Left Ventricular Subendocardial Ischemia in Severe Valvar and Supravalvar Aortic Stenosis

Abstract

Severe valvar aortic stenosis (VAS) and supravalvar aortic stenosis (SVAS) each may cause left ventricular (LV) subendocardial ischemia and infarction, even with patent coronary arteries. LV ischemia in VAS has been related to reduced coronary perfusion relative to raised metabolic requirements, whereas this mechanism of ischemia has not been widely accepted in SVAS because coronary perfusion pressure is higher than normal. LV subendocardial coronary blood flow (CBF) occurs predominantly in diastole and a diastolic pressure-time index (DPTI) was used to estimate it. LV oxygen requirements were estimated from the systolic pressure-time index (SPTI). The ratio DPTI:SPTI (supply:demand) was evaluated as an estimate of the adequacy of subendocardial flow. SVAS was produced acutely in nine dogs and phasic left CBF and distribution of CBF to the LV myocardium were measured. Although mean CBF always rose with aortic constriction, flow in diastole fell from a control of 80% to 34% (P < 0.001) and LV myocardial flow distribution became inhomogeneous with the proportion of flow to subendocardial muscle decreasing 63% (P < 0.001). Departure from the normal homogeneous flow distribution to the LV was predictable from the ratio DPTI:SPTI; values below 0.7 were always associated with relative subendocardial underperfusion. DPTI:SPTI ratios in two patients, one with severe VAS (0.25) and one with SVAS (0.39) were well below values obtained in 18 control patients (1.03 ± 0.23), and were similar to the ratios in dogs with SVAS (0.27 ± 0.08). Both patients had ECG changes suggesting LV ischemia. The mechanism of subendocardial ischemia is thought to be the same in both types of stenosis and its presence is predictable from pressure measurements available at cardiac catheterization.