Several studies, performed during the past 20 years in different experimental animal models of hypertension and in men, have allowed to clarify important pathophysiological and clinical aspects of the hypertensive cardiovascular disease, i.e. the pathological condition characterized by marked structural and functional alterations of the heart induced by arterial hypertension. Epidemiological studies have indeed clearly shown that the prevalence of left ventricular hypertrophy in large hypertensive population samples is markedly high (40-50%) and that the electrocardiographic evidence of cardiac hypertrophy adversely affects patient's prognosis, by significantly increasing cardiovascular morbidity (myocardial infarction, congestive heart failure and cardiac arrhythmias) and mortality (sudden death). It has also been shown that cardiac hypertrophy is characterized by profound functional alterations in myocardial contractility and impairs neural reflex responses to beta-adrenergic stimulation and to deactivation of cardiopulmonary volume receptors, which are involved in physiological conditions in blood volume homeostasis control. Finally, several interventional studies have unequivocally shown that antihypertensive drugs may allow to obtain, even following 3-6 months of treatment, along with a blood pressure reduction, a clearcut regression of cardiac hypertrophy. By improving cardiovascular hemodynamics and neural control of circulation, regression of cardiac structural alterations is associated with a significant reduction in the patient's cardiovascular risk profile.