A major stress hormone that the adrenal glands produce in response to intense physical or emotional stress is adrenaline, also referred to as epinephrine. Profound changes in the cardiovascular system are produced by these drugs, likely due to stimulation of α- or β-adrenergic receptors that would act to increase cardiac work through increasing blood pressure, heart rate and myocardial contractility during myocardial ischemia. Physiologically, at physiological doses adrenaline predominantly leads to vasodilation and coronary blood flow increase by stimulating β₂ receptors in the coronary arteries. Conversely, higher grades of predominant α₁ receptor stimulation lead to systemic vasoconstriction, with subsequent rise in cardiac workload and peripheral resistance. High blood levels of adrenaline (epinephrine) and some aggravating pathophysiological factors, such as arrhythmia, changes in serum potassium, bleeding characteristics, and direct action on the myocardium, are linked to the first phase of myocardial infarction. High levels of adrenaline after an acute MI have been associated with infarct severity, arrhythmogenesis, symptom load and vascular injury based on a clinical biochemistry literature. Adrenaline is a very significative biomarker, it is warning and a target in therapy because appears to be the trigger for maladaptive responses by means of both latter endothelium and electrophysiologic ways. You let me know if details are required for quantitative data tables, receptor specific pathways or pharmacological modulation.