Effect of left ventricular hypertrophy on myocardial blood flow and ventricular performance in systemic hypertension.

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Abstract
The effect of myocardial hypertrophy resulting from chronic pressure overload upon myocardial blood flow (MBF) and left ventricular (LV) performance was studied in 17 hypertensive patients, 9 of whom had left ventricular hypertrophy (LVH), and 9 normotensive controls. Mean LV MBF was measured at cardiac catheterization using the regional 133Xe washout technique. In hypertensive patients with LVH, LV MBF was reduced at rest (35.0 .+-. 5.4 ml/100 g per/min) compared with controls (64.8 .+-. 7.6 ml/100 g per/min, P < 0.01) and hypertensive patients without LVH (62.6 .+-. 14.5 ml/100 g per/min, P < 0.01). Coronary vascular resistance was elevated in the hypertensive patients with LVH (37.6 .+-. 6.6 dyn .cntdot. cm-5g-1, P < 0.01). Ejection fraction, mean velocity of circumferential fiber shortening (MVcf) and end-systolic and end-diastolic volumes were not significantly different among the 3 groups. Peak systolic stress was significantly lower (P < 0.01) in the hypertensive patients with LVH (225 .+-. 45 dyn .cntdot. cm-2 .cntdot. 10-3) than in the controls (385 .+-. 114 dyn .cntdot. cm-2 .times. 10-3) and the hypertensive patients without LVH (395 .+-. 39 dyn .cntdot. cm-2 .cntdot. 10-3). A multivariate regression equation was developed relating MBF to heart rate (HR), MVcf and peak LV wall stress. When MBF was adjusted for differences in stress among patients using the regression equation, there was no significant difference in MBF between hypertensive patients with and without LVH. Resting LV myocardial blood flow is normal in hypertensive patients without LVH. Resting MBF is reduced in controlled hypertensive patients with LVH as a consequence of reduced wall stress. Resting LV performance measured by ejection phase indexes is well preserved in hypertensive patients with and without LVH. Resting MBF in patients with normal coronary arteriograms evidently is related to hemodynamic indexes of the major determinants of myocardial O2 consumption.