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- W2020754803 abstract "Despite numerous studies on cardiac hypertrophy and heart failure, the precise mechanisms by which a well-compensated hypertrophied heart eventually decompensates are not fully understood (1). A major shortcoming of previous experimental studies is that progression from compensated left ventricular (LV) hypertrophy to overt, clinically relevant, congestive heart failure could not be clearly demonstrated in an individual model animal. Aortic banding (2,3), renal artery constriction (4), and coronary artery ligation (5,6) are common procedures used to create animal models for LV hypertrophy or failure. However, these methods have the disadvantages of using specific surgical procedures and of having extremely variable time courses in developing predicted cardiac disorders. In genetic cardiomyopathy in hamsters (7,8) and viral myocarditis in mice (9), rats (10), and rabbits (11) administered cardiotoxic drugs such as adriamycin, heart failure ensues from myocardial cell" @default.
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- W2020754803 date "1996-12-01" @default.
- W2020754803 modified "2023-09-25" @default.
- W2020754803 title "Changes of myocardial contractile state and theintracellular calcium transients during transitions to heart failure: Studies in dahl rat heart failure model" @default.
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- W2020754803 doi "https://doi.org/10.1016/s1071-9164(96)80066-2" @default.
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