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Objectives The aim of this study was to assess the hypothesis that alcohol consumption is associated with onset of atrial fibrillation (AF) and/or heart failure (HF). Background The connection between ethanol intake and AF or HF remains controversial. Methods The study population was 22,824 AF- or HF-free subjects (48% men, age ≥35 years) randomly recruited from the general population included in the Moli-sani study, for whom complete data on HF, AF, and alcohol consumption were available. The cohort was followed up to December 31, 2015, for a median of 8.2 years (183,912 person-years). Incident cases were identified through linkage to the Molise regional archive of hospital discharges. Hazard ratios were calculated using Cox proportional hazard models and cubic spline regression. Results A total of 943 incident cases of HF and 554 of AF were identified. In comparison with never drinkers, both former and occasional drinkers showed comparable risk for developing HF. Drinking alcohol in the range of 1 to 4 drinks/day was associated with a lower risk for HF, with a 22% maximum risk reduction at 20 g/day, independent of common confounders. In contrast, no association of alcohol consumption with onset of AF was observed. Very similar results were obtained after restriction of the analyses to regular or only wine drinkers or according to sex, age, social status, or adherence to the Mediterranean diet. Conclusions Consumption of alcohol in moderation was associated with a lower incidence of HF but not with development of AF.

Aims Surgical endarterectomy is the therapy of choice for atherosclerotic common femoral artery (CFA) obstruction. Recently, some large single-centre series have shown encouraging results for the percutaneous treatment of CFA obstructions. The purpose of this study was to evaluate the safety, feasibility, and one-year efficacy of the endovascular treatment of CFA obstructions with combined use of directional atherectomy (DA) and a paclitaxel-coated balloon (DCB). Methods and results Between January 2012 and July 2014, 30 consecutive patients with severely calcified obstructions of the common femoral artery were treated in our centre using DA followed by DCB dilatation. Provisional stenting was allowed in the case of a suboptimal result. Twenty cases (66%) were isolated CFA interventions, whereas five (17%) and five (17%) also involved inflow and outflow vessels, respectively. Chronic total CFA occlusions (CTO) were recanalised in six cases (20%). Procedural success was achieved in all cases; stenting was needed in three cases (10%). At one year, restenosis and target lesion revascularisation were observed in two of 30 (6.6%) and one of 30 (3.3%) patients, respectively. The secondary patency rate was 96.7%. Conclusions This single-centre prospective study suggests that the combined use of DA and DCB is a safe and effective alternative to surgery, a treatment option for common femoral artery lesions and provides encouraging results in this setting.

AIMS Many studies have analysed the occurrence of acute kidney injury (AKI) after percutaneous coronary intervention (PCI) but there are limited data relating to AKI risk in patients undergoing carotid artery stenting (CAS). The aim of this study was to determine the incidence and predictors of AKI in patients undergoing proximal protected CAS. METHODS AND RESULTS We analysed 456 patients undergoing proximal protected CAS. A binomial multivariate logistic model was developed including patients' clinical and angiographic/procedural characteristics. AKI (defined as an sCr increase ≥0.3 mg/dl or ≥1.5-fold sCr increase from baseline or more than 50% increase from baseline, within 48 hours post procedure) occurred in 155 patients (34%). AKI patients were more frequently affected by hypertension, diabetes, dyslipidaemia and anaemia, and presented lower renal function at baseline. Higher contrast volume to creatinine clearance ratio (2.40±1.44 vs. 2.08±1.15; p=0.01), lower post-procedural mean arterial pressure (MAP) (94.3±17.7 vs. 99.6±18.5 mmHg; p=0.003) and a more frequent post-procedural systolic pressure drop (∆SBP >50 mmHg) (23.9% vs. 14.3%, p=0.01) were observed in the AKI group of patients. At multivariate analysis, independent predictors of AKI were ∆SBP >50 mmHg, diabetes mellitus and dyslipidaemia. CONCLUSIONS AKI can occur quite frequently after proximal protected CAS and is related to clinical and procedural features. These data should be confirmed in larger registries or randomised trials.

BACKGROUND The association of the polyphenol content of human diet with pulmonary function is not yet fully understood. This study aims at evaluating the association of polyphenol consumption with lung function in a novel holistic approach. METHODS A cross-sectional analysis of 4551 women and 5108 men (age ≥35 years) from the Moli-sani study was performed. Participants were randomly recruited from the general population. The EPIC-FFQ was used for the dietary assessment. Polyphenol intakes were calculated using Eurofir-eBASIS, and a polyphenol antioxidant content (PAC) score was constructed to assess the total content of the diet in these nutrients. Pulmonary function maneuvers were performed, and the forced vital capacity (FVC) and forced expiratory volume in the first second (FEV1) were measured; FVC% predicted and FEV1% predicted were computed using the European Community of Coal and Steel prediction equations that included height and age. RESULTS In both genders, in age, height, and energy intake adjusted models, the majority of classes of polyphenols (mg/day) showed a positive association with FEV1, FVC, FEV1% predicted, and FVC% predicted (β-coef >0, P 0, P 0, P

Evidence indicates that Vitamin D deficiency may be associated with increased risk of cardiovascular disease, although findings on risk of heart failure (HF) are controversial. We investigated the relationship between serum Vitamin D and the incidence of hospitalization for HF in a large prospective cohort of Italian adults.19,092 (49% men, age range 35-99 years) HF-free individuals from the Moli-sani study, with complete data on serum Vitamin D (25-hydroxyvitamin) levels and incident hospitalized HF, were analysed. The cohort was followed up for a median of 6.2 years. Baseline serum Vitamin D levels were categorized in deficient (10 ng/mL), insufficient (10-29 ng/mL), and normal (≥30 ng/mL) Incident cases of hospitalization for HF were identified by linkage with the regional hospital discharge registry. Hazard ratios (HRs) were calculated using Cox-proportional hazard models. The prevalence of normal, insufficient or deficient levels of Vitamin D was 12.2%, 79.6% and 8.2%, respectively. During follow-up, 562 admissions to hospital for HF were identified. The incidence of HF was 1.6%, 2.9% and 5.3%, respectively in subjects with normal, insufficient and deficient levels of Vitamin D. After multivariable analysis, individuals with deficiency of Vitamin D had a higher risk of hospitalization for HF (HR: 1.61, 95%CI: 1.06-2.43) than those with normal levels. Further adjustment for subclinical inflammation did not substantially change the association between Vitamin D deficiency and HF.Deficiency of Vitamin D was associated, independently of known HF risk factors, with an increased risk of hospitalization for HF in an Italian adult population.

Aims Doxorubicin is widely used against cancer; however, it can produce heart failure (HF). Among other hallmarks, oxidative stress is a major contributor to HF pathophysiology. The late INa inhibitor ranolazine has proven effective in treating experimental HF. Since elevated [Na+]i is present in failing myocytes, and has been recently linked with reactive oxygen species (ROS) production, our aim was to assess whether ranolazine prevents doxorubicin-induced cardiotoxicity, and whether blunted oxidative stress is a mechanism accounting for such protection. Methods and result In C57BL6 mice, doxorubicin treatment for 7 days produced LV dilation and decreased echo-measured fractional shortening (FS). Ranolazine (305 mg/kg/day) prevented LV dilation and dysfunction when co-administered with doxorubicin. Doxorubicin-induced cardiotoxicity was accompanied instead by elevations in atrial natriuretic peptide (ANP), BNP, connective tissue growth factor (CTGF), and matrix metalloproteinase 2 (MMP2) mRNAs, which were not elevated on co-treatment with ranolazine. Alterations in extracellular matrix remodelling were confirmed by an increase in interstitial collagen, which did not rise in ranolazine-co-treated hearts. Levels of poly(ADP-ribose) polymerase (PARP) and pro-caspase-3 measured by western blotting were lowered with doxorubicin, with increased cleavage of caspase-3, indicating activation of the proapoptotic machinery. Again, ranolazine prevented this activation. Furthermore, in HL-1 cardiomyocytes transfected with HyPer to monitor H2O2 emission, besides reducing the extent of cell death, ranolazine prevented the occurrence of oxidative stress caused by doxorubicin. Interestingly, similar protective results were obtained with the Na+/Ca2+ exchanger (NCX) inhibitor KB-R7943. Conclusions Ranolazine protects against experimental doxorubicin cardiotoxicity. Such protection is accompanied by a reduction in oxidative stress, suggesting that INa modulates cardiac redox balance, resulting in functional and morphological derangements.

AIMS: Doxorubicin is widely used against cancer; however, it can produce heart failure (HF). Among other hallmarks, oxidative stress is a major contributor to HF pathophysiology. The late INa inhibitor ranolazine has proven effective in treating experimental HF. Since elevated [Na+ ]i is present in failing myocytes, and has been recently linked with reactive oxygen species (ROS) production, our aim was to assess whether ranolazine prevents doxorubicin-induced cardiotoxicity, and whether blunted oxidative stress is a mechanism accounting for such protection. METHODS AND RESULT: In C57BL6 mice, doxorubicin treatment for 7 days produced LV dilation and decreased echo-measured fractional shortening (FS). Ranolazine (305 mg/kg/day) prevented LV dilation and dysfunction when co-administered with doxorubicin. Doxorubicin-induced cardiotoxicity was accompanied instead by elevations in atrial natriuretic peptide (ANP), BNP, connective tissue growth factor (CTGF), and matrix metalloproteinase 2 (MMP2) mRNAs, which were not elevated on co-treatment with ranolazine. Alterations in extracellular matrix remodelling were confirmed by an increase in interstitial collagen, which did not rise in ranolazine-co-treated hearts. Levels of poly(ADP-ribose) polymerase (PARP) and pro-caspase-3 measured by western blotting were lowered with doxorubicin, with increased cleavage of caspase-3, indicating activation of the proapoptotic machinery. Again, ranolazine prevented this activation. Furthermore, in HL-1 cardiomyocytes transfected with HyPer to monitor H2 O2 emission, besides reducing the extent of cell death, ranolazine prevented the occurrence of oxidative stress caused by doxorubicin. Interestingly, similar protective results were obtained with the Na+ /Ca2+ exchanger (NCX) inhibitor KB-R7943. CONCLUSIONS: Ranolazine protects against experimental doxorubicin cardiotoxicity. Such protection is accompanied by a reduction in oxidative stress, suggesting that INa modulates cardiac redox balance, resulting in functional and morphological derangements.