5,167 research outputs found
Atrial fibrillation is not associated with increased risk of venous thromboembolism: Results from ARAPACIS study
No full textSerum γ-Glutamyltransferase Concentration Predicts Endothelial Dysfunction in Naïve Hypertensive Patients
No full textBackground: Serum gamma-glutamyltransferase (γ-GT) is recognized as a risk factor for cardiovascular diseases (CV). Traditional cardiovascular risk factors mediate endothelial dysfunction. Aim: to evaluate a possible correlation between serum-GT and endothelium-dependent vasodilation in naive hypertensives. Methods: We enrolled 500 hypertensives. Endothelial function was studied by strain-gauge plethysmography. Receiver operating characteristic (ROC) analysis was used to assess the predictive value of γ-GT and to identify the optimal cut-off value of the same variable for endothelial dysfunction. Results: At univariate linear analysis peak percent increase in acetylcholine (ACh)-stimulated vasodilation was inversely related to γ-GT (r =-0.587), alanine aminotransferase (ALT) (r =-0.559), aspartate aminotransferase (AST) (r =-0.464), age (r =-0.171), body mass index (BMI) (r =-0.152), and fasting glucose (r =-101). In the stepwise multivariate regression model, endothelium-dependent vasodilation was significantly related to γ-GT (β =-0.362), ALT (β =-0.297), AST (β =-0.217), estimated glomerular filtration rate (e-GFR) (β = 0.199), gender (β = 0.166), and smoking (β =-0.061). The ROC analysis demonstrated that the accuracy of γ-GT for identifying patients with endothelial dysfunction was 82.1%; the optimal γ-GT cut-off value for discriminating patients with this alteration was 27 UI/L. Conclusions: Serum γ-GT values, within the normal range, are significantly associated with endothelial dysfunction in hypertensives, and may be considered a biomarker of early vascular damage
Competitive interaction between chronic obstructive pulmonary disease and CHA2DS2-VASc score in predicting incident atrial fibrillation
No full textBackground: Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality, and an emerging risk factor for atrial fibrillation (AF). CHADS2 and CHA2DS2-VASc scores are significantly associated with incident AF independently of other risk factors. The aim of this study was to demonstrate a possible interaction between COPD and CHA2DS2-VASc in predicting incident AF. Methods: This observational prospective cohort study included 4322 Caucasians with cardiovascular risk factors, stratified by CHA2DS2-VASc score (> 2 vs < 2) and presence/absence of COPD. To detect AF appearance, patients underwent, every 6 months, physical examination, standard 12‐lead electrocardiogram and routine laboratory tests. Results: COPD prevalence was significantly higher in patients with CHA2DS2-VASc ≥ 2 vs CHA2DS2-VASc < 2 category (13.3% vs 10.5%, P = 0.009). During the follow-up, 589 cases of AF were documented (3.8 events/100 patients-year). COPD+ showed a significantly higher incidence of AF vs COPD− patients (17.4 vs 8.4 events/100 patients-year, P < 0.0001). In Cox regression models both CHA2DS2-VASc score (HR = 4.70, 95% CI = 3.63–6.08) and COPD (HR = 2.04, 95% CI = 1.69–2.48) significantly predicted the incidence rate of AF; this was also confirmed introducing the two variables into the same Cox model. A significant competitive interaction between CHA2DS2-VASc and COPD was found in a Cox model in patients with CHA2DS2-VASc < 2 (HR = 8.45, 95% CI = 5.20–13.74) than in those with CHA2DS2-VASc ≥ 2. Conclusions: COPD is an independent and strong predictor of incident AF. The presence of COPD increases the HR for incident AF about five times in patients with CHA2DS2VASc score < 2, while the coexistence of a CHA2DS2Vasc score ≥ 2 minimizes the prognostic significance of COPD
Immuno-Mediated Inflammation in Hypertensive Patients with 1-h Post-Load Hyperglycemia
No full textInflammation plays a key role in the pathogenesis/progression of atherosclerosis, and inflammatory molecules contribute to the progression of cardiovascular disease. Subjects with normal post-load glucose tolerance and 1-h post-load plasma glucose >155 mg/dL have an increased risk of subclinical target organ damage and incident diabetes. We aimed to test possible differences in immune-mediated inflammatory parameters in newly-diagnosed hypertensives with or without 1-h post-load hyperglycemia. We enrolled 25 normotensives (NGT) and 50 hypertensives normotolerant on oral glucose tolerance test, further divided into two groups based on 1-h post-load plasma glucose: NGT 1-h ≥ 155 (n = 25) and NGT 1-h < 155 (n = 25). We measured toll-like receptor (TLR) 2, TLR4, nuclear factor kβ (NF-kβ), interleukin (IL)-1β, IL-6, IL-8, IL-10, and tumor necrosis factor (TNF)-α. Hypertensives showed significantly worse metabolic and lipid profiles, and higher values of body mass ass index (BMI), creatinine, and inflammatory parameters, compared to controls. NGT 1-h ≥ 155 had a worse glycometabolic profile and higher values of TLR2 (9.4 ± 4.2 vs. 5.9 ± 2.6 MFI), TLR4 (13.1 ± 3.9 vs. 7.8 ± 2.3 MFI), NF-kβ (0.21 ± 0.07 vs. 0.14 ± 0.04), IL-1β (6.9 ± 3.4 vs. 3.2 ± 2.1 pg/mL), IL-6 (10.8 ± 2.6 vs. 4.1 ± 1.6 pg/mL), IL-8 (27.6 ± 9.3 vs. 13.3 ± 5.6 pg/mL), TNF-α (6.4 ± 2.9 vs. 3.3 ± 1.4 pg/mL), and high-sensitivity C-reactive protein (hs-CRP) (4.8 ± 1.5 vs. 2.7 ± 1.0 mg/dL) in comparison with NGT 1-h < 155. Matsuda-index and 1-h post-load glycemia were retained as major predictors of TLRs and NF-kβ. These results contribute to better characterizing cardiovascular risk in hypertensives
COPD significantly increases cerebral and cardiovascular events in hypertensives
No full textEssential hypertension and chronic obstructive pulmonary disease often coexist in the same patient. The aim of this study was to evaluate whether the addition of chronic obstructive pulmonary disease modifies the risk of cardiovascular events in hypertensives. We enrolled 1728 hypertensives. Study outcomes included fatal and non-fatal cardiovascular stroke and myocardial infarction, and cardiovascular death. During a mean follow-up of 57 months there were 205 major adverse cardiovascular events (2.47 per 100 pts/yr): cardiac (n117; 1.41 per 100 pts/yr) and cerebrovascular (n = 77; 0.93 per 100 pts/yr). In hypertensives with chronic obstructive pulmonary disease we observed a greater number of cardiovascular events than in hypertensives without respiratory disease (133 [5.55 per 100 pts/yr) vs 72 [1.22 per 100 pts/yr], respectively. The addition of chronic obstructive pulmonary disease to hypertension increased the incidence of total and non-fatal stroke of more than nine- (2.42 vs 0.32 per 100 pts/yr) and 11-fold (2.09 vs 0.22 per 100 pts/yr), respectively. The same trend was observed for total (2.88 vs 0.81 per 100 pts/yr) and non-fatal (2.67 vs 0.79 per 100 pts/y) myocardial infarction. The presence of chronic obstructive pulmonary disease in hypertensives significantly increases the risk of stroke, myocardial infarction and major adverse cardiovascular events
Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients
No full text: Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 m2); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 m2). Smoking and COPD were directly and significantly interrelated (Cramer's V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 m2 lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 m2). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions
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