Antiplatelet therapy involves the use of medications that 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 therapy works by blocking platelet activation pathways, thereby reducing the risk of cardiovascular emergencies such as myocardial infarction and stroke.
This treatment 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 and risk balance.
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 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 are reversible and can be adjusted based on patient response, offering more precise treatment options.
Mainly indicated for patients with acute coronary syndrome, post-myocardial infarction recovery, ischemic stroke, or transient ischemic attack. Patients receiving drug-eluting stent placement require long-term dual antiplatelet therapy to prevent in-stent thrombosis.
Also used to prevent limb amputation in diabetic patients with peripheral artery disease and secondary prevention in high-risk deep vein thrombosis patients. In certain cases, combined with anticoagulants, but careful assessment of bleeding risk is necessary.
Most medications are oral, such as aspirin at 75-325 mg daily, and initial loading doses of clopidogrel at 300 mg followed by 75 mg daily. During acute myocardial infarction, loading doses like ticagrelor at 180 mg followed by 90 mg twice daily may be used.
Hospitalized patients may temporarily use intravenous drugs such as glycoprotein IIb/IIIa receptor antagonists. Dosages should be adjusted according to renal function; for severe renal failure, doses should be reduced, for example, prasugrel should be discontinued if creatinine clearance is below 30 ml/min.
Clinical trials have confirmed that it can reduce cardiac mortality in acute coronary syndrome patients by 20-30% and decrease the recurrence risk of stroke by 25%. Long-term monotherapy can effectively delay the progression of atherosclerosis, 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 bruising, with about 5-10% experiencing 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 adjusted before cardiac catheterization.
Special populations require particular attention:
Combining with non-steroidal anti-inflammatory drugs (NSAIDs) significantly increases gastrointestinal bleeding risk; high-risk drugs like indomethacin should be avoided. When combined with warfarin and other anticoagulants, INR monitoring is necessary as bleeding risk increases.
Interactions with antibiotics such as chloramphenicol may affect platelet function, requiring monitoring. When combined with CYP3A4 enzyme inducers, dosage adjustments of newer P2Y12 inhibitors are necessary.
Clinical trials show that dual antiplatelet therapy reduces major cardiac events in ST-segment elevation myocardial infarction (STEMI) patients by 15% within one year. The PLATO trial confirmed that 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 a 30% faster onset of action for newer drugs. The European Society of Cardiology recommends initiating treatment within 48 hours for acute coronary syndrome patients.
Monotherapy with anticoagulants like warfarin can inhibit coagulation factors but is less effective in preventing arterial thrombosis. New oral anticoagulants (NOACs) like dabigatran may be an option for certain patients, but the risks of arterial and venous thrombosis should be evaluated.
Post-surgical patients may consider temporarily stopping antiplatelet therapy in favor of low-dose anticoagulation, though this carries a higher thrombosis risk. If patients cannot tolerate dual therapy after stent placement, extending monotherapy may be considered.
It is generally recommended to take antiplatelet drugs at a fixed time to maintain stable blood drug levels, such as taking them at the same time daily with meals or on an empty stomach, depending on the specific medication. Avoid combining with monoamine oxidase inhibitors or alcohol to reduce gastric mucosal irritation. Consult your doctor for personalized advice based on your health status.
If I notice gum bleeding or skin bruising, does that mean the therapy is working?Minor bleeding signs may be normal reactions 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 whether to adjust the medication dose or switch to another treatment.
Should I suspend exercise or daily activities during antiplatelet therapy?Light exercise such as walking or yoga can be maintained, but high-impact activities or those prone to causing trauma should be avoided. If invasive procedures like endoscopy or tooth extraction are needed, inform healthcare providers in advance 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 use, while those with temporary thrombotic risk may stop after a few months. Do not stop medication on your own; it should be discontinued gradually under a doctor’s guidance to avoid increasing cardiovascular event risks.
Will herbal medicines or vitamin supplements affect the efficacy of antiplatelet therapy?Some herbal supplements (such as ginkgo and fish oil) may enhance anticoagulant effects and increase bleeding risk; excessive vitamin K intake may reduce the effectiveness of some drugs. Always inform your healthcare provider before using any over-the-counter medicines or supplements to avoid drug interactions.
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