Effects of obesity and weight loss on soluble CD40L levels.
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CD40 Ligand↗
Biomedical subjects
Claudio Ferri
Publications and source records attributed to Claudio Ferri.
Controlled analysis of blood pressure sensitivity to sodium intake: interactions with hypertension type.
OBJECTIVE: The contribution of salt intake to the pathogenesis of hypertension holds longstanding interest. Recent studies employed the sensitivity of blood pressure (BP) to salt intake as an intermediate phenotype. The validity of this approach relative to the homogeneity of sodium-sensitive hypertension was investigated while simultaneously controlling multiple putative factors. METHODS: Blood pressure responses to shifts in salt intake were measured in 274 individuals with essential hypertension in steady-state sodium balance on high (200 mEq) and low (10 mEq) sodium intakes. Univariate and multivariate analyses predicted systolic and diastolic sodium sensitivity based on interactions among demographic factors (age, gender, race, body mass index) and hypertensive type [low-renin (LR), modulator (M), non-modulator (NM)]. RESULTS: The influence of hypertension type on systolic salt sensitivity (SSS) depended on gender (P = 0.03). In females, highest SSS was in LR (21, 14, 13 mmHg for LR, M, NM, P = 0.02), while in males highest SSS was in NM (11, 10, 16 mmHg for LR, M, NM, P = 0.07). Age predicted SSS without interacting with other factors, producing a 2.4 mmHg increase per decade (P = 0.02). Hypertension type affected diastolic salt sensitivity (DSS) (P = 0.002) without interacting with other factors. M had less DSS (6 mmHg) than LR (9 mmHg) and NM (11 mmHg) (P < 0.01). CONCLUSIONS: For subjects in sodium balance, the distributions of SSS and DSS were unimodal and the mechanisms mediating SSS and DSS were different. Controlling for multiple demographic factors, at least two hypertensive types have largest BP responses to sodium intake, reducing the usefulness of blood pressure sensitivity to salt intake as an intermediate phenotype.
Adult↗
Mediterranean diet, cocoa and cardiovascular disease: a sweeter life, a longer life, or both?
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Arm↗
Effects of bezafibrate and simvastatin on endothelial activation and lipid peroxidation in hypercholesterolemia: evidence of different vascular protection by different lipid-lowering treatments.
Hypercholesterolemia is combined with enhanced lipid peroxidation, which can promote atherogenesis by inducing endothelial adhesion molecule expression. Statins may protect vascular endothelium in hypercholesterolemia by reducing enhanced plasma levels of low-density lipoprotein and decreasing oxidative stress. Herein, we describe increased circulating levels of soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin and total 8-iso-prostaglandin F(2 alpha) (8-iso-PGF(2 alpha)) concentrations, as indexes of endothelial activation and lipid peroxidation, respectively, in 67 hypercholesterolemic patients compared with 32 normocholesterolemic subjects. Significant cholesterol reductions were achieved in hypercholesterolemic patients after 6 months under either simvastatin (40 mg/d) or bezafibrate (800 mg/d) treatment, given according to a randomized double-blind trial. Simvastatin but not bezafibrate simultaneously reduced soluble adhesin and total 8-iso-PGF(2 alpha) concentrations also. Vitamin E supplementation (400 IU/d) further reduced indexes of endothelial activation and lipid peroxidation in simvastatin-treated patients and significantly reduced the above indexes in bezafibrate-treated patients. Changes in circulating soluble adhesion molecule levels were directly correlated with changes in total 8-iso-PGF(2 alpha) concentrations in simvastatin-treated patients also receiving vitamin E supplementation. All together, our data demonstrated that hypercholesterolemia was combined with endothelial activation and lipid peroxidation, which were efficaciously counteracted by simvastatin but not bezafibrate treatment. Thus, a different vascular protection can be achieved by different lipid-lowering treatments.
Adult↗
Effects of carbon-coated coronary stents on the markers of inflammation, thrombin generation and platelet and endothelial activation.
BACKGROUND: The effects of stent carbon coating on the activation of inflammatory and endothelial cells and of coagulation were assessed in patients undergoing coronary artery stent implantation. METHODS: Forty-four consecutive patients with stable angina and an isolated significant stenosis in a native coronary vessel undergoing stent implantation were randomized to a carbon-coated stent (Carbostent, n = 23) or an uncoated stent with a similar design (Multilink, n = 21). The markers of inflammation, of hemostasis and of platelet and endothelial activation were determined before and 6, 24, 48 and 72 hours after the procedure. RESULTS: Procedural success was achieved in all cases and no patient presented with major in-hospital adverse events. In both the Carbostent and Multilink groups, the median (interquartile range) plasma levels of C-reactive protein significantly increased after the procedure (p < 0.001 and p = 0.002 vs baseline levels, respectively), reaching a peak at 48 hours, without any difference between groups (p = 0.76). Similarly, in both groups the plasma levels of fibrinogen, thrombin-antithrombin III complexes, prothrombin fragments F1 + 2, plasminogen activator inhibitor-1, soluble E-selectin, soluble P-selectin and von Willebrand factor significantly increased after the procedure (all p < 0.05 vs baseline values), without any difference between groups (all p = NS). CONCLUSIONS: This study confirms that the markers of inflammation, of endothelial and platelet activation and of thrombin generation significantly increase after successful coronary artery stent implantation. More importantly, it demonstrates that carbon coating does not modify the biologic response of the vessel wall to stent implantation.
Aged↗
Patterns of myocardial endothelin-1 expression and outcome after cardiac transplantation.
BACKGROUND: Endothelin-1 (ET-1), a potent vasoconstrictor, is released in response to several inflammatory cytokines after heart transplantation. The present study correlated patterns of myocardial ET-1 expression in heart biopsies with acute rejection, post-transplantation ischemic injury, and subsequent development of coronary vasculopathy. METHODS AND RESULTS: Patterns of myocardial ET-1 expression were evaluated in 47 heart transplant recipients at 3 months after transplant. Transplant vasculopathy was documented by coronary angiography at 2 years after transplant. Expression of ET-1 was tabulated for both blood vessels and the interstitium. Vascular ET-1 expression was positive in 7/17 (41%) of patients with greater than grade 2 (International Society Heart Lung Transplant) rejection compared with 3/30 (10%) of patients with grade 0 and grade 1A rejection (P=0.02). Compared with patients with negative interstitial ET-1 expression (n=22), patients with positive interstitial ET-1 expression (n=25) had higher incidence of post-transplantation ischemic injury (52% versus 9%, P=0.002), lower mean episodes of acute rejection (> or = grade 2) during the first 3 months of transplant (1.09+/-0.66 versus 1.86+/-1.6, P=0.048), and more common vasculopathy at 2 years (50% versus 15%, P=0.02), and they tended to have worse survival (83.2% versus 100%, P=0.058). CONCLUSIONS: Vascular ET-1 expression is likely to be associated with acute rejection. Interstitial ET-1 expression, however, is more likely to be associated with post-transplantation ischemic injury and subsequent development of coronary vasculopathy.
Coronary Angiography↗
Prolonged, low dose alpha-tocopherol therapy counteracts intercellular cell adhesion molecule-1 activation.
BACKGROUND: Up-regulation of ICAM-1 at the vascular endothelial level is one of the most important promoters in the slow progression of a healthy vessel to an atherosclerotic one. The current study aimed to evaluate whether low dose of the antioxidant alpha-tocopherol affects the circulating soluble (s) ICAM-1 in healthy subjects. METHODS: Either alpha-tocopherol E (50 I.U./day) or placebo was randomly, double-blindly given to 39 healthy male volunteers (mean age 41.6+/-5.9 years) over a period of 20 weeks. RESULTS: At the baseline, sICAM-1 levels were inversely correlated with alpha-tocopherol concentrations (r=-0.525, p<0.0001). Twenty weeks of alpha-tocopherol supplementation (n=20 subjects) significantly decreased the circulating sICAM-1 levels (from 149.2+/-18.4 to 131.5+/-17.2 microg l(-1), p<0.004) while it increased the alpha-tocopherol concentrations (from 25.8+/-5.0 to 31.2+/-5.7 micromol l(-1), p<0.003). No significant changes in plasma sICAM-1 and alpha-tocopherol levels were observed in placebo-treated subjects (n=19). In actively treated subjects, changes in circulating sICAM-1 were inversely correlated with changes in alpha-tocopherol concentrations (r=-0.597, p=0.005). CONCLUSIONS: Plasma sICAM-1 concentrations are stable in healthy subjects over a period of 20 weeks while they significantly decreased with low dose of alpha-tocopherol. Thus, antioxidant vitamins are likely to counteract with endothelial changes that could potentially trigger the atherogenetic process.
Adult↗
Vitamin E supplementation reduces plasma vascular cell adhesion molecule-1 and von Willebrand factor levels and increases nitric oxide concentrations in hypercholesterolemic patients.
Up-regulation of vascular cell adhesion molecule-1 (VCAM-1) and reduced nitric oxide (NO) availability represent early characteristics of atherosclerosis. To evaluate whether the antioxidant vitamin E affected the circulating levels of soluble VCAM-1 (sVCAM-1) and the plasma metabolite of NO (nitrite+nitrate) in hypercholesterolemic patients, either vitamin E (either 400 IU or 800 IU/d for 8 wk) or placebo were randomly, double-blindly given to 36 hypercholesterolemic patients and 22 age- and sex-matched controls. At baseline hypercholesterolemic patients showed higher plasma sVCAM-1 (microg.liter(-1)) (591.2 +/- 132.5 vs. 505.0 +/- 65.6, P < 0.007) and lower NO metabolite (microM) levels (15.9 +/- 3.4 vs. 29.2 +/- 5.1, P < 0.0001) than controls. In hypercholesterolemic patients, 8 wk vitamin E (but not placebo) treatment significantly decreased circulating sVCAM-1 levels (400 IU: -148.9 +/- 84.6, P < 0.009; 800 IU: -204.0 +/- 75.7, P < 0.0001; placebo: -4.7 +/- 22.6, NS), whereas it increased NO metabolite concentrations (400 IU: +4.0 +/- 1.7, P < 0.02; 800 IU: +5.5 +/- 0.8, P < 0.0001; placebo: +0.1 +/- 1.1, NS) without affecting circulating low- density lipoprotein levels. Changes in both plasma sVCAM-1 and NO metabolite levels showed a trend to significantly correlate (r = -0.515, P = 0.010; and r = 0.435, P = 0.034, respectively) with changes in vitamin E concentrations induced by vitamin E supplementation. In conclusion, isolated hypercholesterolemia both increased circulating sVCAM-1 and reduced NO metabolite concentrations. Vitamin E supplementation counteracts these alterations, thus representing a potential tool for endothelial protection in hypercholesterolemic patients.
Adult↗
Treatment of hypertension and adherence to treatment guidelines in clinical practice: an Italian study.
Despite the results from clinical trials in patients with hypertension and the development of a long list of guidelines for the management of hypertension, many physicians and other healthcare professionals still manage hypertension using approaches that clearly diverge at least partially from the recommendations of these guidelines. Whatever the underlying reasons for physicians' failure to adhere to these guidelines, it is one of the main causes of the high percentage of treated patients with uncontrolled hypertension. This article is a report of the outcomes of a project designed to identify specific discrepancies between hypertension guidelines and clinical practice in Italy then guide the physicians to reach a consensus on hypertension management through discussions with their peers. A total of 1120 internists from all 20 regions in Italy were recruited to participate in workshops conducted between June 2002 and July 2004. They were divided into 57 groups to discuss at least 7 key topics, including the blood pressure level at which to start drug therapy, target-organ damage, isolated systolic hypertension, pulse pressure, clinical trials, generic drugs, and fixed combination drug therapy. The project findings confirmed that the vast majority of internists agree with the guidelines but do not adhere to them completely in clinical practice. Through open discussions that allowed them to identify common viewpoints, the participants may have developed a better awareness of and insight into the guidelines for hypertension management. Hopefully this strategy for group participation will lead to improvements in the management of hypertension throughout Italy.
Guideline Adherence↗