Abstract 4203: Diastolic Wall Strain Can Noninvasively Predict Hemodynamic Deterioration Unassociated with Systolic Dysfunction in Hypertensive Hearts
This study examined whether LV diastolic wall strain (DWS) could noninvasively predict the transition to decompensated diastolic heart failure (DHF) in hypertensive hearts. Dahl salt-sensitive rats fed 0.3 % NaCl diet served as control group (group N: n=8) and those fed 8 % NaCl diet as hypertensive group (group HT: n=15). Serial Doppler echocardiographic studies were performed at age 13, 17 and 19 weeks. At 19 weeks, LV pressure was measured following the echocardiographic study. DWS was calculated as [(end-systolic thickness of LV posterior wall) - (end-diastolic thickness of LV posterior wall)]/(end-systolic thickness of LV posterior wall). Mid-wall fractional shortening (MFS) was not different between two groups at any stage. At 13 weeks (compensatory hypertrophic stage), the transmitral flow velocity curves (TMFV) represented the abnormal relaxation pattern with low E/A ratio in group HT. At 19 weeks (heart failure stage), E/A increased with the elevation of LV end-diastolic pressure and lung weight in group HT. DWS was not different between two groups at 13 weeks, however, its decrease preceded the pseudonormalization of TMFV at 17 weeks in group HT and continued until 19 weeks. The difference between the endocardial and epicardial movements is equal to that between the wall thickness at end-systole and end-diastole (a numerator of DWS). Therefore, based on the linear elastic theory, DWS is considered to decrease with increase of LV wall stiffness. We previously demonstrated that myocardial stiffness constant was elevated at age 17 weeks but not at age 13 weeks in Dahl salt-sensitive rats fed high-salt diet. The current results indicate that DWS is helpful in noninvasively predicting hemodynamic deterioration without the changes in systolic function, which is explained partly by the theory that DWS reflects LV wall stiffness.