Pravastatin and simvastatin improves acetylsalicylic acid‐mediated <i>in vitro</i> blood platelet inhibition

Luzak, Bogusława; Rywaniak, Joanna; Stanczyk, Lidia; Watała, Cezary

doi:10.1111/j.1365-2362.2012.02661.x

Cited by 22 publications

(13 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…37 Statins also improve platelet reactivity in vitro. 38 Treatment of coronary risk factors by optimal medications, with subsequent improvement of endothelial dysfunction, could attenuate enhanced platelet aggregation and reduce cardiovascular events after PCI; however, the clinical evidence is not strong enough at present, and further investigation is encouraged. The precise molecular mechanism of endothelial dysfunction in patients with high RPR after DAPT remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Effects of Endothelial Dysfunction on Residual Platelet Aggregability After Dual Antiplatelet Therapy With Aspirin and Clopidogrel in Patients With Stable Coronary Artery Disease

Fujisue

Sugiyama

Ono

et al. 2013

Circ: Cardiovascular Interventions

View full text Add to dashboard Cite

Background-Dual antiplatelet therapy with aspirin and clopidogrel is widely used in patients with coronary stents. High residual platelet reactivity (high RPR) after dual antiplatelet therapy is associated with increased cardiovascular events. Endothelial function could affect platelet reactivity in vivo. We hypothesized that endothelial dysfunction could be associated with high RPR after dual antiplatelet therapy in patients with stable coronary artery disease. Methods and Results-We screened patients with stable coronary artery disease for cytochrome P450 (CYP) 2C19 genotypes and enrolled 103 patients who lacked CYP2C19*2 or *3 loss-of-function allele to minimize the effect of this gene on high RPR. All patients received aspirin (100 mg/d) and clopidogrel (75 mg/d for long-term treatment or a loading dose of 300 mg) before the following tests. Platelet aggregability was assessed as P2Y12 reaction unit using the VerifyNow System. High RPR was defined as P2Y12 reaction unit ≥230. Peripheral endothelial function was expressed as reactive hyperemia index using reactive hyperemia peripheral arterial tonometry. Fifty-three patients exhibited high RPR. High RPR patients were significantly older, had higher levels of B-type natriuretic peptide, and were predominantly hypertensive compared with non-high RPR patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of Endothelial Dysfunction on Residual Platelet Aggregability After Dual Antiplatelet Therapy With Aspirin and Clopidogrel in Patients With Stable Coronary Artery Disease

Fujisue

Sugiyama

Ono

et al. 2013

Circ: Cardiovascular Interventions

View full text Add to dashboard Cite

show abstract

“…PRV is commercialized generically following the Bristol-Myers Squibb's patent expiration in April 2006 [7] under several brands in solid formulations containing 10, 20, 40 and 80 mg of active pharmaceutical ingredient. Other studies reveals that PRV stimulates angiogenesis in murine models [8] and improves acetylsalicylic acidmediated blood platelet inhibition, in vitro [9], while it has been suggested that statins appear to have therapeutic benefits in diseases that are unrelated to elevated serum cholesterol levels, such as pain and inflammation [10]. The importance of PRV active substance and statins is also revealed by review studies that indicate new therapeutic perspectives of statins in autoimmune diseases and cancer, antiatherosclerotic, anti-inflammatory, antioxidant, immunomodulatory and antithrombotic effects [11].…”

Section: Introductionmentioning

confidence: 99%

Kinetic analysis of solid-state degradation of pure pravastatin versus pharmaceutical formulation

Ledeți

Vlase

Fuliaş

2015

J Therm Anal Calorim

View full text Add to dashboard Cite

In this paper, the kinetic behavior of decomposition of a well-known bioactive substance used for treating dyslipidemia and the prevention of cardiovascular disease drug from statin class, namely pravastatin, was described. The kinetic study was performed on the main decomposition process which occurs at nearly 200°C, for both pure active substance and a generic commercial formulation that contain 40 mg pravastatin per tablet, using Kissinger, Friedman, Kissinger-Akahira-Sunose, FlynnWall-Ozawa and NPK methods. The stability of pravastatin as pure active substance and as tablet was compared by means of kinetic data, and the results suggested that in the solid pharmaceutical formulation, PRV has an increased stability compared to pure active substance.

show abstract

“…Early statin therapy has been shown to acutely affect platelet deposition following vascular injury by reducing granule secretion and thromboxane A 2 release, by nearly 30% [15]. In addition, statins may accentuate the inhibitory effect of aspirin on platelet aggregation [16].…”

Section: Evidence That Statins Have An Early Ef-fect On Platelets Andmentioning

confidence: 99%

“…In MIRACL, 3086 participants were randomized to receive high dose atorvastatin (80mg) within 1-4 days of presentation versus placebo. The primary endpoint of death, MI, and recurrent symptomatic myocardial ischemia at 16 Evidence of an acute benefit of statin therapy was observed in the ARMYDA-ACS (Atorvastatin for Reduction of Myocardial Damage during Angioplasty) study. As with MIRACL, the trial studied high-dose atorvastatin (80 mg) in a much smaller population of 171 patients.…”

Section: Early Clinical Response To Statins In Acute Coronary Syndromesmentioning

confidence: 99%

Anti-Thrombotic Effects of Statins in Acute Coronary Syndromes: At the Intersection of Thrombosis, Inflammation, and Platelet-Leukocyte Interactions

Sexton¹,

Wallace²,

Smyth³

2016

CCR

View full text Add to dashboard Cite

HMG CoA reductase inhibitors, or statins, are standard of care for preventing cardiovascular disease in at-risk populations. Statins are a well-established therapy proven to reduce long-term cardiovascular mortality and morbidity for prevention of secondary cardiovascular events and have become guidelinerecommended therapy following acute myocardial infarction. Emerging data from clinical trials over the last decade indicates that statin therapy may provide broad beneficial effects beyond their primary lipid lowering mechanisms. In coronary heart disease, statins have demonstrated a unique ability to target several cellular pathways, which appear to play an underappreciated role in acute inflammation and subsequent thrombosis. Herein, we review the potential mechanisms where statins may act as antithrombotic agents in the setting of acute coronary syndromes and discuss the clinical implications of these findings.

show abstract

Pravastatin and simvastatin improves acetylsalicylic acid‐mediated in vitro blood platelet inhibition

Cited by 22 publications

References 23 publications

Effects of Endothelial Dysfunction on Residual Platelet Aggregability After Dual Antiplatelet Therapy With Aspirin and Clopidogrel in Patients With Stable Coronary Artery Disease

Effects of Endothelial Dysfunction on Residual Platelet Aggregability After Dual Antiplatelet Therapy With Aspirin and Clopidogrel in Patients With Stable Coronary Artery Disease

Kinetic analysis of solid-state degradation of pure pravastatin versus pharmaceutical formulation

Anti-Thrombotic Effects of Statins in Acute Coronary Syndromes: At the Intersection of Thrombosis, Inflammation, and Platelet-Leukocyte Interactions

Contact Info

Product

Resources

About