Potential mechanisms for infarction after cocaine and other stimulant misuse
| *Intravenous injecting patients. |
| • Vasoconstriction (seen on acute or subacute angiography), with or without superimposed thrombosis/occlusion, either as direct drug effect or secondary to subarachnoid haemorrhage |
| • Cardiac arrhythmias and/or cardiomyopathy (especially with cocaine) causing infarction by embolism or even by hypoperfusion in cases of transient ventricular tachyarrhythmias |
| • Embolism from infective endocarditis* |
| • Cerebral vasculitis |
| • Embolism of venous thrombus or particulate contaminant matter (for example, talc or corn starch) in injecting users, presumably with cardiac right to left shunts* |
| • In the case of cocaine, it may also lead to enhanced thrombus formation due to effects on platelets and depletion of coagulation control proteins (anti-thrombin III and protein C) |