Paolo Pancera

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.

Autonomic system activity and 24-hour blood pressure variations in subjects with normal- and high-tension glaucoma.

PurposeAs suggested by findings of abnormal responses to posture in patients with normal-tension glaucoma (NTG), cardiovascular autoregulation may also be defective in primary open-angle glaucoma (POAG). Patients and MethodsBoth 24-hour ambulatory blood pressure monitoring and the head-up tilt test were performed in 17 subjects with NTG and in 13 subjects with high-tension POAG (ht-POAG). These groups were compared with 17 age-matched healthy individuals. Subjects undergoing cardiovascular therapy were excluded. ResultsNo significant differences in diurnal and nocturnal blood pressure and heart rate were found between the groups. A significant reduction in diurnal heart rate variability was found in NTG (12.1 ± 2.8 bpm) compared with the ht-POAG (15.0 ± 2.4 bpm, P < 0.01) and control groups (15.8 ± 3.0 bpm, P = 0.01]). Nocturnal diastolic blood pressure variability was also reduced in NTG (6.9 ± 2.2 mm Hg) compared with controls (8.6 ± 2.3 mm Hg, P < 0.05]) as was heart rate variability (6.3 ± 1.4 vs 8.3 ± 2.6 in ht-POAG, P < 0.05), suggesting blunted blood pressure and heart rate modulation in NTG subjects. Spectral analysis of short-term heart rate variability showed a significant reduction of total power in the supine position (1064 ± 600 in NTG vs 1688 ± 889 ms2 in controls, P < 0.05]). This was not accompanied either by a physiological reduction in total power or in a high-frequency component during the passive orthostatic stimulus. These differences tend to become more prominent in the clinically more severe forms of NTG (as identified by scores based on the extent of optic disk excavation, visual field damage, and progression of disease). This would suggest a correlation between the extent of autonomic disorder and severity of glaucoma. The &agr; index (root-square of low-frequency heart rate to low-frequency blood pressure ratio) was lower in the supine position in NTG subjects (8.1 ± 3.1 vs 10.6 ± 3.3 ms/mm Hg in controls, P < 0.05), confirming the reduced baroreflex sensitivity. ConclusionsThe results confirm the hypothesis that dysfunction of autonomic control of the cardiovascular response may be a contributing pathogenetic factor in NTG, inducing a chronic ischemia of the optic nerve.

The effects of thromboxane A2 inhibition (Picotamide) and angiotensin II receptor blockade (Losartan) in primary Raynaud's phenomenon

Pancera P, Sansone S, Secchi S, Covi G, Lechi A (University of Verona, Verona, Italy). The effects of thromboxane A2 inhibition (Picotamide) and angiotensin II receptor blockade (Losartan) in primary Raynauds phenomenon. J Intern Med 1997; 242: 373–6.

Effect of losartan on heart rate and blood pressure variability during tilt test and trinitroglycerine vasodilation

OBJECTIVE To define the changes in variability of heart rate and of blood pressure during vasodilation in a group of hypertensive patients treated with an angiotensin II type I (AT1) receptor inhibitor. DESIGN Losartan (50 mg/day at 0800 h) or placebo were administered for 3 weeks according to a single blind, crossover, randomized protocol, to 18 hypertensive patients (16 men and two women, mean age 42 + 3.6 years). Continuous ECG recording and beat-to-beat blood pressure monitoring were carried out with subjects in the supine position and during a head-up tilt test, as well as after sublingual administration of trinitroglycerine. The elaboration of ECG traces in the frequency domain, was carried out using an autoregressive method and measured using the autoregressive moving average technique. RESULTS Orthostatic stimulus, both during treatment with losartan and with placebo, caused a significant decrease in the heart rate high frequency power; on the other hand, the low frequency power appeared unchanged after placebo and was significantly reduced with losartan. Five minutes after the administration of trinitroglycerine, the low frequency power with placebo showed a significant increase (817 -+ 221 versus 465 + 101 ms2, P < 0.03). No change was recorded in total power nor in low frequency or high frequency power during losartan therapy. The ratio of low frequency to high frequency powers showed a sympathetic prevalence during vasodilation only during placebo treatment, whereas a mainly unchanged balance was maintained during losartan treatment Blood pressure variability showed a sympathetic prevalence after upright and trinitroglycerine stimulation only in placebo-treated subjects. CONCLUSIONS Our study demonstrated that vasodilation is not able to evoke an unbalancing of the autonomic modulation in hypertensive patients treated with an AT1 receptor inhibitor, but permits the maintenance of a significant vagal component, thus highlighting the favorable profile of this drug in the autonomic control of circulation.

Pseudomonas septicaemia. A review of 60 cases observed in a university hospital

Epidemiological, clinical features and the pathogenesis of 60 cases of pseudomonas septicaemia, observed over a period of 7 years from 1975 to 1981, are described. The mean frequency of occurrence was 0.40 episodes per 1000 admissions and an incidence of 66 per cent was observed in patients with serious underlying diseases, such as haematological malignancies and neoplasia. Thirty-seven patients had received cytotoxic and immunosuppressive therapy and showed a marked leukopenia, and whenever the leukocyte count fell below 2000/mm3, the prognosis was significantly worse. The most common portals of entry were the respiratory and gastrointestinal tracts. The overall mortality was very high (75 per cent) and mainly related to septic shock. Apart from the very high frequency of this complication (24 patients, 40 per cent of all cases), a typical clinical picture, distinguishing pseudomonas from other Gram-negative septicaemias, did not emerge.

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.

Effects of long-term nicardipine treatment on hemodynamics of large arteries in essential hypertension

SummaryThe effects of the calcium-entry blocker nicardipine on brachial hemodynamics were studied in 22 patients (18 male, 4 female) with essential hypertension, who were treated with 20 mg tid for 1 year. Compliance, characteristic impedance, vascular resistances, and tangential tension were measured before treatment and after 1, 3, and 12 months of treatment by an automatic recording from a B-mode, high-resolution, real-time scanner and pulsed Doppler velocimetry for the calculation of the flow volume. We observed statistically significant variations in compliance and impedance after 1 month (3.21±0.59 dyn−1 cm4 10−7 vs. 1.26±0.16 dyn−1 cm4 10−7 and 50.6±4.7 dyn s cm−5102 vs. 91.4 ±7.3 dyn s cm−5 102, respectively; mean±SEM; p<0.001), while tangential tension was significantly reduced after only 3 months (23.2±2.2 mmHg vs. 25.4±2.3 mmHg cm; p<0.05). The correlation between variations in mean blood pressure and in the hemodynamic parameters studied remained statistically significant throughout the study. Nicardipine improved the parameters of large-artery hemodynamics that favor a normal systolic pulse.

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