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BackgroundCryoballoon-based pulmonary vein isolation (PVI) is a treatment option for atrial fibrillation (AF). Left atrial volume (LAV) and left atrial volume index (LAVi) are important parameters for long term success of PVI. Galectin-3 (Gal-3) and neutrophil to lymphocyte ratio (N/L ratio) are biomarkers to demonstrate the cardiac fibrosis and remodelling.Methods50 patients with symptomatic PAF despite ≥1 antiarrhythmic drug(s), who underwent PVI were enrolled. LAV, LAVi, Gal-3 and N/L ratio were calculated before ablation and after ablation at 6 and 12 months. According to AF recurrence patients were divided into two groups, recurrent AF (n = 14) and non-recurrent AF (n = 36).ResultsIn both groups (recurrent and non-recurrent), initial and 12 months follow-up LAV values were 41.39 ± 18.13 ml and 53.24 ± 22.11 ml vs 48.85 ± 12.89 ml and 42.08 ± 13.85 (p = 0.037). LAVi were 20.9 ± 8.91 ml/m2 and 26.85 ± 11.28 ml/m2 vs 25.36 ± 6.21 and 21.87 ± 6.66 (p = 0.05) for recurrent and non-recurrent AF groups, respectively. In both groups PVI had no significant effect on serum Gal-3 levels and N/L ratio during 12 months follow-up. The comparison between two groups at the end of 12th month showed Gal-3 values of 6.66 ± 4.09 ng/ml and 6.02 ± 2.95 ng/ml (p = 0.516), N/L ratio values of 2.28 ± 1.07 103/μl and 1.98 ± 0.66 103/μl (p = 0.674).ConclusionLAV and LAVi are useful to predict the remodelling of the left atrium and AF recurrence after cryoballoon-based PVI. However, biomarkers such as Gal-3 and N/L ratio are not associated with AF recurrence.

SummaryPulmonary embolism (PE) is a potentially life-threatening condition and the fact that 90% of PE originate from lower limb veins highlights the significance of early detection and treatment of deep vein thrombosis.1) Massive/high risk PE involving circulatory collapse or systemic arterial hypotension is associated with an early mortality rate of approximately 50%, in part from right ventricular (RV) failure.2) Intermediate risk/submassive PE, on the other hand, is defined as PE-related RV dysfunction, troponin and/or B-type natriuretic peptide elevation despite normal arterial pressure. 3)Without prompt treatment, patients with intermediate risk PE may progress to the massive category with a potentially fatal outcome. In patients with PE and right ventricular dysfunction (RVD), in hospital mortality ranges from 5% to 17%, significantly higher than in patients without RVD. 4,5) (Int Heart J 2016; 57: 91-95)

Once-daily dosing of non-vitamin K antagonist oral anticoagulants (NOACs) may increase patient adherence to treatment but may also be associated with a higher risk of bleeding. In this study, we investigated the adherence to once- or twice-daily dosing of NOACs and the risk of bleeding in nonvalvular atrial fibrillation (NVAF) patients. This multicenter cross-sectional study, conducted between 1 September 2015 and 28 February 2016, included 2214 patients receiving NOACs for at least 3 months, due to NVAF. Patients receiving once-daily or twice-daily NOAC doses were 1:1 propensity score matched for baseline demographic characteristics and the presence of other diseases. The medication adherence was assessed by the 8-item Morisky Medication Adherence Scale. Risk factors were investigated in relation to minor and major bleeding. The mean age of patients was 71 ± 10 years, and 53% of the patients were women. The medication adherence was lower in patients receiving twice-daily NOAC doses compared to once-daily-dose group (47% versus 53%, p = 0.001), and there was no difference between the groups in terms of minor (15% versus 16%, p = 0.292) and major bleeding (3% versus 3%, p = 0.796). Independent risk factors for bleeding were non-adherence to medication (OR: 1.62, 95% CI: 1.23-2.14, p = 0.001), presence of 3 or more other diseases (OR: 10.3, 95% CI: 5.3-20.3, p < 0.001), and HAS-BLED (Hypertension, Abnormal renal and liver function, Stroke, Bleeding, Labile INR, Elderly, Drugs or alcohol) score (OR: 4.84, 95% CI: 4.04-5.8, p < 0.001). In summary, the once-daily dose of NOACs was associated with increased patient adherence to medication, while it was not associated with bleeding complications.

Introduction Frailty is a condition of elderly characterized by increased vulnerability to stressful events. Frail patients are more likely to have adverse events. The purposes of this study were to define frailty in patients aged ≥ 70 years with chronic coronary syndrome (CCS) and to evaluate mortality and prognostic significance of frailty in these patients. Methods We included 99 patients, ≥ 70 years old (mean age 74±5.3 years), with diagnosis of CCS. They were followed-up for up to 12 months. The frailty score was evaluated according to the Canadian Study of Health and Aging (CSHA). All patients were divided as frail or non-frail. The groups were compared for their characteristics and clinical outcomes. Results Fifty patients were classified as frail, and 49 patients as non-frail. The 12-month Major Adverse Cardiac Events (MACE) rate was 69.4% in frail patients and 20% in non-frail patients. Frailty increases the risk for MACE as much as 3.48 times. Two patients died in the non-frail group and 11 patients died in the frail group. Frailty increases the risk for death as much as 6.05 times. When we compared the aforementioned risk factors by multivariate analysis, higher CSHA frailty score was associated with increased MACE and death (relative risk [RR] = 22.94, 95% confidence interval [CI] 3.33-158.19, P =0.001, for MACE; RR = 7.41, 95% CI 1.44-38.03, P =0.016, for death). Conclusion Being a frail elderly CCS patient is associated with worse outcomes. Therefore, frailty score should be evaluated for elderly CCS patients as a prognostic marker.

NT-proBNP (5042.1±1626 versus 1417.1±1711.6 pg/ml) and TN-C (1089±348.6 versus 758.5±423.9 ng/ml) levels were significantly higher in the malignant arrhythmia group than that of the benign arrhythmia group (p.

Silent embolic cerebral infarction (SECI) is a major complication of coronary angiography (CAG) and percutaneous coronary intervention (PCI). Patients with stable coronary artery disease (CAD) who underwent CAG with or without PCI were recruited. Cerebral diffusion-weighted magnetic resonance imaging was performed for SECI within 24 hours. Clinical and angiographic characteristics were compared between patients with and without SECI. Silent embolic cerebral infarction occurred in 12 (12%) of the 101 patients. Age, total cholesterol, SYNTAX score (SS), and coronary artery bypass history were greater in the SECI(+) group (65 ± 10 vs 58 ± 11 years,P= .037; 223 ± 85 vs 173 ± 80 mg/dL,P= .048; 30.1 ± 2 vs 15 ± 3,P< .001; 4 [33.3%] vs 3 [3.3%],P= .005). The SECI was more common in the PCI group (8/24 vs 4/77,P= .01). On subanalysis, the SS was significantly higher in the SECI(+) patients in both the CAG and the PCI groups (29.3 ± 1.9 vs 15 ± 3,P< .01; 30.5 ± 1.9 vs 15.1 ± 3.2,P< .001, respectively). The risk of SECI after CAG and PCI increases with the complexity of CAD (represented by the SS). The SS is a predictor of the risk of SECI, a complication that should be considered more often after CAG.

SUMMARY OBJECTIVE: Early diagnosis and risk stratification may provide a better prognosis in pulmonary embolism (PE). Copeptin has emerged as a valuable predictive biomarker in various cardiovascular diseases. The aim of this study was to determine the levels of copeptin in patients with acute PE and to evaluate its relationship with disease severity and PE-related death. METHODS: Fifty-four patients and 60 healthy individuals were included in this study. Copeptin concentrations and right ventricular dysfunction were analyzed. The correlation between copeptin levels and hemodynamic and echocardiographic parameters was examined. After these first measurements, patients were evaluated with PE-related mortality at the one-year follow-up. RESULTS: The copeptin levels were higher in PE patients than in the control group (8.3 ng/mL vs 3.8 ng/mL, p<0.001). Copeptin levels were found to be significantly higher in patients with PE-related death and right ventricular dysfunction (10.2 vs 7.5 ng/ml, p=0.001; 10.5 vs 7.5 ng/ml, p=0.002, respectively). When the cut-off value of copeptin was ≥5.85, its sensitivity and specificity for predicting PE were 71.9% and 85.0%, respectively (AUC=0.762, 95% CI=0.635-0.889, p<0.001). CONCLUSIONS: The copeptin measurement had moderate sensitivity and specificity in predicting the diagnosis of PE, and the copeptin level was significantly higher in patients with PE-related death at the one-year follow-up. Copeptin may be a useful new biomarker in predicting diagnosis, risk stratification, and prognosis of PE.