Atrial fibrillation (AF) is a very common arrhythmia that mainly affects older individuals. The mechanism of atrial fibrillation is complex and is related to the pathogenesis of trigger activation and the perpetuation of arrhythmia. The pulmonary veins in the left atrium arei confirm that onfirm the most common triggers due to their distinct anatomical and electrophysiological properties. As a result, their electrical isolation by ablation is the cornerstone of invasive AF treatment. Multiple factors and comorbidities affect the atrial tissue and lead to myocardial stretch. Several neurohormonal and structural changes occur, leading to inflammation and oxidative stress and, consequently, a fibrotic substrate created by myofibroblasts, which encourages AF perpetuation. Several mechanisms are implemented into daily clinical practice in both interventions in and the medical treatment of atrial fibrillation.

The influence of diabetes mellitus (DM) on platelet reactivity (PR) in prasugrel or ticagrelor treated patients is not well studied. In an observational study involving 777 patients with acute coronary syndrome undergoing percutaneous coronary intervention treated by either prasugrel 10 mg od (n = 315) or ticagrelor 90 mg bid (n = 462), platelet function was assessed using the VerifyNow P2Y12 function assay (in PRU) at one month post intervention. In the overall population, ticagrelor and insulin-treated DM affected PR, with a decrease in log by 0.88 (corresponding to a 58 % decrease in PR) compared to prasugrel-treated patients (p < 0.001), and an increase in log by 0.26 (corresponding to a 30 % increase in PR) compared to non-diabetic patients (p = 0.01), respectively. PR in prasugrel-treated patients differed significantly by DM status: 70.0 (36.3-113.0) in non-diabetic vs 69.0 (44.5-115.3) in non insulin-treated diabetic vs 122.0 (69.0-161.0) in insulin-treated diabetic patients, p for trend = 0.01. No differences were observed in ticagrelor-treated patients. By multivariate analysis, in prasugrel-treated patients insulin-treated DM was the only factor predicting PR, with log of PR increased by 0.42 (corresponding to a 52 % increase in PR) compared to non-diabetic patients (p = 0.001). No factor was found to affect PR in ticagrelor-treated patients. Patients with insulin-treated DM treated with prasugrel post PCI have higher PR, than patients without DM or non insulin-treated diabetic patients treated with this drug. Ticagrelor treated patients have overall lower PR than patients on prasugrel, independent of DM status or insulin treatment. Clinical Trials Gov. NCT01774955

Background: SCN5A mutations may present with different clinical phenotypes such as Brugada syndrome, long QT3 syndrome, sick sinus syndrome, atrial fibrillation, dilated cardiomyopathy, and the least known multifocal ectopic Purkinje-related premature contractions syndrome. Case summary: We report a case of a 29-year-old woman with palpitations due to multifocal premature ventricular complexes (PVCs) and a family history of sudden death. The previous electrophysiological study had shown that PVCs arose from Purkinje fibres but catheter ablation was unsuccessful. Cardiac magnetic resonance (CMR) imaging demonstrated non-ischaemic areas of subendocardial fibrosis at multiple left ventricular (LV) segments with concomitant dilatation and mild systolic impairment. Amiodarone suppressed the ectopy but caused hyperthyroidism. Due to recent pregnancy, she received no antiarrhythmics which resulted in PVC burden increase and further deterioration of the ejection fraction (EF). After gestation, amiodarone was reinitiated and switched to flecainide after implantation of a subcutaneous defibrillator as a safety net. At follow-up, LV function had almost normalized. Genetic analysis confirmed an SCN5A mutation. Discussion: Multifocal ectopic Purkinje-related premature contractions syndrome is associated with SCN5A mutation which in our case (R222Q) is the most common described. Flecainide can be an appropriate treatment option when ablation is ineffective. Defibrillator—even a subcutaneous type—could be implanted in cases of LV dysfunction or scar. PVCs suppression by flecainide and restoration of EF implies an arrhythmia—induced mechanism of LV impairment.

Objectives: Previous studies have demonstrated gaps in achievement of low-density lipoprotein-cholesterol (LDL-C) goals among patients at very high cardiovascular risk. We aimed to investigate lipid treatment patterns, rates and predictors of lipid targets attainment, in such outpatients in an urban area of Greece. Methods: This was a prospective observational study, conducted in 19 outpatient clinics of Western Greece. We recruited patients with established cardiovascular disease (CVD) and/or diabetes mellitus (DM), previously (at least 3 months before baseline assessment) untreated with any lipid lowering medication. Lipid profile assessment was performed at baseline (prior to lipid-lowering treatment initiation) and at follow-up. Lipid lowering treatment choice was at physicians’ discretion and was kept constant until follow-up. Results: We recruited 712 patients with a mean age 61.4 ± 10.4 years, 68.0% males, 43.0% with DM, 64.7% with prior coronary artery disease-CAD. In total, 237/712 (33.3%) of prescribed regimens were of high or very high LDL-C lowering efficacy and out of them 113/237 (47.7%) comprised a combination of statin and ezetimibe. At follow-up the primary target of LDL-C < 70 mg/dL (1.8 mmol/L) was achieved in 71(10.0%) patients. The secondary target of non-HDL-C < 100 mg/dL (2.6 mmol/L) in the subgroup of patients with DM or increased triglycerides levels (>150 mg/dl or 1.7 mmol/L) was achieved in 45(11.6%) of patients. In multivariate logistic regression analysis (AUC = 0.71, 95% CIs 0.65-0.77, p < 0.001) male gender, smoking, baseline LDL-C and very high potency LDL-C lowering regimen emerged as independent predictors of LDL-C goal attainment (OR = 1.88, 95% CIs 1.03-3.44, p = 0.04, OR = 0.57, 95% CIs 0.33-0.96, p = 0.04, OR = 0.98, 95% CIs 0.98-0.99, p < 0.001 and OR = 2.21, 95% CIs 1.15-4.24, p = 0.02 respectively). Conclusions: First-line management of dyslipidemia among very-high cardiovascular risk outpatients in Western Greece is unsatisfactory, with the majority of treated individuals failing to attain the LDL-C and non-HDL-C targets. This finding points out the need for intensification of statin treatment in such patients.

Left bundle branch area pacing (LBBAP) is an emerging pacing method, which may prevent the deleterious effects of right ventricular pacing. The aim of this study is to compare the effects of LBBAP with right ventricular septal pacing (RVSP) in patients with advanced atrioventricular conduction abnormalities and preserved left ventricular ejection fraction. The effect of pacing was evaluated by echocardiographic indices of dyssynchrony, including global myocardial work efficiency (GWE) and peak systolic dispersion (PSD). The primary endpoint was GWE postprocedural, at 3, 6 and 12 months after the procedure. Twenty patients received LBBAP and 18 RVSP. Complete follow-up was accomplished in 37 patients (97.4%), due to the death of a patient (RVSP arm), from non-related cause. GWE was significantly increased in the group of LBBAP compared to RVSP at all timepoints (90.8% in LBBAP vs 85.8% in RVSP group at 12 months, p=0.01). PSD was numerically lower in the LBBAP arm at all timepoints, yet not statistically significant (56.4 msec in LBBP vs 65.1 msec in RVSP arm at 12 months, p=0.178). The implantation time was increased (median 93 min in LBBAP vs 45 min in RVSP group, p<0.01), along with fluoroscopy time and dose area product (DAP), in the arm of LBBAP. There were no severe perioperative acute complications in either group. LBBAP is an emerging and safe technique for patients with a pacing indication. Despite the longer procedural and fluoroscopy time, as well as higher DAP, LBBAP seems to offer better left ventricular synchrony compared to RVSP, according to GWE measurements.