EARLY CHANGES OF THE ARTERIAL CAROTID WALL IN UNCOMPLICATED PRIMARY HYPERTENSIVE PATIENTS - STUDY BY ULTRASOUND HIGH-RESOLUTION B-MODE IMAGING

Arterial hypertension is frequently responsible for arteriosclerotic damage in the carotid region. Nevertheless, there is as yet no general agreement that hypertension is correlated with lesions detected by noninvasive means in the carotid arteries. We studied, by noninvasive echotomographic technique, 70 uncomplicated primary hypertensive individuals without clinically evident end-organ complications and 30 normotensive matched control subjects to detect early lesions of carotid arteries. The presence of other cardiovascular risk factors was assessed, and heart structure and function were studied by echocardiography. Although hypertensive individuals were comparable to control subjects for other risk factors, they showed a marked increase in the thickness of the intimal-medial complex of the carotid wall (0.71+/-0.4 versus 0.56+/-0.2 mm, P<.001 in the right carotid and 0.83+/-0.3 versus 0.58+/-0.2, P<.003 in the left), in left ventricular mass (203+/-52 versus 176+/-37 g, P<.05), and in the prevalence of definite plaques of the carotid wall, both monolaterally and bilaterally (P<.003 by chi(2) test). Among the different factors contributing to the increase in thickness of the carotid artery wall, standing blood pressure, serum triglycerides, and age were found to be the best predictors (they accounted for about 16% of the variability, P<.005). These results indicate that carotid arteries of hypertensive individuals undergo degenerative changes, just as shown for hypercholesterolemic and diabetic patients in other studies. This supports the use of B-mode ultrasound imaging to detect early involvement of the carotid region before the appearance of any end-organ damage of hypertension. Moreover, this finding sheds new light on the relationship between arterial wall damage and insulin resistance, since all the main contributors to intimal-medial thickening are particularly altered in the presence of hyperinsulinemia and increased insulin resistance.