Key result
Gradually developing left ventricular pressure overload in dogs caused moderate hypertrophy but no significant difference in end-diastolic elastic stiffness compared to controls (221 vs 221 g/cm2).
Why the study?
Does gradually developing left ventricular pressure overload alter diastolic myocardial stiffness in a canine model?
Does gradually developing left ventricular pressure overload alter diastolic myocardial stiffness in a canine model?
Absolute Event Rate: 221% vs 221%
p-value: p=not significant
Moderate left ventricular hypertrophy resulting from chronic, gradually developing pressure overload is an adaptive process that maintains normal myocardial stiffness.
Supports adaptive role of moderate hypertrophy in maintaining stiffness; leaves open translation to human pressure-overload states.
The effects of gradually developing left ventricular pressure overload on diastolic myocardial stiffness were studied in a chronic moderate hypertrophy model. A snug aortic band was placed beneath the left coronary artery in six puppies 4.5 wk of age, and hemodynamic studies were performed 33.5 wk later. In all six dogs, moderate pressure gradients (10-58 mmHg) developed across the constriction, and angiographic area of the aortic constriction was significantly smaller than for a control group, 4.9 +/- 0.5 vs. 8.4 +/- 0.8 mm2/kg, (mean +/- SE, P less than 0.05). Increases occurred in left ventricular (LV) wall thickness (1.08 +/- 0.07 vs. 0.83 +/- 0.04 cm, P less than 0.05), LV wall mass (5.2 +/- 0.3 vs. 4.1 +/- 0.2 g/kg, P less than 0.05), and wall thickness-to-radius ratio (0.67 +/- 0.04 vs. 0.50 +/- 0.03, P less than 0.01), whereas no differences were noted in LV end-diastolic pressure (11 +/- 1 vs. 9 +/- 1 mmHg), LV end-diastolic volume (LVEDV, 2.06 +/- 0.22 vs. 2.35 +/- 0.15 ml/kg) or ejection fraction (71 +/- 4 vs. 71 +/- 3%). The values of LV wall mass, LVEDV, and aortic constriction are normalized to body weight. Diastolic LV myocardial stiffness was examined in terms of the elastic stiffness-stress relations. There were small and insignificant differences in end-diastolic stress (17.3 +/- 1.5 vs. 20.4 +/- 3.8 g/cm2), myocardial stiffness constant (Km, 13.7 +/- 5.6 vs. 11.2 +/- 3.3), and end-diastolic elastic stiffness (221 +/- 67 vs. 221 +/- 79 g/cm2) between hypertrophied and control hearts. No significant differences in the elastic stiffness of hypertrophied and normal muscle were observed over the common stress range of 5-25 g/cm2. We conclude that moderate left ventricular hypertrophy in chronic, gradually developing pressure overload is an adaptation process associated with normal myocardial stiffness.
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Serizawa et al. (1982) studied Left ventricular hypertrophy. Aortic banding (gradually developing left ventricular pressure overload) vs. Control group was evaluated on End-diastolic elastic stiffness (g/cm2) (p=not significant). Gradually developing left ventricular pressure overload in dogs caused moderate hypertrophy but no significant difference in end-diastolic elastic stiffness compared to controls (221 vs 221 g/cm2).
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