Adrenaline (epinephrine) is a key stress hormone released by the adrenal glands during acute physical or emotional stress. Its effects on the heart are mediated via α- and β-adrenergic receptors, increasing heart rate, contractility, and blood pressure—potentially exacerbating cardiac stress during myocardial ischemia . At physiological levels, epinephrine primarily activates β₂ receptors in coronary arteries, causing vasodilation and increasing coronary blood flow. However, at high levels, predominant α₁ receptor activation causes systemic vasoconstriction, raising peripheral resistance and cardiac workload . Elevated blood adrenaline (epinephrine) is a hallmark of the acute phase of myocardial infarction and is implicated in multiple pathophysiologic mechanisms—including arrhythmias, alterations in potassium levels, bleeding function, and direct myocardial injury. Collectively, clinical biochemistry research establishes that acute MI initiates a marked adrenaline surge, tied to infarct severity, arrhythmogenesis, symptom burden, and vascular injury. While adrenaline serves as an important biomarker, it also seems to drive maladaptive responses through electrophysiologic and endothelial pathways—making it both a risk signal and a potential therapeutic target. Let me know if you’d like to integrate quantitative data tables, explore receptor-specific pathways, or discuss therapeutic modulation strategies in more depth.