Table 5

 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)