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. Additional Indexing Words: Regional coronary blood flow Radioactive microspheres Myocardial supply:demand relationship Tension-time index Diastolic pressure time index L EFT VENTRICULAR SUBENDOCARDIAL pairment ISCHEMIA and infarction may occur in subendoca patients with valvar aortic stenosis and unobstructaortic sten ed coronary arteries.1-3 The cause of this ischemia develop ai is thought to be the concurrence of increased ings suggE myocardial oxygen requirements and relative imsubendoca reports by Phasic coronary blood flow Coronary perfusion pressure Systolic pressure time index of coronary flow to left ventricular rdial muscle. Patients with supravalvar osis and patent coronary arteries may also ngina pectoris, electrocardiographic findestive of left ventricular ischemia, and irdial fibrosis and infarction.4 Recent

Ultrasonic Myocardial Tissue Characterization in Patients With Hypertrophic Cardiomyopathy and Pressure-Overloaded Hypertrophy by Backscattered Energy Temporal Analysis.

“…34,35 Huysman et al reported that the volume fraction of nonmyocyte tissue in the subendocardial myocardium increased as heart weight increased, independent of the type of pressure overload. 36 Therefore, in patients with POH, increased subendocardial connective tissue may result in lower CVIB values in endocardial ROIs.…”

Difference in Coronary Blood Flow Dynamics between Patients with Hypertension and Those with Hypertrophic Cardiomyopathy.

“…In patients with left ventricular hypertrophy (LVH), it has been reported that myocardial ischemia may occur in the absence of epicardial coronary artery disease (1)(2)(3)(4)(5). It has been suggested that an imbalance between oxygen supply and demand due to the greatly increased myocardial mass might be a mechanism for myocardial ischemia (6).…”

Balloon dilation angioplasty of peripheral pulmonary stenosis associated with Williams syndrome

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