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Antiplatelet Therapy and Cardiovascular Diseases
Research Guide
What is Antiplatelet Therapy and Cardiovascular Diseases?
Antiplatelet therapy in cardiovascular diseases is the use of drugs such as aspirin, clopidogrel, and ticagrelor to inhibit platelet aggregation and prevent thrombotic events like myocardial infarction, stroke, and stent thrombosis, particularly following percutaneous coronary intervention.
This field encompasses 61,609 papers on antiplatelet agents including aspirin, clopidogrel, ticagrelor, prasugrel, and their roles in secondary prevention of cardiovascular events. Research examines efficacy in acute coronary syndromes, stroke, and post-percutaneous coronary intervention settings, alongside factors like platelet reactivity, genetic polymorphisms such as CYP2C19 genotype, and bleeding risks. Key trials compare these agents head-to-head, showing differences in reducing vascular death, myocardial infarction, or stroke rates.
Topic Hierarchy
Research Sub-Topics
Clopidogrel Resistance and Platelet Reactivity
This sub-topic investigates high on-treatment platelet reactivity during clopidogrel therapy, using light transmission aggregometry and VerifyNow assays. Researchers correlate reactivity with ischemic outcomes post-PCI.
CYP2C19 Polymorphisms in Antiplatelet Therapy
Studies genotype CYP2C19 loss-of-function alleles (*2, *3) predicting clopidogrel hyporesponsiveness, conducting pharmacogenetic trials for genotype-guided therapy. Meta-analyses assess clinical impact.
Dual Antiplatelet Therapy Duration
This area compares 6-12 vs. 24-36 months DAPT post-PCI via trials like DAPT and PEGASUS, balancing ischemic vs. bleeding risks using scores like DAPT score and PRECISE-DAPT.
Ticagrelor versus Clopidogrel in ACS
Researchers analyze PLATO and PEGASUS-TIMI 54 trials demonstrating ticagrelor's superior efficacy over clopidogrel in reducing CV death/MI/stroke in ACS, examining dyspnea mechanisms.
Bleeding Risk Assessment in Antiplatelet Therapy
This sub-topic develops and validates risk scores (CRUSADE, HAS-BLED) predicting major bleeding on DAPT, incorporating anemia, renal function, and prior events for net clinical benefit analysis.
Why It Matters
Antiplatelet therapy reduces occlusive vascular events in high-risk patients, including those with acute myocardial infarction, ischaemic stroke, or after percutaneous coronary intervention. The Antiplatelet Trialists Collaboration (2002) meta-analysis of randomised trials demonstrated that aspirin or another oral antiplatelet drug protects against death, myocardial infarction, and stroke in such groups. In acute coronary syndromes, Wallentin et al. (2009) found ticagrelor versus clopidogrel reduced death from vascular causes, myocardial infarction, or stroke rates without increasing overall major bleeding. Wiviott et al. (2007) reported prasugrel versus clopidogrel lowered ischemic events including stent thrombosis by significant margins but raised major bleeding risks, including fatal cases, informing personalized therapy to balance thrombotic and hemorrhagic outcomes in clinical practice.
Reading Guide
Where to Start
'Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients' by Antiplatelet Trialists Collaboration (2002), as it provides foundational evidence on antiplatelet benefits across high-risk groups with 6898 citations.
Key Papers Explained
The Antiplatelet Trialists Collaboration (2002) meta-analysis establishes baseline antiplatelet efficacy in high-risk patients. Yusuf et al. (2001) build on this by showing clopidogrel plus aspirin benefits in acute coronary syndromes without ST-elevation. Wallentin et al. (2009) and Wiviott et al. (2007) then compare newer agents, with 'Ticagrelor versus Clopidogrel in Patients with Acute Coronary Syndromes' demonstrating ticagrelor superiority and 'Prasugrel versus Clopidogrel in Patients with Acute Coronary Syndromes' highlighting prasugrel's ischemic benefits despite bleeding risks. Zhang et al. (2014) extend dual therapy evidence to stroke prevention.
Paper Timeline
Most-cited paper highlighted in red. Papers ordered chronologically.
Advanced Directions
Field centers on genetic polymorphisms, platelet reactivity, and bleeding risk modulation in antiplatelet use post-percutaneous coronary intervention, per the topic cluster description. No recent preprints or news available; frontiers involve CYP2C19-guided therapy and personalized regimens.
Papers at a Glance
Frequently Asked Questions
What is the efficacy of ticagrelor compared to clopidogrel in acute coronary syndromes?
In patients with acute coronary syndromes with or without ST-segment elevation, ticagrelor compared with clopidogrel significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke. This was achieved without an increase in the rate of overall major bleeding. Wallentin et al. (2009) in 'Ticagrelor versus Clopidogrel in Patients with Acute Coronary Syndromes' reported these findings from the PLATO trial.
How does prasugrel perform against clopidogrel in patients undergoing percutaneous coronary intervention?
In acute coronary syndromes patients scheduled for percutaneous coronary intervention, prasugrel therapy reduced rates of ischemic events, including stent thrombosis, compared to clopidogrel. However, it increased the risk of major bleeding, including fatal bleeding. Wiviott et al. (2007) in 'Prasugrel versus Clopidogrel in Patients with Acute Coronary Syndromes' documented these results, with overall mortality unchanged.
What are the benefits of adding clopidogrel to aspirin in acute coronary syndromes without ST-segment elevation?
Clopidogrel added to aspirin benefits patients with acute coronary syndromes without ST-segment elevation by further reducing ischemic events. It increases the risk of major bleeding. Yusuf et al. (2001) in 'Effects of Clopidogrel in Addition to Aspirin in Patients with Acute Coronary Syndromes without ST-Segment Elevation' confirmed these effects.
What does evidence show for aspirin plus clopidogrel in secondary prevention after stroke?
Aspirin plus clopidogrel serves as secondary prevention for non-cardioembolic stroke or transient ischemic attack. Zhang et al. (2014) in 'Aspirin plus Clopidogrel as Secondary Prevention after Stroke or Transient Ischemic Attack: A Systematic Review and Meta-Analysis' systematically reviewed short-, middle-, and long-term efficacy and safety.
What is the role of antiplatelet therapy in high-risk patients per meta-analyses?
Aspirin or another oral antiplatelet drug protects most patients at increased risk of occlusive vascular events, including prior myocardial infarction, stroke, or peripheral arterial disease. The Antiplatelet Trialists Collaboration (2002) in their 'Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients' established this across diverse high-risk groups.
Open Research Questions
- ? How do genetic polymorphisms like CYP2C19 genotype influence clopidogrel efficacy and outcomes in percutaneous coronary intervention patients?
- ? What strategies optimize platelet reactivity monitoring to balance thrombotic events and bleeding risks in antiplatelet regimens?
- ? Which patient subgroups derive the greatest net benefit from ticagrelor or prasugrel over clopidogrel without excessive bleeding?
Recent Trends
The field includes 61,609 works on antiplatelet therapy in cardiovascular diseases, focusing on aspirin, clopidogrel, ticagrelor, platelet reactivity, genetic polymorphisms, and bleeding risks in percutaneous coronary intervention contexts.
No growth rate data over 5 years provided, and no recent preprints or news in the last 12 months available.
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