LEFT-VENTRICULAR HYPERTROPHY AND IMPAIRED DIASTOLIC FILLING IN ESSENTIAL-HYPERTENSION - DIASTOLIC MECHANISMS FOR SYSTOLIC DYSFUNCTION DURING EXERCISE

Left ventricular ejection fraction is normal at rest but may respond abnormally to exercise in many patients with essential hypertension. To assess the determinants of the abnormal ejection fraction response to exercise, we performed radionuclide angiography at rest and during exercise in 41 hypertensive patients without coronary artery disease. In 22 patients (group 1), the ejection fraction increased more than 5% during exercise; in the other 19 patients (group 2), the ejection fraction either increased by less than 5% or decreased with exercise. Left ventricular diastolic filling was impaired at rest in patients in group 2 compared with group 1, with reduced peak filling rate (2.5 ± 0.4 vs. 3.1 ± 0.7 end-diastolic volume/sec; p < 0.01) and prolonged time to peak filling rate (175 ± 28 vs. 153 ± 22 msec; p < 0.01). Impaired diastolic filling in group 2 was associated with less augmentation in end-diastolic volume during exercise compared with group 1 (p < 0.01). These observations were not dependent on the threshold value that was arbitrarily chosen to define an abnormal ejection fraction response, as there were significant correlations for the entire group between the magnitude of change in ejection fraction with exercise and both the resting peak filling rate (r = 0.46) and the change in end-diastolic volume with exercise (r = 0.62). Echocardiographic left ventricular mass index was greater in group 2 than in group 1 (141 ± 32 vs. 114 ± 25 g/m2; p < 0.01), and for the entire group was significantly related to peak filling rate (r = -0.50) and time to peak filling rate (r = 0.53). Thus, the abnormal ejection fraction response to exercise in patients with hypertension is related to greater left ventricular mass index and impaired diastolic filling, leading to inadequate augmentation of end-diastolic volume during exercise to maintain systolic function. These findings support the concept that exercise-induced systolic dysfunction in hypertensive patients with left ventricular hypertrophy arises predominantly from diastolic mechanisms.