Objective: The aim of the study is to evaluate the effect of moderate Sicilian red wine consumption on cardiovascular risk factors and, in particular, on some inflammatory biomarkers. Methods: A total of 48 subjects of both sexes who were nondrinkers or rare drinkers of moderate red wine were selected and randomly subdivided into two groups assigned to receive with a crossover design a Sicilian red wine (Nero d'Avola or Etna Torrepalino) during meals: Group A (n ¼ 24), in whom the diet was supplemented for 4 weeks with 250 ml/day of red wine, followed by 4 weeks when they returned to their usual wine intake; and Group B (n ¼ 24), in whom the usual wine intake was maintained for 4 weeks, followed by 4 weeks when the diet was supplemented with 250 ml/day of red wine. The following were values measured in all tests: blood glucose, total and HDL-cholesterol and triglycerides, LDL-cholesterol, LDL/HDL ratio, apolipoproteins A1 and B, Lp(a), plasma C-reactive protein, TGFb1, D-Dimer, Factor VII , PAI Ag, t-PA Ag, fibrinogen, oxidized LDL Ab, total plasma antioxidant capacity. Results: At the end of the red wine intake period, LDL/HDL, fibrinogen, factor VII, plasma C-reactive protein and oxidized LDL Ab were significantly decreased, while HDL-C, Apo A1,TGFb1, t-PA, PAI and total plasma antioxidant capacity were significantly increased. Conclusions: Our results show a positive effect of two Sicilian red wines on many risk factors and on some inflammatory biomarkers, suggesting that a moderate consumption of red wine in the adult population is a positive component of the Mediterranean diet.

Several studies have stressed the involvement of inflammation in the pathophysiology of acute brain ischemia, but the role of immunoinflammatory activation in diabetic stroke patients has not yet been fully evaluated. The aim of our study was to evaluate immunoinflammatory activation of acute phase of stroke in relation to time of symptoms onset, diabetic state and diagnostic subtype. We enrolled 60 patients (32 diabetics; 28 non-diabetics) with acute ischemic stroke and 123 subjects without acute ischemic stroke, and measured levels of IL-lP, TNF-a, IL-6, IL-I0, E-selectin, P-selectin, sICAM-l, sVCAM-l, VWF, 24-72 hand 7-10 days after stroke onset; TPA, PAI-l plasma levels at 24-72h. Our stroke patients exhibited significantly higher plasma levels of cytokines, selectins, adhesion molecules and PAl-I, and diabetic stroke patients exhibited higher plasma levels of PAI-l in comparison with non-diabetic ones. Lacunar strokes in comparison with those non-lacunar exhibited significantly lower levels of TNF-a and ILI-P, P-selectin and ICAM-l. Moreover, diabetic patients with lacunar strokes exhibited a minor grade ofimmunoinflammatory activation ofthe acute phase at 24-72h and 7-10 days after stroke onset. The minor grade of immunoinflammatory activation of patients with lacunar strokes, particularly diabetic ones, could be related to the minor extension of the infarct size, owing to the typical microvascular disease of diabetic subjects which could also explain the reported better outcome of this subtype of ischemic stroke.The epidemiologic relationship between diabetes and stroke is well confirmed (I), but the clinical and prognostic profile of ischemic stroke in diabetic patients in comparison with non-diabetic ones and in relation to diagnostic subtype, appears unclear (2-3). An immunoinflammatory cascade (4) involving endothelial and coagulation functions represents the pathogenetic background of neuronal damage in ischemic stroke. Indeed, there is evidence that brain injury, secondary to arterial occlusion, is characterized by acute local inflammation (5). Moreover, during reperfusion after acute ischemia, polymorphonuclear neutrophils (PMN) are believed to exacerbate tissue damage by both the physical obstruction of vessels and the release of oxygen radicals, proinflammatory cytokines and cytolytic enzymes (4-5). Thus, if clinical and prognostic differences exist between diabetic and non-diabetic

Our data suggest that TGFbeta1 levels are positively associated with BMI, MBP and UAE in hypertensive subjects. This also indicates that TGFbeta1 overproduction might be considered a pathophysiology mechanism of progressive renal function impairment in obese hypertensives.

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This study was designed to evaluate coagulation and fibrinolysis activity and their relationship with left ventricular function in young obese subjects with central fat distribution. We assessed coagulation and fibrinolysis activity by evaluation of factor VII activity, fibrinogen and plasminogen, plasminogen activator inhibitor (PAl), and tissue plasminogen activator antigen basally (tPA1) and after venous occlusion (tPA2). These measures were evaluated in young (<40 years) obese subjects with central fat distribution (n = 19) and in comparable lean subjects (n = 20). Blood glucose, triglycerides, total and high-density lipoprotein (HDL) cholesterol, apolipoprotein (apo) A1 and apo B, fasting immunoreactive insulin, and lipoprotein(a) levels were also measured by current methods. Left ventricular ejection fraction (LVEF) and peak filling rate (PFR) determined by radionuclide angiocardiography and left ventricular mass (LVM) and LVM indexed for body height (LVM/H) determined by echocardiographic study were calculated. Central obesity was evaluated by the waist to hip ratio (WHR) according to the criteria of the Italian Consensus Conference of Obesity. Factor VII (P < .001), fibrinogen (P < .001), plasminogen (P < .001), PAl activity (P < .001), tPA1 (P < .02), fasting blood glucose (P < .01), apo B (P < .02), and immunoreactive insulin (P < .01) were significantly higher in obese than in lean subjects. In contrast, HDL cholesterol (P < .01), tPA2 (P < .01), LVEF (P < .001), and PFR (P < .02) were significantly lower in obese than in lean subjects. In all subjects, WHR correlated directly with fibrinogen and inversely with tPA2; LVEF correlated inversely with tPA1, PAl, and fibrinogen; and PFR correlated inversely with factor VII activity. Multiple regression analysis indicated that WHR and PAl were independent predictors of LVEF. These results indicate that obese subjects with central fat distribution are characterized by a hypercoagulable state associated with a silent left ventricular dysfunction. Such alterations might be responsible for the higher cardiovascular risk in subjects with central obesity. Copyright © 1995 by W.B, Saunders Company OBESITY is an important risk factor for cardiovascular disease, especially when there is a central fat distribution. Several indications suggest an independent role of obesity in promoting cardiovascular disease; however, this has not been universally accepted. 1 In addition, recent follow-up results of the Harvard Growth Study indicate that the risk of morbidity from coronary heart disease and atherosclerosis increased among men and women who had been overweight in adolescence. 2 The effects of obesity in adolescence on adult mortality have been demonstrated to reflect the central deposition of fat that occurs in adolescence.3, 4On the other hand, alterations in hemostatic function are emerging predictors of coronary heart disease or cardiac events. In fact, some epidemiological data indicate that activated coagulation and impaired fibrinolytic function might be associa...