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Background and Objectives: Patients with chronic total occlusions of the coronary arteries are either treated with PCI or referred for surgical revascularization. We analyzed the patients with chronic occluded coronary arteries that were surgically treated and aimed to describe the anatomical characteristics, revascularization rates, and in-hospital outcomes achieved with coronary artery bypass grafting. Methods: Angiographic data of 2005 patients with coronary artery disease treated in our institution between January 2005 and December 2014 were retrospectively analyzed. A total of 1111 patients with at least one coronary total occlusion were identified. We reviewed the preoperative coronary angiograms and surgical protocols to determine the presence, localization, and revascularization of coronary occlusions. We also evaluated the perioperative data and in-hospital outcomes. Results: The median age of the study population was 68 years (25th–75th percentiles, 61.0–74.0). Three-vessel disease was present in 94.8% of patients and the rest (5.8%) had a two-vessel disease. The localizations of the occlusions were as follows: 68.4% in the RCA system, 26.4% in the LAD, and 28.5% in the LCX system. Multiple occlusions were present in 22.6% of the patients. Complete coronary total occlusion revascularization was achieved in 86.1% of the patients. The overall in-hospital mortality was 2.3%. The median in-hospital stay was 14.0 days. After logistic regression analysis, age (odds ratio 3.44 [95% confidence interval, 1.81–6.53], p < 0.001, for a 10-year increase) and the presence of peripheral artery disease (odds ratio 3.32 [1.39–7.93], p = 0.007) were the only statistically significant independent predictors of in-hospital mortality. Conclusions: A high revascularization rate and favorable in-hospital outcomes are achieved with coronary artery bypass surgery in patients with multi-vessel diseases and coronary total occlusions. Older age and the presence of peripheral artery disease are independent predictors of in-hospital mortality. A long-term follow-up and the type of graft (arterial vs. venous) used would bring more useful data for this type of revascularization.

Abstract Thromboembolism and stroke are dreaded complications in atrial fibrillation (AF). Established risk stratification models identify susceptible patients, but their discriminative properties are poor. Atrial cardiomyopathy (ACM) is associated to thromboembolism and stroke in smaller studies, but the modalities used for ACM-diagnosis (MRI and endocardial mapping) are unsuitable for widespread population screening. We aimed to investigate an ECG-based diagnosis of ACM using amplified p-wave analysis (APWA) for stratification of thromboembolic risk and cardiovascular outcome. In this case–control study, ACM-staging was performed using APWA on digital 12-lead sinus rhythm-ECGs in patients with LAA-thrombus and a propensity-score-matched control-cohort. Left atrial contractile function and thrombi were evaluated by transesophageal echocardiography (TEE). Outcome for MACCE including death was assessed using official registries and structured phone interviews. Left-atrial appendage [LAA]-thrombi and appropriate sinus rhythm-ECGs for ACM-staging were found in 109 of 4086 patients that were matched 1:1 to control patients without thrombus (218 patients in total). Both cohorts were comparable regarding cardiovascular risk factors, anticoagulants and CHA2DS2-VASC-score. ACM-stages 1 to 3 (equivalent to no, moderate and extensive ACM) were found in 63 (57.8%), 36 (33.0%) and 10 (9.2%) of patients without and 3 (2.8%), 23 (21.1%) and 83 (76.1%) of patients with LAA-thrombi. Atrial contractile function decreased from ACM-stages 1 to 3 (LAA-flow velocities 38 ± 16 cm/s, 31 ± 15 cm/s and 21 ± 12 cm/s; p

BackgroundAtrial fibrillation (AF) is the most common arrhythmia and a significant burden for healthcare systems worldwide. Presence of relevant atrial cardiomyopathy (ACM) is related to persistent AF and increased arrhythmia recurrence rates after pulmonary vein isolation (PVI).ObjectiveTo investigate the association of left atrial pressure (LAP), left atrial electrical [invasive atrial activation time (IAAT) and amplified p-wave duration (aPWD)] and mechanical [left atrial emptying fraction (LA-EF) and left atrial strain (LAS)] functional parameters with the extent of ACM and their impact on arrhythmia recurrence following PVI.Materials and MethodsFifty patients [age 67 (IQR: 61–75) years, 78% male] undergoing their first PVI for persistent AF were prospectively included. LAP (maximum amplitude of the v-wave), digital 12-lead electrocardiogram, echocardiography and high-density endocardial contact mapping were acquired in sinus rhythm prior to PVI. Arrhythmia recurrence was assessed using 72-hour Holter electrocardiogram at 6 and 12 months post PVI.ResultsRelevant ACM (defined as left atrial low-voltage extent ≥2 cm2 at

BackgroundThere is limited evidence of long‐term impact of right ventricular pacing on left ventricular (LV) systolic function in pacemaker recipients with preserved LV ejection fraction (LVEF). The objective of the study was to evaluate the outcome and echocardiographic course of baseline preserved LVEF in a large cohort of pacemaker recipients with respect to pacing indication and degree of right ventricular pacing. Methods and ResultsWe enrolled 991 patients (73±10 years, 54% male) with baseline normal (>55%) LVEF (n=791) or mildly reduced (41–55%) LVEF (n=200) who had paired echocardiographic data on LV systolic function recorded at implantation and last follow‐up. According to pacing indication, patients were divided into atrioventricular block group A (n=500) and sinus node disease group B (n=491). Main outcome measures were all‐cause mortality and deterioration of LV function ≥2 LVEF categories at last follow‐up. Patients were followed for an average of 44 months. Death from any cause occurred in 166 (17%), and deterioration of LV function ≥2 LVEF categories in 56 (6%) patients. There was no significant difference in outcome between group A and group B either in patients with normal LVEF or in those with mildly reduced LVEF. Mean percentage of right ventricular pacing was not predictive of outcome. ConclusionsIn a large cohort of pacemaker recipients with predominantly normal LVEF, clinically relevant LV dysfunction develops rather infrequently. No significant difference in all‐cause mortality and development of severe LV dysfunction is observed between patients with atrioventricular block and sinus node disease. Accordingly, de novo biventricular pacing cannot be recommended for patients with preserved LVEF.

Abstract??The ischemic preconditioning biological phenomenon has been explored to identify putative pharmacologic agents to mimic this cytoprotective program against cellular ischemic injury. Diazoxide administration confers this cytoprotection, however, whether this is via direct activation of the putative mitochondrial KATP(mKATP) channel which was originally proposed has been questioned. Here, we present data supporting an alternate hypothesis evoking mitochondrial respiratory inhibition rather than mKATPchannel activation, as a mediating event in the diazoxide-activated cytoprotective program. Mitochondrial respiration and reactive oxygen species (ROS) production was measured in digitonin-permeabilized C2C12 myotubes, allowing for the modulation of mKATPconductance by changing the potassium concentration of the medium (0?130 mM). Diazoxide dose-dependently attenuated succinate-supported respiration, an effect that was independent of mKATPchannel conductance. Similarly, 5-hydroxydecanoate (5-HD), a putative mKATPchannel blocker, released diazoxide-induced respiratory inhibition independently of potassium concentration. Since diazoxide-induced cytoprotection and respiratory inhibition are both integrally linked to ROS generation we repeated above experiments following ROS generation using DCF fluorescence. Cytoprotective doses of diazoxide increased ROS generation independently of potassium concentration and 5-HD inhibited ROS production under the same conditions. Collectively these data support the hypothesis that diazoxide-mediated cytoprotection is independent of the conductance of the mKATPchannel and rather implicate mitochondrial respiratory inhibition-triggered ROS signaling. [ABSTRACT FROM AUTHOR]