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RAS inhibition is more effective than beta‐blockade in preventing dilated cardiomyopathy in the Syrian Cardiomyopathic Hamster (SCH).
Author(s) -
Crespo Maria J,
Cruz Nildris,
Escobales Nelson
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a869-c
Subject(s) - dilated cardiomyopathy , blockade , cardiomyopathy , medicine , cardiology , hamster , beta (programming language) , pharmacology , heart failure , receptor , computer science , programming language
Heart failure (HF) is a debilitating disease that involves, in the compensation phase, activation of the renin‐angiotensin (RAS) and adrenergic systems. These endocrine compensations, however, lead to worsening of the condition. To evaluate the role of these systems on the development of dilated cardiomyopathy, we treated 1‐month‐old SCH with enalapril (25mg/kg/d) plus losartan (10mg/kg/d) or carvedilol (1 mg/kg/d) for 5 months. Left ventricular end diastolic‐ and systolic‐ volumes (LVEDV and LVESV), ejection fraction (EF), and left ventricular posterior wall thickness (LVPWT) were determined by echocardiography. Results indicate that LVEDV and LVESV decreased 30% and 62%, respectively (P<0.05) during RAS blockade, while EF increased 42% (P<0.05). By contrast, carvedilol only reduced LVESV by 28% (P<0.05) and increased EF by 18% (P<0.05). While beta‐blockade did not prevent posterior wall thickness reduction, RAS inhibition maintained normal wall thickness (0.11 ± 0.01 cm). These results suggest that early suppression of RAS is more effective than beta‐blockade in preventing the development of cardiomyopathy in this animal model. Supported by a grant from NIH (2 SO6 GM08224).