ABSTRACT
It is now accepted that besides left ventricular hypertrophy (LVH) that characterizes hypertensive heart disease (HHD), changes in the composition of myocardial tissue (i.e. remodeling) develop in the hypertensive heart.1 Whereas LVH provides the adaptive response of the cardiomyocyte compartment to pressure overload in an attempt to normalize systolic wall stress, myocardial remodeling is mostly the consequence of a number of neurohormonally and cytokine-mediated pathological processes occurring both in the cardiomyocyte and the noncardiomyocyte compartments of the hypertensive heart. Some of these processes are related to the exaggerated loss of cardiomyocytes due to apoptosis and the excessive accumulation of collagen type I and III fibers in the myocardium. This chapter deals with the potential molecular mechanisms involved in both the origin and the consequences of apoptosis and fibrosis in HHD.
