Question:
A 21-year-old man presents with sudden onset chest pain. His ECG shows ST-segment elevation in leads II, III, aVF, V5, and V6, and echocardiography reveals concentric left ventricular hypertrophy. What is the most likely cause?
A 21-year-old man presents with sudden onset chest pain. His ECG shows ST-segment elevation in leads II, III, aVF, V5, and V6, and echocardiography reveals concentric left ventricular hypertrophy. What is the most likely cause?
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In cocaine-induced chest pain or myocardial infarction, the initial pharmacological treatment includes Benzodiazepines (to reduce sympathetic drive) and Nitroglycerin (for coronary vasodilation). Pure Beta-blockers are classically avoided due to the theoretical risk of "unopposed alpha" stimulation, which could worsen the coronary vasospasm.
Updated On: Sep 3, 2026
- TCA toxicity
- Antihistamine toxicity
- Chronic cocaine overdose
- Antipsychotic toxicity
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The Correct Option is C
Solution and Explanation
Concept:
The clinical scenario involves an exceptionally young patient (21 years old) presenting with an acute ST-elevation myocardial infarction (STEMI) affecting the inferior (II, III, aVF) and lateral (V5, V6) walls.
Additionally, an echocardiogram shows concentric Left Ventricular Hypertrophy (LVH).
Myocardial infarction in a patient in their early twenties is extremely rare and strongly points toward an illicit toxicological etiology rather than classical atherosclerotic coronary artery disease.
Explanation:
• Cocaine is a potent sympathomimetic drug that inhibits the reuptake of norepinephrine, dopamine, and serotonin at synaptic clefts.
• In the cardiovascular system, the massive surge of catecholamines causes profound alpha-adrenergic receptor-mediated coronary artery vasoconstriction and vasospasm.
• Cocaine also increases myocardial oxygen demand (via severe tachycardia and hypertension) and promotes a pro-thrombotic state through platelet activation.
• This combination of extreme vasospasm and thrombosis can precipitate an acute STEMI, even in young individuals with completely clean, healthy coronary arteries.
• Furthermore, chronic cocaine use leads to sustained, severe episodes of hypertension. Over time, the heart adapts to this high afterload by developing concentric Left Ventricular Hypertrophy, explaining the echo findings.
• Tricyclic antidepressant (TCA) toxicity (Option A) causes cardiac arrhythmias (widened QRS, prolonged QT) due to sodium channel blockade, not classically localized STEMI or structural LVH.
• Antihistamine and Antipsychotic toxicities similarly cause QT prolongation or anticholinergic toxidromes, not acute coronary syndromes.
Final answer:
The combination of an acute STEMI in a very young patient with structural evidence of chronic hypertension (LVH) is a classic presentation of chronic cocaine abuse.
The clinical scenario involves an exceptionally young patient (21 years old) presenting with an acute ST-elevation myocardial infarction (STEMI) affecting the inferior (II, III, aVF) and lateral (V5, V6) walls.
Additionally, an echocardiogram shows concentric Left Ventricular Hypertrophy (LVH).
Myocardial infarction in a patient in their early twenties is extremely rare and strongly points toward an illicit toxicological etiology rather than classical atherosclerotic coronary artery disease.
Explanation:
• Cocaine is a potent sympathomimetic drug that inhibits the reuptake of norepinephrine, dopamine, and serotonin at synaptic clefts.
• In the cardiovascular system, the massive surge of catecholamines causes profound alpha-adrenergic receptor-mediated coronary artery vasoconstriction and vasospasm.
• Cocaine also increases myocardial oxygen demand (via severe tachycardia and hypertension) and promotes a pro-thrombotic state through platelet activation.
• This combination of extreme vasospasm and thrombosis can precipitate an acute STEMI, even in young individuals with completely clean, healthy coronary arteries.
• Furthermore, chronic cocaine use leads to sustained, severe episodes of hypertension. Over time, the heart adapts to this high afterload by developing concentric Left Ventricular Hypertrophy, explaining the echo findings.
• Tricyclic antidepressant (TCA) toxicity (Option A) causes cardiac arrhythmias (widened QRS, prolonged QT) due to sodium channel blockade, not classically localized STEMI or structural LVH.
• Antihistamine and Antipsychotic toxicities similarly cause QT prolongation or anticholinergic toxidromes, not acute coronary syndromes.
Final answer:
The combination of an acute STEMI in a very young patient with structural evidence of chronic hypertension (LVH) is a classic presentation of chronic cocaine abuse.
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