P-1 Remodeling of Myocardial Gap Junctions and its Correlation with Cardiac Contractility in Diabetic Rats

Abstract

not available at time of printing. Poster Sessions 1: Heart Failure/Myocardial Diseases P-1 Remodeling of Myocardial Gap Junctions and its Correlation with Cardiac Contractility in Diabetic Rats Dong-Feng Yeih1, Pen-Chih Liao1, Ho-Tsung Hsin1, Kuo-Chin Chen1, Ai-Hsian Li1, Yung-Zu Tseng2. 1Department of Cardiology, Far-Eastern Memorial Hospital, Taiwan, 2Department of Cardiology, National Taiwan University, Taiwan Introduction: Gap junctions play an essential role in coupling adjacent cardiomyocytes, ensuring organized propagation of action potential and synchronizing beating in cardiomyocytes. However, it remains unclear that temporal remodeling of myocardial gap junctions and its relation to cardiac contractility in diabetic rats. Methods: Male Wistar rats, weighing 250 to 300 grams, were randomized to injection with either vehicle or streptozotocin (50mg, IP). Invasive hemodynamic studies with simultaneous recordings of left ventricular pressure and aortic flow signals were done at 4, 8 and 12 weeks after injection. Maximal systolic elastance (Emax) and maximum theoretical flow (Qmax) were assessed by curve fitting techniques; protein expression of non-phosphorylated Cx43 (P0) and total amount of Cx43 (T) in the left ventricle by western blotting analysis. Results: Emax was significantly lower in diabetic rats than in controls and Emax was significantly depressed with time in diabetic groups. On the other hand, Qmax was preserved and cardiac output was maintained in diabetic rats. Protein expression of total Cx43 was persistently attenuated in diabetic groups, while P0 was enhanced at 8 and 12 weeks after injection. The ratio of P0 to T was significantly increased with time, which correlated well with the declines in Emax in diabetic rats. Conclusions: Temporal remodeling of myocardial gap junctions, with persistently lower total Cx43 and gradually increased non-phosphorylated Cx43 and the ratio of P0 to T, occurred in the evolution of systolic dysfunction in diabetic rats. P-2 Quantification of Left Ventricular Diastolic Dynamics in Normal and Diseased Myocardium by Speckle-Tracking Echocardiography Kaoru Dohi1, Katsuya Onishi2, Takeshi Takamura1, Emiyo Sugiura1, Hiroshi Nakajima1, Kazuhide Ichikawa1, Masaki Tanabe1, Hiroya Tamada1, Masatoshi Miyahara1, Mashio Nakamura1, Masaaki Ito1. 1Department of Cardiology, Mie University Graduate School of Medicine, Japan, 2Department of Molecular and Laboratory Medicine, Mie University Graduate School of Medicine, Japan Background: The present study aimed to quantify left ventricular (LV) diastolic dynamics and to elucidate their relations to systolic properties in normal and diseased myocardium. Methods: 50 patients with hypertensive LV hypertrophy (LVH: EF 61±8%, QRS 96±16ms), 50 patients with dilated cardiomyopathy (DCM: EF 31±10%, QRS 121±32ms), and 50 normal controls (Control: EF 5±6%, QRS 89±9ms) had echo-study with speckle-tracking strain and strain rate imaging. To quantify LV diastolic relaxation and segmental synchrony, global peak relaxation rate (PRR) during early diastole and standard deviation (SD) of the 18 segmental time-to-PRR (TPRR-SD) were calculated from apical 4-, 2-, and long axis views. To elucidate the relations between diastolic and systolic properties, global peak systolic strain (PSS) and SD of the segmental time-to-peak PSS (TPSS-SD) were also evaluated. Results: LV relaxation and diastolic synchrony were significantly impaired in LVH and was more prominent in DCM (PRR: 0.8±0.3* 1/s in LVH, 0.5±0.2*# 1/s in DCM, and 1.2±0.3 1/s in Control, TPRR-SD: 55±16*ms in LVH, 79±35*# ms in DCM, and 42±13ms in Control, *p < 0.05 vs. Control and #p < 0.05 vs. LVH, respectively). There were strong correlations between PSS and PRR, and TPRR-SD and TPSS-SD (r = 0.83 and r = 0.83, p < 0.05, respectively). Conclusion: Speckle-tracking echocardiography quantified LV diastolic dynamics and exhibited the strong relation to systolic properties.