DIMINISHED CONTRACTILE RESERVE IN PATIENTS WITH LEFT-VENTRICULAR HYPERTROPHY AND INCREASED END-SYSTOLIC STRESS DURING DOBUTAMINE STRESS ECHOCARDIOGRAPHY

Left ventricular hypertrophy (LVH) is associated with decreased contra ctile response to inotropic stimulation in animal models, but this has not been documented in humans. To determine whether LVH is associated with decreased myocardial contractile reserve, we measured left ventr icular mass, heart rate-corrected velocity of circumferential fiber sh ortening (Vcf(c)), end-systolic stress, and LV ejection fraction (LVEF ) in patients with LVH and increased end-systolic stress (n = 6) and i n patients without LVH (n = 7) who had a normal response to dobutamine stress echocardiography (increased LVEF and no wall motion abnormalit ies). The afterload-dependent indexes of left ventricular systolic per formance were normal at baseline and showed significant increases at p eak dobutamine dose (LVH group: Vcf(c) 0.91 +/- 0.11 to 1.76 +/- 0.59, p = 0.006; LVEF 49 +/- 5 to 65 +/- 6, p = 0.001; group without LVH: V cf, 1.16 +/- 0.24 to 1.99 +/- 0.36, p = 0.001; LVEF 61 +/- 6 to 68 +/- 6, p = 0.05). The Vcf(c)/ end-systolic stress relation, a load-indepe ndent index of myocardial contractility, rose in a dose-dependent fash ion in both groups, but the increment was significantly less for patie nts with LVH (p <0.02), suggesting a blunted myocardial contractile re serve to inotropic stimulation. The change in heart rate-corrected vel ocity of circumferential fiber shortening per unit of change in end-sy stolic stress in each patient at each dobutamine dose showed a linear and inverse relationship. The increment in heart rate-corrected veloci ty of circumferential fiber shortening for a given reduction in end-sy stolic stress was larger in patients without LVH than in patients with LVH (p = 0.01). These results suggest that in patients with LVH and i ncreased end-systolic stress, ventricular performance is maintained at the expense of limited myocordial contractile reserve, and that inotr opic stimulation unmasks this abnormality, despite a normal response i n LVEF and velocity of circumferential fiber shortening. This approach may identify patients with LVH at risk of developing systolic dysfunc tion and heart failure. (C) 1996 by Excerpta Medica, Inc.