Abstract. Pancera P, Ribul R, Presciuttini B, Lechi A (Universita Á di Verona, Italy). Prevalence of carotid artery kinking in 590 consecutive subjects evaluated by Echocolordoppler. Is there a correlation with arterial hypertension? J Intern Med 2000; 248: 7±12.Objective. To assess a possible correlation between high blood pressure and prevalence of kinking in carotid arteries. Design. Between July 1, 1997 and December 31, 1998, we evaluated the subjects submitted to Echocolordoppler examination of carotid arteries. Setting. Patients were examined at the Laboratory for Noninvasive Vascular Diagnostics of the University Hospital in Verona. Subjects.F ratio, 1/1.2; mean age, 67 years; range, 36±86 years). Main outcome measures. An Echocolordoppler ultrasonograph to evaluate by means of the standard longitudinal and transverse scans the usual parameters of both intima-to-lumen interface and flow.Moreover, particular attention was paid to the analysis of the conformational characteristic of the vessels. Kinking has been classified in three classes according to the degree of bending. All the subjects were asked to compile a questionnaire that provided us with the clinical history.Results. The prevalence of hypertension in the subjects with kinking appeared higher than in subjects without this abnormality (x 2 = 6.44, P , 0.02). We found also a significant association between kinking and transitory ischaemic attacks (x 2 = 6.987, P , 0.01). Conclusions. The high prevalence of kinking in the hypertensives agrees with the pathogenetical hypothesis ascribing a role to the high endoluminal pressure. The presence of hypertension and kinking of the internal carotid artery suggests that they could be additive risk factors in the pathophysiology of a transitory ischaemic attack.

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Haemodynamic changes in the carotid and brachial arteries produced by single doses of four anti-hypertensive drugs (nicardipine, enalapril, atenolol, and urapidil) have been studied in 12 patients with essential hypertension. Measurements were performed noninvasively using a mechanographic method and B-mode pulsed Doppler ultrasonography. Within 7 h all of the drugs had caused a significant reduction in blood pressure, whereas heart rate showed a significant change only after atenolol. All the drugs produced a marked reduction in brachial pulse-wave velocity. Only nicardipine caused a significant reduction in vessel wall tension both in the carotid and brachial arteries, while brachial peripheral resistance was significantly reduced by all the drugs except atenolol. Neither atenolol nor enalapril caused any significant reduction in carotid peripheral resistance. The results show that all four antihypertensive drugs led to a beneficial increase in arterial compliance despite their different effects on peripheral resistance.

(-216.1 ng 24 h-1, 95% CI -276.5, -155.8; P < 0.001), together with an increase in systolic (+7.8 mm Hg, 95% CI +3.1, +12.3; P < 0.01) and diastolic (+3.9 mm Hg, 95% CI +1.2, +6.6; P < 0.01) blood pressure; it had no significant effect on regional vascular resistances (+4.7 mm Hg ml-l s, 95% CI -5.6, +15.0). Effects of ibuprofen on renal prostanoid synthesis were less marked, and there was no change in indices of renal function or hydro-electrolytic balance. 5 The haemodynamic effects of amlodipine may be partially antagonised by ibuprofen, which mainly determines inhibition of extrarenal prostanoid synthesis. It is suggested that this antagonism is attributable not so much to a direct effect of the calcium antagonist on prostacyclin synthesis as to an alteration in vascular tone, dependent on prostacyclin and perhaps other vasodilatory prostanoids.

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