Biological adaptation of the myocardium to chronic mechanical overload. Molecular determinants of the autonomic nervous system

Abstract

Cardiac hypertrophy due to chronic mechanical overload is the physiological reaction of the heart to a disease, but is not a disease itself. The hypertrophied heart is both quantitatively and qualitatively modified, and these changes allow the heart to produce normal active tension at a low cost in terms of heat production. The biological cascade which finally leads to hypertrophy includes a trigger which is likely to be mechanical stretch, the phosphoinisitol pathway and a target at the level of DNA. Most of the physiological alterations observed during cardiac overload include changes in systolic and diastolic function and arrhythmias. The components of the autonomous nervous system are also greatly modified and their regulation is a rather complex issue. Future research to elucidate these mechanisms centres on the regulation process and the possibilities offered by gene transfer.