Abstract 17337: Assessment of Myocardial Damage and Decompensated Physiology Based on the Stress-Strain Relation in Hypertensive Heart Failure Rat Model
Backgrounds: Previous studies suggested that the extent of the left ventricular wall strain is significantly determined by wall stress and myocardial contractility. Accordingly, the aim of the study was to evaluate the hypothesis that the stress-adjusted-strain well reflects disease pathophysiology in hypertensive heart failure.
Methods: Dahl salt-sensitive rat were fed low-(Control, n=41) or high-salt diet (HT-group, n=33) from 6 to 16 weeks-of-age and serially studied every 2 week by speckle tracking echocardiography. Longitudinal strain (LS) was measured and end-systolic meridional wall stress was calculated. Hemodynamics and the slope of the end-diastolic P-V relation (EDPVR), an index of left ventricular stiffness, was calculated using conductance catheter system. Mid-lateral wall of LV was pathologically analyzed for subendocardial, mid-wall, and subepicardial layer %-area- fibrosis.
Results: HT-rats developed progressive LV hypertrophy and decompensated heart failure at 16 weeks with preserved ejection fraction. Extent of subendocardial fibrosis was similar to that of control-group up to 12 weeks, and substantially increased at 14 weeks (10±3%, 3.2±0.7%, p=0.002). Based on pathological analysis, 14 weeks was determined as the on-set period of the pathological change developed. Stress-strain relation was linear from 6 to 12 weeks (LS = 28 − 0.22×Stress, r=0.16, p=0.03), and after 14 weeks, strain showed smaller value relative to that regression line. Expected-LS value was calculated based on the stress-strain relation regression formula 6 to 12 weeks in corresponding to each stress. And delta-LS was defined as the difference between measured-LS and expected-LS. Delta-LS significantly related to endocardial fibrosis (r=0.49, p=0.03), chamber stiffness constant from EDPVR (r=0.51, p=0.01) and lung/body weight ratio (r=0.68, p<0.001).
Conclusions: LV wall stress adjusted longitudinal strain may reflect tissue fibrosis, chamber stiffness, and lung-congestion in hypertensive heart failure. It may be important to take the wall stress into account in assessing longitudinal strain to detect hypertensive myocardial damage and decompensated physiology.
- © 2012 by American Heart Association, Inc.