PP.08.10

Abstract

Objective: This study aimed to observed the relationships of myocardial collagen with myocardial deformation and left ventricular global function in SHR, to investigate the role of collagen accumulation in the development of cardiac dysfunction in hypertension. Design and method: SHR were randomly divided into 9 groups and studied at different weeks(from 12 to 84wks, and WKY rats at the similar weeks of age as control. Conventional parameters and 2DSE measurements including LV longitudinal, radial and circumferential strain (SL, SR, SC) were acquired echocardiographically, and invasive LVEDP and LV ± dp/dtmax were detected within 24hrs after echo exam, and collagen volume fraction (CVF) in subendocardial and subepicardial myocardiumwere observed histologically. Results: (1)RWT and LVMI increased with age in SHR, and reached the peak at 75–84 wks (p < 0.05), and the difference from WKY found after 75 wks (p < 0.05); (2) 2DSE drived SL, SC and SR in SHR increased progressively from 12 to 28 wks(p < 0.05), and SL declined at 45 wks (p < 0.05), while SC, SR decreased at 75wks(p < 0.05), all reached to the minimum at 84wks (p < 0.05), and the difference between SHR and WKY occurred after 66wks; (3) CVF in SHR increased with age, with the subendocardial exceeding the epicardial myocardium from 66wks, especially after 75 wks (p < 0.05), and higher than WKY after 66wks; 4) LV ± dp/dtmax increased from 12 to 28 wks and decreased from 36 to 82wks in SHR(p < 0.05), whereas LVEDP increased from 36 to 82wk, different from those in WKY. (5) Subendocardial CVF correlates negatively with SL (r = −0.47, p = 0.002) and SR, SC(−0.37 ∼ −0.41, p < 0.05), LVEDP correlated with CVF (r = 0.57, p < 0.01). Conclusions: Pathological myocardial fibrosis concerned with hypertension begins at 66 weeks of age in SHR, with interstitial collagen developing from inner to out layer of myocardium; and the development of fibrosis might contribute to the progression of damaged multi-dimensional systolic strain, where longitudinal strain involved firstly and LVEF declines when all directions of systolic strain reduced, which might provide a mechanical and pathological basis for the investigation of the development in hypertensive cardiac dysfunction.