TY - JOUR
T1 - Diminished contractile reserve in patients with left ventricular hypertrophy and increased end-systolic stress during dobutamine stress echocardiography
AU - Fontanet, Héctor L.
AU - Pérez, Julio E.
AU - Dávila-Román, Víctor G.
N1 - Funding Information:
From the Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri; and the Department of Cardiology, llniversitv of South Florida. Tamaa. Florida. Dr. Da&Roman was supported in part by a Minority’Sdientist Development Award from the American Heart Association, Dallas, Texas. Manuscript received January 3 1, 1996; revised manuscript received and accepted May 6, 1996. Address for reprints: Victor G. D&la-Roman, MD, Cardiovascular Division, Box 8086, Washington University School of Medicine, 660 South Euclid Ave, St. Louis, Missouri 63 1 10.
PY - 1996
Y1 - 1996
N2 - Left ventricular hypertrophy (LVH) is associated with decreased contractile 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 ventricular mass, heart rate-corrected velocity of circumferential fiber shortening (Vcfc), end-systolic stress, and LV ejection fraction (LVEF) in patients with LVH and increased end-systolic stress (n = 6) and in patients without LVH (n = 7) who had a normal response to dobutamine stress echocardiography (increased LVEF and no wall motion abnormalities). The afterload-dependent indexes of left ventricular systolic performance were normal at baseline and showed significant increases at peak dobutamine dose (LVH group: Vcfc 0.91 ± 0.11 to 1.76 ± 0.59, p = 0.006; LVEF 49 ± 5 to 65 ± 6, p = 0.001; group without LVH: Vcfc 1.16 ± 0.24 to 1.99 ± 0.36, p = 0.001; LVEF 61 ± 6 to 68 ± 6, p = 0.05). The Vcfc/ end-systolic stress relation, a load-independent index of myocardial contractility, rose in a dosedependent fashion in both groups, but the increment was significantly less for patients with LVH (p <0.02), suggesting a blunted myocardial contractile reserve to inotropic stimulation. The change in heart rate-corrected velocity of circumferential fiber shortening per unit of change in end-systolic stress in each patient at each do-butamine dose showed a linear and inverse relationship. The increment in heart rate-corrected velocity of circumferential fiber shortening for a given reduction in end-systolic stress was larger in patients without LVH than in patients with LVH (p = 0.01). These results suggest that in patients with LVH and increased end-systolic stress, ventricular performance is maintained at the expense of limited myocardial contractile reserve, and that inotropic stimulation unmasks this abnormality, despite a normal response in LVEF and velocity of circumferential fiber shortening. This approach may identify patients with LVH at risk of developing systolic dysfunction and heart failure.
AB - Left ventricular hypertrophy (LVH) is associated with decreased contractile 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 ventricular mass, heart rate-corrected velocity of circumferential fiber shortening (Vcfc), end-systolic stress, and LV ejection fraction (LVEF) in patients with LVH and increased end-systolic stress (n = 6) and in patients without LVH (n = 7) who had a normal response to dobutamine stress echocardiography (increased LVEF and no wall motion abnormalities). The afterload-dependent indexes of left ventricular systolic performance were normal at baseline and showed significant increases at peak dobutamine dose (LVH group: Vcfc 0.91 ± 0.11 to 1.76 ± 0.59, p = 0.006; LVEF 49 ± 5 to 65 ± 6, p = 0.001; group without LVH: Vcfc 1.16 ± 0.24 to 1.99 ± 0.36, p = 0.001; LVEF 61 ± 6 to 68 ± 6, p = 0.05). The Vcfc/ end-systolic stress relation, a load-independent index of myocardial contractility, rose in a dosedependent fashion in both groups, but the increment was significantly less for patients with LVH (p <0.02), suggesting a blunted myocardial contractile reserve to inotropic stimulation. The change in heart rate-corrected velocity of circumferential fiber shortening per unit of change in end-systolic stress in each patient at each do-butamine dose showed a linear and inverse relationship. The increment in heart rate-corrected velocity of circumferential fiber shortening for a given reduction in end-systolic stress was larger in patients without LVH than in patients with LVH (p = 0.01). These results suggest that in patients with LVH and increased end-systolic stress, ventricular performance is maintained at the expense of limited myocardial contractile reserve, and that inotropic stimulation unmasks this abnormality, despite a normal response in LVEF and velocity of circumferential fiber shortening. This approach may identify patients with LVH at risk of developing systolic dysfunction and heart failure.
UR - http://www.scopus.com/inward/record.url?scp=0030294031&partnerID=8YFLogxK
U2 - 10.1016/S0002-9149(96)00592-9
DO - 10.1016/S0002-9149(96)00592-9
M3 - Article
C2 - 8916483
AN - SCOPUS:0030294031
SN - 0002-9149
VL - 78
SP - 1029
EP - 1035
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 9
ER -