Cardiomyopathy in general is defined as a disease of the heart muscle. The purpose of this study is to test the hypothesis that sodium-hydrogen exchanger (NHE1) abnormality is a common cause of cardiac and vascular failures in hereditary cardiomyopathy of the hamster. We verified whether heart failure is accompanied by vascular abnormalities in NHE1.
In order to conduct this study we used complementary techniques such as measurement of mean arterial pressure, cardiac and vascular cells intracellular Ca2+, Na+ and NHE1 levels as well as real 3D confocal microscopy and Western blot.
Our results show an increase in intracellular Ca2+ and Na+ that is associated with an increase in NHE1 levels and activities in both cardiac and vascular myocytes. In addition, these abnormalities were accompanied by necrosis and hypertrophy of cardiomyocytes but not of vascular myocytes. Furthermore, in addition to these cardiac and vascular defects, a decrease in mean arterial pressure was observed during the development of hereditary cardiomyopathy of the hamster. No changes in aortic thickness and the density of elastin were observed.
In conclusion, our results suggest that hereditary cardiomyopathy is not only a cardiac disease but is also a vascular disease where NHE1 could be a common cause and that treatment with a NHE1 blocker would prevent not only the development of cardiac failure but also vascular failure.