[Biological bases of ventricular remodeling]

Cardiac hypertrophy commonly observed in clinical practice is not a disease but a physiological reaction to disease, usually hypertensive or coronary. It involves changes in gene expression, often species specific, which account for the thermodynamic adaptation of the cardiac muscle to new conditions of load; some of these changes may have deleterious effects and explain changes in diastolic compliance and the arrhythmogenicity of hypertrophied hearts. The most important changes are in the myosin content and certain membrane proteins. Many hormonal factors also play a role in ventricular remodeling including angiotensin II and, independently, aldosterone.