Background: Among various intracellular signaling cascades associated with cardiac hypertrophy, the involvement of calcineurin (CaN; Ca2+- calmodulin dependent 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 findings attribute clinical significance to serum CaN, the present investigation was conducted 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 ventricular hypertrophy, dilated cardiomyopathy and acute myocardial infarction. Serum contents of CaN and calmodulin were determined and activities of CaN as well as of acid and alkaline phosphatases were assayed and correlated with 2D echocardiography findings. The results were compared with those obtained from age-matched healthy volunteers. Results: Serum CaN activity, but not of acid or alkaline phosphatases, 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 increases were observed in acute myocardial infarction and dilated cardiomyopathy. Conclusions: Positive correlations observed between serum CaN activity and enhanced left ventricular mass in cardiac hypertrophy suggest that assaying serum CaN activity may be useful in the diagnosis and management of left ventricular hypertrophy.
- Cardiac hypertrophy
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine