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.

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.

Total Clinical Course and Autopsy Findings of Left Ventricular Outflow Tract Obstruction Due to Sigmoid Septum: Histologically Proven Isolated Basal Septal Hypertrophy.

We herein report the total course and autopsy findings of a woman who complained of chest discomfort and had plasma B-type natriuretic peptide 43 pg/mL and left ventricular outflow tract obstruction (with a resting pressure gradient of 181 mmHg) due to sigmoid septum at 73 years of age. Betaxolol and verapamil decreased her pressure gradient to 14 mmHg, but the pressure gradient (101 mmHg) again worsened. The betaxolol dose was increased and cibenzoline was added, resulting in a pressure gradient ≤21 mmHg. An autopsy was performed after death from a urinary tract infection at 80 years of age. The absence of any disarray of cardiac myocytes was confirmed.