M. Ribul

Prevalence of carotid artery kinking in 590 consecutive subjects evaluated by Echocolordoppler. Is there a correlation with arterial hypertension

Abstract. Pancera P, Ribul R, Presciuttini B, Lechi A (Università 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.

Changes in peripheral hemodynamics and vasodilating prostaglandins after high-dose short-term ibuprofen in chronically treated hypertensive patients

The use of cyclooxygenase inhibitors has been seen to reduce the efficacy of many antihypertensive drugs. However, cyclooxygenase inhibitors are normally non-selective because they affect both vascular tissue, where the endothelial prostanoids exert principally a vasodilatory action, and the kidneys, where they also play an important role in regulating hydroelectrolytic metabolism by redistribution of intraparenchymal flow. To evaluate the relative importance of vascular district in the hypertensive patient, we administered ibuprofen - a drug acting with only a minimal antagonist activity. A group of 20 male hypertensives were randomly allocated, according to a single-blind protocol, to treatment with amlodipine (A, 10 mg/day) or lisinopril (L, 20 mg/day). Blood pressure was significantly reduced after 30 days, with a mean difference of -21.75 mmHg for systolic blood pressure (SBP) (95% confidence interval (Cl): -27.46 to -16.04; P< 0.0001) and -14.15 mmHg for diastolic blood pressure (DBP) (95% Cl: -17.13 to -11.17; P< 0.0001). Brachial artery compliance showed a mean increase of 1.657 x 10(-7) dyn-1 cm(4) (95% Cl: 1.188 to 2.126; P<0.001), and forearm resistances showed a mean decrease of -41.973 mmHg ml(-1)s (95% Cl: -75.479 to -8.467; P = 0.017). Changes in compliance were significantly related to those in SBP (r= -0.546; P= 0.013). The administration of ibuprofen (400 mg, three times a day for 3 days) was accompanied by a slight but significant increase in SBP, but not in brachial artery compliance or forearm resistances. Only SBP was affected, showing a mean increase of 4.25 mmHg (95% Cl: 1.26 to 7.24; P = 0.008). There was also reduced urinary excretion of PGI(2) and TXA(2) metabolites. The mean change in 6-keto-PGF(1 alpha) and 2,3-dinor-6-keto-PGF(1 alpha) was 45.71 ng per g urinary creatinine (uCr) (95% Cl: -0.16 to-91.25; P= 0.049) and -73.17 ng (g uCr)(-1) (95% Cl: -38.81 to -107.53; P<0.001), respectively. The mean decrease in TXA(2) catabolites was highly significant: -39.2 ng (g uCr)(-1) (95% Cl: -18.17 to-60.22; P< 0.001) and -102.87 ng (g uCr)(-1) (95% Cl: -61.86 to -143.88; P< 0.001) for TXB(2) and 2,3-dinor-TXB(2), respectively. Our study highlighted an inverse correlation between changes in blood pressure and those in urinary 2,3-dinor-6-keto-PGF(1alpha) excretion, irrespective of antihypertensive regimen. This suggests that, in the hypertensive patient treated with NSAIDs, inhibition of vascular prostanoid synthesis may play an important role in countering the efficacy of an important vascular tone regulatory mechanism.

Changes in the haemodynamics of large arteries induced by single doses of nicardipine, enalapril, atenolol and urapidil.

SummaryHaemodynamic changes in the carotid and brachial arteries produced by single doses of four antihypertensive 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.

Modifications in peripheral hemodynamics and left ventricular function in hypertensives treated with nicardipine slow release

Dear Sir, Hemodynamic factors like compliance, characteristic impedance, and peripheral resistance contribute to afterload, an extremely important factor in left ventricular hypertrophy [1,2]. Against this background, we set out to evaluate the action of nicardipine in hypertension [3,4], relating changes in arterial parameters to those in the left ventricular myocardium. We studied 12 male patients (mean age 41 years, range 34-50 years) with mild to moderate essential hypertension, t reated with nicardipine slow release (40 mg twice daily). Peripheral and cardiac hemodynamic parameters were examined basally and after 1 and 6 months treatment. Blood pressure was recorded with a previously validated [5] automatic apparatus (Dinamap 845XT, Critikon, Johnson & Johnson, Tampa, FL). Hemodynamic parameters were recorded using a plethysmographic method for the measurement of pulse wave velocity (variability ± 6%). By means of a Duplex scanner (Diasonics CV 400, Diasonics, Milpitas, CA) with a 10 Mhz probe and a longitudinal power of resolution of 0.3-0.4 mm, we also measured the diameter (variability ± 4%) of the brachial and common carotid arteries, as well as volume flow (variability ± 8%). In the common carotid, diameter was always measured 2 cm from the beginning of the bulbar dilatation, to avoid any mismeasurements. At the same observation times, patients were also subjected to M-mode, two-dimensional echocardiogram and US-Doppler study of transmittal flows. Echocardiograms were analyzed by a previously described computerized system [6]. Means were compared by Students t test for paired data, with allowance for the correction of Bonferroni. Results after 1 month showed a statistically significant reduction in systolic and diastolic blood pressure (147 -3/93 ± 2 vs. 169 ± 7/106 _+ 2 mmHg, mean ± SEM, p < 0.001), which was maintained after 6 months (149 _ 3/94 +__ 2 mmHg, p < 0.001). Over the same period, heart rate showed a slight but never statistically significant increase (first month vs. basal: 69 ± 2 vs. 66 ± 3 beats/min, sixth month: 71 ± 3 beats/min, p ns). The diameter of the brachial (BAD) and common carotid arteries (CCAD), the variations in hemodynamic parameters after 1 and 6 months, and the echocardiographic results are shown in Table 1. Important findings were the improvement of peripheral hemodynamics and also the shift of mass/volume index, show-. ing an increase of the volume in relation to the mass in the left ventricle. Nicardipine SR exerts a significant effect on blood pressure [7], reducing afterload, and on the left ventricular myocardium, improving diastolic compliance and inducing a gradual reduction of hypertrophy. The balanced combination of these actions determines regression of altered left ventricular morphology and function caused by overload, normalizing ventricular performance [8]. In the heart, significant reduction of posterior wall (PWTD) and interventricular septum thickness (IVSTD) was observed, as well as favorable remodeling of the geometry with a significant increase in the end-diastolic transverse diameter of the left ventricle and shortening of its longitudinal diameter, resulting in an increase of end-diastolic volume (EDV). In addition, there was a marked improvement in diastolic function evaluated by the time of isovolumetric relaxation, the percentage contribution of rapid filling (RF/ EDV) and atrial systole to total left ventricular filling (AS/EDV), and the speed of filling (dv/dt) during diastole. When other classes of drugs are used, in the event of actual left ventricular hypertrophy, vascular