Abstract

SUMMARY 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, nine of whom had left ventricular hypertrophy (LVH), and nine normotensive controls. Mean LV MBF was measured at cardiac catheterization using the regional xenon-133 washout technique. In hypertensive patients with LVH, LV MBF was reduced at rest (35.0 ± 5.4 ml/100 g/min) compared with controls (64.8 ± 7.6 ml/100 g/min, p < 0.01) and hypertensive patients without LVH (62.6 ± 14.5 ml/ 100 g/min, p < 0.01). Coronary vascular resistance was also elevated in the hypertensive patients with LVH (37.6 ± 6.6 dyn * cm−5g−1, p < 0.01). In contrast, ejection fraction, mean velocity of circumferential fiber shortening(MVcf) and end-systolic and end-diastolic volumes were not significantly different among the three groups. Peak systolic stress was significantly lower (p < 0.01) in the hypertensive patients with LVH (225 ± 45 dyn * cm−2 X 10−8) than in the controls (385 ± 114 dyne cm−2 X 10−8) and the hypertensive patients without LVH (395 ± 39 dyn. cm−2 X 10−8). A multivariate regression equation was developed relating MBF to heart rate (HR), MVcf, and peak LV wall stress: MBF = 22.2 MVcf + 10.6 stress + 0.38 HR- 48.2 (r = 0.89, p < 0.01). 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. These results indicate that (1) resting LV myocardial blood flow is normal in hypertensive patients without LVH; (2) resting MBF Is redSuced in controlled hypertensive patients with LVH as a consequence of reduced wall stress; and (3) resting LV performance measured by ejection phase indexes is well preserved in hypertensive patients with and without LVH. These results also provide additional evidence that resting MBF in patients with normal coronary arteriograms is related to hemodynamic indexes of the major determinants of myocardial oxygen consumption.

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