Dynamic left ventricular outflow tract obstruction in a patient with acute coronary syndrome and without the apical akinesia: Potential alternative mechanisms causing a dynamic left ventricular outflow tract obstruction other than a compensatory basal hyperkinesis

Abstract

The mechanism for dynamic left ventricular outflow tract obstruction (LVOTO) after acute coronary syndromes (ACS) is thought to be apical infarction with compensatory hyperkinesia of the residual normally perfused basal segments of the myocardium. However, herein, we report a patient with ACS and dynamic LVOTO (peak gradient of 250 mm Hg at rest) that could not be secondary to apical akinesia. We propose a potential alternative mechanism leading to dynamic LVOTO in ACS, namely, the interplay between sigmoid septum, basal hyperkinesis, and outflow tract narrowing induced by afterload reduction due to acute myocardial ischemia itself.

The Role of Focused 2-Dimensional Echocardiography in Managing Left Ventricular Outflow Tract Obstruction Mimicking Cardiogenic Shock

“…6 It is hypothesized that an acute ischemic event of the LV causes intraventricular afterload reduction in the nonischemic region, leading to hypercontractility. 7 This is often exacerbated by acute maladaptation following extensive territory ischemia, such as changes in LV chamber size, relative hypovolemia, tachyarrhythmias, excessive catecholamine administration, and vasodilation. In this situation, cardiac output and end-organ perfusion are compromised, and the clinical features mimic CS.…”