Coca

coronary artery disease, cardiomyopathy, heart failure, arrhythmia, valvular disease

Pre-existing cardiovascular disease dramatically elevates the risk of myocardial infarction and sudden cardiac death with cocaine use. Frequent cocaine users have a 7-fold higher MI risk even without prior cardiac disease; pre-existing conditions multiply this further.

Concurrent use of beta-adrenergic blockers with cocaine is absolutely contraindicated. Unopposed alpha stimulation causes severe hypertension and coronary vasospasm. This is a well-established clinical contraindication in emergency medicine.

uncontrolled hypertension, tachyarrhythmias

Standard stimulant class contraindication applied by mechanism. Cocaine's sympathomimetic cardiovascular effects pose extreme risk in uncontrolled hypertension and tachyarrhythmias.

Schizophrenia spectrum disorders and psychosis vulnerability are amplified by cocaine use. Cocaine-induced psychosis prevalence reaches up to 86.5% in some clinical populations. Sensitization — not tolerance — occurs for psychosis risk.

Hepatic impairment prolongs cocaine and norcocaine exposure, increasing risk of hepatotoxicity and systemic toxicity. Norcocaine itself is hepatotoxic, creating a compounding risk in patients with pre-existing liver disease.

hyperthyroidism, pheochromocytoma

Standard stimulant class contraindication. Endogenous catecholamine excess from hyperthyroidism or pheochromocytoma is dangerously amplified by cocaine's norepinephrine reuptake inhibition and alpha-adrenergic stimulation.

Cocaine use in pregnancy is associated with placental abruption, adverse neonatal outcomes, and functional brain connectivity alterations in neonates. Absolute contraindication across all coca preparations including leaf and tea.

Prenatal cocaine exposure is associated with functional brain connectivity alterations in neonates. This applies to all coca preparations, as even coca leaf and tea produce measurable blood cocaine levels.

Concurrent MAOI therapy with cocaine poses theoretical risk of hypertensive crisis and serotonin syndrome. No clinical case reports of this specific combination were identified; severity assessment is based on pharmacological mechanism only.

Concurrent TCA use with cocaine produces additive cardiovascular toxicity via combined sodium channel blockade and norepinephrine reuptake inhibition. Evidence is mechanism-based; no controlled clinical study was retrieved.