The present paper provides a critical overview of left ventricular hypertrophy (LVH) and structural changes of carotid arteries as surrogate end points for antihypertensive treatments. LVH is known to be associated with a number of pathophysiologic alterations underlying cardiovascular risk. The quantification of left ventricular mass is feasible and well standardized by echocardiography, even if the reproducibility of measurements is still limited. LVH has been clearly demonstrated to be an independent predictor for cardiovascular morbidity and mortality, and recent data suggest that left ventricular geometric pattern and depressed myocardial function may represent additional risk factors. Although clinical trials have shown that an adequate blood pressure control can be associated with a significant reduction in left ventricular mass, the prognostic impact of LVH regression is still debated. Serial measurements of the carotid artery intima-media complex by B-mode ultrasound have been proposed as an accurate noninvasive approach for the evaluation of progression and regression of the atherosclerotic process over time. The methodology of measurement is not as well standardized as that of LVH, and the reproducibility of measurements is too close to the magnitude of structural changes over time. In addition, sounder data are required concerning the pathophysiologic relationship between carotid lesions and clinical events.

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