Sexual Activity As a Trigger of Myocardial Infarction/Ischemia

Abstract

Landmark studies by Muller, Mittleman, Tofler and others have suggested that acute myocardial infarctions (MIs) may be triggered by certain phenomena (1–4). It is believed that these triggers, often initiated by an increase in catecholamines and sympathetic nervous system activity, ultimately lead to a disruption of the vulnerable atherosclerotic plaque. Increases in sympathetic vascular tone and sympathetic/catecholamine-related increases in heart rate, blood pressure, ventricular contractility, platelet aggregability, hematocrit, and reductions in fibrinolysis may all contribute (2). For example, an increase in ventricular contractility with changes in dP/dT (change in ventricular pressure over time) and an increase in coronary tone can increase the sheer-stress of blood flowing across a vulnerable atherosclerotic plaque. These mechanical forces may then contribute to rupture of a thin fibrous cap overlying the lipid pool of the plaque. Lipid, foam cells, and tissue factors escape into the lumen of the artery, contributing to platelet aggregation, fibrin deposition, and thrombus, which can then obstruct flow through the coronary artery, causing acute MI and/or sudden death. Reduction in flow also results from an increase in stimulation of alpha sympathomimetic receptors. Increases in heart rate and blood pressure during emotional or physical stress increase oxygen demand, and if O₂ supply is limited by coronary stenosis, coronary artery vasospasm, or flow limiting intra-coronary thrombus, ischemia will be worsened.