niacin and Apoplexy
niacin has been researched along with Apoplexy in 34 studies
Niacin: A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.
vitamin B3 : Any member of a group of vitamers that belong to the chemical structural class called pyridines that exhibit biological activity against vitamin B3 deficiency. Vitamin B3 deficiency causes a condition known as pellagra whose symptoms include depression, dermatitis and diarrhea. The vitamers include nicotinic acid and nicotinamide (and their ionized and salt forms).
nicotinic acid : A pyridinemonocarboxylic acid that is pyridine in which the hydrogen at position 3 is replaced by a carboxy group.
Research Excerpts
| Excerpt | Relevance | Reference |
|---|---|---|
| "In Atherothrombosis Intervention in Metabolic Syndrome with low HDL/High Triglycerides: Impact on Global Health Outcomes (AIM-HIGH) trial, addition of extended-release niacin (ERN) to simvastatin in participants with established cardiovascular disease, low high-density lipoprotein cholesterol, and high triglycerides had no incremental benefit, despite increases in high-density lipoprotein cholesterol." | 9.17 | Extended-release niacin therapy and risk of ischemic stroke in patients with cardiovascular disease: the Atherothrombosis Intervention in Metabolic Syndrome with low HDL/High Triglycerides: Impact on Global Health Outcome (AIM-HIGH) trial. ( Anderson, DC; Boden, WE; Chaitman, BR; Cruz-Flores, S; Goldstein, LB; Grant, S; Kostuk, WJ; Padley, RJ; Sila, CA; Teo, KK; Weintraub, WS, 2013) |
| " In our study, patients were randomized, on average, 6 days after an acute myocardial infarction and/or percutaneous transluminal coronary angioplasty secondary to unstable angina, to pravastatin (combined, when necessary, with cholestyramine and/or nicotinic acid) to achieve low-density lipoprotein cholesterol levels of < or =130 mg/dl (group A, n = 70)." | 9.09 | Beneficial effects of pravastatin (+/-colestyramine/niacin) initiated immediately after a coronary event (the randomized Lipid-Coronary Artery Disease [L-CAD] Study). ( Agrawal, R; Arntz, HR; Fischer, F; Schnitzer, L; Schultheiss, HP; Stern, R; Wunderlich, W, 2000) |
| "To examine the effects of combination with levamlodipine and bisoprolol on stroke in rats." | 7.79 | Effects of combination therapy with levamlodipine and bisoprolol on stroke in rats. ( Gui, H; Guo, YF; Huang, GZ; Liu, JG; Liu, X; Yang, YL; Zhang, JM, 2013) |
| "In this study we examined the effect of combination treatment of experimental stroke with Niaspan, a prolonged-release formulation of Niacin (vitamin B3), and Simvastatin, a cholesterol-lowering drug, on functional outcome, axonal damage, axonal density and the of Iba-1 immunoreactive microglia expression in the ischemic brain of rats." | 7.76 | Combination treatment of experimental stroke with Niaspan and Simvastatin, reduces axonal damage and improves functional outcome. ( Chen, J; Chopp, M; Cui, X; Lu, M; Roberts, C; Shehadah, A, 2010) |
| "Niacin treatment of stroke promotes synaptic plasticity and axon growth, which is mediated, at least partially, by the brain-derived neurotrophic factor/tropomyosin-related kinase B pathways." | 7.76 | Niacin treatment of stroke increases synaptic plasticity and axon growth in rats. ( Buller, B; Chen, J; Chopp, M; Cui, X; Ion, M; Roberts, C; Zacharek, A, 2010) |
| "Niacin is a safe and effective means of raising HDL, yet its role in stroke prevention is not well characterized." | 6.44 | Niacin for stroke prevention: evidence and rationale. ( Keener, A; Sanossian, N, 2008) |
| "In Atherothrombosis Intervention in Metabolic Syndrome with low HDL/High Triglycerides: Impact on Global Health Outcomes (AIM-HIGH) trial, addition of extended-release niacin (ERN) to simvastatin in participants with established cardiovascular disease, low high-density lipoprotein cholesterol, and high triglycerides had no incremental benefit, despite increases in high-density lipoprotein cholesterol." | 5.17 | Extended-release niacin therapy and risk of ischemic stroke in patients with cardiovascular disease: the Atherothrombosis Intervention in Metabolic Syndrome with low HDL/High Triglycerides: Impact on Global Health Outcome (AIM-HIGH) trial. ( Anderson, DC; Boden, WE; Chaitman, BR; Cruz-Flores, S; Goldstein, LB; Grant, S; Kostuk, WJ; Padley, RJ; Sila, CA; Teo, KK; Weintraub, WS, 2013) |
| " In our study, patients were randomized, on average, 6 days after an acute myocardial infarction and/or percutaneous transluminal coronary angioplasty secondary to unstable angina, to pravastatin (combined, when necessary, with cholestyramine and/or nicotinic acid) to achieve low-density lipoprotein cholesterol levels of < or =130 mg/dl (group A, n = 70)." | 5.09 | Beneficial effects of pravastatin (+/-colestyramine/niacin) initiated immediately after a coronary event (the randomized Lipid-Coronary Artery Disease [L-CAD] Study). ( Agrawal, R; Arntz, HR; Fischer, F; Schnitzer, L; Schultheiss, HP; Stern, R; Wunderlich, W, 2000) |
| "Moderate- to high-quality evidence suggests that niacin does not reduce mortality, cardiovascular mortality, non-cardiovascular mortality, the number of fatal or non-fatal myocardial infarctions, nor the number of fatal or non-fatal strokes but is associated with side effects." | 4.95 | Niacin for primary and secondary prevention of cardiovascular events. ( Arpagaus, A; Briel, M; Hemkens, LG; Nordmann, AJ; Olu, KK; Saccilotto, R; Schandelmaier, S, 2017) |
| "Therapeutic benefit of niacin, fibrates, and cholesteryl ester transfer protein (CETP) inhibitors on cardiovascular events (all cause mortality, coronary heart disease mortality, non-fatal myocardial infarction, and stroke)." | 4.90 | Effect on cardiovascular risk of high density lipoprotein targeted drug treatments niacin, fibrates, and CETP inhibitors: meta-analysis of randomised controlled trials including 117,411 patients. ( Francis, DP; Keene, D; Price, C; Shun-Shin, MJ, 2014) |
| "To examine the effects of combination with levamlodipine and bisoprolol on stroke in rats." | 3.79 | Effects of combination therapy with levamlodipine and bisoprolol on stroke in rats. ( Gui, H; Guo, YF; Huang, GZ; Liu, JG; Liu, X; Yang, YL; Zhang, JM, 2013) |
| "Niaspan, an extended-release formulation of niacin (vitamin B3), has been widely used to increase high density lipoprotein (HDL) cholesterol and to prevent cardiovascular diseases and stroke." | 3.77 | Combination treatment with low-dose Niaspan and tissue plasminogen activator provides neuroprotection after embolic stroke in rats. ( Chen, J; Chopp, M; Cui, Y; Lu, M; Roberts, C; Shehadah, A; Zhang, L, 2011) |
| "In this study we examined the effect of combination treatment of experimental stroke with Niaspan, a prolonged-release formulation of Niacin (vitamin B3), and Simvastatin, a cholesterol-lowering drug, on functional outcome, axonal damage, axonal density and the of Iba-1 immunoreactive microglia expression in the ischemic brain of rats." | 3.76 | Combination treatment of experimental stroke with Niaspan and Simvastatin, reduces axonal damage and improves functional outcome. ( Chen, J; Chopp, M; Cui, X; Lu, M; Roberts, C; Shehadah, A, 2010) |
| "Niaspan, an extended-release formulation of Niacin (vitamin B3), has been widely used to increase high density lipoprotein (HDL) cholesterol and to prevent cardiovascular diseases and stroke." | 3.76 | Niaspan treatment induces neuroprotection after stroke. ( Chen, J; Chopp, M; Cui, Y; Ion, M; Kapke, A; Roberts, C; Shehadah, A; Zacharek, A, 2010) |
| "Niacin treatment of stroke promotes synaptic plasticity and axon growth, which is mediated, at least partially, by the brain-derived neurotrophic factor/tropomyosin-related kinase B pathways." | 3.76 | Niacin treatment of stroke increases synaptic plasticity and axon growth in rats. ( Buller, B; Chen, J; Chopp, M; Cui, X; Ion, M; Roberts, C; Zacharek, A, 2010) |
| " In this study, we investigated whether the Niacin-mediated increase of HDL regulates angiogenesis and thereby improves functional outcome after stroke." | 3.74 | Niaspan increases angiogenesis and improves functional recovery after stroke. ( Chen, J; Chopp, M; Cui, X; Feldkamp, CS; Jiang, H; Kapke, A; Lu, M; Roberts, C; Zacharek, A; Zhang, C, 2007) |
| "Niacin has potentially favourable effects on lipids, but its effect on cardiovascular outcomes is uncertain." | 2.78 | HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment. ( , 2013) |
| "Niacin use was associated with a significant reduction in the composite endpoints of any CVD event (OR: 0." | 2.49 | The current state of niacin in cardiovascular disease prevention: a systematic review and meta-regression. ( Karas, RH; Lavigne, PM, 2013) |
| "Niacin is a safe and effective means of raising HDL, yet its role in stroke prevention is not well characterized." | 2.44 | Niacin for stroke prevention: evidence and rationale. ( Keener, A; Sanossian, N, 2008) |
| "Stroke is an uncommon disease in childhood with an estimated incidence of 1 to 6 per 100,000 and stenoocclusive arteriopathy is the main risk factor of recurrent pediatric arterial ischemic stroke (AIS)." | 1.46 | Elevated serum lipoprotein(a) as a risk factor for combined intracranial and extracranial artery stenosis in a child with arterial ischemic stroke: A case report. ( Han, JY; Kim, HJ; Lee, IG; Park, J; Shin, S, 2017) |
| "Combination treatment of stroke with BMSCs and Niaspan in T1DM rats increases white matter remodeling and additively increases BMSC monotherapy induced myelination and synaptic plasticity after stroke in T1DM rats." | 1.39 | Combination BMSC and Niaspan treatment of stroke enhances white matter remodeling and synaptic protein expression in diabetic rats. ( Chen, J; Chopp, M; Ning, R; Roberts, C; Venkat, P; Yan, T; Ye, X; Zacharek, A, 2013) |
| "Niaspan treatment of stroke increases vascular stabilization, decreases brain hemorrhage and blood-brain-barrier (BBB) leakage in T1DM rats." | 1.39 | Niaspan attenuates the adverse effects of bone marrow stromal cell treatment of stroke in type one diabetic rats. ( Chen, J; Chopp, M; Lu, M; Ning, R; Roberts, C; Venkat, P; Yan, T; Ye, X; Zacharek, A, 2013) |
| "Niaspan treatment of stroke in T1DM rats inhibits HMGB1/RAGE, TLR4 and MMP-9 expression which may contribute to the reduced inflammatory response after stroke in T1DM rats." | 1.37 | Niaspan reduces high-mobility group box 1/receptor for advanced glycation endproducts after stroke in type-1 diabetic rats. ( Chen, J; Chopp, M; Cui, X; Liu, X; Roberts, C; Yan, T; Ye, X; Zacharek, A, 2011) |
Research
Studies (34)
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 4 (11.76) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 9 (26.47) | 29.6817 |
| 2010's | 21 (61.76) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
Authors
| Authors | Studies |
|---|---|
| Schandelmaier, S | 1 |
| Briel, M | 1 |
| Saccilotto, R | 1 |
| Olu, KK | 1 |
| Arpagaus, A | 1 |
| Hemkens, LG | 1 |
| Nordmann, AJ | 1 |
| Han, JY | 1 |
| Kim, HJ | 1 |
| Shin, S | 1 |
| Park, J | 1 |
| Lee, IG | 1 |
| Ponce, OJ | 1 |
| Larrea-Mantilla, L | 1 |
| Hemmingsen, B | 1 |
| Serrano, V | 1 |
| Rodriguez-Gutierrez, R | 1 |
| Spencer-Bonilla, G | 1 |
| Alvarez-Villalobos, N | 1 |
| Benkhadra, K | 1 |
| Haddad, A | 1 |
| Gionfriddo, MR | 1 |
| Prokop, LJ | 1 |
| Brito, JP | 1 |
| Murad, MH | 1 |
| Gui, H | 1 |
| Guo, YF | 1 |
| Liu, X | 2 |
| Zhang, JM | 1 |
| Yang, YL | 1 |
| Huang, GZ | 1 |
| Liu, JG | 1 |
| Teo, KK | 1 |
| Goldstein, LB | 1 |
| Chaitman, BR | 1 |
| Grant, S | 1 |
| Weintraub, WS | 1 |
| Anderson, DC | 1 |
| Sila, CA | 1 |
| Cruz-Flores, S | 1 |
| Padley, RJ | 1 |
| Kostuk, WJ | 1 |
| Boden, WE | 1 |
| Ye, X | 3 |
| Yan, T | 3 |
| Chopp, M | 8 |
| Zacharek, A | 6 |
| Ning, R | 2 |
| Venkat, P | 2 |
| Roberts, C | 8 |
| Chen, J | 8 |
| Lu, M | 4 |
| Nuñez-Figueredo, Y | 1 |
| Ramírez-Sánchez, J | 1 |
| Delgado-Hernández, R | 1 |
| Porto-Verdecia, M | 1 |
| Ochoa-Rodríguez, E | 1 |
| Verdecia-Reyes, Y | 1 |
| Marin-Prida, J | 1 |
| González-Durruthy, M | 1 |
| Uyemura, SA | 1 |
| Rodrigues, FP | 1 |
| Curti, C | 1 |
| Souza, DO | 1 |
| Pardo-Andreu, GL | 1 |
| Rahman, M | 1 |
| Muhammad, S | 1 |
| Khan, MA | 1 |
| Chen, H | 1 |
| Ridder, DA | 1 |
| Müller-Fielitz, H | 1 |
| Pokorná, B | 1 |
| Vollbrandt, T | 1 |
| Stölting, I | 1 |
| Nadrowitz, R | 1 |
| Okun, JG | 1 |
| Offermanns, S | 2 |
| Schwaninger, M | 2 |
| Keene, D | 1 |
| Price, C | 1 |
| Shun-Shin, MJ | 1 |
| Francis, DP | 1 |
| Verdoia, M | 1 |
| Schaffer, A | 1 |
| Suryapranata, H | 1 |
| De Luca, G | 1 |
| Silverman, MG | 1 |
| Ference, BA | 1 |
| Im, K | 1 |
| Wiviott, SD | 1 |
| Giugliano, RP | 1 |
| Grundy, SM | 1 |
| Braunwald, E | 1 |
| Sabatine, MS | 1 |
| Robinson, JG | 1 |
| Keener, A | 1 |
| Sanossian, N | 1 |
| Bitzur, R | 1 |
| Cohen, H | 1 |
| Kamari, Y | 1 |
| Shaish, A | 1 |
| Harats, D | 1 |
| Shehadah, A | 3 |
| Cui, X | 4 |
| Cui, Y | 2 |
| Ion, M | 2 |
| Kapke, A | 2 |
| Buller, B | 1 |
| Zhang, L | 1 |
| Diep, F | 1 |
| Lavigne, PM | 1 |
| Karas, RH | 1 |
| HABENICHT, J | 1 |
| FRUHMANN, H | 1 |
| SCIAGRA, A | 1 |
| NUTI, A | 1 |
| MENTHA, J | 1 |
| STEPONAVICIUS, J | 1 |
| Mullard, AJ | 1 |
| Reeves, MJ | 1 |
| Jacobs, BS | 1 |
| Kothari, RU | 1 |
| Birbeck, GL | 1 |
| Maddox, K | 1 |
| Stoeckle-Roberts, S | 1 |
| Wehner, S | 1 |
| Jiang, H | 1 |
| Zhang, C | 1 |
| Feldkamp, CS | 1 |
| Arntz, HR | 1 |
| Agrawal, R | 1 |
| Wunderlich, W | 1 |
| Schnitzer, L | 1 |
| Stern, R | 1 |
| Fischer, F | 1 |
| Schultheiss, HP | 1 |
| Lee, BY | 1 |
| Thurmon, TF | 1 |
| Klungel, OH | 1 |
| Heckbert, SR | 1 |
| de Boer, A | 1 |
| Leufkens, HG | 1 |
| Sullivan, SD | 1 |
| Fishman, PA | 1 |
| Veenstra, DL | 1 |
| Psaty, BM | 1 |
Clinical Trials (6)
Trial Overview
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| AIM HIGH: Niacin Plus Statin to Prevent Vascular Events[NCT00120289] | Phase 3 | 3,414 participants (Actual) | Interventional | 2005-09-30 | Terminated (stopped due to AIM-HIGH was stopped on the recommendation of the DSMB because of lack of efficacy of niacin in preventing primary outcome events.) | ||
| A Pilot Study Evaluating a Ketogenic Diet Concomitant to Nivolumab and Ipilimumab in Patients With Metastatic Renal Cell Carcinoma[NCT05119010] | 60 participants (Anticipated) | Interventional | 2023-03-24 | Recruiting | |||
| A Randomized, Double-Blind, Parallel Group Study to Evaluate the Efficacy and Safety of Bempedoic Acid 180 Mg + Ezetimibe 10 Mg Fixed-Dose Combination Compared to Bempedoic Acid, Ezetimibe, and Placebo Alone in Patients Treated With Maximally Tolerated St[NCT03337308] | Phase 3 | 382 participants (Actual) | Interventional | 2017-10-23 | Completed | ||
| A Randomized Controlled Intervention Study to Assess the Effect of Bergamot Juice on LDL Cholesterol Level in Healthy Subjects[NCT05589636] | 44 participants (Anticipated) | Interventional | 2022-02-10 | Recruiting | |||
| Post-prandial Effects of Extra Virgin Olive Oil on Endothelial Function in Adults at Risk for Type 2 Diabetes: A Randomized Crossover Controlled Trial[NCT04025281] | 20 participants (Actual) | Interventional | 2019-07-09 | Completed | |||
| The Impact of Consumption of Eggs in the Context of Plant-Based Diets on[NCT04316429] | 35 participants (Actual) | Interventional | 2020-06-09 | Completed | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Trial Outcomes
Cardiovascular Mortality
(NCT00120289)
Timeframe: Time to first event measured from date of randomization through last follow-up visit (common termination), for an average of 36 months follow-up, maximum 66 months.
| Intervention | participants (Number) |
|---|---|
| ERN + Simvastatin | 45 |
| Placebo + Simvastatin | 38 |
Composite End Point of CHD Death, Nonfatal MI, Ischemic Stroke, Hospitalization for Non-ST Segment Elevation Acute Coronary Syndrome (ACS), or Symptom-driven Coronary or Cerebral Revascularization
(NCT00120289)
Timeframe: Time to first event measured from date of randomization through last follow-up visit (common termination) for an average of 36 months follow-up, maximum 66 months.
| Intervention | participants (Number) |
|---|---|
| ERN + Simvastatin | 282 |
| Placebo + Simvastatin | 274 |
Composite Endpoint of CHD Death, Non-fatal MI, High-risk ACS or Ischemic Stroke
(NCT00120289)
Timeframe: Time to first event measured from date of randomization through last follow-up visit (common termination) for an average of 36 months follow-up, maximum 66 months
| Intervention | participants (Number) |
|---|---|
| ERN + Simvastatin | 171 |
| Placebo + Simvastatin | 158 |
Composite Endpoint of CHD Death, Non-fatal MI, or Ischemic Stroke
(NCT00120289)
Timeframe: Time to first event measured from date of randomization through last follow-up visit (common termination) for an average of 36 months follow-up, maximum 66 months
| Intervention | participants (Number) |
|---|---|
| ERN + Simvastatin | 156 |
| Placebo + Simvastatin | 138 |
Percent Change From Baseline to Week 12 in Apolipoprotein B (Apo B)
Blood samples were drawn after a minimum 10-hour fast (water was allowed) at pre-specified intervals. Samples were collected and analyzed for apo B. Baseline was defined as the predose Day 1/Week 0 value. Percent change from baseline in apo B was analyzed using ANCOVA with treatment group and randomization stratification as a factors and baseline apo B as a covariate. Percent change from baseline was calculated as: ([apo B value at Week 12 minus Baseline value] divided by [Baseline Value]) multiplied by 100. (NCT03337308)
Timeframe: Baseline; Week 12
| Intervention | Percent change (Least Squares Mean) |
|---|---|
| Bempedoic Acid 180 mg + Ezetimibe 10 mg FDC | -24.6 |
| Bempedoic Acid 180 mg | -11.8 |
| Ezetimibe 10 mg | -15.3 |
| Placebo | 5.5 |
Percent Change From Baseline to Week 12 in High-density Lipoprotein Cholesterol (HDL-C)
Blood samples were drawn after a minimum 10-hour fast (water was allowed) at pre-specified intervals. Samples were collected and analyzed for HDL-C. Baseline was defined as the mean of the HDL-C values from Week -2 and predose Day 1/Week 0. Percent change from baseline was calculated as: ([HDL-C value at Week 12 minus Baseline value] divided by [Baseline Value]) multiplied by 100. (NCT03337308)
Timeframe: Baseline; Week 12
| Intervention | Percent change (Mean) |
|---|---|
| Bempedoic Acid 180 mg + Ezetimibe 10 mg FDC | -5.59 |
| Bempedoic Acid 180 mg | -5.40 |
| Ezetimibe 10 mg | -2.11 |
| Placebo | -0.54 |
Percent Change From Baseline to Week 12 in High-sensitivity C-reactive Protein (hsCRP)
Blood samples were drawn after a minimum 10-hour fast (water was allowed) at pre-specified intervals. Samples were collected and analyzed for hsCRP. Baseline was defined as the predose Day 1/Week 0 value. Percent change from baseline in hsCRP was analyzed using a non-parametric analysis. Percent change from baseline was calculated as: ([hsCRP value at Week 12 minus Baseline value] divided by [Baseline Value]) multiplied by 100. (NCT03337308)
Timeframe: Baseline; Week 12
| Intervention | Percent Change (Median) |
|---|---|
| Bempedoic Acid 180 mg + Ezetimibe 10 mg FDC | -35.1 |
| Bempedoic Acid 180 mg | -31.9 |
| Ezetimibe 10 mg | -8.2 |
| Placebo | 21.6 |
Percent Change From Baseline to Week 12 in Low-density Lipoprotein Cholesterol (LDL-C)
Blood samples were drawn after a minimum 10-hour fast (water was allowed) at pre-specified intervals. Samples were collected and analyzed for LDL-C. Baseline was defined as the mean of the LDL-C values from Week -2 and predose Day 1/Week 0. Percent change from baseline in LDL-C was analyzed using analysis of covariance (ANCOVA) with treatment group and randomization stratification as a factors and baseline LDL-C as a covariate. Percent change from baseline was calculated as: ([LDL-C value at Week 12 minus Baseline value] divided by [Baseline Value]) multiplied by 100. For LDL-C, if measured LDL-C value was available, measured LDL-C was used. (NCT03337308)
Timeframe: Baseline; Week 12
| Intervention | Percent Change (Least Squares Mean) |
|---|---|
| Bempedoic Acid 180 mg + Ezetimibe 10 mg FDC | -36.2 |
| Bempedoic Acid 180 mg | -17.2 |
| Ezetimibe 10 mg | -23.2 |
| Placebo | 1.8 |
Percent Change From Baseline to Week 12 in Non-high-density Lipoprotein Cholesterol (Non-HDL-C)
Blood samples were drawn after a minimum 10-hour fast (water was allowed) at pre-specified intervals. Samples were collected and analyzed for non-HDL-C. Baseline was defined as the mean of the non-HDL-C values from Week -2 and predose Day 1/Week 0. Percent change from baseline in non-HDL-C was analyzed using ANCOVA with treatment group and randomization stratification as a factors and baseline non-HDL-C as a covariate. Percent change from baseline was calculated as: ([non-HDL-C value at Week 12 minus Baseline value] divided by [Baseline Value]) multiplied by 100. (NCT03337308)
Timeframe: Baseline; Week 12
| Intervention | Percent change (Least Squares Mean) |
|---|---|
| Bempedoic Acid 180 mg + Ezetimibe 10 mg FDC | -31.9 |
| Bempedoic Acid 180 mg | -14.1 |
| Ezetimibe 10 mg | -19.9 |
| Placebo | 1.8 |
Percent Change From Baseline to Week 12 in Total Cholesterol (TC)
Blood samples were drawn after a minimum 10-hour fast (water was allowed) at pre-specified intervals. Samples were collected and analyzed for TC. Baseline was defined as the mean of the TC values from Week -2 and predose Day 1/Week 0. Percent change from baseline in TC was analyzed using ANCOVA with treatment group and randomization stratification as a factors and baseline TC as a covariate. Percent change from baseline was calculated as: ([TC value at Week 12 minus Baseline value] divided by [Baseline Value]) multiplied by 100. (NCT03337308)
Timeframe: Baseline; Week 12
| Intervention | Percent change (Least Squares Mean) |
|---|---|
| Bempedoic Acid 180 mg + Ezetimibe 10 mg FDC | -26.4 |
| Bempedoic Acid 180 mg | -12.1 |
| Ezetimibe 10 mg | -16.0 |
| Placebo | 0.7 |
Percent Change From Baseline to Week 12 in Triglycerides (TGs)
Blood samples were drawn after a minimum 10-hour fast (water was allowed) at pre-specified intervals. Samples were collected and analyzed for TGs. Baseline was defined as the mean of the TGs values from Week -2 and predose Day 1/Week 0. Percent change from baseline was calculated as: ([TGs value at Week 12 minus Baseline value] divided by [Baseline Value]) multiplied by 100. (NCT03337308)
Timeframe: Baseline; Week 12
| Intervention | Percent change (Mean) |
|---|---|
| Bempedoic Acid 180 mg + Ezetimibe 10 mg FDC | -7.90 |
| Bempedoic Acid 180 mg | 7.94 |
| Ezetimibe 10 mg | -2.46 |
| Placebo | 5.47 |
Reviews
11 reviews available for niacin and Apoplexy
| Article | Year |
|---|---|
Niacin for primary and secondary prevention of cardiovascular events.
Topics: Adult; Aged; Cardiovascular Diseases; Humans; Middle Aged; Myocardial Infarction; Niacin; Primary Pr | 2017 |
Lipid-Lowering Agents in Older Individuals: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.
Topics: Aged; Aged, 80 and over; Cardiovascular Diseases; Coronary Artery Disease; Diabetes Mellitus; Fibric | 2019 |
Effect on cardiovascular risk of high density lipoprotein targeted drug treatments niacin, fibrates, and CETP inhibitors: meta-analysis of randomised controlled trials including 117,411 patients.
Topics: Amides; Anticholesteremic Agents; Cholesterol Ester Transfer Proteins; Coronary Disease; Esters; Fib | 2014 |
Effects of HDL-modifiers on cardiovascular outcomes: a meta-analysis of randomized trials.
Topics: Anticholesteremic Agents; Cardiovascular Diseases; Cholesterol Ester Transfer Proteins; Diabetes Mel | 2015 |
Nutritional or pharmacological activation of HCA(2) ameliorates neuroinflammation.
Topics: 3-Hydroxybutyric Acid; Adenylyl Cyclases; Animals; Brain; Brain Ischemia; Diet, Ketogenic; Dimethyl | 2015 |
Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions: A Systematic Review and Meta-analysis.
Topics: Cardiovascular Diseases; Cholesterol, LDL; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhib | 2016 |
Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions: A Systematic Review and Meta-analysis.
Topics: Cardiovascular Diseases; Cholesterol, LDL; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhib | 2016 |
Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions: A Systematic Review and Meta-analysis.
Topics: Cardiovascular Diseases; Cholesterol, LDL; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhib | 2016 |
Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions: A Systematic Review and Meta-analysis.
Topics: Cardiovascular Diseases; Cholesterol, LDL; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhib | 2016 |
LDL reduction: how low should we go and is it safe?
Topics: Allylamine; Anticholesteremic Agents; Azetidines; Cholesterol, LDL; Colesevelam Hydrochloride; Coron | 2008 |
Niacin for stroke prevention: evidence and rationale.
Topics: Carotid Artery Diseases; Cholesterol, HDL; Cholesterol, LDL; Clinical Trials as Topic; Humans; Niaci | 2008 |
Triglycerides and HDL cholesterol: stars or second leads in diabetes?
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Coronary Disease; Diabetes Complications | 2009 |
Triglycerides and HDL cholesterol: stars or second leads in diabetes?
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Coronary Disease; Diabetes Complications | 2009 |
Triglycerides and HDL cholesterol: stars or second leads in diabetes?
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Coronary Disease; Diabetes Complications | 2009 |
Triglycerides and HDL cholesterol: stars or second leads in diabetes?
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Coronary Disease; Diabetes Complications | 2009 |
The current state of niacin in cardiovascular disease prevention: a systematic review and meta-regression.
Topics: Cardiovascular Diseases; Cholesterol, HDL; Humans; Hypolipidemic Agents; Incidence; Niacin; Randomiz | 2013 |
Raising HDL cholesterol: a worthwhile goal?
Topics: Cholesterol, HDL; Drug Combinations; Estrogen Replacement Therapy; Exercise; Guidelines as Topic; He | 2002 |
Trials
3 trials available for niacin and Apoplexy
Other Studies
20 other studies available for niacin and Apoplexy
| Article | Year |
|---|---|
Elevated serum lipoprotein(a) as a risk factor for combined intracranial and extracranial artery stenosis in a child with arterial ischemic stroke: A case report.
Topics: Child; Dyslipidemias; Humans; Intracranial Arteriosclerosis; Lipoprotein(a); Male; Niacin; Risk Fact | 2017 |
Effects of combination therapy with levamlodipine and bisoprolol on stroke in rats.
Topics: Animals; Antihypertensive Agents; Baroreflex; Bisoprolol; Drug Therapy, Combination; Heart Rate; Mal | 2013 |
Combination BMSC and Niaspan treatment of stroke enhances white matter remodeling and synaptic protein expression in diabetic rats.
Topics: Animals; Brain; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Lipoproteins, HDL; Mesen | 2013 |
Niaspan attenuates the adverse effects of bone marrow stromal cell treatment of stroke in type one diabetic rats.
Topics: Animals; Blood-Brain Barrier; Diabetes Mellitus, Type 1; Disease Models, Animal; Ectodysplasins; Int | 2013 |
JM-20, a novel benzodiazepine–dihydropyridine hybrid molecule, protects mitochondria and prevents ischemic insult-mediated neural cell death in vitro.
Topics: Animals; Benzodiazepines; Brain Ischemia; Calcium; Cell Death; Cerebellum; Cytochromes c; Dihydropyr | 2014 |
The β-hydroxybutyrate receptor HCA2 activates a neuroprotective subset of macrophages.
Topics: 3-Hydroxybutyric Acid; Animals; Brain; Diet, Ketogenic; Macrophages; Mice; Mice, Knockout; Monocytes | 2014 |
Combination treatment of experimental stroke with Niaspan and Simvastatin, reduces axonal damage and improves functional outcome.
Topics: Amyloid beta-Protein Precursor; Animals; Axons; Brain; Brain Ischemia; Calcium-Binding Proteins; Del | 2010 |
Niaspan treatment induces neuroprotection after stroke.
Topics: Animals; Brain Infarction; Delayed-Action Preparations; Disease Models, Animal; Infarction, Middle C | 2010 |
Niacin treatment of stroke increases synaptic plasticity and axon growth in rats.
Topics: Analysis of Variance; Animals; Axons; Blotting, Western; Brain-Derived Neurotrophic Factor; Cells, C | 2010 |
Niaspan reduces high-mobility group box 1/receptor for advanced glycation endproducts after stroke in type-1 diabetic rats.
Topics: Animals; Brain; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; HMGB Proteins; Male; Nia | 2011 |
Combination treatment with low-dose Niaspan and tissue plasminogen activator provides neuroprotection after embolic stroke in rats.
Topics: Animals; Drug Therapy, Combination; Intracranial Embolism; Male; Neuroprotective Agents; Niacin; Rat | 2011 |
Cholesterol conundrum.
Topics: Azetidines; Cholesterol, HDL; Cholesterol, LDL; Ezetimibe; Heart Diseases; Humans; Hydroxymethylglut | 2011 |
[Early therapy of apoplexy with sodium nicotinate].
Topics: Cerebral Hemorrhage; Humans; Niacin; Nicotinic Acids; Secondary Prevention; Sodium; Stroke | 1953 |
[ON THE TREATMENT OF APOPLEXY WITH COMPLAMIN (7-(2-HYDROXY-3-(N-2-HYDROXYETHYL-N-METHYLAMINO)PROPYL)THEOPHYLLINE NICOTINATE].
Topics: Cerebrovascular Disorders; Geriatrics; Humans; Niacin; Nicotinic Acids; Stroke; Theophylline; Xanthi | 1963 |
[Research on the action of vasoactive drugs on cerebral circulation in patients suffering from apoplectic strokes. II. Action of nicotinic acid].
Topics: Brain; Cerebrovascular Circulation; Niacin; Nicotinic Acids; Stroke | 1959 |
[Administration of nicotinic acid in cerebral circulatory disorders, especially in states following apoplexy with hemiplegia].
Topics: Cerebral Hemorrhage; Cerebrovascular Circulation; Hemiplegia; Humans; Niacin; Nicotinic Acids; Strok | 1951 |
Lipid testing and lipid-lowering therapy in hospitalized ischemic stroke and transient ischemic attack patients: results from a statewide stroke registry.
Topics: Aged; Anticoagulants; Cholestyramine Resin; Clofibric Acid; Female; Hospital Records; Hospitalizatio | 2006 |
Niaspan increases angiogenesis and improves functional recovery after stroke.
Topics: Angiopoietin-1; Animals; Bromodeoxyuridine; Cells, Cultured; Cholesterol; Cholesterol, HDL; Disease | 2007 |
Nutritional disorders among workers in North China during national turmoil.
Topics: Adult; China; Female; Food Deprivation; Humans; Male; Middle Aged; Niacin; Nutrition Disorders; Oxyg | 2001 |
Lipid-lowering drug use and cardiovascular events after myocardial infarction.
Topics: Cholesterol; Clofibrate; Cohort Studies; Coronary Artery Disease; Coronary Disease; Female; Humans; | 2002 |