Recently, Jessica L Mega and others from Harvard Brigham and Women’s Hospital have detailed the pharmacological aspects of antiplatelet and anticoagulant drugs in the Lancet, and this article summarizes the article in 10 areas. Antithrombotic drugs include anticoagulants and antiplatelet agents and are commonly used to treat a variety of cardiovascular diseases. The efficacy and safety of antithrombotic drugs should be carefully weighed when administering antithrombotic therapy. 2. Oral antiplatelet agents target platelet adhesion, activation, or aggregation to prevent thrombosis. Small doses of aspirin selectively inhibit cyclooxygenase-1 (COX-1), producing an antiplatelet effect, while large doses inhibit both COX-1 and COX-2, exerting anti-inflammatory and analgesic effects. Aspirin permanently and irreversibly inactivates platelets for 7-10 days. After oral administration, aspirin is rapidly absorbed through the gastrointestinal tract, reaching maximum plasma concentrations in 30 minutes (regular aspirin) to 4 hours (enterosoluble form). Therefore, chewable 150-325 mg of regular aspirin is recommended for patients with acute coronary syndromes to achieve rapid clinical effects. 3. P2Y12 receptor inhibitors such as clopidogrel, prasugrel, and tigretol may produce further antiplatelet effects in addition to aspirin. Both clopidogrel and prasugrel are precursors that require biotransformation in vivo to be effective. 600 mg loading dose of clopidogrel produces antiplatelet effects within 2 hours, while 60 mg loading dose of prasugrel is effective within 30 minutes. Both take 7-10 days to eliminate after discontinuation of the drug. To date, no clinical studies have shown that individualized clopidogrel dosing based on genetic testing is effective, and no clinical studies have found sustained worsening of regression with the combination of proton pump inhibitors. Prasugrel is contraindicated in patients with prior stroke or transient ischemia (TIA) because of the increased risk of bleeding, and is not recommended for use in older adults over 75 years of age. 4. Tegretol inhibits P2Y12 receptors by a unique mechanism and has a faster elimination time after discontinuation than clopidogrel and prasugrel, requiring a loading dose of 180 mg at initiation followed by 90 mg twice daily maintenance. Although tegretol inhibits platelets by 40% in 30 minutes, it takes at least 4 hours to achieve effective inhibition in patients with ST-segment elevation myocardial infarction. Concomitant administration of Tegretol with potent CYP3A4 inhibitors and inducers, CYP3A4 enzyme substrates (simvastatin and lovastatin), and grapefruit juice should be avoided. 5. Vorapaxar and atopaxar are thrombin receptor antagonists that inhibit platelet aggregation. Vorapaxar is approved by the FDA for patients with myocardial infarction and peripheral vascular disease, but not for patients with prior stroke, TIA, or intracranial hemorrhage. 6. Vitamin K antagonists such as warfarin are the most commonly used oral anticoagulants. Warfarin interferes with the synthesis of vitamin K-dependent coagulation factors, including coagulation factors II, VII, IX, X, protein S, and protein C. Due to indirect inhibition of vitamin K-dependent coagulation factors, warfarin has a half-life of 40 hours, which is associated with a delayed clinical effect of 48-72 hours. Administration of vitamin K or infusion of coagulation factors reverses the effects of warfarin. Because of the narrow therapeutic window of warfarin and the tendency to interact with other drugs or food, frequent monitoring is required for its use. 7. Non-vitamin K oral anticoagulants (NOACs) include direct thrombin inhibitors (dabigatran) and Xa factor inhibitors (rivaroxaban, apixaban, and edoxaban). These drugs have a rapid onset of action, are partially excreted by the kidneys, and require dose adjustment based on the degree of renal insufficiency. Each drug has the potential for drug interactions with other drugs, including P-glycoprotein substrates (e.g., verapamil, dronedarone, and amiodarone). After initial treatment, conventional doses of NOACs are generally used in the treatment of venous thromboembolism, but lower doses are sometimes used in the extended phase of secondary prevention. 9. Overall, in the Atrial Fibrillation Stroke Prevention Trial, all four NOACs reduced the risk of intracranial hemorrhage compared with warfarin, but also increased the risk of gastrointestinal bleeding (dabigatran, rivaroxaban, and edoxaban). 10. NOAC drugs do not require routine monitoring. However, if necessary, prothrombin time can be used for qualitative assessment of Xa factor inhibitors and activated partial thromboplastin time (APTT) can be used for monitoring of direct thrombin inhibitors. There are no direct antidotes for these drugs.