Akademik Veri Yönetim Sistemi
Journal of Cardiac Failure, cilt.11, sa.8, ss.638-644, 2005 (SCI-Expanded)
Background: The mechanisms of cardiac remodeling during chronic heart failure remain poorly defined. We sought to advance a chronic canine model of nonischemic cardiomyopathy. Methods and Results: Male dogs (n = 6) received decremental right ventricular apical tachypacing (12 months) to achieve and maintain stable left ventricular (LV) dysfunction. After 10 months of tachypacing, 120 beats/min was sufficient to maintain stable LV dysfunction. Electrocardiography, echocardiography, and tissue Doppler imaging were done to evaluate electrophysiology, LV dimensions and function, and dyssynchrony during normal sinus rhythm. The 6-minute walk test was used to evaluate functional capacity. We observed increases in both QRS duration (P < .0001) and QRS amplitude (P < .0001). LV fractional shortening was reduced from a baseline of 38.0 ± 1.4% to 11.2 ± 1.4% (P < .0001). LV end-diastolic dimension increased from 3.8 ± 0.1 cm at baseline to 5.3 ± 0.3 cm (P < .0001); LV end-systolic dimension increased from 2.3 ± 0.1 cm to 4.7 ± 0.2 cm (P < .0001). LV mass increased from 85.9 ± 3.5 g at baseline to 179 ± 13.7 g (P < .0001). There was evidence of LV dyssynchrony (P < .04) during both normal sinus rhythm and right ventricular tachypacing, compared with control dogs. The distance a dog walked in 6 minutes was significantly less at 12 months compared with normal controls (540 ± 32 m versus 277 ± 64 m, P < .008). Conclusion: This nonischemic model of canine cardiomyopathy reproduces many aspects of chronic human heart failure including reduced fractional shortening, dilated ventricular dimensions, increased LV mass, decreased functional capacity, and dyssynchrony. © 2005 Elsevier Inc. All rights reserved.