The immediate effects of cocaine consumption include the narrowing of arteries and an increased likelihood of clot formation. This drug induces tachycardia, elevated blood pressure, heightened demand for oxygen by the heart, and greater vascular stress. Cocaine leads to the constriction of coronary arteries in a manner that depends on the dose, with about 5 to 6 percent of patients presenting to the emergency department (ED) for cocaine-related issues experiencing cardiac ischemia. When present in the bloodstream at high levels, cocaine's adverse impact on the heart's pumping strength can result in a sudden weakening of the left ventricle's function, potentially leading to heart failure. Additionally, cocaine can trigger irregular heart rhythms, either through its direct effect on the heart muscle or as a result of the stress from reduced blood supply to the heart. Although rare, severe complications like aortic dissection and rupture have been reported following cocaine use. Due to cocaine’s effect on potassium and sodium blockade, the QRS and QTc may also be prolonged, contributing to ventricular dysrhythmias such as ventricular tachycardia, frequent premature ventricular contraction, or Torsades de Pointes.
Over the long term, chronic cocaine use accelerates the development of arterial plaque. Additionally, cocaine use triggers platelet activation, α granule secretion, and the development of microaggregates containing platelets. This suggests that cocaine, even when used in the modest amounts common among sporadic users, can facilitate thrombus formation and heighten the risk for ischemic incidents in otherwise healthy people.
