ticlopidine and Cardiovascular Diseases studies

Ticlopidine: An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.
ticlopidine : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group.

Cardiovascular Diseases: Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.

Research Excerpts

Excerpt	Relevance	Reference
"Discontinuing aspirin after short-term dual antiplatelet therapy (DAPT) was evaluated as a bleeding reduction strategy."	9.34	Effect of Ticagrelor Monotherapy vs Ticagrelor With Aspirin on Major Bleeding and Cardiovascular Events in Patients With Acute Coronary Syndrome: The TICO Randomized Clinical Trial. ( Ahn, CM; Cho, DK; Cho, JY; Cho, S; Cho, YH; Choi, D; Her, AY; Hong, BK; Hong, MK; Hong, SJ; Jang, Y; Jeon, DW; Kim, BK; Kim, JS; Kim, YH; Ko, YG; Kwon, H; Nam, CM; Shin, DH; Suh, Y; Yoo, SY; Yun, KH, 2020)
"Ticagrelor reduced cardiovascular events compared with clopidogrel in PLATO without increasing overall major bleeding."	9.22	Impact of glycoprotein IIb/IIIa inhibitors on the efficacy and safety of ticagrelor compared with clopidogrel in patients with acute coronary syndromes: Analysis from the Platelet Inhibition and Patient Outcomes (PLATO) Trial. ( Bansilal, S; Becker, RC; Cannon, CP; Harrington, RA; Himmelmann, A; Husted, S; James, SK; Katus, HA; Lopes, RD; Neely, B; Shimada, YJ; Steg, PG; Storey, RF; Wallentin, L; Wiviott, SD, 2016)
"Rectal indomethacin has been proven to be effective for prevention of post-ERCP pancreatitis (PEP) but its impact on bleeding after biliary sphincterotomy (BABES) and cardiovascular mortality has not been extensively studied."	9.19	Does rectal indomethacin given for prevention of post-ERCP pancreatitis increase bleeding after biliary endoscopic sphincterotomy or cardiovascular mortality?: Post hoc analysis using prospective clinical trial data. ( Patai, Á; Patai, ÁV; Solymosi, N, 2014)
"Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed."	9.16	Prasugrel versus clopidogrel for acute coronary syndromes without revascularization. ( Ardissino, D; Armstrong, PW; Aylward, PE; Bhatt, DL; Boden, WE; Brown, EB; Cinteză, M; Clemmensen, P; Corbalan, R; Cornel, JH; Dalby, AJ; Fox, KA; Gasparovic, V; Goodman, SG; Gottlieb, S; Goudev, AR; Gurbel, PA; Hamm, C; Hochman, JS; Huber, K; Leiva-Pons, JL; Lokhnygina, Y; Martinez, F; McGuire, DK; McLendon, RC; Merkely, B; Nicolau, JC; Ohman, EM; Oto, A; Parkhomenko, A; Pavlides, G; Prabhakaran, D; Roe, MT; Ruzyllo, W; Topacio, GO; Tseng, CD; White, HD; Winters, KJ, 2012)
"The significant clinical benefit and overall safety of ticagrelor compared with clopidogrel in acute coronary syndrome patients in the PLATO cohort were not found to depend on age."	9.16	Ticagrelor versus clopidogrel in elderly patients with acute coronary syndromes: a substudy from the prospective randomized PLATelet inhibition and patient Outcomes (PLATO) trial. ( Bach, RG; Becker, RC; Cannon, CP; Heras, M; Horrow, J; Husted, S; James, S; Katus, H; Lopes, RD; Mahaffey, KW; Morais, J; Storey, RF; Wallentin, L; Wojdyla, D, 2012)
"To observe the effects of upstream versus downstream application of tirofiban on platelet aggregation and clinical outcomes (major adverse cardiovascular event, MACE) in patients with high-risk non-ST-segment elevation acute coronary syndromes (NSTE-ACS) undergoing percutaneous coronary intervention (PCI)."	9.14	[Effects of upstream tirofiban versus downstream tirofiban on platelet aggregation and clinical outcomes in patients with high-risk acute coronary syndromes undergoing percutaneous coronary interventions]. ( Cheng, WJ; Guo, YH; Li, YP; Liu, T; Liu, YY; Ma, HY; Shi, DM; Xie, Y; Zhao, YX; Zhou, YJ, 2009)
"In acute coronary syndrome patients with chronic kidney disease, ticagrelor compared with clopidogrel significantly reduces ischemic end points and mortality without a significant increase in major bleeding but with numerically more non-procedure-related bleeding."	9.14	Ticagrelor versus clopidogrel in acute coronary syndromes in relation to renal function: results from the Platelet Inhibition and Patient Outcomes (PLATO) trial. ( Aylward, P; Buck, KK; Budaj, A; Cannon, CP; Cornel, JH; Harrington, RA; Horrow, J; James, S; Katus, H; Keltai, M; Lewis, BS; Parikh, K; Storey, RF; Szummer, K; Wallentin, L; Wojdyla, D, 2010)
" 25,086 individuals with acute coronary syndromes and intended early PCI were randomly assigned to double-dose (600 mg on day 1, 150 mg on days 2-7, then 75 mg daily) versus standard-dose (300 mg on day 1 then 75 mg daily) clopidogrel, and high-dose (300-325 mg daily) versus low-dose (75-100 mg daily) aspirin."	9.14	Double-dose versus standard-dose clopidogrel and high-dose versus low-dose aspirin in individuals undergoing percutaneous coronary intervention for acute coronary syndromes (CURRENT-OASIS 7): a randomised factorial trial. ( Ajani, AE; Avezum, A; Bassand, JP; Budaj, A; Chrolavicius, S; Di Pasquale, G; Eikelboom, JW; Faxon, DP; Fox, KA; Gao, P; Granger, CB; Jolly, SS; Joyner, CD; Macaya, C; Mehta, SR; Montalescot, G; Niemela, K; Rupprecht, HJ; Steg, PG; Tanguay, JF; White, HD; Widimsky, P; Yusuf, S, 2010)
"In patients with an acute coronary syndrome who were referred for an invasive strategy, there was no significant difference between a 7-day, double-dose clopidogrel regimen and the standard-dose regimen, or between higher-dose aspirin and lower-dose aspirin, with respect to the primary outcome of cardiovascular death, myocardial infarction, or stroke."	9.14	Dose comparisons of clopidogrel and aspirin in acute coronary syndromes. ( Afzal, R; Bassand, JP; Chrolavicius, S; Diaz, R; Eikelboom, JW; Fox, KA; Granger, CB; Jolly, S; Joyner, CD; Mehta, SR; Pogue, J; Rupprecht, HJ; Widimsky, P; Yusuf, S, 2010)
"A number of reports have demonstrated that obesity is a risk factor for a reduced clopidogrel pharmacodynamic response."	8.95	Obesity and Inflammation and Altered Clopidogrel Pharmacokinetics and Pharmacodynamics. ( Monte, SV; Norgard, NB, 2017)
"To determine the effectiveness and safety of thienopyridine derivatives (ticlopidine and clopidogrel) versus aspirin for preventing serious vascular events (stroke, myocardial infarction (MI) or vascular death) in patients at high risk, and specifically in patients with a previous TIA or ischaemic stroke."	8.85	Thienopyridine derivatives versus aspirin for preventing stroke and other serious vascular events in high vascular risk patients. ( Hankey, GJ; Mason, G; Maurice, JB; Sudlow, CL; Wedderburn, CJ, 2009)
"The most widely studied and prescribed antiplatelet agent for the prevention of stroke and other serious vascular events among high vascular risk patients is aspirin."	8.80	Thienopyridine derivatives (ticlopidine, clopidogrel) versus aspirin for preventing stroke and other serious vascular events in high vascular risk patients. ( Dunbabin, DW; Hankey, GJ; Sudlow, CL, 2000)
"The reasons for postdischarge adenosine diphosphate receptor inhibitor (ADPri) switching among patients with myocardial infarction (MI) are unclear."	7.85	Switching of adenosine diphosphate receptor inhibitor after hospital discharge among myocardial infarction patients: Insights from the Treatment with Adenosine Diphosphate Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events after ( Anstrom, KJ; Baker, BA; Cohen, DJ; Effron, MB; Henry, TD; McCoy, LA; Messenger, JC; Peterson, ED; Wang, TY; Zettler, ME, 2017)
"Despite the growing use of clopidogrel, limited data exist regarding the prognostic significance of chronic clopidogrel therapy in patients sustaining acute coronary syndrome (ACS)."	7.83	Prior chronic clopidogrel therapy is associated with increased adverse events and early stent thrombosis. ( Asher, E; Atar, S; Beigel, R; Fefer, P; Hammerman, H; Herscovici, R; Matetzky, S; Mazin, I; Polak, A; Regev, E; Sabbag, A; Shlomo, N; Zahger, D, 2016)
"We analysed clinical and pharmacological factors influencing resistance to clopidogrel in 250 patients with cardiovascular diseases during 18 months."	7.81	[CLINICAL AND PHARMACOLOGICAL FACTORS INFLUENCING RESISTANCE TO CLOPIDOGREL IN PATIENTS WITH CARDIOVASCULAR DISEASES]. ( Aksenova, MG; Dobrovol'skiĭ, AV; Kirillov, MIu; Kopylov, FIu; Mesitskaia, DF; Nikitina, IuM; Syrkin, AL, 2015)
"The aim of the present study was to evaluate clopidogrel treatment after incident myocardial infarction (MI) in patients with and without chronic kidney disease (CKD)."	7.80	Benefit of clopidogrel therapy in patients with myocardial infarction and chronic kidney disease-a Danish nation-wide cohort study. ( Blicher, TM; Hommel, K; Kamper, AL; Kristensen, SL; Madsen, M; Olesen, JB; Torp-Pedersen, C, 2014)
"To characterize the clinical presentation of a cohort of patients with coronary artery disease (CAD) and aspirin reactions."	7.79	Characterization of aspirin allergies in patients with coronary artery disease. ( Feng, CH; Stevenson, DD; White, AA, 2013)
"A total of 10,101 patients aged 18 years or older with a diagnosis of acute coronary syndrome (ACS) made during a hospitalization or emergency department visit between 2001 and 2008 and who had their first clopidogrel prescription within 90 days after their ACS diagnosis were included in the study."	7.78	Effect of the clopidogrel-proton pump inhibitor drug interaction on adverse cardiovascular events in patients with acute coronary syndrome. ( Bhurke, SM; Bursac, Z; Franks, AM; Li, C; Martin, BC; Said, Q, 2012)
"To estimate the clinical effectiveness associated with clopidogrel treatment after myocardial infarction (MI) in patients with diabetes."	7.78	Association of clopidogrel treatment with risk of mortality and cardiovascular events following myocardial infarction in patients with and without diabetes. ( Andersson, C; Gislason, GH; Køber, L; Lyngbæk, S; Nguyen, CD; Nielsen, M; Torp-Pedersen, C, 2012)
"In the PLATO trial of ticagrelor versus clopidogrel for treatment of acute coronary syndromes, ticagrelor reduced the composite outcome of cardiovascular death, myocardial infarction, and stroke, but increased events of major bleeding related to non-coronary artery bypass graft (CABG)."	7.76	Effect of CYP2C19 and ABCB1 single nucleotide polymorphisms on outcomes of treatment with ticagrelor versus clopidogrel for acute coronary syndromes: a genetic substudy of the PLATO trial. ( Armstrong, M; Barratt, BJ; Becker, RC; Horrow, J; Husted, S; James, S; Katus, H; Shah, SH; Steg, PG; Storey, RF; Wallentin, L, 2010)
"To assess the prognosis of patients presenting with an acute coronary syndrome (ACS) despite chronic clopidogrel therapy (CCT)."	7.75	Prognosis of patients suffering an acute coronary syndrome while already under chronic clopidogrel therapy. ( Bonello, L; De Labriolle, A; Kent, KM; Lemesle, G; Pichard, AD; Roy, P; Satler, LF; Steinberg, DH; Suddath, WO; Torguson, R; Waksman, R, 2009)
" The calculated concentrations were used to determine the pharmacokinetic parameters of the analytes."	6.79	Clinical pharmacokinetics of clopidogrel and its metabolites in patients with cardiovascular diseases. ( Burchardt, P; Danielak, D; Główka, F; Karaźniewicz-Łada, M; Komosa, A; Kruszyna, L; Lesiak, M, 2014)
" Whether this is worth both the risk of non-compliance with twice-a-day dosing in real-life patients lacking the same motivation as their trial-volunteer counterparts, and the 2000-fold difference in incremental cost, is the remaining matter for debate."	6.48	Quantitative comparison of clopidogrel 600 mg, prasugrel and ticagrelor, against clopidogrel 300 mg on major adverse cardiovascular events and bleeding in coronary stenting: synthesis of CURRENT-OASIS-7, TRITON-TIMI-38 and PLATO. ( Davies, JE; Francis, DP; Nijjer, SS, 2012)
"Aspirin has been convincingly shown to reduce stroke and death in men with transient ischemic attacks (it may possibly be beneficial to women also), myocardial infarction and death in patients with unstable angina, thromboembolic complications associated with artificial heart valves in patients receiving oral anticoagulants (although gastrointestinal bleeding is prohibitive with this combination), and thrombotic occlusion of silicone rubber arteriovenous cannulae in uremic patients undergoing hemodialysis."	6.15	Clinical trials evaluating platelet-modifying drugs in patients with atherosclerotic cardiovascular disease and thrombosis. ( Harker, LA, 1986)
"HPR-aspirin was persistent 75days later in 36% patients."	5.43	High platelet reactivity on aspirin in patients with acute ST elevation myocardial infarction. ( Dillinger, JG; Drouet, L; Henry, P; Saeed, A; Sideris, G; Silberman, SM; Sollier, CB; Spagnoli, V; Voicu, S, 2016)
"Discontinuing aspirin after short-term dual antiplatelet therapy (DAPT) was evaluated as a bleeding reduction strategy."	5.34	Effect of Ticagrelor Monotherapy vs Ticagrelor With Aspirin on Major Bleeding and Cardiovascular Events in Patients With Acute Coronary Syndrome: The TICO Randomized Clinical Trial. ( Ahn, CM; Cho, DK; Cho, JY; Cho, S; Cho, YH; Choi, D; Her, AY; Hong, BK; Hong, MK; Hong, SJ; Jang, Y; Jeon, DW; Kim, BK; Kim, JS; Kim, YH; Ko, YG; Kwon, H; Nam, CM; Shin, DH; Suh, Y; Yoo, SY; Yun, KH, 2020)
"Ticlopidine is an antiplatelet agent that has been proven efficacious in preventing vascular events in patients with a history of vasculopathy."	5.30	Ticlopidine-associated pancytopenia: implications of an acetylsalicylic acid alternative. ( Armstrong, PW; Brown, NE; Gill, S; Majumdar, S, 1997)
"Ticagrelor reduced cardiovascular events compared with clopidogrel in PLATO without increasing overall major bleeding."	5.22	Impact of glycoprotein IIb/IIIa inhibitors on the efficacy and safety of ticagrelor compared with clopidogrel in patients with acute coronary syndromes: Analysis from the Platelet Inhibition and Patient Outcomes (PLATO) Trial. ( Bansilal, S; Becker, RC; Cannon, CP; Harrington, RA; Himmelmann, A; Husted, S; James, SK; Katus, HA; Lopes, RD; Neely, B; Shimada, YJ; Steg, PG; Storey, RF; Wallentin, L; Wiviott, SD, 2016)
"Rectal indomethacin has been proven to be effective for prevention of post-ERCP pancreatitis (PEP) but its impact on bleeding after biliary sphincterotomy (BABES) and cardiovascular mortality has not been extensively studied."	5.19	Does rectal indomethacin given for prevention of post-ERCP pancreatitis increase bleeding after biliary endoscopic sphincterotomy or cardiovascular mortality?: Post hoc analysis using prospective clinical trial data. ( Patai, Á; Patai, ÁV; Solymosi, N, 2014)
" Across the baseline ST-segment depression strata, there was a consistent treatment benefit with ticagrelor versus clopidogrel on vascular death/myocardial infarction."	5.17	Quantitative ST-depression in acute coronary syndromes: the PLATO electrocardiographic substudy. ( Armstrong, PW; Fu, Y; Harrington, RA; James, S; Katus, H; Storey, RF; Wallentin, L; Westerhout, CM, 2013)
"Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed."	5.16	Prasugrel versus clopidogrel for acute coronary syndromes without revascularization. ( Ardissino, D; Armstrong, PW; Aylward, PE; Bhatt, DL; Boden, WE; Brown, EB; Cinteză, M; Clemmensen, P; Corbalan, R; Cornel, JH; Dalby, AJ; Fox, KA; Gasparovic, V; Goodman, SG; Gottlieb, S; Goudev, AR; Gurbel, PA; Hamm, C; Hochman, JS; Huber, K; Leiva-Pons, JL; Lokhnygina, Y; Martinez, F; McGuire, DK; McLendon, RC; Merkely, B; Nicolau, JC; Ohman, EM; Oto, A; Parkhomenko, A; Pavlides, G; Prabhakaran, D; Roe, MT; Ruzyllo, W; Topacio, GO; Tseng, CD; White, HD; Winters, KJ, 2012)
"The significant clinical benefit and overall safety of ticagrelor compared with clopidogrel in acute coronary syndrome patients in the PLATO cohort were not found to depend on age."	5.16	Ticagrelor versus clopidogrel in elderly patients with acute coronary syndromes: a substudy from the prospective randomized PLATelet inhibition and patient Outcomes (PLATO) trial. ( Bach, RG; Becker, RC; Cannon, CP; Heras, M; Horrow, J; Husted, S; James, S; Katus, H; Lopes, RD; Mahaffey, KW; Morais, J; Storey, RF; Wallentin, L; Wojdyla, D, 2012)
"Among patients with high on-treatment reactivity after PCI with drug-eluting stents, the use of high-dose clopidogrel compared with standard-dose clopidogrel did not reduce the incidence of death from cardiovascular causes, nonfatal myocardial infarction, or stent thrombosis."	5.15	Standard- vs high-dose clopidogrel based on platelet function testing after percutaneous coronary intervention: the GRAVITAS randomized trial. ( Angiolillo, DJ; Aragon, JR; Berger, PB; Bertrand, OF; Cannon, CP; Garratt, KN; Kandzari, DE; Lee, MS; Manoukian, SV; Price, MJ; Puri, S; Robbins, M; Schork, NJ; Spriggs, D; Stillablower, ME; Stillabower, ME; Stinis, CT; Tanguay, JF; Teirstein, PS; Topol, EJ, 2011)
"Two randomized, controlled trials conducted between October 2006 and April 2007: a symptom drug box trial using direct-to-consumer ads for a histamine-2 blocker and a proton-pump inhibitor to treat heartburn, and a prevention drug box trial using direct-to-consumer ads for a statin and clopidogrel to prevent cardiovascular events."	5.14	Using a drug facts box to communicate drug benefits and harms: two randomized trials. ( Schwartz, LM; Welch, HG; Woloshin, S, 2009)
"To observe the effects of upstream versus downstream application of tirofiban on platelet aggregation and clinical outcomes (major adverse cardiovascular event, MACE) in patients with high-risk non-ST-segment elevation acute coronary syndromes (NSTE-ACS) undergoing percutaneous coronary intervention (PCI)."	5.14	[Effects of upstream tirofiban versus downstream tirofiban on platelet aggregation and clinical outcomes in patients with high-risk acute coronary syndromes undergoing percutaneous coronary interventions]. ( Cheng, WJ; Guo, YH; Li, YP; Liu, T; Liu, YY; Ma, HY; Shi, DM; Xie, Y; Zhao, YX; Zhou, YJ, 2009)
"Clopidogrel therapy may be more effective in current smokers, but it may also confer a greater bleeding risk than in nonsmokers."	5.14	Smoking, clopidogrel, and mortality in patients with established cardiovascular disease. ( Berger, JS; Berger, PB; Bhatt, DL; Fox, KA; Hacke, W; Lincoff, AM; Montalescot, G; Shao, M; Steg, PG; Steinhubl, SR; Topol, EJ, 2009)
"In acute coronary syndrome patients with chronic kidney disease, ticagrelor compared with clopidogrel significantly reduces ischemic end points and mortality without a significant increase in major bleeding but with numerically more non-procedure-related bleeding."	5.14	Ticagrelor versus clopidogrel in acute coronary syndromes in relation to renal function: results from the Platelet Inhibition and Patient Outcomes (PLATO) trial. ( Aylward, P; Buck, KK; Budaj, A; Cannon, CP; Cornel, JH; Harrington, RA; Horrow, J; James, S; Katus, H; Keltai, M; Lewis, BS; Parikh, K; Storey, RF; Szummer, K; Wallentin, L; Wojdyla, D, 2010)
" 25,086 individuals with acute coronary syndromes and intended early PCI were randomly assigned to double-dose (600 mg on day 1, 150 mg on days 2-7, then 75 mg daily) versus standard-dose (300 mg on day 1 then 75 mg daily) clopidogrel, and high-dose (300-325 mg daily) versus low-dose (75-100 mg daily) aspirin."	5.14	Double-dose versus standard-dose clopidogrel and high-dose versus low-dose aspirin in individuals undergoing percutaneous coronary intervention for acute coronary syndromes (CURRENT-OASIS 7): a randomised factorial trial. ( Ajani, AE; Avezum, A; Bassand, JP; Budaj, A; Chrolavicius, S; Di Pasquale, G; Eikelboom, JW; Faxon, DP; Fox, KA; Gao, P; Granger, CB; Jolly, SS; Joyner, CD; Macaya, C; Mehta, SR; Montalescot, G; Niemela, K; Rupprecht, HJ; Steg, PG; Tanguay, JF; White, HD; Widimsky, P; Yusuf, S, 2010)
"In patients with an acute coronary syndrome who were referred for an invasive strategy, there was no significant difference between a 7-day, double-dose clopidogrel regimen and the standard-dose regimen, or between higher-dose aspirin and lower-dose aspirin, with respect to the primary outcome of cardiovascular death, myocardial infarction, or stroke."	5.14	Dose comparisons of clopidogrel and aspirin in acute coronary syndromes. ( Afzal, R; Bassand, JP; Chrolavicius, S; Diaz, R; Eikelboom, JW; Fox, KA; Granger, CB; Jolly, S; Joyner, CD; Mehta, SR; Pogue, J; Rupprecht, HJ; Widimsky, P; Yusuf, S, 2010)
"The present study suggested benefit of tailored antiplatelet therapy during elective PCI with GP IIb/IIIa antagonist for clopidogrel nonresponders without increased bleeding risk."	5.13	Glycoprotein IIb/IIIa inhibitors improve outcome after coronary stenting in clopidogrel nonresponders: a prospective, randomized study. ( Alessi, MC; Bali, L; Bonnet, JL; Cuisset, T; Frere, C; Lambert, M; Morange, PE; Moro, PJ; Mouret, JP; Quilici, J, 2008)
" Overall, clopidogrel plus aspirin was not significantly more effective than aspirin alone in reducing the rate of myocardial infarction, stroke, or death from cardiovascular causes."	5.12	Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. ( Berger, PB; Bhatt, DL; Black, HR; Boden, WE; Booth, J; Brennan, DM; Cacoub, P; Cohen, EA; Creager, MA; Easton, JD; Fabry-Ribaudo, L; Flather, MD; Fox, KA; Hacke, W; Haffner, SM; Hamm, CW; Hankey, GJ; Johnston, SC; Mak, KH; Mas, JL; Montalescot, G; Pearson, TA; Steg, PG; Steinhubl, SR; Topol, EJ; Weber, MA, 2006)
"The Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance (CHARISMA) study was designed to evaluate the efficacy and safety of clopidogrel plus aspirin versus placebo plus aspirin in patients with established coronary, cerebral, or peripheral arterial disease or in patients with multiple risk factors for atherothrombosis who have not yet sustained an ischemic event."	5.11	Clopidogrel added to aspirin versus aspirin alone in secondary prevention and high-risk primary prevention: rationale and design of the Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance (CHARISMA) trial. ( Bhatt, DL; Topol, EJ, 2004)
"In this phase 2 study, which was designed to assess safety when administered at the time of percutaneous coronary intervention, prasugrel and clopidogrel both resulted in low rates of bleeding."	5.11	Randomized comparison of prasugrel (CS-747, LY640315), a novel thienopyridine P2Y12 antagonist, with clopidogrel in percutaneous coronary intervention: results of the Joint Utilization of Medications to Block Platelets Optimally (JUMBO)-TIMI 26 trial. ( Antman, EM; Behounek, BD; Braunwald, E; Carney, RJ; Lazzam, C; McCabe, CH; McKay, RG; Murphy, SA; Weerakkody, G; Winters, KJ; Wiviott, SD, 2005)
"This study meta-analysed randomized, double-blind, placebo controlled trials in patients with intermittent claudication of the lower limbs comparing ticlopidine to placebo in order to test the hypothesis that the drug, a pure antiplatelet agent, is able to reduce the incidence of thrombotic cardio-vascular events on atherosclerotic arteries in these patients."	5.06	Is it possible to reduce the risk of cardiovascular events in subjects suffering from intermittent claudication of the lower limbs? ( Boissel, JP; Destors, JM; Peyrieux, JC, 1989)
" With respect to intracranial hemorrhage, aspirin + clopidogrel yielded worse outcomes than 7 treatments, including placebo, apixaban, aspirin, aspirin + dipyridamole, cilostazol, clopidogrel, and dabigatran (OR, 2."	4.95	The Efficacy and Safety of 3 Types of Interventions for Stroke Prevention in Patients With Cardiovascular and Cerebrovascular Diseases: A Network Meta-analysis. ( Chang, S; Chang, Y; Lu, S; Sun, Q; Zhang, Y, 2017)
"The available evidence demonstrates that the use of clopidogrel plus aspirin in people at high risk of cardiovascular disease and people with established cardiovascular disease without a coronary stent is associated with a reduction in the risk of myocardial infarction and ischaemic stroke, and an increased risk of major and minor bleeding compared with aspirin alone."	4.95	Clopidogrel plus aspirin versus aspirin alone for preventing cardiovascular events. ( Bellesini, M; Donadini, MP; Middeldorp, S; Squizzato, A; Takeda, A, 2017)
"A number of reports have demonstrated that obesity is a risk factor for a reduced clopidogrel pharmacodynamic response."	4.95	Obesity and Inflammation and Altered Clopidogrel Pharmacokinetics and Pharmacodynamics. ( Monte, SV; Norgard, NB, 2017)
" We sought to determine the effect of switching from clopidogrel to a novel P2Y12 receptor inhibitor on the occurrence of major adverse cardiovascular events (MACE) and bleeding."	4.93	The impact of switching P2Y12 receptor inhibitor therapy during index hospitalization: a systematic review. ( Chandrasekhar, J; Froeschl, M; Hibbert, B; May, ML; Mehran, R; So, D, 2016)
"Although the addition of aspirin to clopidogrel resulted in small relative reductions in major cardiovascular events, myocardial infarction, and stroke, it also resulted in a relative increase in major bleeding events."	4.88	Effects of combined aspirin and clopidogrel therapy on cardiovascular outcomes: a systematic review and meta-analysis. ( He, J; Lu, J; Qin, YY; Wei, X; Wu, MJ; Xu, JF; Ye, XF; Zhou, YH, 2012)
"In those who have already survived myocardial infarction (MI) or stroke, or have had a transient ischaemic episode (TIA), daily low dose aspirin (ASA) reduces the risk of recurrences by an amount that greatly exceeds the risk of serious bleeding (secondary prevention)."	4.88	Primary prevention of ischaemic cardiovascular disorders with antiplatelet agents. ( Meade, T, 2012)
"Studies that reported clopidogrel metabolism, platelet reactivity or clinically relevant outcomes (cardiovascular disease [CVD] events and bleeding), and information on CYP2C19 genotype were included."	4.87	CYP2C19 genotype, clopidogrel metabolism, platelet function, and cardiovascular events: a systematic review and meta-analysis. ( Casas, JP; Hingorani, AD; Holmes, MV; Perel, P; Shah, T, 2011)
" Aspirin and, more recently, clopidogrel are among the most important treatments of cardiovascular diseases."	4.86	[Long-term use of oral antiplatelet therapy: from studies to practice]. ( Helft, G, 2010)
"To summarize the pharmacokinetic and pharmacodynamic properties of ticagrelor, a selective P2Y12 receptor antagonist, and evaluate its role in the treatment of patients with acute coronary syndromes (ACS)."	4.86	Efficacy and safety of ticagrelor: a reversible P2Y12 receptor antagonist. ( Anderson, SD; Epstein, BJ; Shah, NK; Yim, J, 2010)
"We performed this meta-analysis to update the clinical evidences on the relation between clopidogrel non-responsiveness and clinical outcomes in patients with coronary artery disease (CAD) who underwent percutaneous coronary intervention."	4.86	Clopidogrel non-responsiveness and risk of cardiovascular morbidity. An updated meta-analysis. ( Abbate, R; Gensini, GF; Giusti, B; Gori, AM; Marcucci, R; Sofi, F, 2010)
"Among patients treated with clopidogrel for percutaneous coronary intervention, carriage of even 1 reduced-function CYP2C19 allele appears to be associated with a significantly increased risk of major adverse cardiovascular events, particularly stent thrombosis."	4.86	Reduced-function CYP2C19 genotype and risk of adverse clinical outcomes among patients treated with clopidogrel predominantly for PCI: a meta-analysis. ( Anderson, JL; Antman, EM; Bliden, K; Cannon, CP; Collet, JP; Danchin, N; Giusti, B; Gurbel, P; Horne, BD; Hulot, JS; Kastrati, A; Mega, JL; Montalescot, G; Neumann, FJ; Sabatine, MS; Shen, L; Sibbing, D; Simon, T; Steg, PG; Trenk, D; Wiviott, SD, 2010)
" Monotherapy with either aspirin or clopidogrel, reduces the rate of stroke, myocardial infarction, and cardiovascular death in patients suffering from peripheral arterial disease."	4.85	Antiplatelet therapy after endovascular intervention: does combination therapy really work and what is the optimum duration of therapy? ( Milani, RV, 2009)
"Oral antiplatelet therapy with clopidogrel and aspirin is an important and widely prescribed strategy to prevent ischemic events in patients with cardiovascular diseases."	4.85	Recent developments in clopidogrel pharmacology and their relation to clinical outcomes. ( Antonino, MJ; Gurbel, PA; Tantry, US, 2009)
"The present review focuses on the roles of thromboxane A2 (TxA2) in arterial thrombosis, atherogenesis, vascular stent-related ischemic events and renal proteinuria."	4.85	Effect of pharmaceutical interventions targeting thromboxane receptors and thromboxane synthase in cardiovascular and renal diseases. ( Alberts, P; Bounameaux, H; Fontana, P; Mann, J; Sakariassen, KS; Sorensen, AS, 2009)
"To determine the effectiveness and safety of thienopyridine derivatives (ticlopidine and clopidogrel) versus aspirin for preventing serious vascular events (stroke, myocardial infarction (MI) or vascular death) in patients at high risk, and specifically in patients with a previous TIA or ischaemic stroke."	4.85	Thienopyridine derivatives versus aspirin for preventing stroke and other serious vascular events in high vascular risk patients. ( Hankey, GJ; Mason, G; Maurice, JB; Sudlow, CL; Wedderburn, CJ, 2009)
"Aspirin should be used to treat patients with acute myocardial infarction (MI) and continued indefinitely to reduce vascular death, nonfatal MI, and nonfatal stroke."	4.84	Antiplatelet therapy in the treatment of atherothrombotic disease: considering the evidence. ( Aronow, WS, 2007)
"To quantify the impact of clopidogrel plus aspirin on the individual outcomes of death, myocardial infarction, or stroke in patients with established cardiovascular disease, or in patients with multiple risk factors for vascular disease."	4.84	Incremental effect of clopidogrel on important outcomes in patients with cardiovascular disease: a meta-analysis of randomized trials. ( Bavry, AA; Bhatt, DL; Duggal, S; Helton, TJ; Kumbhani, DJ; Roukoz, H, 2007)
"Clopidogrel has demonstrated improved outcomes for patients with acute coronary syndromes in several large randomized controlled trials."	4.84	Clopidogrel: who, when, and how? ( Cannon, CP, 2007)
"The most widely studied and prescribed antiplatelet agent for the prevention of stroke and other serious vascular events among high vascular risk patients is aspirin."	4.80	Thienopyridine derivatives (ticlopidine, clopidogrel) versus aspirin for preventing stroke and other serious vascular events in high vascular risk patients. ( Dunbabin, DW; Hankey, GJ; Sudlow, CL, 2000)
"Clopidogrel plus aspirin is associated with a reduced risk for myocardial infarction and ischemic stroke and an increased risk for major bleeding compared with aspirin alone among patients at high risk for or with an established cardiovascular disease but without a coronary stent."	3.88	Aspirin Plus Clopidogrel vs Aspirin Alone for Preventing Cardiovascular Events Among Patients at High Risk for Cardiovascular Events. ( Bellesini, M; Donadini, MP; Squizzato, A, 2018)
"Data on the clinical impact of gender in "real-life" patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI), receiving clopidogrel, prasugrel, or ticagrelor are limited."	3.85	Gender-related differences in antiplatelet treatment patterns and outcome: Insights from the GReekAntiPlatElet Registry. ( Alexopoulos, D; Davlouros, P; Deftereos, S; Goudevenos, J; Hamilos, M; Kanakakis, I; Lekakis, J; Sitafidis, G; Vavouranakis, M; Xanthopoulou, I, 2017)
"The reasons for postdischarge adenosine diphosphate receptor inhibitor (ADPri) switching among patients with myocardial infarction (MI) are unclear."	3.85	Switching of adenosine diphosphate receptor inhibitor after hospital discharge among myocardial infarction patients: Insights from the Treatment with Adenosine Diphosphate Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events after ( Anstrom, KJ; Baker, BA; Cohen, DJ; Effron, MB; Henry, TD; McCoy, LA; Messenger, JC; Peterson, ED; Wang, TY; Zettler, ME, 2017)
"Despite the growing use of clopidogrel, limited data exist regarding the prognostic significance of chronic clopidogrel therapy in patients sustaining acute coronary syndrome (ACS)."	3.83	Prior chronic clopidogrel therapy is associated with increased adverse events and early stent thrombosis. ( Asher, E; Atar, S; Beigel, R; Fefer, P; Hammerman, H; Herscovici, R; Matetzky, S; Mazin, I; Polak, A; Regev, E; Sabbag, A; Shlomo, N; Zahger, D, 2016)
"Proton pump inhibitors (PPIs) reduce gastrointestinal bleeding events but may alter clopidogrel metabolism."	3.83	Impact of Proton Pump Inhibitor Use on the Comparative Effectiveness and Safety of Prasugrel Versus Clopidogrel: Insights From the Treatment With Adenosine Diphosphate Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events After Acu ( Baker, BA; Cohen, DJ; Effron, MB; Faries, DE; Jackson, LR; Ju, C; McCoy, LA; Messenger, JC; Peterson, ED; Wang, TY; Zettler, M, 2016)
"This study was conducted to determine whether there is additive benefit of dual-antiplatelet therapy (DAPT) with aspirin (acetylsalicylic acid [ASA]) and clopidogrel compared with ASA monotherapy among patients with symptomatic peripheral arterial disease."	3.81	Association of dual-antiplatelet therapy with reduced major adverse cardiovascular events in patients with symptomatic peripheral arterial disease. ( Amsterdam, EA; Anderson, DR; Armstrong, EJ; Bang, H; Freischlag, JA; Laird, JR; Singh, GD; Yeo, KK, 2015)
"CYP2C19 genotype and the residual platelet reactivity (RPR) were measured in 361 coronary heart disease patients (male, mean age 69yrs), and the risk of cardiovascular events over a 3-month follow-up was assessed to evaluate the impact of co-administration of esomeprazole during dual antiplatelet therapy with aspirin and clopidogrel."	3.81	Impact of esomeprazole on platelet reactivity and clinical outcome according to CYP2C19 genotype in coronary heart disease patients during dual antiplatelet therapy. ( Akasaka, T; Arima, Y; Hokimoto, S; Kaikita, K; Kumagae, N; Morita, K; Nakagawa, K; Ogawa, H; Oniki, K; Sakamoto, K; Tabata, N; Tsujita, K; Yamamoto, E, 2015)
"We analysed clinical and pharmacological factors influencing resistance to clopidogrel in 250 patients with cardiovascular diseases during 18 months."	3.81	[CLINICAL AND PHARMACOLOGICAL FACTORS INFLUENCING RESISTANCE TO CLOPIDOGREL IN PATIENTS WITH CARDIOVASCULAR DISEASES]. ( Aksenova, MG; Dobrovol'skiĭ, AV; Kirillov, MIu; Kopylov, FIu; Mesitskaia, DF; Nikitina, IuM; Syrkin, AL, 2015)
"Patients on prasugrel had fewer cardiovascular events as compared to patients on clopidogrel twice daily with no difference in bleeding events."	3.81	Comparing prasugrel to twice daily clopidogrel post percutaneous coronary intervention in a Veterans Affairs population. ( Khatri, S; Pierce, T, 2015)
"The aim of the present study was to evaluate clopidogrel treatment after incident myocardial infarction (MI) in patients with and without chronic kidney disease (CKD)."	3.80	Benefit of clopidogrel therapy in patients with myocardial infarction and chronic kidney disease-a Danish nation-wide cohort study. ( Blicher, TM; Hommel, K; Kamper, AL; Kristensen, SL; Madsen, M; Olesen, JB; Torp-Pedersen, C, 2014)
"Clopidogrel is safer than ticagrelor in regard to bleeding."	3.79	Clopidogrel is safer than ticagrelor in regard to bleeds: a closer look at the PLATO trial. ( Biondi-Zoccai, G; Chatterjee, S; D'Ascenzo, F; DiNicolantonio, JJ; Niazi, AK; Tomek, A, 2013)
"To characterize the clinical presentation of a cohort of patients with coronary artery disease (CAD) and aspirin reactions."	3.79	Characterization of aspirin allergies in patients with coronary artery disease. ( Feng, CH; Stevenson, DD; White, AA, 2013)
" Phenotyping of platelet response to clopidogrel was a better predictor of stent thrombosis than genotyping."	3.78	Phenotyping vs. genotyping for prediction of clopidogrel efficacy and safety: the PEGASUS-PCI study. ( Delle-Karth, G; Grzybowski, T; Huber, K; Jilma, B; Kozinski, M; Kubica, J; Lang, IM; Linkowska, K; Maurer, G; Neunteufl, T; Siller-Matula, JM, 2012)
" In the management of aspirin-related uncomplicated peptic ulcers in patients requiring antiplatelet therapies, continuing aspirin plus a powerful proton pump inhibitor is the choice of treatment."	3.78	New look at antiplatelet agent-related peptic ulcer: an update of prevention and treatment. ( Hsu, PI, 2012)
"Simulated cohort of patients with acute coronary syndrome scheduled to undergo percutaneous coronary intervention (PCI), consisting of three arms: those receiving genotype-guided antiplatelet therapy with clopidogrel or prasugrel, those receiving clopidogrel regardless of genotype, and those receiving prasugrel regardless of genotype."	3.78	Cost-effectiveness of cytochrome P450 2C19 genotype screening for selection of antiplatelet therapy with clopidogrel or prasugrel. ( Beitelshees, AL; Daniel Mullins, C; Onukwugha, E; Reese, ES, 2012)
"A total of 10,101 patients aged 18 years or older with a diagnosis of acute coronary syndrome (ACS) made during a hospitalization or emergency department visit between 2001 and 2008 and who had their first clopidogrel prescription within 90 days after their ACS diagnosis were included in the study."	3.78	Effect of the clopidogrel-proton pump inhibitor drug interaction on adverse cardiovascular events in patients with acute coronary syndrome. ( Bhurke, SM; Bursac, Z; Franks, AM; Li, C; Martin, BC; Said, Q, 2012)
"To estimate the clinical effectiveness associated with clopidogrel treatment after myocardial infarction (MI) in patients with diabetes."	3.78	Association of clopidogrel treatment with risk of mortality and cardiovascular events following myocardial infarction in patients with and without diabetes. ( Andersson, C; Gislason, GH; Køber, L; Lyngbæk, S; Nguyen, CD; Nielsen, M; Torp-Pedersen, C, 2012)
"One possible cause of stent thrombosis is an insufficient effect of clopidogrel."	3.77	Optimizing of thienopyridine therapy by multiple electrode platelet aggregometry in clopidogrel low responders undergoing PCI. ( Behr, T; Behr, W; Kuch, B; von Scheidt, W, 2011)
"We conducted a retrospective cohort study to assess CV outcomes of 9753 patients taking dual antiplatelet therapy of aspirin plus clopidogrel with or without a PPI after hospitalization for acute coronary syndrome (ACS)."	3.77	Relationship between cardiovascular outcomes and proton pump inhibitor use in patients receiving dual antiplatelet therapy after acute coronary syndrome. ( Chen, PF; Hsiao, FY; Huang, WF; Mullins, CD; Tsai, YW; Wen, YW, 2011)
" Carriers of this polymorphism have a higher incidence of stent thrombosis and cardiovascular death, whilst on the thienopyridine clopidogrel."	3.76	Prasugrel, Māori, and personalised medicine in New Zealand. ( Gladding, P; Webster, M; White, H, 2010)
"We genotyped ABCB1 in 2932 patients with acute coronary syndromes undergoing percutaneous intervention who were treated with clopidogrel (n=1471) or prasugrel (n=1461) in the TRITON-TIMI 38 trial."	3.76	Genetic variants in ABCB1 and CYP2C19 and cardiovascular outcomes after treatment with clopidogrel and prasugrel in the TRITON-TIMI 38 trial: a pharmacogenetic analysis. ( Antman, EM; Braunwald, E; Close, SL; Mega, JL; Sabatine, MS; Shen, L; Simon, T; Walker, JR; Wiviott, SD, 2010)
"In the PLATO trial of ticagrelor versus clopidogrel for treatment of acute coronary syndromes, ticagrelor reduced the composite outcome of cardiovascular death, myocardial infarction, and stroke, but increased events of major bleeding related to non-coronary artery bypass graft (CABG)."	3.76	Effect of CYP2C19 and ABCB1 single nucleotide polymorphisms on outcomes of treatment with ticagrelor versus clopidogrel for acute coronary syndromes: a genetic substudy of the PLATO trial. ( Armstrong, M; Barratt, BJ; Becker, RC; Horrow, J; Husted, S; James, S; Katus, H; Shah, SH; Steg, PG; Storey, RF; Wallentin, L, 2010)
"To examine the risk for adverse cardiovascular outcomes related to concomitant use of PPIs and clopidogrel compared with that of PPIs alone in adults hospitalized for myocardial infarction."	3.76	Proton-pump inhibitors are associated with increased cardiovascular risk independent of clopidogrel use: a nationwide cohort study. ( Abildstrøm, SZ; Ahlehoff, O; Charlot, M; Gislason, G; Hansen, PR; Jørgensen, CH; Køber, L; Madsen, JK; Norgaard, ML; Sørensen, R; Torp-Pedersen, C, 2010)
"The aim of the study was to evaluate the effect of the concomitant treatment with proton-pump inhibitors (PPIs) and clopidogrel on the incidence of stent thrombosis, acute coronary syndrome (ACS) and death in patients who underwent percutaneous coronary intervention (PCI) and stent implantation."	3.76	Impact of concomitant treatment with proton pump inhibitors and clopidogrel on clinical outcome in patients after coronary stent implantation. ( Brozovic, I; Farhan, S; Geppert, A; Huber, K; Jarai, R; Siller-Matula, J; Smetana, P; Tentzeris, I; Wojta, J, 2010)
"Among persons treated with clopidogrel, carriers of a reduced-function CYP2C19 allele had significantly lower levels of the active metabolite of clopidogrel, diminished platelet inhibition, and a higher rate of major adverse cardiovascular events, including stent thrombosis, than did noncarriers."	3.75	Cytochrome p-450 polymorphisms and response to clopidogrel. ( Antman, EM; Brandt, JT; Braunwald, E; Close, SL; Hockett, RD; Macias, W; Mega, JL; Sabatine, MS; Shen, L; Walker, JR; Wiviott, SD, 2009)
"To assess the prognosis of patients presenting with an acute coronary syndrome (ACS) despite chronic clopidogrel therapy (CCT)."	3.75	Prognosis of patients suffering an acute coronary syndrome while already under chronic clopidogrel therapy. ( Bonello, L; De Labriolle, A; Kent, KM; Lemesle, G; Pichard, AD; Roy, P; Satler, LF; Steinberg, DH; Suddath, WO; Torguson, R; Waksman, R, 2009)
"This study was conducted to compare the risk of recurrent hospitalization for major gastrointestinal (GI) complications (peptic ulcer, bleeding, and perforation) in patients at high GI risk who require ongoing antiplatelet therapy (aspirin [acetylsalicylic acid] or clopidogrel) with or without proton pump inhibitors (PPIs)."	3.75	A comparison of aspirin and clopidogrel with or without proton pump inhibitors for the secondary prevention of cardiovascular events in patients at high risk for gastrointestinal bleeding. ( Chang, PY; Chen, PF; Hsiao, FY; Huang, WF; Kuo, KN; Tsai, YW; Wen, YW, 2009)
"(1) For patients with acute coronary syndromes who have undergone percutaneous angioplasty and stenting, the best-assessed treatment for preventing relapses is a combination of aspirin and clopidogrel; (2) Prasugrel, an antiplatelet drug belonging the same chemical class as clopidogrel, is authorized in the EU for use in this indication; (3) Clinical evaluation is based on a randomized double-blind trial comparing prasugrel + aspirin versus clopidogrel + aspirin in 13 608 patients with acute coronary syndromes, half of whom were treated for at least 15 months."	3.75	Prasugrel: new drug. After angioplasty and stenting: continue to use aspirin + clopidogrel. ( , 2009)
"The current standard of care for anti-thrombotic therapy with primary PCI for acute ST elevation myocardial infarction (STEMI) is aspirin, clopidogrel, unfractionated heparin and platelet glycoprotein IIb/IIIa inhibitors."	3.74	What anti-thrombotic therapy is best with primary PCI for acute ST elevation myocardial infarction: how should the HORIZONS trial change current practice? ( Brodie, BR, 2008)
"A literature search was conducted using EMBASE (1980-January 2008), PubMed (1966-January 2008), Google, and a manual search of the reference lists using the search terms gastrointestinal bleed, gastrointestinal hemorrhage, peptic ulcer hemorrhage, ASA, aspirin, Plavix, clopidogrel, and PPI."	3.74	Single antiplatelet therapy for patients with previous gastrointestinal bleeds. ( Ackman, ML; Gellatly, RM, 2008)
" The cost-effectiveness of longer combination therapy depends critically on the balance of thrombotic event rates, durable efficacy, and the increased bleeding rate in patients taking clopidogrel."	3.73	A cost-effectiveness analysis of combination antiplatelet therapy for high-risk acute coronary syndromes: clopidogrel plus aspirin versus aspirin alone. ( Heidenreich, PA; Schleinitz, MD, 2005)
"(1) Aspirin reduces acute-phase mortality after myocardial infarction, and also reduces the risk of myocardial infarction and death in patients with unstable angina."	3.70	Antiplatelet drugs in cardiovascular prevention: coronary events: acute phase and secondary prevention. ( , 2000)
"Peripheral artery disease is considered to be a manifestation of systemic atherosclerosis with associated adverse cardiovascular and limb events."	2.84	Ticagrelor versus Clopidogrel in Symptomatic Peripheral Artery Disease. ( Baumgartner, I; Berger, JS; Blomster, J; Fowkes, FG; Heizer, G; Held, P; Hiatt, WR; Jones, WS; Katona, BG; Mahaffey, KW; Millegård, M; Norgren, L; Patel, MR; Reist, C, 2017)
"Most retinal or subretinal hemorrhages in eyes enrolled in CATT were less than 1 DA."	2.82	Association between Antiplatelet or Anticoagulant Drugs and Retinal or Subretinal Hemorrhage in the Comparison of Age-Related Macular Degeneration Treatments Trials. ( Ahmed, O; Daniel, E; Grunwald, JE; Maguire, MG; Martin, DF; Ying, GS, 2016)
" The calculated concentrations were used to determine the pharmacokinetic parameters of the analytes."	2.79	Clinical pharmacokinetics of clopidogrel and its metabolites in patients with cardiovascular diseases. ( Burchardt, P; Danielak, D; Główka, F; Karaźniewicz-Łada, M; Komosa, A; Kruszyna, L; Lesiak, M, 2014)
"Healthy subjects (n = 160; ages 20 to 53 years; homozygous CYP2C19 extensive metabolizer genotype; no nicotine for 6 weeks, prescription drugs for 4 weeks, over-the-counter drugs for 2 weeks, and no caffeine or alcohol for 72 h; confined; restricted diet) received clopidogrel 75 mg/day for 9 days, at which time clopidogrel pharmacokinetic and pharmacodynamic endpoints were measured."	2.78	Clopidogrel pharmacokinetics and pharmacodynamics vary widely despite exclusion or control of polymorphisms (CYP2C19, ABCB1, PON1), noncompliance, diet, smoking, co-medications (including proton pump inhibitors), and pre-existent variability in platelet f ( Barnard, MR; Bhatt, DL; Brooks, JK; Frelinger, AL; Lampa, M; Lee, RD; Michelson, AD; Mulford, DJ; Nigam, A; Nudurupati, S; Wu, J, 2013)
"Ticlopidine pretreatment did not significantly influence the risk of death or myocardial infarction in patients randomized to abciximab."	2.70	Ticlopidine pretreatment before coronary stenting is associated with sustained decrease in adverse cardiac events: data from the Evaluation of Platelet IIb/IIIa Inhibitor for Stenting (EPISTENT) Trial. ( Ellis, SG; Lincoff, AM; Steinhubl, SR; Topol, EJ; Wolski, K, 2001)
"Substantial evidence suggests that genetic predisposition plays a vital role in the physiopathology of this complex disease."	2.55	Cardiovascular pharmacogenetics: a promise for genomically-guided therapy and personalized medicine. ( El Amri, H; Zaiou, M, 2017)
"Aspirin was associated with increased bleeding risks when combined with non-steroidal anti-inflammatory drugs, clopidogrel and selective serotonin reuptake inhibitors compared with monotherapy."	2.53	Bleeding Risk with Long-Term Low-Dose Aspirin: A Systematic Review of Observational Studies. ( García Rodríguez, LA; Hennekens, CH; Lanas, A; Martín-Pérez, M; Rothwell, PM, 2016)
" Importantly, these drug-drug interactions have prognostic implications, since patients with high on-treatment platelet reactivity associated with reduced clopidogrel metabolism have an increased risk of ischemia."	2.52	Drug-drug interactions between clopidogrel and novel cardiovascular drugs. ( Angiolillo, DJ; Gaudio, C; Greco, C; Marazzi, G; Pelliccia, F; Rollini, F, 2015)
"To assess the impact of smoking on clinical and pharmacodynamic response to clopidogrel."	2.50	The impact of smoking on clinical efficacy and pharmacodynamic effects of clopidogrel: a systematic review and meta-analysis. ( Chai, H; Chen, M; Huang, DJ; Li, Q; Liu, W; Luo, XL; Peng, Y; Ren, X; Wang, XQ; Zhang, C; Zhao, ZG, 2014)
" Most pharmacokinetic and pharmacodynamic studies in vivo were conducted using small sample sizes and were single centered, resulting in conflicting data."	2.49	Pharmacodynamic impacts of proton pump inhibitors on the efficacy of clopidogrel in vivo--a systematic review. ( Chen, J; Chen, SY; Lian, JJ; Luo, TC; Zeng, XQ, 2013)
"In this meta-analysis, TAT was associated with significantly effective outcomes for TLR and TVR without any increase in major adverse events but was associated with tolerance issues compared with DAT after DES implantation."	2.49	Cilostazol added to aspirin and clopidogrel reduces revascularization without increases in major adverse events in patients with drug-eluting stents: a meta-analysis of randomized controlled trials. ( Bonneau, HN; Kaneda, H; Koo, BK; Nagai, R; Sakurai, R, 2013)
" Whether this is worth both the risk of non-compliance with twice-a-day dosing in real-life patients lacking the same motivation as their trial-volunteer counterparts, and the 2000-fold difference in incremental cost, is the remaining matter for debate."	2.48	Quantitative comparison of clopidogrel 600 mg, prasugrel and ticagrelor, against clopidogrel 300 mg on major adverse cardiovascular events and bleeding in coronary stenting: synthesis of CURRENT-OASIS-7, TRITON-TIMI-38 and PLATO. ( Davies, JE; Francis, DP; Nijjer, SS, 2012)
" Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired."	2.48	Comparative pharmacokinetics and pharmacodynamics of platelet adenosine diphosphate receptor antagonists and their clinical implications. ( Ferro, A; Floyd, CN; Passacquale, G, 2012)
" Therefore the optimal dosage and duration of clopidogrel therapy is of utmost importance."	2.48	Clinical use of clopidogrel. ( Byrne, RA; Sarafoff, N; Sibbing, D, 2012)
" In consideration for prescribing DAPT (drug, dosage and duration) the clinician will have to weigh the potential benefits (reduction in death from cardiovascular causes, nonfatal myocardial infarction, and nonfatal stroke) and risks (severe or life-threatening bleeding) for each and every patient."	2.48	Dual antiplatelet therapy for primary and secondary prevention. ( Dhruvakumar, S; Gerula, C; Kaluski, E; Klapholz, M; Maher, J; Mathur, AP; Mazza, V; Waller, AH, 2012)
" Until further reliable controlled data are available, this potential, but currently unproven, clinical interaction can be minimized by widely separating the dosing of clopidogrel and PPI."	2.46	NSAID-induced gastrointestinal and cardiovascular injury. ( Chan, FK; Ng, SC, 2010)
" We conclude that the benefits of prasugrel are overestimated, and the risks, especially during chronic use are underestimated."	2.45	Prasugrel development - claims and achievements. ( Kopyleva, O; Serebruany, V; Shalito, I, 2009)
" In addition to this, clopidogrel has also been widely used with better long term administration results in patients with atherosclerotic disease."	2.45	Current problems, new opportunities and future directions of anti-platelet therapy - increasing role of novel antiplatelet agents in cardiovascular diseases. ( Akram, F; Akram, S; Postuła, M, 2009)
" For antiplatelet agents, the most important risk is excess bleeding, especially as emerging evidence suggests that excess bleeding is associated with adverse long-term outcomes; thus prevention and management of excess bleeding is critically important."	2.45	Safety and tolerability of antiplatelet therapies for the secondary prevention of atherothrombotic disease. ( Spinler, SA, 2009)
" The improved efficacy of multiple-drug therapy is associated with an increased risk of bleeding, which raises the issue of the dosing of these drugs."	2.45	Antiplatelet agents. ( Spectre, G; Varon, D, 2009)
" As an alternative, new ADP receptor antagonists with better bioavailability and improved pharmacokinetics, e."	2.44	Thienopyridines in cardiovascular disease: focus on clopidogrel resistance. ( Huber, K; Schrör, K; Siller-Matula, J; Wojta, J, 2007)
"Ticlopidine is an inhibitor of platelets function in vivo."	2.43	[Place of ticlopidine in antiplatelet treatment]. ( Goch, A; Goch, JH; Wlazłowski, R, 2005)
"Atorvastatin has protective effects against membrane lipid peroxidation at pharmacologic concentrations."	2.42	Hypothesis: atorvastatin has pleiotropic effects that translate into early clinical benefits on cardiovascular disease. ( Hennekens, CH; Novela, C, 2004)
"Ticlopidine was first shown to decrease major events compared with placebo or aspirin in patients with stroke or recent transient ischemic attack."	2.40	The antiplatelet effects of ticlopidine and clopidogrel. ( Cannon, CP; Loscalzo, J; Sharis, PJ, 1998)
" There have been a limited number of studies investigating the pharmacokinetic profile of the drug."	2.39	Clinical pharmacokinetics of ticlopidine. ( Desager, JP, 1994)
"Ticlopidine is a new antiplatelet agent with a distinct mechanism of action."	2.38	Ticlopidine and antiplatelet therapy. ( Flores-Runk, P; Raasch, RH, 1993)
"Postoperative complications were similar in the 2 groups."	1.46	Poor prognosis after surgery for intertrochanteric fracture in elderly patients with clopidogrel treatment: A cohort study. ( Chen, X; Liu, Z; Ren, J; Sun, T; Wang, J; Wang, X; Zhang, J, 2017)
"HPR-aspirin was persistent 75days later in 36% patients."	1.43	High platelet reactivity on aspirin in patients with acute ST elevation myocardial infarction. ( Dillinger, JG; Drouet, L; Henry, P; Saeed, A; Sideris, G; Silberman, SM; Sollier, CB; Spagnoli, V; Voicu, S, 2016)
" However, no data are available regarding its impact on adverse clinical outcomes in patients undergoing percutaneous coronary intervention (PCI)."	1.39	Comparison of clinical efficacy and safety of clopidogrel resinate with clopidogrel bisulfate in patients undergoing percutaneous coronary intervention. ( Chang, K; Cho, JS; Chung, WS; Her, SH; Jeong, SH; Kim, CJ; Kim, PJ; Park, MW; Seung, KB; Yim, HW, 2013)
"High platelet reactivity (HPR) under treatment with clopidogrel or aspirin is associated with adverse outcome."	1.39	Dual non-responsiveness to antiplatelet treatment is a stronger predictor of cardiac adverse events than isolated non-responsiveness to clopidogrel or aspirin. ( Christ, G; Delle-Karth, G; Drucker, C; Huber, K; Jilma, B; Maurer, G; Neunteufl, T; Siller-Matula, JM; Tolios, A, 2013)
"Regardless of dose, adjusted odds ratios associating clopidogrel use with the study endpoint were statistically significant and followed a dose-response pattern."	1.39	Gastrointestinal events with clopidogrel: a nationwide population-based cohort study. ( Grove, EL; Jørgensen, NR; Schwarz, P; Vestergaard, P; Würtz, M, 2013)
"No choroidal or retrobulbar hemorrhages occurred in any patient."	1.37	Comparison of hemorrhagic complications of warfarin and clopidogrel bisulfate in 25-gauge vitrectomy versus a control group. ( Albert, MA; Compton, CJ; Feist, RM; Frederick, PA; Gupta, SR; Heersink, MJ; Hill, ML; Mason, JO; Neimkin, MG; Thomley, ML; Vail, RS; White, MF, 2011)
" Management is currently limited to dosing alteration and introduction of other antiplatelet agents."	1.37	Resistance to aspirin and clopidogrel therapy. ( Alam, S; Assaad, S; Beresian, J; Bitar, A; Charafeddine, K; Khoury, M; Musallam, KM; Taher, AT, 2011)
"Diabetes and more specially type 2 diabetes are a major cardiovascular risk factor."	1.36	[Antiplatelet agents and diabetes mellitus]. ( Bal dit Sollier, C; Drouet, L; Henry, P, 2010)
"Aspirin did not inhibit and did not interfere with the effects of clopidogrel or cangrelor using this test."	1.35	Measurement of platelet P-selectin for remote testing of platelet function during treatment with clopidogrel and/or aspirin. ( Fox, SC; Heptinstall, S; May, JA; Neubert, U; Shah, A, 2009)
" The improved efficacy of multiple drug therapy is associated with an increased risk of bleeding, which raises the issue of the dosing of these drugs."	1.35	Frontiers in platelet inhibition. ( Shai, E; Spectre, G; Varon, D, 2009)
" One hundred sixty-one patients on 100 mg of aspirin co-medication underwent elective coronary stenting and were given an initial dosage of 600 mg clopidogrel, followed by 75 mg clopidogrel daily."	1.35	How to optimise clopidogrel therapy? Reducing the low-response incidence by aggregometry-guided therapy modification. ( Engelhardt, A; Lask, S; Mügge, A; Neubauer, H, 2008)
"Thrombotic thrombocytopenic purpura is a syndrome characterized by hemolytic anemia, thrombocytopenia, neurological symptoms, fever and renal dysfunction."	1.32	Thrombotic thrombocytopenic purpura associated with ticlopidine. ( Kandemir, G; Orhan, B; Oztürk, A; Türken, O; Yaylaci, M, 2003)
"Aspirin treatment for primary prevention is safe and useful at an annual coronary event risk > or = 1."	1.32	[Anticoagulation and antiaggregation in cardiac patients]. ( Meyer, BJ, 2003)
"(2) Aspirin has essentially gastrointestinal adverse effects, whose incidence can be limited by prescribing a daily dose below 350 mg."	1.31	Antiplatelet drugs in cardiovascular prevention: take adverse effects and costs into account. ( , 2000)
"Ticlopidine is an antiplatelet agent that has been proven efficacious in preventing vascular events in patients with a history of vasculopathy."	1.30	Ticlopidine-associated pancytopenia: implications of an acetylsalicylic acid alternative. ( Armstrong, PW; Brown, NE; Gill, S; Majumdar, S, 1997)

Research

Studies (535)

Authors

Clinical Trials (83)

Trial Overview

Trial Outcomes

P2Y12 Reaction Unit (PRU)

Timeframe	Studies, this research(%)	All Research%
pre-1990	3 (0.56)	18.7374
1990's	18 (3.36)	18.2507
2000's	193 (36.07)	29.6817
2010's	317 (59.25)	24.3611
2020's	4 (0.75)	2.80

Authors	Studies
Lyu, SQ	1
Zhu, J	1
Wang, J	3
Wu, S	1
Zhang, H	1
Shao, XH	1
Yang, YM	1
Kirac, D	1
Yaman, AE	1
Doran, T	1
Mihmanli, M	1
Keles, EC	1
Girotra, S	1
Stebbins, A	1
Wruck, L	1
Marquis-Gravel, G	1
Gupta, K	1
Farrehi, P	1
Benziger, CP	1
Effron, MB	3
Whittle, J	1
Muñoz, D	1
Kripalani, S	1
Anderson, RD	1
Jain, SK	1
Polonsky, TS	1
Ahmad, FS	1
Roe, MT	2
Rothman, RL	1
Harrington, RA	4
Hernandez, AF	1
Jones, WS	2
Kim, BK	1
Hong, SJ	1
Cho, YH	1
Yun, KH	1
Kim, YH	1
Suh, Y	1
Cho, JY	1
Her, AY	1
Cho, S	1
Jeon, DW	1
Yoo, SY	1
Cho, DK	1
Hong, BK	1
Kwon, H	1
Ahn, CM	1
Shin, DH	1
Nam, CM	1
Kim, JS	1
Ko, YG	2
Choi, D	1
Hong, MK	1
Jang, Y	2
Ostroumova, OD	1
Kochetkov, AI	1
Pereverzev, AP	1
Kravchenko, EV	1
Kazjulin, AN	1
Andreev, DN	2
Pavleeva, EE	1
Tian, KP	1
Guan, J	1
Cai, LL	1
Li, YR	1
Deng, XL	1
Liu, QY	1
Zheng, BX	1
Cong, YL	1
Xanthopoulou, I	2
Davlouros, P	1
Deftereos, S	1
Hamilos, M	1
Sitafidis, G	1
Kanakakis, I	1
Vavouranakis, M	1
Goudevenos, J	1
Lekakis, J	2
Alexopoulos, D	3
Piccolo, R	1
Gargiulo, G	1
Franzone, A	1
Santucci, A	1
Ariotti, S	1
Baldo, A	1
Tumscitz, C	1
Moschovitis, A	1
Windecker, S	2
Valgimigli, M	4
Sun, Q	1
Chang, S	1
Lu, S	1
Zhang, Y	2
Chang, Y	1
Buhatem Medeiros, F	1
Pepe Medeiros de Rezende, N	1
Bertoldi Franco, J	1
Porrio de Andrade, AC	1
Timerman, L	1
Gallottini, M	1
Itagiba Neves, IL	1
Ortega, KL	1
Hernandez-Suarez, DF	1
Scott, SA	2
Tomey, MI	1
Melin, K	1
Lopez-Candales, A	1
Buckley, CE	1
Duconge, J	1
Tan, SSN	1
Fong, AYY	1
Mejin, M	1
Gerunsin, J	1
Kong, KL	1
Chin, FYY	1
Tiong, LL	1
Lim, MSH	1
Asri, S	1
Khiew, NZ	1
Voon, CY	1
Mohd Amin, NH	1
Cham, YL	1
Koh, KT	1
Oon, YY	1
Ong, TK	1
Yee, J	1
Kumar, V	1
Anuwatworn, A	1
Petrasko, M	1
Stys, A	1
Zafar, MU	1
Baber, U	2
Smith, DA	1
Sartori, S	1
Contreras, J	1
Rey-Mendoza, J	1
Linares-Koloffon, CA	1
Escolar, G	1
Mehran, R	3
Fuster, V	3
Badimon, JJ	1
Zhang, J	1
Chen, X	1
Liu, Z	1
Wang, X	1
Ren, J	1
Sun, T	1
Kim, JB	1
Choi, BG	1
Rha, SW	2
Seo, HS	1
Choi, SY	1
Byun, JK	1
Na, JO	1
Choi, CU	1
Kim, EJ	1
Park, CG	1
Oh, DJ	1
Tzimas, P	1
Tsoumani, M	1
Giannakis, D	1
Kalantzi, K	1
Petrou, A	1
Chantzichristos, V	1
Sofikitis, N	1
Papadopoulos, G	1
Milionis, H	2
Tselepis, A	1
Squizzato, A	4
Bellesini, M	2
Takeda, A	1
Middeldorp, S	3
Donadini, MP	2
Laine, M	1
Frere, C	3
Bonello, L	6
Lader, E	1
Turner, RM	2
Fontana, V	1
Bayliss, M	1
Whalley, S	1
Santoyo Castelazo, A	1
Pirmohamed, M	2
Mazlan-Kepli, W	1
Dawson, J	1
Berry, C	1
Walters, M	1
Pultar, J	1
Wadowski, PP	1
Panzer, S	9
Gremmel, T	10
Tousoulis, D	3
Siasos, G	3
Zaromitidou, M	1
Oikonomou, E	1
Maniatis, K	1
Kioufis, S	1
Kokkou, E	1
Papavassiliou, AG	1
Stefanadis, C	3
Agewall, S	1
Cattaneo, M	1
Collet, JP	4
Andreotti, F	1
Lip, GY	2
Verheugt, FW	3
Huber, K	7
Grove, EL	7
Morais, J	2
Husted, S	4
Wassmann, S	1
Rosano, G	1
Atar, D	1
Pathak, A	1
Kjeldsen, K	1
Storey, RF	7
Remková, A	1
Janušicová, A	1
Remko, M	1
Liu, Y	2
Liu, N	2
Li, W	2
Shao, H	2
Zhi, H	1
Li, J	1
Hayasaka, M	1
Takahashi, Y	1
Nishida, Y	1
Yoshida, Y	1
Hidaka, S	1
Asai, S	1
Chen, J	4
Chen, SY	1
Lian, JJ	1
Zeng, XQ	1
Luo, TC	1
Mischnik, M	1
Boyanova, D	1
Hubertus, K	1
Geiger, J	1
Philippi, N	1
Dittrich, M	1
Wangorsch, G	1
Timmer, J	1
Dandekar, T	1
Capranzano, P	3
Capodanno, D	1
Stiefelhagen, P	2
Villacorta, AS	1
Villacorta Junior, H	1
Batista, MJ	1
Gomes, RV	1
Macedo, LA	1
Helmuth, B	1
Mesquita, ET	1
McKenzie, JL	1
Douglas, G	1
Bazargan, A	1
Kopp, CW	7
Seidinger, D	5
Koppensteiner, R	8
Steiner, S	9
Sorich, MJ	2
Polasek, TM	1
Wiese, MD	1
Johnson, JA	2
Cavallari, LH	3
Weeke, P	2
Roden, DM	3
Gerson, LB	2
Zhao, ZG	1
Chen, M	1
Peng, Y	1
Chai, H	1
Liu, W	1
Li, Q	1
Ren, X	1
Wang, XQ	1
Luo, XL	1
Zhang, C	1
Huang, DJ	1
Armstrong, PW	3
Westerhout, CM	1
Fu, Y	1
Katus, H	4
James, S	4
Wallentin, L	5
Würtz, M	4
Lordkipanidzé, M	2
Park, MW	1
Jeong, SH	1
Her, SH	1
Kim, PJ	1
Cho, JS	1
Kim, CJ	1
Chung, WS	1
Seung, KB	1
Yim, HW	1
Chang, K	1
López, J	1
Morales, C	1
Avanzas, P	1
Callejo, F	1
Hernández-Vaquero, D	1
Llosa, JC	1
Siller-Matula, JM	4
Jilma, B	4
Tsoumani, ME	2
Kalantzi, KI	2
Goudevenos, IA	1
Tselepis, AD	2
DiNicolantonio, JJ	2
D'Ascenzo, F	1
Tomek, A	1
Chatterjee, S	1
Niazi, AK	1
Biondi-Zoccai, G	1
Gladding, PA	1
Wilhelm, TJ	1
Post, S	1
Moertl, D	2
Coory, M	1
Pekarsky, BA	1
Chua, D	1
Nishi, C	1
Knauér, NIu	1
Lifshits, GI	1
Voronina, EN	1
Koleda, NV	1
Gus'kova, EV	1
Fischer, C	1
Lümmen, G	1
Karaźniewicz-Łada, M	3
Danielak, D	3
Burchardt, P	2
Kruszyna, L	1
Komosa, A	1
Lesiak, M	1
Główka, F	3
Rubboli, A	1
Oldgren, J	1
Marìn, F	1
Lip, G	1
Suh, JW	2
Cha, MJ	1
Lee, SP	2
Chae, IH	2
Bae, JH	1
Kwon, TG	1
Bae, JW	1
Cho, MC	1
Kim, HS	3
Maev, IV	1
Samsonov, AA	1
Godilo-Godlevskiĭ, VA	1
Dicheva, DT	1
Chen, Y	1
Tang, Y	1
Huang, X	1
Xie, Y	2
Ford, I	1
Scott, NW	1
Herd, V	1
Mitchell, LR	1
Williams, DJ	1
Brittenden, J	1
Jeong, YH	4
Bliden, KP	3
Shuldiner, AR	3
Tantry, US	9
Gurbel, PA	11
del Castillo-Carnevali, H	1
Barrios Alonso, V	1
Zamorano Gómez, JL	1
Tan, DS	1
Yeo, AH	1
Ho, HK	1
Wee, HL	1
Ong, HY	1
Ay, C	1
Otto, CM	1
Xhelili, E	1
Hokimoto, S	3
Mizobe, M	1
Akasaka, T	2
Arima, Y	2
Kaikita, K	3
Nakagawa, K	3
Ogawa, H	3
Wisman, PP	1
Roest, M	1
Asselbergs, FW	1
de Groot, PG	1
Moll, FL	1
van der Graaf, Y	1
de Borst, GJ	1
Wang, Q	1
Ljung, R	1
Lagergren, J	1
Lu, Y	1
Rubiś, B	1
Oszkinis, G	1
Maggioni, AP	1
Park, Y	3
Jung, JM	1
Kim, K	1
Koh, JS	1
Park, JR	1
Hwang, SJ	2
Kwak, CH	2
Hwang, JY	2
Kim, S	1
Fornós-Garrigós, A	1
Orozco-Beltrán, D	1
Gil-Guillén, VF	1
Puig-Barberà, J	1
Fluixa, C	1
Fernández, A	1
Blicher, TM	1
Hommel, K	1
Kristensen, SL	1
Torp-Pedersen, C	3
Madsen, M	1
Kamper, AL	1
Olesen, JB	1
Daels, FP	1
Gaizauskas, A	1
Rioja, J	1
Varshney, AK	1
Erkan, E	1
Ozgok, Y	1
Melekos, M	1
de la Rosette, JJ	1
Williams, JM	1
Tuttle-Newhall, JE	1
Schnitzler, M	1
Dzebisashvili, N	1
Xiao, H	1
Axelrod, D	1
Mogal, H	1
Lentine, KL	1
Musunuru, K	1
Slavik, L	1
Ulehlova, J	1
Krcova, V	1
Hlusi, A	1
Indrakova, J	1
Hutyra, M	1
Galuszka, J	1
Indrak, K	1
Patel, PA	1
Fleisher, LA	1
Goldsweig, AM	1
Reid, KJ	1
Gosch, K	1
Tang, F	1
Fang, MC	1
Maddox, TM	2
Chan, PS	1
Cohen, DJ	4
Pinnarelli, L	1
Mayer, F	1
Bauleo, L	1
Agabiti, N	1
Kirchmayer, U	1
Belleudi, V	1
Di Martino, M	1
Autore, C	1
Ricci, R	1
Violini, R	1
Fusco, D	1
Davoli, M	1
Perucci, CA	1
Davila, CD	1
Vargas, F	1
Huang, KH	1
Monaco, T	1
Dimou, A	1
Rangaswami, J	1
Figueredo, VM	1
Huynh, K	1
Singh, S	1
Kullo, IJ	1
Pardi, DS	1
Loftus, EV	1
Patai, Á	1
Solymosi, N	1
Patai, ÁV	1
Mesitskaia, DF	2
Nikitina, IuM	2
Lomakin, OV	1
Shchekochikhin, DIu	1
Kopylov, FIu	2
Lanas, A	5
Gargallo, CJ	1
Liu, J	2
Zhao, D	1
Qi, Y	1
Sun, J	1
Wang, Y	1

Trial	Phase	Enrollment	Study Type	Start Date	Status
[NCT02494895]	Phase 4	3,056 participants (Anticipated)	Interventional	2015-08-01	Recruiting
PROlonging Dual Antiplatelet Treatment In Patients With Coronary Artery Disease After Graded Stent-induced Intimal Hyperplasia studY[NCT00611286]	Phase 4	1,700 participants (Anticipated)	Interventional	2006-12-31	Completed
Randomized 2x2 Factorial Trial Comparing the Cre8 Amphilimus-sirolimus Eluting Stent vs. the Synergy Everolimus-eluting Stent and a Personalized vs. Standard Duration of Dual Antiplatelet Therapy in All-comers Patients Undergoing Percutaneous Coronary Int[NCT04135989]	Phase 4	2,106 participants (Anticipated)	Interventional	2020-01-01	Active, not recruiting
Comparative Study of the Antithrombotic Effects of Ticagrelor and Clopidogrel in Type 2 Diabetic Patients[NCT01823510]	Phase 4	20 participants (Actual)	Interventional	2013-07-31	Completed
Associations of the Pharmacogenetic and Pharmacokinetic Factors With Clopidogrel Low Response and Clinical Outcome in Patients With Coronary Stent Implantation: a Registration Study[NCT01968499]		1,805 participants (Actual)	Observational [Patient Registry]	2011-03-31	Completed
Comparison of Age-related Macular Degeneration Treatments Trials: Lucentis-Avastin Trial (CATT)[NCT00593450]	Phase 3	1,208 participants (Actual)	Interventional	2008-02-29	Completed
The Effect of Remote Ischemic Preconditioning on Myocardial Injury After Noncardiac Surgery in Patients at a High Risk of Cardiac Events[NCT05733208]		766 participants (Anticipated)	Interventional	2023-05-06	Recruiting
Comparative Study of Clinical Efficacy and Safety of Different Clopidogrel Salts in Patients With Cardiovascular Disease. A Multi-center Non-interventional Clinical Trial.[NCT02126982]		1,500 participants (Actual)	Observational	2012-10-31	Completed
Study of the Effect of Eicosapentaenoic Acid (EPA) on Markers of Atherothrombosis in Patients With Type-2 Diabetes[NCT06129526]	Phase 4	450 participants (Anticipated)	Interventional	2023-12-31	Not yet recruiting
The TRANSLATE-ACS Study: Treatment With ADP Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events After Acute Coronary Syndrome[NCT01088503]		12,227 participants (Actual)	Observational	2010-03-31	Completed
REACTIC-TAVI Trial: Platelet REACtivity According to TICagrelor Dose After Transcatheter AorticValve Implantation. A Pilot Study.[NCT04331145]	Phase 4	40 participants (Actual)	Interventional	2020-06-23	Completed
Global Multicenter, Open-label, Randomized, Event-driven, Active-controlled Study Comparing a rivAroxaban-based Antithrombotic Strategy to an antipLatelet-based Strategy After Transcatheter aortIc vaLve rEplacement (TAVR) to Optimize Clinical Outcomes[NCT02556203]	Phase 3	1,653 participants (Actual)	Interventional	2015-12-16	Terminated (stopped due to Imbalance in the efficacy and safety endpoints between treatment arms in favor of comparator)
A Randomized, Double-blind, Parallel Group, Multicentre Phase IIIb Study to Compare Ticagrelor With Clopidogrel Treatment on the Risk of Cardiovascular Death, Myocardial Infarction and Ischemic Stroke in Patients With Established Peripheral Artery Disease[NCT01732822]	Phase 3	13,885 participants (Actual)	Interventional	2012-12-04	Completed
Platelet-Oriented Inhibition in New TIA and Minor Ischemic Stroke (POINT) Trial[NCT00991029]	Phase 3	4,881 participants (Actual)	Interventional	2010-05-28	Terminated (stopped due to The trial was halted by the DSMB.)
The AHEAD Study: Monitoring Anticoagulated Patients Who Suffer Head Injury[NCT02461498]		3,556 participants (Actual)	Observational	2011-07-31	Completed
Comparison of Platelet Inhibitory Effect With Adjunctive Cilostazol Versus High Maintenance-dose ClopidogrEL in Acute Myocardial Infarction Patients According to CYP2C19 Polymorphism[NCT00915733]	Phase 4	80 participants (Actual)	Interventional	2009-05-31	Completed
ReAssessment of Anti-Platelet Therapy Using an InDividualized Strategy in Patients With ST-segment Elevation Myocardial Infarction[NCT01452139]	Phase 2/Phase 3	102 participants (Actual)	Interventional	2011-09-30	Completed
A Multicenter Prospective observationaL Study to evAluate the effecT of Clopidogrel on the prEvention of Major vascuLar Events According to the gEnotype of Cytochrome P450 2C19 in Ischemic Stroke paTients; PLATELET Study[NCT04072705]		2,927 participants (Actual)	Observational	2019-09-20	Completed
A Comparison of CS-747 and Clopidogrel in Acute Coronary Syndrome Subjects Who Are to Undergo Percutaneous Coronary Intervention[NCT00097591]	Phase 3	13,619 participants (Actual)	Interventional	2004-11-30	Completed
Genotype Guided Comparison of Clopidogrel and Prasugrel Outcomes Study[NCT00995514]		4,471 participants (Actual)	Observational	2009-10-31	Terminated (stopped due to Administrative reasons)
Pharmacogenetics of Clopidogrel in Acute Coronary Syndromes[NCT03347435]		889 participants (Actual)	Interventional	2013-06-30	Terminated (stopped due to Ethics Committe decision)
The Effect of Inducing the Cytochrome P450 System on the Pharmacodynamic Efficacy of Clopidogrel[NCT01330589]		0 participants (Actual)	Interventional	2011-04-30	Withdrawn (stopped due to Inability to enroll subjects and changes in standard of care for PCI)
ReAssessment of Anti-Platelet Therapy Using an InDividualized Strategy Based on GENetic Evaluation (The RAPID GENE Study)[NCT01184300]	Phase 2/Phase 3	200 participants (Actual)	Interventional	2010-08-31	Completed
Cost-effectiveness of CYP2C19 Genotype Guided Treatment With Antiplatelet Drugs in Patients With ST-segment-elevation Myocardial Infarction Undergoing Immediate PCI With Stent Implantation: Optimization of Treatment (POPular Genetics).[NCT01761786]	Phase 4	2,700 participants (Actual)	Interventional	2011-06-30	Completed
Testing Numeric Formats for Presenting Data About Treatment Benefits and Harms[NCT00950014]		2,944 participants (Actual)	Interventional	2009-08-31	Completed
A Phase III, Multicenter, Multinational, Randomized, Parallel Group, Double-blind Trial of Clopidogrel Versus Placebo in High-risk Patients Aged 45 Years and Older, at Risk of Atherothrombotic Events, and Who Are Receiving Background Therapy Including Low[NCT00050817]	Phase 3	15,603 participants (Actual)	Interventional	2002-10-31	Completed
Pragmatic Randomized Controlled Trial Comparing Treatment Effectiveness of Guideline Indicated Anti-platelet Therapy for Acute Coronary Syndrome in Patients With Chronic Kidney Disease[NCT03150667]	Phase 4	220 participants (Anticipated)	Interventional	2017-04-10	Recruiting
Reversal of the Anti-platelet Effects of Ticagrelor in Healthy Persons and Patients With Coronary Artery Disease[NCT02383771]	Phase 4	64 participants (Actual)	Interventional	2015-03-31	Completed
DPP-4 Inhibitors in Patients With Type 2 Diabetes and Acute Myocardial Infarction:Effects on Platelet Function[NCT02377388]	Phase 3	74 participants (Actual)	Interventional	2017-02-07	Completed
Efficacy of H2 Receptor Antagonist in Prevention of Thienopyridine-related Peptic Ulcer[NCT02418312]		228 participants (Actual)	Interventional	2012-01-31	Completed
Pantoprazole Versus Famotidine for the Prevention of Recurrent Peptic Ulcers in Thienopyridine Users - a Double-blind Randomized Controlled Trial[NCT02551744]		101 participants (Actual)	Interventional	2012-07-31	Completed
A Single-center, Randomized, Open-label, Controlled, Dose-escalating, Parallel-group Study to Assess the Anti-platelet Effect of Berberine in Patients Receiving Aspirin and Clopidogrel After Percutaneous Coronary Intervention[NCT03378934]	Phase 4	64 participants (Anticipated)	Interventional	2018-09-26	Recruiting
A Randomised, Double-blind, Parallel Group, Phase 3, Efficacy and Safety Study of Ticagrelor Compared With Clopidogrel for Prevention of Vascular Events in Patients With Non-ST or ST Elevation Acute Coronary Syndromes (ACS) [PLATO- a Study of PLATelet Inh[NCT00391872]	Phase 3	18,624 participants (Actual)	Interventional	2006-10-31	Completed
Evaluation of Platelet Aggregation and Adenosine Levels in Patients With Coronary Artery Disease and Chronic Kidney Dysfunction Taking Dual Antiplatelet Therapy With Aspirin and Clopidogrel or Ticagrelor[NCT03039205]	Phase 2	90 participants (Actual)	Interventional	2017-11-07	Completed
Intensified Antiplatelet Therapy in Post-PCI Patients With High On-treatment Platelet Reactivity: the OPTIMA-2 Trial[NCT01955200]	Phase 4	1,724 participants (Actual)	Interventional	2013-10-05	Completed
WilL LOWer Dose Aspirin be More Effective Following ACS? (WILLOW-ACS)[NCT02741817]	Phase 4	20 participants (Actual)	Interventional	2016-06-26	Completed
Randomized, Multinational, Double-blind Study, Comparing a High Loading Dose Regimen of Clopidogrel Versus Standard Dose in Patients With Unstable Angina or Myocardial Infarction Managed With an Early Invasive Strategy.[NCT00335452]	Phase 3	25,086 participants (Actual)	Interventional	2006-06-30	Completed
A Randomized Controlled Trial of Influenza Vaccine to Prevent Adverse Vascular Events: A Pilot Study[NCT01945268]	Phase 4	107 participants (Actual)	Interventional	2015-04-30	Completed
A Randomized Controlled Trial of Influenza Vaccine to Prevent Adverse Vascular Events[NCT02762851]	Phase 4	5,000 participants (Anticipated)	Interventional	2016-06-30	Recruiting
A Randomized, Double-Blind, Double-Dummy, Parallel Group, Phase 3 Efficacy and Safety Study of CGT-2168 Compared With Clopidogrel to Reduce Upper Gastrointestinal Events Including Bleeding and Symptomatic Ulcer Disease[NCT00557921]	Phase 3	5,000 participants (Anticipated)	Interventional	2007-12-31	Terminated (stopped due to Terminated by Sponsor)
The Efficacy and Safety of Proton Pump Inhibitor ( in Patients With Moderate Bleeding Risk and Coronary Artery Disease Undergoing Percutaneous Coronary: A Randomised, Open ,Compared With Control[NCT05820048]	Phase 4	300 participants (Anticipated)	Interventional	2023-05-01	Not yet recruiting
Genotype Guided Versus Conventional Approach in Selection of Oral P2Y12 Receptor Blocker in Chinese Patients Suffering From Acute Coronary Syndrome[NCT01994941]	Phase 4	133 participants (Actual)	Interventional	2013-08-31	Completed
Prospective Multi-center Registry of Genotyping Related Clopidogrel in Percutaneous Coronary Intervention Patients[NCT02707445]		5,000 participants (Actual)	Interventional	2011-09-30	Completed
Evaluating Pharmacogenomic Variants for Cardiology Therapeutics: the Lighthouse Pilot (Association Between Genetic Variant Scores and P2Y12 Inhibitor Effects)[NCT04702113]		300 participants (Actual)	Interventional	2020-12-03	Completed
[NCT01032668]	Phase 3	192 participants (Actual)	Interventional	2008-09-30	Completed
Prognostic Models for People With Stable Coronary Artery Disease[NCT01609465]		300,000 participants (Anticipated)	Observational	2010-01-31	Active, not recruiting
Individualizing Dual Antiplatelet Therapy After Percutaneous Coronary Intervention - The IDEAL-PCI Registry[NCT01515345]	Phase 3	1,008 participants (Actual)	Interventional	2011-07-31	Completed
GRAVITAS: Gauging Responsiveness With A VerifyNow Assay-Impact On Thrombosis And Safety[NCT00645918]		2,800 participants (Actual)	Interventional	2008-06-30	Completed
Laboratory Implications of Non Obstructive Atherosclerotic Plaques Identified by Multiple Detector Coronary Angiotomography[NCT03632785]		90 participants (Actual)	Observational	2017-03-27	Completed
Effect of Modifying Anti-platelet Treatment to Ticagrelor in Patients With Diabetes and Low Response to Clopidogrel[NCT01643031]	Phase 4	500 participants (Anticipated)	Interventional	2012-08-31	Not yet recruiting
MONET BRIDGE(Maintenance Of aNtiplatElet Therapy in Patients With Coronary Stenting Undergoing Surgery) - (Mantenimento Della Terapia Antiaggregante Nei Pazienti Portatori di Stent Coronarico Candidati a Chirurgia)[NCT03862651]	Phase 2	140 participants (Anticipated)	Interventional	2019-06-01	Not yet recruiting
Multicenter, Prospective Cohort of Patient With Coronary Stents Undergoing Non Cardiac Surgery or Invasive Procedures.[NCT01045850]		1,312 participants (Actual)	Observational	2006-02-28	Completed
Pharmacogenomics of Anti-Platelet Interventions (The PAPI Study)[NCT00799396]	Phase 4	682 participants (Actual)	Interventional	2006-07-31	Completed
Escalating Clopidogrel by Involving a Genetic Strategy - Thrombolysis In Myocardial Infarction 56[NCT01235351]	Phase 2	335 participants (Actual)	Interventional	2010-10-31	Completed
Can Pharmacogenomic Testing Improve Response and Avoid Adverse Effects With Clopidogrel Therapy? A Biospecimen Bank for Genetic and Genomic Investigation of Clopidogrel.[NCT01611545]		130 participants (Actual)	Observational	2012-06-30	Completed
Role of Clopidogrel in Preventing Exacerbations in Patients With Severe COPD: An Open-label Randomized Controlled Trial.[NCT06021990]	Phase 3	162 participants (Anticipated)	Interventional	2023-10-01	Recruiting
Clopidogrel Hyper-Responsiveness: Incidence and Associated Outcomes in Patients With Cerebral Aneurysms[NCT05945563]		208 participants (Anticipated)	Observational [Patient Registry]	2023-01-17	Recruiting
Antiplatelet Resistance Research in Patients With Peripheral Arterial Revascularization[NCT03953547]		88 participants (Actual)	Observational	2018-01-01	Completed
Role of Innate and Adaptive Immunity After Acute Myocardial Infarction BATTLE-AMI Study (B And T Types of Lymphocytes Evaluation in Acute Myocardial Infarction)[NCT02428374]	Phase 4	300 participants (Anticipated)	Interventional	2015-05-31	Recruiting
Dual Antiplatelet Therapy in Patients With Aspirin Resistance Following Coronary Artery Bypass Grafting[NCT01159639]	Phase 4	200 participants (Actual)	Interventional	2010-06-30	Completed
A Comparison of Prasugrel and Clopidogrel in Acute Coronary Syndrome Subjects With Unstable Angina/Non-ST-Elevation Myocardial Infarction Who Are Medically Managed[NCT00699998]	Phase 3	9,326 participants (Actual)	Interventional	2008-06-30	Completed
Assessment of Platelet REACtivity After Transcatheter Aortic Valve Implantation[NCT02224066]	Phase 4	65 participants (Actual)	Interventional	2016-01-31	Completed
Antiplatelet Therapy in Elderly Patients Undergoing Percutaneous Coronary Intervention[NCT04999293]		1,505 participants (Actual)	Observational	2021-07-20	Completed
Clopidogrel Resistance and Platelet Reactivity in Hispanic Females Undergoing Percutaneous Coronary Intervention[NCT01796873]		150 participants (Anticipated)	Observational	2012-01-31	Recruiting
A Phase 1, Randomized, Open-Label, 2-Period, Crossover Design Study to Assess the Effects of Multiple Oral Doses of Dexlansoprazole, Lansoprazole, Omeprazole or Esomeprazole on the Steady-State Pharmacokinetics and Pharmacodynamics of Clopidogrel in Healt[NCT00942175]	Phase 1	160 participants (Actual)	Interventional	2009-12-31	Completed
Biological Efficacy of Clopidogrel 600 mg Loading Dose Followed by 75 mg Maintenance Dose After Implantation of Drug-eluting Stents in Patients With Diabetes Mellitus or Metabolic Syndrome (SPACE)[NCT00298428]		159 participants (Actual)	Interventional	2006-05-31	Completed
Gastrointestinal Ulceration in Patients on Dual Antiplatelet Therapy After Percutaneous Coronary Intervention[NCT00413309]		30 participants (Anticipated)	Interventional	2006-04-30	Completed
Antiplatelet Therapy in Acute Mild-Moderate Ischemic Stroke (ATAMIS): a Parallel Randomized, Open-label, Multicenter, Prospective Study[NCT02869009]	Phase 3	3,000 participants (Actual)	Interventional	2016-11-30	Completed
Impact of the Degree of Peri-Interventional Platelet Inhibition After Loading With Clopidogrel on Early Clinical Outcome of Elective Coronary Stent Placement[NCT00457236]		800 participants	Observational	2003-03-31	Active, not recruiting
Ticagrelor With Aspirin or Alone in High-Risk Patients After Coronary Intervention[NCT02270242]	Phase 4	9,006 participants (Actual)	Interventional	2015-07-31	Completed
A Randomized, Open-label, Active-controlled, Parallel-group Study to Investigate the Platelet Inhibition of Ticagrelor Versus Clopidogrel in Patients With Stable Coronary Artery Disease and Type 2 Diabetes Mellitus After Recent Elective Percutaneous Coron[NCT02748330]	Phase 4	40 participants (Actual)	Interventional	2016-06-30	Completed
A Phase III Randomized Trial of Warfarin Plus Antiplatelet Therapy Versus Antiplatelet Therapy Alone in Patients With Peripheral Vascular Disease[NCT00125671]	Phase 3	2,400 participants	Interventional	2000-01-31	Active, not recruiting
Efficacy and Safety of Apixaban in Reducing Restenosis and Limb Loss in Subjects With Symptomatic Peripheral Artery Disease (PAD) Undergoing Infrapopliteal Endovascular Peripheral Revascularization Procedures in Patients With Critical Limb[NCT04229264]	Phase 3	200 participants (Anticipated)	Interventional	2020-01-09	Recruiting
DUAL Pathway Inhibition (Low-dose Rivaroxaban and Aspirin) as Compared to Aspirin Only to Improve Endothelial Function in Peripheral Artery Disease.[NCT04218656]	Phase 4	159 participants (Actual)	Interventional	2020-06-08	Completed
Prospective Pilot Study- Does Mean Platelet Volume Change With Clopidogrel in Patients With Stable Angina Undergoing Percutaneous Coronary Intervention?[NCT02550301]		100 participants (Anticipated)	Observational	2015-09-30	Not yet recruiting
Optimized Antiplatelet Therapy With Aspirin and Clopidogrel Improves Mortality Compared to Standard Treatment.[NCT01796691]		600 participants (Actual)	Observational	2009-01-31	Completed
Optimizing Therapy With Aspirin and Clopidogrel. The BOchum CLopidogrel and Aspirin Plan to Improve Dual Antiplatelet Therapy.[NCT01212302]		500 participants (Actual)	Interventional	2008-10-31	Completed
PPD Trial Pilot Study: Plavix, Prasugrel and Drug Eluting Stents[NCT01103843]		1,000 participants (Anticipated)	Interventional	2010-04-30	Recruiting
The Role of Multiple Electrode Aggregometry in Detection of Clopidogrel Resistance in Diabetic Patients With Coronary Artery Disease and Prediction of Clinical Outcomes. A Comparative-method, Non Interventional, Single Center Study.[NCT01991093]		280 participants (Actual)	Observational	2014-06-30	Completed
Effects of Prolonged Dual Antiplatelet Therapy With Clopidogrel Plus Acetylsalicylic Acid (ASA) After Percutaneous Lower Extremity Revascularization in Patients With Peripheral Arterial Disease[NCT02798913]	Phase 3	300 participants (Anticipated)	Interventional	2016-01-31	Recruiting
A Randomized, Single Center Trial to Assess the Endothelial Function With Ticagrelor Monotherapy Compared to Aspirin Monotherapy in Patients With History of Acute Coronary Syndrome[NCT03881943]	Phase 4	200 participants (Actual)	Interventional	2017-01-31	Completed
Aspirin Impact on Platelet Reactivity in Acute Coronary Syndrome Patients on Novel P2Y12 Inhibitors Therapy[NCT02049762]	Phase 4	29 participants (Actual)	Interventional	2015-06-30	Completed
The Association Between Plasma or Platelet microRNAs and Clopidogrel Low Response and Its Mechanism[NCT02447809]	Phase 4	400 participants (Anticipated)	Interventional	2015-01-31	Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Platelet reactivity by measuring P2Y12 Reaction Unit using Accumetrics VerifyNow (NCT01823510)
Timeframe: up to 7 days

Platelet Reactivity

Intervention	percentage of baseline PRU (Mean)
	2 hour post-loading dose	6 hour post-loading dose	5-7 days of maintenance dosing
Clopidogrel + Aspirin	77.8	66.8	62.7
Ticagrelor + Aspirin	14.8	8.2	14.5

Platelet reactivity by Multiplate Analyzer (NCT01823510)
Timeframe: up to 7 days

Platelet Reactivity Index (PRI)

Intervention	percentage of baseline Unit (Mean)
	2 hour post-loading dose	6 hour post-loading dose	5-7 days of maintenance dosing
Clopidogrel + Aspirin	54.5	43.6	45.5
Ticagrelor + Aspirin	20.5	20.6	24.2

Platelet reactivity index by Vasodilator-Stimulated Phosphoprotein phosphorylation (VASP) assay. (NCT01823510)
Timeframe: up to 7 days

Thrombus Formation

Intervention	percentage of baseline PRI (Mean)
	2 hour post-loading dose	6 hour post-loading dose	5-7 days of maintenance dosing
Clopidogrel + Aspirin	85.8	82.5	68.4
Ticagrelor + Aspirin	21.8	17.8	17.2

Thrombus formation in Badimon Perfusion Chamber high-shear) (ex vivo model of thrombosis). (NCT01823510)
Timeframe: up to 7 days

Area of Lesion

Area of Lesion Change From Baseline

Average Cost of Drug/Patient

Change From Baseline in Visual-acuity Score (Continuous)

Intervention	percentage of baseline size (Mean)
	2 hour post loading dose	6 hours post loading dose	5-7 days of maintenance dose
Clopidogrel + Aspirin	84.4	79.8	82.6
Ticagrelor + Aspirin	66.9	59.9	68.9

Intervention	mm^2 (Mean)
1-Lucentis Monthly	6.6
2-Avastin Monthly	6.5
3-Lucentis as Needed	7.3
4-Avastin as Needed	7.0

Intervention	mm^2 (Mean)
1-Lucentis Monthly	-0.1
2-Avastin Monthly	0.3
3-Lucentis as Needed	0.6
4-Avastin as Needed	1.3

Intervention	US dollars per patient (Mean)
1-Lucentis Monthly	23400
2-Avastin Monthly	595
3-Lucentis as Needed	13800
4-Avastin as Needed	385

"Visual acuity testing was performed with the Electronic Visual Tester (EVA) following the ETDRS protocol. VA score is measured as number of letters read correctly. The VA score change is the difference of the VA score at 1 Year and the VA score at baseline.~In this study, the outcome VA score change is ranged from -71 to 52, with the higher VA score change the better visual acuity improvement." (NCT00593450)
Timeframe: Baseline and 1 Year

Change in Diastolic Blood Pressure From Baseline

Change in Systolic Blood Pressure From Baseline

Number of Treatments

Retinal Thickness Plus Subfoveal-fluid Thickness at Fovea

Retinal Thickness Plus Subfoveal-fluid Thickness Change From Baseline at Fovea

Total Thickness at Fovea

Total Thickness Change From Baseline at Fovea

Visual-acuity Score and Snellen Equivalent (Continuous)

Intervention	No. of Letters (Mean)
1-Lucentis Monthly	8.5
2-Avastin Monthly	8.0
3-Lucentis as Needed	6.8
4-Avastin as Needed	5.9

Intervention	mm Hg (Mean)
1-Lucentis Monthly	-0.9
2-Avastin Monthly	-1.4
3-Lucentis as Needed	-1.9
4-Avastin as Needed	-2.1

Intervention	mm Hg (Mean)
1-Lucentis Monthly	-2.1
2-Avastin Monthly	-5.4
3-Lucentis as Needed	-5.2
4-Avastin as Needed	-4.5

Intervention	Number of Treatments (Mean)
1-Lucentis Monthly	11.7
2-Avastin Monthly	11.9
3-Lucentis as Needed	6.9
4-Avastin as Needed	7.7

Intervention	μm (Mean)
1-Lucentis Monthly	152
2-Avastin Monthly	172
3-Lucentis as Needed	166
4-Avastin as Needed	172

Intervention	μm (Mean)
1-Lucentis Monthly	-100
2-Avastin Monthly	-79
3-Lucentis as Needed	-81
4-Avastin as Needed	-79

Intervention	μm (Mean)
1-Lucentis Monthly	266
2-Avastin Monthly	300
3-Lucentis as Needed	294
4-Avastin as Needed	308

Intervention	μm (Mean)
1-Lucentis Monthly	-196
2-Avastin Monthly	-164
3-Lucentis as Needed	-168
4-Avastin as Needed	-152

"Visual acuity testing was performed with the Electronic Visual Tester (EVA) following the ETDRS protocol. VA score is measured as number of letters read correctly.~In this study, the outcome VA score is ranged from 0 to 97, with the higher score the better visual acuity." (NCT00593450)
Timeframe: at 1 Year

Change From Baseline Visual-acuity Score (Frequency)

Dye Leakage on Angiogram

Fluid on Optical Coherence Tomography

Visual-acuity Score and Snellen Equivalent (Frequency)

Factors Associated With Initial ADP Receptor Inhibitor Selection at Enrollment: Duke Coronary Artery Disease (CAD) Index

Intervention	No. of Letters (Mean)
1-Lucentis Monthly	68.8
2-Avastin Monthly	68.4
3-Lucentis as Needed	68.4
4-Avastin as Needed	66.5

Intervention	Participants (Number)
	Increase of ≥15 letters	Increase of 5-14 letters	Change of ≤4 letters	Decrease of 5-14 letters	Decrease of ≥15 letters
1-Lucentis Monthly	97	90	62	19	16
2-Avastin Monthly	83	98	50	18	16
3-Lucentis as Needed	71	103	75	23	13
4-Avastin as Needed	76	90	59	23	23

Intervention	Participants (Number)
	Absent	Present	Data missing
1-Lucentis Monthly	167	97	20
2-Avastin Monthly	153	100	12
3-Lucentis as Needed	133	137	15
4-Avastin as Needed	111	145	15

Intervention	Participants (Number)
	Absent	Present	Data missing
1-Lucentis Monthly	124	151	9
2-Avastin Monthly	69	188	8
3-Lucentis as Needed	68	203	14
4-Avastin as Needed	52	214	5

Intervention	Participants (Number)
	83-97 letters, 20/12-20	68-82 letters, 20/25-40	53-67 letters, 20/50-80	38-52 letters, 20/100-160	≤37 letters, ≤20/200
1-Lucentis Monthly	42	149	52	23	18
2-Avastin Monthly	45	134	47	21	18
3-Lucentis as Needed	38	141	66	23	17
4-Avastin as Needed	40	127	57	24	23

The Duke CAD Index is a validated composite measure of angiographic burden, which assigns prognostic weights 1 through 100. Higher scores indicate greater angiographic burden and are associated with poorer prognosis. (NCT01088503)
Timeframe: Day 0 (study enrollment)

Factors Associated With Initial ADP Receptor Inhibitor Selection at Enrollment: Pre-Procedure Hemoglobin

Percentage of Participants With Definite or Probable Stent Thrombosis (ST) Events

Intervention	units on a scale (Mean)
Prasugrel	40.36
Other	41.87

Intervention	grams/deciliter (g/dL) (Mean)
Prasugrel	14.59
Other	14

Academic Research Consortium (ARC) criteria were used to define ST. Definite ST is angiographic or pathologic confirmation of partial or total thrombotic occlusion within the peri-stent region, and at least 1 of the following additional criteria: acute ischemic symptoms; ischemic electrocardiogram changes; elevated cardiac biomarkers. Probable ST is any unexplained death within 30 days of stent implantation; any MI, which is related to documented acute ischemia in the territory of the implanted stent without angiographic confirmation of ST and in the absence of any other obvious cause. Events that occurred more than 7 days after medication was switched or discontinued were excluded from the analysis. Observed (unadjusted) percentages of participants with ST events are presented. Kaplan-Meier analysis was used to estimate the percentage of participants with a definite or probable ST event. (NCT01088503)
Timeframe: Baseline through 15 months

Percentage of Participants With MACE and Who Had No Prior History of Transient Ischemic Attack (TIA)/Stroke, Weigh ≥60 Kilograms (kg), and Are Age <75 Years

Intervention	percentage of participants (Number)
Prasugrel	1.35
Clopidogrel	1.79

MACE is defined as a composite of all-cause death, MI, stroke, or unplanned coronary revascularization. Events that occurred more than 7 days after medication was switched or discontinued were excluded from the analysis. Observed (unadjusted) percentages of participants with MACE, as well as the statistical analyses adjusted for baseline cohort differences, are presented. Percentage of participant = (number of participants with events / number of participants treated) * 100. (NCT01088503)
Timeframe: Baseline through 12 months

Percentage of Participants With Major Adverse Cardiovascular Events (MACE)

Intervention	percentage of participants (Number)
Prasugrel	12.67
Clopidogrel	15.89

MACE is defined as a composite of all-cause death, myocardial infarction (MI), stroke, or unplanned coronary revascularization. Events that occurred more than 7 days after medication was switched or discontinued were excluded from the analysis. Observed (unadjusted) percentages of participants with MACE, as well as the statistical analyses adjusted for baseline cohort differences, are presented. Percentage of participants = (number of participants with events in 12 months/ number of participants treated) * 100. (NCT01088503)
Timeframe: Baseline through 12 months

Factors Associated With Initial Adenosine Diphosphate (ADP) Receptor Inhibitor Selection at Enrollment

Intervention	percentage of participants (Number)
Prasugrel	13.14
Clopidogrel	17.12

Factors are drug-eluting stent (DES) vs. bare metal stent (BMS) placement, other (no stent) vs. BMS, STEMI, other race, cardiogenic shock occurred within 24 hours, male, European Quality of Life Questionnaire-5 Dimension Health State Score (EQ-5D) - United States (US) Index =1 vs. <1, married, diabetes, and other vs. BMS placement. The EQ-5D US index is a participant-rated, health-related, quality-of-life instrument based on US population. Scores range from -0.11 to 1.0 with 1.0 = perfect health. (NCT01088503)
Timeframe: Day 0 (study enrollment)

Percentage of Participants With Cumulative Severe or Moderate Bleeding Events

Intervention	participants (Number)
	Received DES	Received only BMS	STEMI	Other Race (Non-Caucasian)	Cardiogenic Shock on Presentation	Male Participants	EQ-5D US index = 1 vs. <1	Married Participants	Participant has Diabetes	No BMS or DES
Other	6282	2491	4508	1049	176	6342	3873	5601	2472	331
Prasugrel	2365	672	1831	365	79	2451	1516	2044	767	86

Bleeding events were collected utilizing the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) definition of bleeding. Non-coronary artery bypass grafting (CABG)-related GUSTO severe or life-threatening bleeding is any intracranial hemorrhage (ICH) OR any bleeding event resulting in substantial hemodynamic compromise requiring treatment. Non-CABG-related GUSTO moderate bleeding is any bleeding event resulting in the need for transfusion that is not considered a GUSTO severe or life-threatening bleed. Additional bleeding events are fatal bleeding or ICH, or any non -fatal surgical-related bleeding events leading to ≥4 units of red cell transfusion. Observed (unadjusted) percentages of participants with bleeding events, as well as the statistical analyses adjusted for baseline cohort differences, are presented. Percentage of participants = (number of participants with events / number of participants treated) * 100. (NCT01088503)
Timeframe: Baseline, 1, 6, 12 and 15 months

Percentage of Participants With MACE Over 1, 6 and 15 Months

Intervention	percentage of participants (Number)
	Baseline	1 month	6 months	12 months	15 months
Clopidogrel	0.45	1.62	2.77	3.86	4.21
Prasugrel	0.54	1.22	1.93	2.72	3.10

MACE is defined as a composite of all-cause death, MI, stroke, or unplanned coronary revascularization. Events that occurred more than 7 days after medication was switched or discontinued were excluded from the analysis. Observed (unadjusted) percentages of participants with MACE are presented. Kaplan-Meier analysis was used to estimate the percentage of participants with a MACE event. (NCT01088503)
Timeframe: Baseline through 1, 6 and 15 months

Number of Participants With Cardiovascular Death or Thromboembolic Event

Intervention	percentage of participants (Number)
	1 month	6 months	15 months
Clopidogrel	5.40	12.04	19.13
Prasugrel	4.63	9.64	14.26

Composite of CV-death, any stroke, myocardial infarction (MI), symptomatic valve thrombosis, pulmonary embolism (PE), deep vein thrombosis (DVT), and non-central nervous system (CNS) systemic embolism (per adjudication). (NCT02556203)
Timeframe: Through study completion, on average 16 months

Number of Participants With Composite Bleeding Endpoint of BARC (Bleeding Academic Research Consortium) 2, 3, or 5 Bleeds

Intervention	Participants (Count of Participants)
Rivaroxaban (Xarelto, BAY59-7939)	83
Antiplatelet	68

Composite of BARC 2,3 or 5 bleedings (NCT02556203)
Timeframe: Through study completion, on average 16 months

Number of Participants With Death or First Thromboembolic Event (DTE)

Intervention	Participants (Count of Participants)
Rivaroxaban (Xarelto, BAY59-7939)	148
Antiplatelet	85

Death or first adjudicated thromboembolic event (DTE), defined as composite of all-cause death, any stroke, myocardial infarction (MI), symptomatic valve thrombosis, pulmonary embolism (PE), deep vein thrombosis (DVT), and non-central nervous system (CNS) systemic embolism. (NCT02556203)
Timeframe: Through study completion, on average 14 months

Number of Participants With Death or First Thromboembolic Event (DTE)

Intervention	Participants (Count of Participants)
Rivaroxaban (Xarelto, BAY59-7939)	68
Antiplatelet	63

Number of Participants With ISTH (International Society on Thrombosis and Haemostasis) Major Bleeds

Intervention	Participants (Count of Participants)
Rivaroxaban (Xarelto, BAY59-7939)	105
Antiplatelet	78

ISTH major bleeds (NCT02556203)
Timeframe: Through study completion, on average 16 months

Number of Participants With Net-clinical Benefit

Intervention	Participants (Count of Participants)
Rivaroxaban (Xarelto, BAY59-7939)	49
Antiplatelet	30

The net-clinical-benefit defined as the adjudicated composite of all-cause death, any stroke, myocardial infarction, symptomatic valve thrombosis, pulmonary embolism, deep vein thrombosis, non-CNS systemic embolism (efficacy); VARC life-threatening, disabling and VARC major bleeds (safety). (NCT02556203)
Timeframe: Through study completion, on average 16 months

Number of Participants With Primary Bleeding Event (PBE)

Intervention	Participants (Count of Participants)
Rivaroxaban (Xarelto, BAY59-7939)	137
Antiplatelet	100

PBE is defined according to VARC (Valve Academic Research Consortium) definitions as the adjudicated composite of: Life-threatening, disabling or major bleeding. (NCT02556203)
Timeframe: Through study completion, on average 16 months

Number of Participants With TIMI (Thrombolysis In Myocardial Infarction) Major / Minor Bleeds

Intervention	Participants (Count of Participants)
Rivaroxaban (Xarelto, BAY59-7939)	46
Antiplatelet	31

Composite of TIMI major and minor bleedings (NCT02556203)
Timeframe: Through study completion, on average 16 months

ALI

Intervention	Participants (Count of Participants)
Rivaroxaban (Xarelto, BAY59-7939)	42
Antiplatelet	24

Participants with ALI. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

All-cause Mortality

Intervention	Participant (Number)
Ticagrelor 90 mg bd	117
Clopidogrel 75 mg od	115

Participants with all-cause death. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Any Amputation Caused by PAD

Intervention	Participant (Number)
Ticagrelor 90 mg bd	628
Clopidogrel 75 mg od	635

Participants with any amputation caused by peripheral arterial disease (PAD). If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Any Revascularisation (Coronary, Peripheral [Limb, Mesenteric, Renal, Carotid and Other])

Intervention	Participant (Number)
Ticagrelor 90 mg bd	179
Clopidogrel 75 mg od	208

Participants with any revascularization. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Composite of Cardiovascular (CV) Death/MI/Ischemic Stroke

Intervention	Participant (Number)
Ticagrelor 90 mg bd	1211
Clopidogrel 75 mg od	1250

Participants with CV death, myocardial infarction (MI) or ischemic stroke. If no event, censoring occurs at the minimum of (primary analysis censoring date (PACD), last endpoint assessment date, non-CV death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Composite of CV Death, MI, and All-cause Stroke (Ischemic or Hemorrhagic)

Intervention	Participants (Number)
Ticagrelor 90 mg bd	751
Clopidogrel 75 mg od	740

Participants with CV death, MI or all-cause stroke. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, non-CV death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Composite of CV Death, MI, Ischemic Stroke, and ALI

Intervention	Participant (Number)
Ticagrelor 90 mg bd	766
Clopidogrel 75 mg od	759

Participants with CV death, MI, ischemic stroke or acute limb ischemia (ALI). If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, non-CV death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

CV Death

Intervention	Participant (Number)
Ticagrelor 90 mg bd	839
Clopidogrel 75 mg od	833

Participants with CV death. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, non-CV death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

CV-related Hospitalization

Intervention	Participant (Number)
Ticagrelor 90 mg bd	363
Clopidogrel 75 mg od	343

Participants with hospitalization associated with CV death, hospitalization due to MI, ischemic stroke, lower extremity revascularization, major amputation due to PAD, transient ischemic attack (TIA), coronary revascularization or unstable angina. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Lower Extremity Revascularization

Intervention	Participant (Number)
Ticagrelor 90 mg bd	1312
Clopidogrel 75 mg od	1314

Participants with lower extremity revascularization (LER). If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Major Amputation Caused by PAD

Intervention	Participant (Number)
Ticagrelor 90 mg bd	846
Clopidogrel 75 mg od	892

Participants with major amputation caused by PAD. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Participants with MI. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Net Clinical Benefit (Composite of All-cause Mortality/MI/Ischemic Stroke/ALI/Major Amputation/Fatal Bleeding/Intracranial Bleeding)

Participants with all-cause death, MI, ischemic stroke, ALI, major amputation, fatal bleeding or intracranial bleeding. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Net Clinical Benefit (Composite of All-cause Mortality/MI/Ischemic Stroke/ALI/Major Amputation/TIMI Major Bleeding)

Participants with all-cause death, MI, ischemic stroke, ALI, major amputation or Thrombolysis in Myocardial Infarction (TIMI) major bleeding. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Net Clinical Benefit (Composite of All-cause Mortality/MI/Ischemic Stroke/Fatal Bleeding/Intracranial Bleeding)

Participants with all-cause death, MI, ischemic stroke, fatal bleeding or intracranial bleeding. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Net Clinical Benefit (Composite of CV Death/MI/Ischemic Stroke/Fatal Bleeding/Intracranial Bleeding)

Participants with CV death, MI, ischemic stroke, fatal bleeding or intracranial bleeding. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, non-CV death date) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Non-CV Death

Participants with non-CV death. If no event, censoring occurs at the minimum of (PACD, last endpoint assessment date, CV death) (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

PLATO Major Bleeding Events

Participants with PLATO major bleeding event. If no event, censoring occurs at the minimum of (last endpoint assessment date, death date, 7 days after last dose of study drug) (NCT01732822)
Timeframe: From the date of first dose and up to and including 7 days following the date of last dose of study drug

Premature Permanent Discontinuation of Study Drug Due to Any Bleeding Event

Participants with a permanent discontinuation of study drug due to any bleeding event. If no event, censoring occurs at the minimum of (last endpoint assessment date, death date, 7 days after last dose of study drug) (NCT01732822)
Timeframe: From the date of first dose and up to and including 7 days following the date of last dose of study drug

TIMI Major Bleeding Events

Participants with TIMI major bleeding event. If no event, censoring occurs at the minimum of (last endpoint assessment date, death date, 7 days after last dose of study drug) (NCT01732822)
Timeframe: From the date of first dose and up to and including 7 days following the date of last dose of study drug

TIMI Major or Minor Bleeding Events

Participants with TIMI major or minor bleeding event. If no event, censoring occurs at the minimum of (last endpoint assessment date, death date, 7 days after last dose of study drug) (NCT01732822)
Timeframe: From the date of first dose and up to and including 7 days following the date of last dose of study drug

Change in ABI/TBI From Baseline

"Change in ankle brachial index (ABI) / toe brachial index (TBI).~Ankle brachial index (ABI) is the ratio of blood pressures from the ankle and arm and is used for diagnosing peripheral arterial occlusive disease (PAOD):~Normal: 1 to 1.29 Borderline: 0.91 to 0.99 Mild PAOD: 0.71 to 0.90 Medium severe PAOD: 0.41 to 0.7 Severe PAOD: <0.4~Toe brachial index (TBI) is the ratio between the toe pressure and the higher brachial pressure, used for diagnosing PAOD when the ABI cannot be used:~Normal: >0.7 Mild: 0.5-0.7 Moderate: 0.35-0.5 Moderate-Severe: <0.35 and toe pressure 40 mmHg Severe: <0.35 and toe pressure < 30 mmHg" (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Changes in Fontaine Stage

"Progression of the clinical/symptomatic status of the limb by changes in Fontaine stage.~Stage I - Asymptomatic Stage IIa - Intermittent claudication after more than 200 meters of pain free walking Stage IIb - Intermittent claudication after less than 200 meters of walking Stage III - Rest pain Stage IV - Ischemic ulcers or gangrene" (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Changes in Rutherford Classification

"Progression of the clinical/symptomatic status of the limb by changes in Rutherford classification.~Category 0 - Asymptomatic Category 1 - Mild claudication Category 2 - Moderate claudication - The distance that delineates mild, moderate and severe claudication is not specified in the Rutherford classification, but is mentioned in the Fontaine classification as 200 meters.~Category 3 - Severe claudication Category 4 - Rest pain Category 5 - Ischemic ulceration not exceeding ulcer of the digits of the foot Category 6 - Severe ischemic ulcers or frank gangrene" (NCT01732822)
Timeframe: From randomization to PACD, an average of 2.5 years

Composite of Ischemic Stroke, Myocardial Infarction, Death From Ischemic Vascular Causes, or Major Hemorrhage

Secondary efficacy outcome: Number of participants with ischemic stroke, myocardial infarction, death from ischemic vascular causes, or major hemorrhage (NCT00991029)
Timeframe: Up to 90 days

Composite of Ischemic Stroke, Myocardial Infarction, or Death From Ischemic Vascular Causes

Primary efficacy outcome: Number of Participants with Ischemic Stroke, Myocardial Infarction, or Death From Ischemic Vascular Causes (NCT00991029)
Timeframe: Up to 90 days

Death From Any Cause

Other safety outcome: Number of Participants with Death from any cause (NCT00991029)
Timeframe: up to 90 days

Death From Ischemic Vascular Causes

Secondary efficacy outcome: Number of participants with Death from ischemic vascular causes (NCT00991029)
Timeframe: Up to 90 days

Hemorrhagic Stroke

Other safety outcome: Number of participants with Hemorrhagic stroke (NCT00991029)
Timeframe: up to 90 days

Ischemic or Hemorrhagic Stroke

Secondary efficacy outcome: Number of participants with Ischemic or hemorrhagic stroke (NCT00991029)
Timeframe: Up to 90 days

Ischemic Stroke

Secondary efficacy outcome:Number of participants with Ischemic stroke (NCT00991029)
Timeframe: Up to 90 days

Major Hemorrhage

Primary safety outcome: Number of Participants with major hemorrhage (NCT00991029)
Timeframe: Up to 90 days

Major Hemorrhage Other Than Intracranial Hemorrhage

Other safety outcome: Number of Participants with Major hemorrhage other than intracranial hemorrhage (NCT00991029)
Timeframe: up to 90 days

Minor Hemorrhage

Other safety outcome:Number of Participants with Minor hemorrhage (NCT00991029)
Timeframe: up to 90 days

Myocardial Infarction

Secondary efficacy outcome: Number of participants with Myocardial infarction (NCT00991029)
Timeframe: Up to 90 days

Other Symptomatic Intracranial Hemorrhage

Other safety outcome: Number of participants with other symptomatic intracranial hemorrhage (NCT00991029)
Timeframe: up to 90 days

Symptomatic Intracerebral Hemorrhage

Other safety outcome: Number of participants with Symptomatic intracerebral hemorrhage (NCT00991029)
Timeframe: up to 90 days

Number of Subjects Reaching the Composite Endpoint of All-Cause Death, Nonfatal Myocardial Infarction (MI), or Nonfatal Stroke

The endpoint in this measure is a combination of all-cause death, nonfatal MI, or nonfatal stroke. Results are reported for the All ACS population. (NCT00097591)
Timeframe: Randomization up to 15 months

Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), Nonfatal Stroke, or Rehospitalization for Cardiac Ischemic Events

The endpoint in this measure is a combination of CV death, nonfatal MI, nonfatal stroke, or rehospitalization for cardiac ischemic events. Results are reported for the All ACS population. (NCT00097591)
Timeframe: Randomization up to 15 months

Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), or Nonfatal Stroke

The endpoint in this measure is a combination of CV death, nonfatal MI, or nonfatal stroke. Results are reported for the All ACS population for the 30 and 90 day periods. (NCT00097591)
Timeframe: Randomization to 30 days; randomization to 90 days

Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), or Nonfatal Stroke

The endpoint in this measure is a combination of CV death, nonfatal MI, or nonfatal stroke. The data is presented by the study population, which is represented as follows: 1) subjects who presented with unstable angina and non-ST-segment elevation myocardial infarction (UA/NSTEMI), 2) subjects who presented with ST segment elevation myocardial infarction (STEMI), and 3) all subjects with acute coronary syndromes (ACS) (i.e. all subjects with UA/NSTEMI or STEMI). (NCT00097591)
Timeframe: Randomization up to 15 months

Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), or Urgent Target Vessel Revascularization (UTVR)

The endpoint in this measure is a combination of CV death, nonfatal MI, or UTVR. Results are reported for the All ACS subject population for the 30 and 90 day periods. (NCT00097591)
Timeframe: Randomization to 30 days; randomization to 90 days

Number of Treated Subjects With Non-Coronary Artery Bypass Graft (CABG) Related Thrombolysis In Myocardial Infarction (TIMI) Study Group Major and Minor Bleeding Events

TIMI classification for major and minor bleeding in the subset of subjects who did not undergo a coronary artery bypass operation (CABG) were defined as follows: Major bleeding: any intracranial hemorrhage (ICH) OR any clinically overt bleeding (including bleeding evident on imaging studies) associated with a fall in hemoglobin (Hgb) of ≥5 grams/deciliter (gm/dL)from baseline. Minor Bleeding: any clinically overt bleeding associated with a fall in Hgb of ≥3 gm/dL but <5 gm/dL from baseline. Major bleeding events were further examined as events that were deemed life threatening and/or fatal. (NCT00097591)
Timeframe: First dose of study drug up to 15 months (while at risk)

Number of Participants With Healed Peptic Ulcer

Follow-up endoscopy was performed at the end of the 6th month (NCT02418312)
Timeframe: 6 months

Number of Participants With Ulcer Recurrence

Follow-up endoscopy was performed at the end of the 6th month (NCT02551744)
Timeframe: six month

Participants With Any Event From the Composite of All-cause Mortality, MI, and Stroke

Participants with death from any cause, MI, or stroke. If no event, censoring occurs at the earliest of patient withdrawal of consent or date of scheduled withdrawal from therapy. ITT analysis of whole population. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: Randomization up to 12 months

Participants With Any Event From the Composite of Death From Vascular Causes, MI (Including Silent), Stroke, Recurrent Ischemia, Transient Ischemic Attack (TIA) and Other Arterial Thrombotic Events.

Participants with death from vascular causes, MI, stroke, recurrent ischemia, or other thrombotic events. If no event, censoring occurs at the earliest of patient withdrawal consent or date of scheduled withdrawal from therapy. ITT analysis of whole population. Events were adjudicated. (NCT00391872)
Timeframe: Randomization up to 12 months

Participants With Any Event From the Composite of Death From Vascular Causes, MI, and Stroke for the Subgroup of Patients With Intent for Invasive Management at Randomization

Participants with death from vascular causes, MI, or stroke. If no event, censoring occurs at the earliest of patient withdrawal consent or date of scheduled withdrawal from therapy. ITT analysis of intent for invasive management population. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: Randomization up to 12 months

Participants With Any Event From the Composite of Death From Vascular Causes, Myocardial Infarction (MI), and Stroke

Participants with death from vascular causes, MI, or stroke. If no event, censoring occurs at the earliest of patient withdrawal consent or date of scheduled withdrawal from therapy. Intention To Treat (ITT) analysis of whole population. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: Randomization up to 12 months

Participants With Any Major Bleeding Event

Participants with major (fatal/life-threatening or other) bleed by a study protocol scale based on need for treatment, number of transfusions, hemoglobin decrease, and other factors. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: First dosing up to 12 months

Participants With Coronary Artery Bypass Graft (CABG) Major Bleeding

Participants with a major CABG-related bleed by a study protocol scale based on need for treatment, number of transfusions, hemoglobin decrease, and other factors. All CABG surgeries were submitted for adjudication by an endpoint committee as potential bleeds. (NCT00391872)
Timeframe: First dosing up to 12 months

Participants With Coronary Artery Bypass Graft (CABG) Major Fatal/Life-threatening Bleeding

Number of participants with a major fatal/life-threatening CABG-related bleed by a study protocol scale based on need for treatment, number of transfusions, hemoglobin decrease, and other factors. All CABG surgeries were submitted for adjudication by an endpoint committee as potential bleeds. (NCT00391872)
Timeframe: First dosing up to 12 months

Participants With Death From Any Cause

Participants with death from any cause. If no event, censoring occurs at the earliest of patient withdrawal consent or date of scheduled withdrawal from therapy. ITT (intention to treat) analysis of whole population. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: Randomization up to 12 months

Participants With Death From Vascular Causes

Participants with death from vascular causes. If no event, censoring occurs at the earliest of patient withdrawal consent or date of scheduled withdrawal from therapy. ITT (intention to treat) analysis of whole population. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: Randomization up to 12 months

Participants With Major or Minor Bleeding

Participants with major (fatal/life-threatening or other) or minor bleed by a study protocol scale based on need for treatment, number of transfusions, hemoglobin decrease, and other factors. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: First dosing up to 12 months

Participants With MI Event

Participants with MI event. If no event, censoring occurs at the earliest of patient withdrawal consent or date of scheduled withdrawal from therapy. ITT (intention to treat) analysis of whole population. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: Randomization up to 12 months

Participants With Non-CABG (Coronary Artery Bypass Graft) Related Major Bleeding

Participants with non CABG related major (fatal/life-threatening or other) bleed by a study protocol scale based on need for treatment, number of transfusions, hemoglobin decrease, and other factors. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: First dosing up to 12 months

Participants With Non-procedural Major Bleeding

Participants with non-procedural major bleed by a study protocol scale based on need for treatment, number of transfusions, hemoglobin decrease, and other factors. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: First dosing up to 12 months

Participants With Stroke

Participants with stroke. If no event, censoring occurs at the earliest of patient withdrawal consent or date of scheduled withdrawal from therapy. ITT (intention to treat) analysis of whole population. Events were adjudicated by an endpoint committee. (NCT00391872)
Timeframe: Randomization up to 12 months

Participants With Ventricular Pauses of Greater Than or Equal to 3 Seconds in Patients Monitored by Holter 24 Hour ECG Recorders for 1 Week at 1 Month Following Randomization

Number of participants who were observed to have at least 1 ventricular pause of at least 3 seconds. Population is all patients who were observed over 2 week-long periods. Pauses were flagged algorithmically and confirmed by TIMI cardiologists. (NCT00391872)
Timeframe: 1-week period following randomization

Participants With Ventricular Pauses of Greater Than or Equal to 3 Seconds in Patients Monitored by Holter 24-hour ECG Recorders for 1 Week Following Randomization

Number of participants who were observed to have at least 1 ventricular pause of at least 3 seconds. Population is all patients who were observed over 2 week-long periods. Pauses were flagged algorithmically and confirmed by Thrombolysis in Myocardial Infarction (TIMI) group cardiologists. (NCT00391872)
Timeframe: 1-week period following randomization

First Occurrence of CV Death / MI / Stroke - Interaction Clopidogrel Treatment Regimen and ASA Dose Level

First Occurrence of CV Death / MI / Stroke - ASA Dose Comparison

First Occurrence of CV Death / MI / Stroke - Clopidogrel Treatment Regimen Comparison

"The primary endpoint is the first occurrence of any of the following events:~Cardiovascular death (any death with a clear cardiovascular or unknown cause),~Myocardial Infarction (diagnosis of new Myocardial Infarction (MI) - nonfatal or fatal)~Stroke (presence of a new focal neurologic deficit thought to be vascular in origin, with signs or symptoms lasting more than 24 hours - nonfatal or fatal)~reported between the randomization and Day 30 (inclusive), and validated by the blinded Event Adjudication Committee (EAC)." (NCT00335452)
Timeframe: 30 days

First Occurrence of CV Death / MI / Stroke - Clopidogrel Treatment Regimen Comparison in PCI Subgroup

Occurrence of Major Bleeding - ASA Dose Level Comparison

Occurrence of Major Bleeding - Clopidogrel Dose Regimen Comparison

Major bleeding is defined as any severe bleeding (associated with any of the following: death, leading to a drop in hemoglobin ≥ 5 g/dl, significant hypotension with the need for inotropic agents, symptomatic intracranial hemorrhage, requirement for surgery or for a transfusion ≥ 4 units of red blood cells or equivalent whole blood) and other major bleeding (significantly disabling bleeding, or intraocular bleeding leading to significant loss of vision or bleeding requiring transfusion of 2-3 units of red blood cells or equivalent whole blood) after validation by the independent EAC. (NCT00335452)
Timeframe: 30 days

Occurrence of Stent Thrombosis - Clopidogrel Treatment Regimen Comparison

This includes definite stent thrombosis (confirmed by angiography or evidence of recent thrombus determined at autopsy or by examination of tissue retrieved following thrombectomy) and probable stent thrombosis (unexplained death having occurred after intracoronary stenting or, MI related to acute ischemia in the territory of the implanted stent without angiographic confirmation and in the absence of any obvious cause) after validation by the EAC. (NCT00335452)
Timeframe: 30 days

Any Bleeding Event

"Bleeding classified by the TIMI hemorrhage classification scheme:~Minor: any clinically overt sign of hemorrhage (including imaging) that is associated with a hemoglobin drop of 3 to < 5 g/dL~Major: (1) if it is intracranial, or (2) clinically significant overt signs of hemorrhage associated with a drop inhemoglobin of > 5 g/dL" (NCT01515345)
Timeframe: 30days

Definite Stent Thrombosis

"The angiographic or pathological confirmation of stent thrombosis is called definite stent thrombosis" (NCT01515345)
Timeframe: 30 days

Probable Stent Thrombosis

"Probable stent thrombosis is considered to have occurred in case of~any unexplained death within the first 30 days.~any MI that is related to documented acute ischemia in the territory of the implanted stent without angiographic confirmation of stent thrombosis and in the absence of any other obvious cause, irrespective of the time after the index procedure" (NCT01515345)
Timeframe: 30days

Changes in Platelet Function in Response to Clopidogrel

Baseline minus post clopidogrel/pre-aspirin platelet rich plasma (PRP) maximum aggregation. (NCT00799396)
Timeframe: Measured at baseline, and after clopidogrel treatment

Changes in Platelet Function in Response to Clopidogrel Plus Aspirin

Baseline minus post clopidogrel/post-aspirin platelet rich plasma (PRP) maximum aggregation (NCT00799396)
Timeframe: Measured at baseline, and after clopidogrel plus aspirin treatment

Comparisons of Vasodilator-stimulated Phosphoprotein (VASP) Phosphorylation Platelet Reactivity Index (PRI)

The outcome measurement was on-treatment PRI determined through flow cytometric assessment of phosphorylation status of VASP. (NCT01235351)
Timeframe: Approximately every 2 weeks for 8 weeks

Comparisons of Vasodilator-stimulated Phosphoprotein (VASP) Phosphorylation Platelet Reactivity Index (PRI)

The outcome measurement was on-treatment PRI determined through flow cytometric assessment of phosphorylation status of VASP. (NCT01235351)
Timeframe: Approximately every 2 weeks for 8 weeks

Percentage of Participants With a Composite Endpoint of All-cause Death, MI, or Stroke

The percentage of participants is the total number of participants experiencing an all-cause death, nonfatal MI, or nonfatal stroke divided by number of participants in the treatment arm. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

Percentage of Participants With a Composite Endpoint of Cardiovascular (CV) Death, Myocardial Infarction (MI), or Stroke

The percentage of participants is the total number of participants experiencing a CV death, nonfatal MI, or nonfatal stroke divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

Percentage of Participants With a Composite Endpoint of CV Death and MI

The percentage of participants is the total number of participants experiencing a CV death or nonfatal MI divided by number of participants in the treatment arm. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

Percentage of Participants With a Composite Endpoint of CV Death, MI, Stroke, or Re-hospitalization for Recurrent Unstable Angina (UA)

The percentage of participants is the total number of participants experiencing a CV death, nonfatal MI, nonfatal stroke or re-hospitalization for a recurrent UA divided by number of participants in the treatment arm. Endpoints events were adjudicated by the Clinical Endpoint Committee. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

Biomarker Measurements of Inflammation/Hemodynamic Stress: Brain Natriuretic Peptide (BNP)

Brain natriuretic peptide (BNP) is secreted by the ventricles of the heart in response to hemodynamic stress and is a biomarker associated with increased CV risk. Results are presented as geometric least squares means (Geometric LS means). Geometric LS means were adjusted for treatment + baseline value + clopidogrel status at randomization. (NCT00699998)
Timeframe: Day 30 and 6 Months

Biomarker Measurements of Inflammation/Hemodynamic Stress: C-Reactive Protein (CRP)

C-Reactive Protein (CRP) is a biomarker associated with inflammation and increased CV risk. Results are presented as geometric least squares means (Geometric LS means). Geometric LS means were adjusted for treatment + baseline value + clopidogrel status at randomization. (NCT00699998)
Timeframe: Day 30 and Month 6

Economic and Quality of Life Outcomes

Seattle Angina Questionnaire (SAQ) is a validated, disease-specific questionnaire containing 11 questions (Q) yielding 5 summary scales related to angina: physical limitations, angina stability, angina frequency, treatment satisfaction and disease perception. In this study only angina frequency and the physical limitations scales were assessed. Anginal Frequency was assessed using Q3 and Q4 which consists of a Likert scale ranging from 1 to 6 (higher values equals better quality of life) to assess how often a patient is having symptoms now. Physical limitations was assessed using Q1 which contains 9 items each assessed via Likert scale ranging from 1 to 6 (higher values equals better quality of life) to assess how much a participant's condition is hampering their ability to do what they want to do. Scale scores are transformed to a 0-100 by subtracting the lowest possible score, dividing by the range of the scale, and multiplying by 100. Higher values equal better quality of life. (NCT00699998)
Timeframe: Baseline and follow-up (24 months)

Genotyping Related to Drug Metabolism

Variation in the genes encoding the cytochrome P450 (CYP) enzymes (CYP2C19) can reduce the ability to metabolize clopidogrel and a reduced platelet response and have been associated with increased rates of CV events including CV death. Participants were classified as extensive metabolizers (EM); reduced metabolizers (RM); or unknown (UNK) metabolizers based on their CYP2C19 genotype. Possible extensive metabolizer (EM) phenotypes include EM=extensive metabolizer, UM=ultra-rapid metabolizer, and EM (non-UM) that are not UM. Possible reduced metabolizer (RM) phenotypes include IM=intermediate metabolizer and PM=poor metabolizer. Genotypes associated with each predicted phenotype are presented; predicted phenotype is presented first followed by the genotype. Percentage=(number of participants with the predicted phenotype and genotype divided by the total number of participants per arm) multiplied by 100. (NCT00699998)
Timeframe: Baseline

Platelet Aggregation Measures

Platelet aggregation was measured by as measured by Accumetrics Verify Now™ P2Y12. Results were reported in P2Y12 Reaction Units (PRU). PRU represents the rate and extent of adenosine (ADP)-stimulated platelet aggregation. Lower values indicate greater P2Y12 platelet inhibition and lower platelet activity and aggregation. ANCOVA Model was used and values were corrected for treatment + baseline value + clopidogrel status at randomization. (NCT00699998)
Timeframe: Day 30 and 12 Months

Summary of All Deaths

All deaths, regardless of possible relatedness, with the exception of 1 event, were adjudicated by the Clinical Endpoint Committee (CEC) and are reported in this table. The 1 event which was not adjudicated was a result of the revocation of consent by the participant prior to their death. Deaths possibly related to study drug in the opinion of the investigator are also contained in the Serious Adverse Event (SAE) module. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

Pharmacodynamic Parameter Maximum Platelet Aggregation (MPA) From Aggregometry (Turbidimetric) With 5 µM Adenosine Diphosphate.

Maximum platelet aggregation (MPA) from aggregometry (turbidimetric) with 5 µM adenosine diphosphate. (NCT00942175)
Timeframe: 24-hour post Day 9 dose in each period.

Pharmacodynamic Parameter MPA From Aggregometry (Turbidimetric) With 20 µM Adenosine Diphosphate.

MPA from aggregometry (turbidimetric) with 20 µM adenosine diphosphate. (NCT00942175)
Timeframe: 24-hour post Day 9 dose in each period.

Pharmacodynamic Parameter Platelet Reactivity Index (PRI) From Vasodilator-stimulated Phosphoprotein (VASP) Phosphorylation State (Flow Cytometry).

PRI is the platelet reactivity index from VASP phosphorylation state (flow cytometry). (NCT00942175)
Timeframe: 24-hour post Day 9 dose in each period.

Pharmacokinetic Parameter Area Under the Plasma Concentration Versus Time Curve (AUC) From Time 0 to Time of the Last Quantifiable Concentration (AUC[0-tlqc]) of Clopidogrel's Active Metabolite.

Area under the plasma concentration versus time curve (AUC(0-tlqc)) is a measure of total plasma exposure to the drug from Time 0 to Time of the Last Quantifiable Concentration (AUC[0-tlqc]). (NCT00942175)
Timeframe: Day 9 of each period

Pharmacokinetic Parameter Peak Plasma Concentration (Cmax) of Clopidogrel's Active Metabolite.

Maximum observed plasma concentration (Cmax) is the peak plasma concentration of a drug after administration, obtained directly from the plasma concentration-time curve. (NCT00942175)
Timeframe: Day 9 of each period

Number of Participants With BARC Type 2, 3, or 5

Number of participants with first occurrence of clinically relevant bleeding episode, defined as Bleeding Academic Research Consortium (BARC) Types 2, 3 or 5 bleeding. BARC bleeding types range from 0 (no bleeding) to 5 (fatal bleeding). (NCT02270242)
Timeframe: 12 months after randomization

Number of Participants With Ischemic Episode

Number of participants with first occurrence of confirmed all-cause death, non-fatal myocardial infarction or stroke. (NCT02270242)
Timeframe: 12 months after randomization

Number of Participants Who Were Responders or Low-Responders of Antiplatelet Therapy as a Result of Whole Blood Aggregometry Testing (See Outcome Measure Description)

"In patients treated with aspirin and clopidogrel aggregometry was performed and depending on the results the patients were either responder or low-responder of antiplatelet therapy.~The following definitions were used for clopidogrel low response (CLR: >5 ohm when stimulated with adenosine diphosphate (ADP) 5 μM) and ASA low response (ALR: >0 ohm;stimulated with arachidonic acid 10 μM) with the ChronoLog 590 aggregometer. In the case of low-response alternative antiplatelet therapy was modified according to the study plan (see protocol section)." (NCT01212302)
Timeframe: 2 years

Intervention	Change in ABI/TBI (Mean)
	ABI - 6 months N = 6184(Tica), 6319(Clopi)	ABI - End of treatment N = 4951(Tica), 5073(Clopi)	TBI - 6 months N = 55(Tica), 48(Clopi)	TBI - End of treatment N = 36(Tica), 21(Clopi)
Clopidogrel 75 mg od	0.011	0.016	0.036	-0.065
Ticagrelor 90 mg bd	0.016	0.022	0.050	0.059

Intervention	Participant (Number)
	Stage I - End of treatment	Stage IIa - End of treatment	Stage IIb - End of treatment	Stage III - End of treatment	Stage IV - End of treatment	Missing - End of treatment
Clopidogrel - Stage I	743	230	56	9	4	250
Clopidogrel - Stage IIa	723	1956	311	15	7	724
Clopidogrel - Stage IIb	198	557	450	23	10	370
Clopidogrel - Stage III	33	33	38	23	5	60
Clopidogrel - Stage IV	19	21	15	12	13	45
Ticagrelor - Stage I	775	227	45	7	7	248
Ticagrelor - Stage IIa	683	1948	269	24	7	743
Ticagrelor - Stage IIb	171	560	469	12	5	403
Ticagrelor - Stage III	15	41	39	31	1	59
Ticagrelor - Stage IV	26	28	19	7	13	47

Intervention	Participant (Number)
	Category 0 - End of treatment	Category 1/2 - End of treatment	Category 3 - End of treatment	Category 4 - End of treatment	Category 5 - End of treatment	Category 6 - End of treatment	Missing - End of treatment
Clopidogrel - Cat 0	743	230	56	9	2	2	250
Clopidogrel - Cat 1/2	723	1956	311	15	6	1	724
Clopidogrel - Cat 3	198	557	450	23	6	4	370
Clopidogrel - Cat 4	33	33	38	23	4	1	60
Clopidogrel - Cat 5	13	18	12	11	12	0	34
Clopidogrel - Cat 6	6	3	3	1	1	0	11
Ticagrelor - Cat 0	775	227	45	7	5	2	248
Ticagrelor - Cat 3	171	560	469	12	3	2	403
Ticagrelor - Cat 4	15	41	39	31	1	0	59
Ticagrelor - Cat 5	23	23	13	4	11	0	33
Ticagrelor - Cat 6	3	5	6	3	0	2	14
Ticagrelor - Stage II	683	1948	269	24	4	3	743

Intervention	Participants (Number)
	All ACS (Through 30 days)	All ACS (Through 90 days)
Clopidogrel	502	573
Prasugrel	389	462

Intervention	Participants (Number)
	UA/NSTEMI (n=5044, n=5030)	STEMI (n=1769, n=1765)	All ACS (n=6813, n=6795)
Clopidogrel	565	216	781
Prasugrel	469	174	643

Intervention	Participants (Number)
	TIMI Major or Minor Bleeding	TIMI Major Bleeding	TIMI Major Bleeding - Life-threatening (LT)	LT - Fatal	LT - Symptomatic intracranial hemorrage (ICH)	LT - Requiring inotropes	LT - Requiring surgical intervention	LT - Requiring transfusion (>=4 units)	TIMI Minor Bleeding
Clopidogrel	231	111	56	5	17	8	19	30	125
Prasugrel	303	146	85	21	19	21	19	45	164

Intervention	participants (Number)
Proton Pump Inhibitor Group	1
Histamine-2 Receptor Antagonist Group	7

Intervention	participants (Number)
Clopidogrel 300/75/75 mg + ASA Low Dose	267
Clopidogrel 300/75/75 mg + ASA High Dose	290
Clopidogrel 600/150/75 mg + ASA Low Dose	282
Clopidogrel 600/150/75 mg + ASA High Dose	240

Intervention	participants (Number)
	CV death/MI/Stroke	- CV death	- MI (fatal or not)	- Stroke (fatal or not)
Clopidogrel + ASA High Dose	527	211	251	65
Clopidogrel + ASA Low Dose	546	231	260	55

Intervention	participants (Number)
	Major bleeding	- Severe bleeding	- Major but not severe bleeding
Clopidogrel + ASA High Dose	282	216	73
Clopidogrel + ASA Low Dose	285	215	74

Intervention	participants (Number)
	Stent trombosis	- Definite	- Probable
Clopidogrel 300/75/75 mg + ASA	200	111	89
Clopidogrel 600/150/75 mg + ASA	135	58	77

Intervention	% of PRI (Mean)
	Clopidogrel 75 mg	Clopidogrel 150 mg
CYP2C19*2 Non-Carriers	57.5	46.9

Intervention	% of PRI (Mean)
	Clopidogrel 75 mg	Clopidogrel 150 mg	Clopidogrel 225 mg	Clopidogrel 300 mg
CYP2C19*2 Carriers	71.0	62.4	54.0	50.1

Intervention	percentage of participants with an event (Number)
Prasugrel: <75 Years of Age	10.61
Prasugrel: 75 Years of Age or Older	27.04
Clopidogrel: <75 Years of Age	11.12
Clopidogrel: 75 Years of Age or Older	26.83

Intervention	percentage of participants with an event (Number)
Prasugrel: <75 Years of Age	10.06
Prasugrel: 75 Years of Age or Older	24.64
Clopidogrel: <75 Years of Age	10.96
Clopidogrel: 75 Years of Age or Older	24.13

Intervention	percentage of participants with an event (Number)
Prasugrel: <75 Years of Age	9.61
Prasugrel: 75 Years of Age or Older	22.53
Clopidogrel: <75 Years of Age	10.21
Clopidogrel: 75 Years of Age or Older	22.69

Intervention	percentage of participants with an event (Number)
Prasugrel: <75 Years of Age	12.13
Prasugrel: 75 Years of Age or Older	26.27
Clopidogrel: <75 Years of Age	12.83
Clopidogrel: 75 Years of Age or Older	25.67

Intervention	picograms per milliliter (pg/mL) (Geometric Mean)
	Day 30	6 Months (n=725, 125, 701, 174)
Clopidogrel: <75 Years of Age	319.345	250.982
Clopidogrel: 75 Years of Age or Older	951.359	722.750
Prasugrel: <75 Years of Age	313.494	253.434
Prasugrel: 75 Years of Age or Older	1082.396	770.132

Intervention	milligrams per liter (mg/L) (Geometric Mean)
	Day 30	6 Months (n=755, 143, 745, 178)
Clopidogrel: <75 Years of Age	2.287	2.149
Clopidogrel: 75 Years of Age or Older	2.226	1.543
Prasugrel: <75 Years of Age	2.330	2.272
Prasugrel: 75 Years of Age or Older	2.441	1.593

Intervention	units on a scale (Mean)
	Baseline, physical limitations	Baseline, angina frequency	24 Months, physical limitations (n=420, 412)	24 Months, angina frequency (n=420, 412)
Clopidogrel	67.0	73.1	74.5	89.5
Prasugrel	67.8	73.6	75.1	89.7

Intervention	percentage participants with geneotype (Number)
	UM, 1/17	UM, 17/17	EM (non-UM), 1/1	IM, 1/2	IM, 1/3	IM, 1/4	IM, 1/6	IM, 1/8	PM, 2/2	PM, 2/3	PM, 2/4	PM, 2/6	PM, 2/8	PM, 3/3	UNK, 1/10	UNK, 1/13	UNK, 1/9	UNK, 1/9, 9/17	UNK, 13/17	UNK, 2/13	UNK, 2/17	UNK, 2/9	UNK, 3/17	UNK, 4/17	UNK, 4/9	UNK, 6/17	UNK, 8/17	UNK, 9/17	UNK, Undefined genotype
Clopidogrel: <75 Years of Age	25.1	5.4	35.7	19.8	0.5	0.1	0.0	0.4	4.3	0.3	0.2	0.0	0.0	0.2	0.1	0.0	0.0	0.0	0.0	0.0	6.8	0.1	0.0	0.2	0.0	0.0	0.1	0.0	0.5
Clopidogrel: 75 Years of Age or Older	21.8	4.3	41.2	19.7	0.6	0.3	0.2	0.3	3.8	0.3	0.2	0.0	0.0	0.0	0.0	0.0	0.0	0.0	0.0	0.0	6.2	0.0	0.3	0.0	0.0	0.2	0.0	0.0	0.6
Prasugrel: <75 Years of Age	24.0	5.1	38.8	18.6	0.8	0.4	0.0	0.1	3.9	0.3	0.0	0.0	0.0	0.0	0.0	0.0	0.1	0.0	0.0	0.0	6.3	0.0	0.1	0.2	0.0	0.0	0.2	0.0	0.7
Prasugrel: 75 Years of Age or Older	25.0	3.6	42.1	18.3	0.6	0.0	0.2	0.5	2.2	0.2	0.2	0.0	0.0	0.0	0.0	0.2	0.2	0.0	0.0	0.0	6.1	0.0	0.0	0.2	0.0	0.0	0.0	0.0	0.6

Intervention	P2Y12 Reaction Units (PRU) (Least Squares Mean)
	Day 30	Month 12 (n=386, 76, 400, 103)
Clopidogrel: <75 Years of Age	193.489	199.003
Clopidogrel: 75 Years of Age or Older	200.285	181.360
Prasugrel: <75 Years of Age	93.280	94.529
Prasugrel: 75 Years of Age or Older	151.872	135.096

Intervention	participants (Number)
	Congestive Heart Failure	Cardiogenic Shock	Cardiac Rupture	Myocardial Infarction	Dysrhythmia	Stent Thrombosis	Directly Related to Revascularization-CABG or PCI	Intracranial Hemorrhage	Non-Hemorrhagic Stroke	Sudden death due to cardiovascular event	Pulmonary Embolism	Stroke, unknown type	Other Cardiovascular Event	Cardiovascular event, unknown type	Accidental	Trauma	Hemorrhage, not intracranial	Infection	Malignancy	Suicide	Other Non-Cardiovascular event	Cause unknown (nonadjudicated event)
Clopidogrel: <75 Years of Age	13	10	0	24	6	0	1	4	4	70	2	0	0	45	1	0	0	16	14	0	8	0
Clopidogrel: 75 Years of Age or Older	23	9	0	21	3	0	1	1	3	43	1	0	1	45	1	1	4	17	11	0	6	0
Prasugrel: <75 Years of Age	10	8	0	16	5	0	1	2	4	75	0	0	6	40	1	2	1	14	14	1	8	0
Prasugrel: 75 Years of Age or Older	21	4	1	24	2	0	1	1	4	39	1	1	1	41	0	3	1	21	7	0	4	1

Intervention	percentage of MPA (Mean)
PPI Group 1: Regimen A	28.1
PPI Group 1: Regimen B	30.8
PPI Group 2: Regimen A	34.6
PPI Group 2: Regimen C	36.2
PPI Group 3: Regimen A	34.2
PPI Group 3: Regimen D	42.5
PPI Group 4: Regimen A	29.3
PPI Group 4: Regimen E	38.2

Intervention	percentage of MPA (Mean)
PPI Group 1: Regimen A	36.7
PPI Group 1: Regimen B	41.6
PPI Group 2: Regimen A	43.1
PPI Group 2: Regimen C	46.3
PPI Group 3: Regimen A	43.5
PPI Group 3: Regimen D	53.5
PPI Group 4: Regimen A	39.3
PPI Group 4: Regimen E	47.9

Intervention	percent inhibition (Mean)
PPI Group 1: Regimen A	42.3
PPI Group 1: Regimen B	46.4
PPI Group 2: Regimen A	41.3
PPI Group 2: Regimen C	43.0
PPI Group 3: Regimen A	47.9
PPI Group 3: Regimen D	59.1
PPI Group 4: Regimen A	46.5
PPI Group 4: Regimen E	58.0

Intervention	ng*hr/ML (Mean)
PPI Group 1: Regimen A	41.69
PPI Group 1: Regimen B	36.42
PPI Group 2: Regimen A	41.25
PPI Group 2: Regimen C	37.75
PPI Group 3: Regimen A	37.78
PPI Group 3: Regimen D	26.28
PPI Group 4: Regimen A	42.35
PPI Group 4: Regimen E	31.23

Intervention	ng/mL (Mean)
PPI Group 1: Regimen A	39.14
PPI Group 1: Regimen B	30.01
PPI Group 2: Regimen A	38.85
PPI Group 2: Regimen C	29.33
PPI Group 3: Regimen A	38.25
PPI Group 3: Regimen D	22.55
PPI Group 4: Regimen A	40.98
PPI Group 4: Regimen E	24.69