La. Ferrara et al., EARLY CHANGES OF THE ARTERIAL CAROTID WALL IN UNCOMPLICATED PRIMARY HYPERTENSIVE PATIENTS - STUDY BY ULTRASOUND HIGH-RESOLUTION B-MODE IMAGING, Arteriosclerosis and thrombosis, 14(8), 1994, pp. 1290-1296
Arterial hypertension is frequently responsible for arteriosclerotic d
amage in the carotid region. Nevertheless, there is as yet no general
agreement that hypertension is correlated with lesions detected by non
invasive means in the carotid arteries. We studied, by noninvasive ech
otomographic technique, 70 uncomplicated primary hypertensive individu
als without clinically evident end-organ complications and 30 normoten
sive matched control subjects to detect early lesions of carotid arter
ies. The presence of other cardiovascular risk factors was assessed, a
nd heart structure and function were studied by echocardiography. Alth
ough 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 carot
id wall, both monolaterally and bilaterally (P<.003 by chi(2) test). A
mong the different factors contributing to the increase in thickness o
f the carotid artery wall, standing blood pressure, serum triglyceride
s, and age were found to be the best predictors (they accounted for ab
out 16% of the variability, P<.005). These results indicate that carot
id 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 e
nd-organ damage of hypertension. Moreover, this finding sheds new ligh
t on the relationship between arterial wall damage and insulin resista
nce, since all the main contributors to intimal-medial thickening are
particularly altered in the presence of hyperinsulinemia and increased
insulin resistance.