A growing body of evidence indicates that the clustering of metabolic and hemodynamic abnormalities characterizing the metabolic syndrome is associated with a prevalence of subclinical damage in a variety of organs, such as left ventricular hypertrophy, thickening or atherosclerotic plaques of carotid arteries, microalbuminuria and deranged renal function. This is clinically relevant since these markers of target organ damage are associated with an increased risk of cardiovascular fatal and nonfatal events. The contribution of the metabolic syndrome to target organ damage in hypertensives is presumably responsible for a substantial increase in cardiovascular fatal and nonfatal events. Thus, target organ damage should be routinely searched for in hypertensives with metabolic syndrome in order to define initial therapeutic strategies and to monitor treatment-induced protection.