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Left ventricular hypertrophy in the SS‐16BN/Mcwi model of HCM results in accelerated cardiac morbidity
Author(s) -
Kriegel Alison Jessica,
Greene Andrew Seth
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.21.5.a584-b
Subject(s) - medicine , cardiology , afterload , ejection fraction , muscle hypertrophy , fibrosis , left ventricular hypertrophy , heart failure , hypertrophic cardiomyopathy , ventricular hypertrophy , cardiac function curve , cardiomyopathy , concentric hypertrophy , hypertensive heart disease , endocrinology , ventricle , blood pressure
The SS‐16 BN /Mcwi (SSBN16) is a consomic rat model of hypertrophic cardiomyopathy resulting from the introgression of chromosome 16 from the Brown Norway rat onto the genetic background of the SS/Mcwi (Dahl Salt‐Sensitive (SS)). SS rats are a model of left ventricular hypertrophy due to increased afterload from hypertension. Unlike SS rats, SSBN16 rats do not exhibit hypertension on a low (1%) or high (4%) salt diet. Despite being normotensive, SSBN16 rats undergo left ventricular hypertrophy and an associated decline in cardiac function. At 36 weeks of age 4 out of 9 SSBN16 rats on a low salt diet either died or were unable to stand and exhibited labored breathing. Before euthanasia of surviving animals (n=7) transthoracic echocardiography was performed and cardiac function was compared to that of 18 week old SSBN16 rats (n=20). We observed a 19% reduction in fractional shortening (55.21%±1.87 and 44.72%±1.59 respectively). The rats also exhibited systolic dysfunction at 36 weeks of age as their ejection fraction dropped by 9% and end systolic volume more than doubled. Left ventricular tissue revealed extensive perivascular fibrosis in all animals and increased myocyte diameter in those in poor health. The absence of hypertension, accelerated morbidity and the rapid progression to pathological heart failure in SSBN16 compared to SS suggests a unique mechanism of cardiac disease in this model. Support HL 29587, HL66579