Cocaine‑Induced Prothrombotic Mechanisms and Cardiovascular Risk

Mechanisms of Thrombosis

Cocaine raises plasminogen‑activator inhibitor levels, fostering thrombus formation in both arterial and venous beds. 1
Cocaine increases platelet count and enhances platelet activation, leading to hyper‑aggregability. 1
Cocaine elevates pro‑thrombotic biomarkers—including C‑reactive protein, von Willebrand factor, and fibrinogen—indicating a systemic pro‑coagulant state. 1
Cocaine accelerates atherosclerosis, producing plaque formation that is prone to superimposed thrombosis even in young individuals. 1

Acute coronary artery thrombosis occurs shortly after cocaine ingestion and is a major cause of myocardial infarction (MI) in young adults. 1
MI is diagnosed in 0.7 %–6 % of cocaine‑using patients who present to emergency departments with chest pain. 1
The mean age of patients experiencing cocaine‑related MI is approximately 38 years. 2
Autopsy examinations of young cocaine users reveal coronary atherosclerosis with overlying thrombus formation. 1

The American Heart Association states that cocaine‑induced myocardial ischemia results from (1) increased myocardial oxygen demand, (2) reduced oxygen supply via coronary vasoconstriction, (3) a pro‑thrombotic state, and (4) accelerated atherosclerosis. 4
Concurrent use of cocaine and cigarette smoking produces synergistic vasoconstriction and markedly higher thrombotic risk compared with either substance alone. 5