Anticoagulants
Anticoagulants are drugs that block steps in the coagulation cascade to prevent or treat venous thromboembolism, cardioembolic stroke, and valve thrombosis. Direct oral anticoagulants are first-line for most nonvalvular indications, while warfarin, titrated to an INR of 2 to 3, remains required for mechanical valves and high-risk antiphospholipid syndrome; parenteral heparins bridge and cover renal failure or urgent reversal needs.
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What this article covers
- Overview
Anticoagulants slow fibrin clot formation by inhibiting steps of the coagulation cascade, distinct from antiplatelet agents, which block platelet aggregation.
- Epidemiology
Scale of use: Among the most prescribed drug classes, driven by AF, whose prevalence rises with age, and by VTE, which affects roughly 1 in 1,000 adults yearly.
- Risk factors
Age over 75 years: An independent bleeding risk factor, and it raises AF stroke risk through the CHA2DS2-VASc score.
- Pathophysiology
Vitamin K antagonism: Warfarin inhibits hepatic vitamin K epoxide reductase, blocking carboxylation of factors II, VII, IX, X, and proteins C and S; protein C falls first, causing a transient prothrombotic state.
- Clinical features
Effective anticoagulation: Absence of the target thrombotic event, easy bruising, and minor mucosal bleeding, expected findings that do not alone require stopping therapy.
- Differential diagnosis
The relevant differential is the competing agent chosen between for the same indication, each with the discriminator that decides it.
- Diagnosis
The choice of an anticoagulant is established by confirming the indication, quantifying thrombotic and bleeding risk, and obtaining the labs each drug requires.
- Management
First, stabilize any active hemorrhage before starting any agent, then match the class to indication and renal function, dose, monitor, and adjust.
- Complications
Major hemorrhage: About 1% to 3% of warfarin patients per year and about 3% of UFH-treated patients; intracranial hemorrhage carries the highest mortality.
- Prognosis
Efficacy in VTE treatment: DOACs are at least as effective as warfarin for preventing recurrent VTE, with less central nervous system and fatal bleeding.
- Prevention
Renal function reassessment: Recheck creatinine clearance every 6 to 12 months, switching agents before accumulation causes bleeding.
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- Pulmonary embolism
Pulmonary embolism is thrombus, usually from a lower-extremity deep vein thrombosis, obstructing the pulmonary arterial circulation and causing V/Q mismatch, right ventricular strain, and hypoxemia. Diagnosis follows Wells criteria (with PERC in low-risk patients) to sequence D-dimer, CT pulmonary angiography, and V/Q scanning, and management is risk-stratified anticoagulation escalating to thrombolysis or embolectomy for hemodynamic instability.
- Heparin-induced thrombocytopenia
Heparin-induced thrombocytopenia is an immune, prothrombotic drug reaction in which IgG antibodies against platelet factor 4-heparin complexes activate platelets, causing venous and arterial thrombosis alongside a paradoxical falling platelet count. The danger is clotting, not bleeding, so management is to stop all heparin immediately and start a non-heparin anticoagulant while avoiding platelet transfusion and premature warfarin.
- Antiphospholipid syndrome
Antiphospholipid syndrome is an acquired autoimmune thrombophilia in which antiphospholipid antibodies cause recurrent venous and arterial thrombosis and pregnancy morbidity, paradoxically prolonging the aPTT in vitro while promoting clotting in vivo. Diagnosis requires a qualifying clinical event plus a laboratory antibody confirmed positive on two occasions at least 12 weeks apart, and thrombotic disease is treated with indefinite warfarin rather than a DOAC.
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- Antiplatelet agents
Antiplatelet agents block platelet activation and aggregation to prevent arterial thrombosis. Aspirin irreversibly inhibits cyclooxygenase-1, and P2Y12 inhibitors such as clopidogrel, ticagrelor, and prasugrel block adenosine diphosphate-driven platelet activation. Aspirin 81 mg daily anchors secondary prevention, and dual antiplatelet therapy with aspirin plus a P2Y12 inhibitor is first-line after acute coronary syndrome or coronary stenting.
- Cancer-associated venous thromboembolism
Deep vein thrombosis or pulmonary embolism occurring in a patient with active malignancy, driven by tumor-derived procoagulant activity plus stasis and vascular injury. Diagnosis is confirmed by compression ultrasonography or CT pulmonary angiography, and first-line treatment is apixaban, rivaroxaban, or low molecular weight heparin continued while cancer is active.