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Background: Among various intracellular signaling cascades associated with cardiac hypertrophy, the involvement of calcineurin(CaN; Ca2+-calmodulin dependen t protein phosphatase) is gaining credence because of its enhanced activity in ventricular myocardium and the ability of CaN inhibitors to prevent pressure-overload hypertrophy. Since our recent finding s attribute clinical significance to serum CaN, the present investigation was co nducted to evaluate its significance in cardiac hypertrophy. Methods: The study group comprised of patients diagnosed for hypertensive hypertrophy, hypertrophic cardiomyopathy, chronic coronary artery disease with compensatory left ventricu lar hypertrophy, dilated cardiomyopathy and acute myocardial infarction. Serum c ontents of CaN and calmodulin were determined and activities of CaN as well as o f acid and alkaline phosphatases were assayed and correlated with 2D echocardiog raphy findings. The results were compared with those obtained from age-matched healthy volunteers. Results: Serum CaN activity, but not of acid or alkaline pho sphatases, was significantly enhanced by 2-fold in hypertensive hypertrophy, 3 -fold in hypertrophic cardiomyopathy and 3.75-fold in chronic coronary artery disease associated with left ventricular hypertrophy, unaccompanied by changes i n serum contents of calmodulin and CaN. No such increases were observed in acute myocardial infarction and dilated cardiomyopathy. Conclusions: Positive correla tions observed between serum CaN activity and enhanced left ventricular mass in cardiac hypertrophy suggest that assaying serum CaN activity may be useful in th e diagnosis and management of left ventricular hypertrophy.
Background: Among various intracellular signaling cascades associated with cardiac hypertrophy, the involvement of calcineurin (CaN; Ca2 + -calmodulin dependen t protein phosphatase) is gaining credence because of its enhanced activity in ventricular myocardium and the ability of CaN inhibitors to prevent pressure-overload hypertrophy Since our recent finding s attribute clinical significance to serum CaN, the present investigation was co nducted to evaluate its significance in cardiac hypertrophy. Methods: The study group composed of patients diagnosed for hypertensive hypertrophy, hypertrophic cardiomyopathy, chronic coronary artery disease with compensatory left ventricu lar hypertrophy, dilated cardiomyopathy and acute myocardial infarction. Serum c ontents of CaN and calmodulin were determined and activities of CaN as well as of acid and alkaline phosphatases were assayed and correlated with 2D echocardiog raphy findings. The results were compared with those obtained from age-matc hed healthy volunteers. Results: Serum CaN activity, but not of acid or alkaline pho sphatases, was significantly enhanced by 2-fold in hypertensive hypertrophy, 3-fold in hypertrophic cardiomyopathy and 3.75-fold in chronic coronary artery disease associated with left ventricular hypertrophy , unaccompanied by changes in serum contents of calmodulin and CaN. No such amplities were observed in acute myocardial infarction and dilated cardiomyopathy. Conclusions: Positive correla tions observed between serum CaN activity and enhanced left ventricular mass in cardiac hypertrophy suggest that assaying serum CaN activity may be useful in th e diagnosis and management of left ventricular hypertrophy.