Antiplatelet therapy is a pharmacological approach used to inhibit platelet activation and aggregation, primarily aimed at preventing arterial occlusive diseases caused by thrombus formation. Platelets aggregate at sites of vascular injury to form clots to stop bleeding, but excessive activation can lead to the rupture of atherosclerotic plaques and the formation of lethal thrombi. This treatment works by blocking platelet activation pathways, thereby reducing the risk of cardiovascular emergencies such as myocardial infarction and stroke.
This therapy is widely used in primary and secondary prevention of cardiovascular diseases. Common medications include aspirin, clopidogrel, and others. Physicians select monotherapy or combination therapy based on the patient’s risk level and comorbidities to achieve optimal antithrombotic effects while balancing bleeding risks.
Antiplatelet drugs are mainly divided into three categories: 1) Cyclooxygenase (COX) inhibitors like aspirin, which irreversibly inhibit prostaglandin synthesis within platelets; 2) P2Y12 receptor antagonists such as clopidogrel and prasugrel, which block ADP-induced platelet aggregation; 3) Phosphodiesterase inhibitors like cilostazol, which increase intracellular cAMP in platelets to inhibit activation.
Combination strategies such as “dual antiplatelet therapy” (DAPT) combine drugs with different mechanisms, for example, post-stent placement treatment. Newer drugs like ticagrelor have reversible effects, allowing adjustment based on patient response for more precise therapy.
Mainly indicated for acute coronary syndrome, recovery phase after myocardial infarction, ischemic stroke, or transient ischemic attack. Patients receiving drug-eluting stent implantation require long-term dual antiplatelet therapy to prevent in-stent thrombosis.
Also used to prevent limb amputation in diabetic patients with peripheral arterial disease and secondary prevention in high-risk deep vein thrombosis patients. In certain cases, anticoagulants may be combined, but bleeding risks must be carefully evaluated.
Most medications are administered orally, such as aspirin at 75-325 mg daily, with a loading dose of 300 mg for clopidogrel followed by 75 mg daily. During acute myocardial infarction, loading doses like ticagrelor 180 mg followed by 90 mg twice daily may be used.
Hospitalized patients may receive short-term intravenous medications, such as glycoprotein IIb/IIIa receptor antagonists. Dosages should be adjusted based on renal function; for example, prasugrel should be discontinued if creatinine clearance is below 30 ml/min.
Clinical trials have confirmed that antiplatelet therapy can reduce cardiac mortality by 20-30% in acute coronary syndrome patients and decrease recurrent stroke risk by 25%. Long-term monotherapy effectively delays atherosclerosis progression, and dual therapy can reduce stent thrombosis rates to below 1%.
The most serious risk is bleeding complications, including gastrointestinal bleeding and intracranial hemorrhage, with higher risks in elderly patients. Common side effects include gastrointestinal discomfort and skin petechiae; about 5-10% of patients may experience non-fatal bleeding.
Contraindications include active internal bleeding, recent history of intracranial hemorrhage, and severe liver dysfunction. Medication should be discontinued at least 5-7 days before surgery, and doses should be adjusted prior to cardiac catheterization.
Special populations require particular attention:
Concurrent use with non-steroidal anti-inflammatory drugs (NSAIDs) significantly increases gastrointestinal bleeding risk; high-risk drugs like indomethacin should be avoided. When combined with anticoagulants such as warfarin, INR monitoring is necessary as bleeding risk increases.
Interactions with antibiotics like chloramphenicol may affect platelet function, requiring monitoring. New P2Y12 inhibitors may require dose adjustments when used with CYP3A4 enzyme inducers.
Clinical trials show that dual antiplatelet therapy reduces major cardiac events in ST-elevation myocardial infarction (STEMI) patients by 15% within one year. The PLATO trial confirmed prasugrel reduces cardiac death risk by 19% compared to clopidogrel in STEMI patients.
Long-term follow-up studies indicate a 40% reduction in recurrent myocardial infarction rates among chronic users, with newer drugs providing a 30% faster onset of action. The European Society of Cardiology recommends initiating treatment within 48 hours for acute coronary syndrome patients.
Pure anticoagulants like warfarin inhibit clotting factors but are less effective for arterial thrombosis prevention. New oral anticoagulants (NOACs) such as dabigatran may be options for certain patients, but arterial and venous thrombotic risks must be evaluated.
Surgical patients may consider temporarily stopping antiplatelet therapy in favor of low-dose anticoagulation, though this carries a higher risk of thrombosis. For patients with drug-eluting stents who cannot tolerate dual therapy, extending monotherapy may be considered.
It is generally recommended to take antiplatelet medications at the same time each day to maintain stable blood drug levels, such as with meals or on an empty stomach, depending on the specific drug. Avoid combining with monoamine oxidase inhibitors or alcohol to reduce gastric mucosal irritation. Consult your doctor for personalized advice and adjustments based on your health status.
If I notice gum bleeding or skin bruising, does that mean the antiplatelet therapy is working?Minor bleeding signs may be normal responses to platelet inhibition, but if bleeding persists or worsens (such as blood in stool, urine, or severe headache), seek medical attention immediately. Your doctor will assess the severity and may adjust the medication dose or switch therapies.
Should I suspend exercise or daily activities during antiplatelet therapy?Light activities such as walking or yoga are generally safe, but high-impact or trauma-prone activities should be avoided. If invasive procedures like endoscopy or tooth extraction are planned, inform your healthcare provider beforehand to evaluate bleeding risks and adjust medication timing accordingly.
How long is the typical duration of antiplatelet therapy? Can I stop it on my own?The duration depends on the disease; for example, post-myocardial infarction patients may require long-term therapy, while others at temporary risk may stop after a few months. Do not discontinue medication without medical advice; your doctor will evaluate thrombotic risks and guide gradual discontinuation to prevent cardiovascular events.
Will herbal medicines or vitamin supplements affect the efficacy of antiplatelet therapy?Some herbal supplements (like ginkgo or fish oil) may enhance anticoagulant effects and increase bleeding risk; excessive vitamin K intake may reduce drug effectiveness. Always inform your healthcare provider before using any non-prescription drugs or supplements to avoid interactions.
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