Objective: The use of combination antiretroviral therapy has decreased AIDS–related mortality. It has been observed that treated AIDS patients now have a greater cardiovascular mortality and early organ damage even without hypertension. Goals of our study have been to determine whether 1) in normotensive AIDS patients with or without renal damage there are functional (arterial stiffening) and structural (carotid wall thickening) large artery alterations and whether 2) this leads to alterations in an important predictor of cardiovascular events, i.e. central blood pressure (BP). Design and Methods: We studied 40 treated, normotensive, normocholesterolemic, euglycemic AIDS patients, with (n = 20, age 52.0 ± 2.6 years; BP 131/77 ± 4/2 mmHg, means ± SE) or without (n = 20, age 44.0 ± 2.0 years; BP 130/76 ± 2/1 mmHg) renal damage, and 20 healthy controls (C, age 52.0 ± 1.0 years; BP 124/77 ± 2/1 mmHg). Renal damage was defined by microalbuminuria and/or glomerular filtration rate < 60 ml/min. Arterial distensibility was measured by aorto-femoral Pulse Wave Velocity (PWV), central systolic BP by tonometry (Sphygmocor) and carotid artery intima-media thickness (IMT) by semi-automatic echotracking (WTS). Results: Compared to C AIDS patients without renal damage showed similar values of carotid IMT (543 ± 26 vs 554 ± 24 μm), PWV (11.0 ± 0.5 vs 10.3 ± 0.4 m/sec) and central BP (117 ± 2/77 ± 1 vs 115 ± 2/70 ± 3 mmHg). In contrast, all values were greater in AIDS patients with renal damage (IMT: 608 ± 26 μm, PWV: 11.0 ± 0.5 and central BP130 ± 3/77 ± 2 mmHg), the difference being statistically significant (+ 13 mmHg, p < 0.05) for central systolic BP. In AIDS patients, PWV showed a not significant correlation with creatinine (r = 0.3) and filtration rate, both when measured by Cokroft-Gault and by MDRD (r = 0.35 and 0.31) formula, while automatically calculated IMT and systolic BP significantly correlated between each other (r = 0.4). Conclusion: In normotensive AIDS patients with no major cardiovascular risk factors there is no apparent alteration in arterial structure and function. This alteration is evident in AIDS patients with renal damage, leading to a greater central BP value that might account for their increased cardiovascular risk.

Aims. The aim of our study was to measure carotid intima-media thickness (cIMT) and risk factors associated with its development and progression, and to evaluate arterial wall characteristics through integrated backscatter analysis (IBS) in HIV patients. Methods. Perspective cohort study enrolling 44 HIV patients treated with antiretroviral drugs who underwent standard B Mode cIMT measurement and tissue characterization of carotid wall by means of dedicated software by acoustic densitometry, at time 0 and 2 years later. Major findings. Cross-sectional evaluation performed at baseline found that cIMT value correlated significantly with age (r - 0.42, p - 0.005) and systolic blood pressure (r - 0.31, p - 0.04). No correlation was found between cIMT and CD4, HIV-RNA, triglycerides or total cholesterol. There was no difference between the group with versus the group with no protease inhibitors treatment. cIMT progression during 2 years of observation was statistically significant (median, interquartile range [IQR]: 0.005, 0-0.031). No correlation was found between IBS and duration of disease and kind of therapy, whereas a significant association was found between cIMT and IBS (r = 0.33, p = 0.03). No noticeable changes of IBS were observed during 2 years observation. Conclusions. Classic risk factors greatly affect cIMT than time of HIV infection, duration of antiretroviral therapy exposure and use of protease inhibitors. IBS is a promising technique for the evaluation of arterial wall composition in HIV patients.

Introduction.Low-grade inflammation has been shown to be related with arterial stiffness in several clinical conditions.Aim.To test the impact of C-reactive protein (CRP) on arterial stiffness in a large number of hypertensive patients, in comparison with more conventional risk factors, such as age, systolic blood pressure, and lipid variables.Methods.We studied 259 consecutive hypertensive non-diabetic patients (138 males, age range 19-86 years) on treatment with several antihypertensive agents in various combinations and dosages.Arterial stiffness was measured twice by carotid-femoral pulse wave velocity (PWV, Complior) and the mean of the values used for data analysis.Other measurements consisted of blood pressure (BP, sphygmomanometry), heart rate (HR, palpatory method), body mass index (BMI), serum total cholesterol, HDL-cholesterol, triglycerides and glucose.CRP was measured by high sensitivity hymmunochimic turbinometric technique.Results.In the whole group of patients mean age (±SE) was 52±0.8 years, BMI 26±0.2 g/m2, BP (systolic/diastolic), 142±1/87+0.6 mmHg, HR 66±0.6 b/min; serum total cholesterol, HDL cholesterol, triglycerides and glucose were 197±2.1,54±0.8,130±5 and 88.5 ±1.3 mg/dl respectively.Mean CRP was 3.2±0.3(mg/l) and PWV 10.9±0.9 m/sec.PWV individual values did not correlate with lipid variables, while they showed a correlation with age (r=0.29,p<0.0001), systolic BP (r= 0.25, p<0.0001), glycaemia (r= 0.12, p<0.04),BMI (r=0.16,p< 0.05) and CRP (r=0.18,p<0.003).The correlation between CRP and PWV remained significant (p<0.01)when a stepwise multivariate analysis including all variables showing a significant correlation in the bivariate analysis was performed.Conclusions.In treated hypertensive patients CRP is independently related to arterial stiffness.

Use of local arterial distensibility measurements by change in carotid artery diameter divided by pulse pressure has limitations because blood pressure is often taken in a vessel distant or at a time different from where and when change in diameter is taken. In 92 subjects (23 to 91 years of age), carotid artery diameter was continuously measured ecographically, whereas blood pressure was continuously measured simultaneously tonometrically on the contralateral artery, the 2 signals being synchronized via 2 EKGs. Within each cardiac cycle, there was a linear relationship between the changes in vessel diameter and the changes in blood pressure during either the protomesosystole or the diastole after the dicrotic notch. The diastolic slope was displaced upward and steeper than the systolic slope, the pressure-diameter loop showing a hysteresis. Both slopes showed a high reproducibility when data were averaged over a several-second period. There were small differences between consecutive cardiac cycles, suggesting that modulation of arterial mechanical response to continuous changes in intravascular pressure may undergo physiological variations. In the 92 subjects, systolic and diastolic slopes correlated significantly with distensibility values obtained by Reneman formula and exhibited a close inverse relationship with each subject's age and systolic blood pressure, thereby showing the ability to reflect age- and pressure-dependent large artery stiffening. This method may allow precise assessment of man's arterial mechanical properties within each cardiac cycle. This highly dynamic assessment may help to collect information on properties of normal and altered large elastic arteries and the mechanisms involved in disease.

Diabetes is associated with a reduction of arterial distensibility. Limited information exists regarding whether or how early this appears in the course of the disease. We studied 54 normoglycemic, normotensive, healthy offspring of 2 parents with type 2 diabetes mellitus and 55 age- and sex-matched healthy control subjects. Carotid diastolic diameter and systodiastolic change were measured by echo tracking (Wall Track System) and wall thickness by echocolor Doppler (Sonos 5500, Philips). Pulse pressure was measured by a semiautomatic device positioned on the brachial artery and arterial distensibility calculated by Reneman formula. Blood pressure, blood glucose, glycohemoglobin, and insulin sensitivity (homeostasis model assessment index) were normal or only slightly elevated and by and large similar in the 2 groups. Compared with control subjects, offspring of diabetic parents showed similar carotid diameters at diastole and a reduced increase in carotid diameter at systole (-16%), a reduced carotid artery distensibility (-30%), and an increased pulse pressure (+21.8%), all differences being statistically significant (P<0.05) and persisting in subgroups with elevated or normal body mass index values (<25 and >or=25 kg/m(2)). Carotid artery wall thickness was not different between the 2 groups. Thus, subjects with predisposition to diabetes show carotid artery stiffening even in the absence of blood pressure alterations, as well as substantial alterations of glucose metabolism, body mass index, and changes in carotid wall thickness. This suggests that, in diabetes, alterations in arterial mechanical properties represent an early phenomenon, which may occur in the absence of metabolic and blood pressure alterations.

Objective Systemic sclerosis (SSc) is characterized by an altered nitric oxide (NO): endothelin I ratio and by endothelial dysfunction. Aims To verify the effects of prostaglandin E1 (PGE1) α-cyclodestrin treatment on endothelial function, quantified as flow-mediated dilation (FMD) of the radial artery. Methods In 16 women with SSc (age 57 ± 2.7 years, means ± SE) in whom a diagnosis of SSc had been made several years earlier (7.1 ± 1.2 years), FMD was evaluated by an echotracking technique on the radial artery, using trinitroglycerin vasodilation as a non-endothelial measure of the vessel's ability to increase its diameter maximally. FMD was evaluated after 4 months washout period and after 4 months cyclic infusion of PGE1 α-cyclodestrin. Expired NO was measured at the same time. Results PGE1 α-cyclodestrin cyclic infusions did not modify systolic and diastolic blood pressure, heart rate or trinitroglycerin radial artery vasodilation. On the other hand, it induced a marked and significant increase in FMD of the radial artery, which was also accompanied by an increase in blood flow and expired NO. Conclusions Endothelial dysfunction and reduced FMD associated with SSc are improved by cyclic treatment with PGE1 α-cyclodestrin. This effect occurs together with a concomitant increase in expired NO, suggesting its direct positive influence on endothelial function. It may also partly explain the clinical beneficial effect of the drug in SSc.