niacin and Stroke
niacin has been researched along with Stroke 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.
Stroke: A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)
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 Stroke
| 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 Stroke
Other Studies
20 other studies available for niacin and Stroke
| 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 |