His bundle pacing (HBP) can reverse left ventricular (LV) remodeling in patients with right ventricular (RV) pacing-induced cardimyopathy (PICM) but may be unable to correct infranodal atrioventricular block (AVB).  https://www.selleckchem.com/products/pds-0330.html  Left bundle branch pacing (LBBP) results in rapid LV activation and may be able to reliably pace beyond the site of AVB. Our study was conducted to assess the feasibility, safety, and outcomes of permanent LBBP in infranodal AVB and PICM patients. Patients with infranodal AVB and PICM who underwent LBBP for cardiac resynchronization therapy (CRT) were included. Clinical evaluation and echocardiographic and electrocardiographic assessments were recorded at baseline and follow-up. Permanent LBBP upgrade was successful in 19 of 20 patients with a median follow-up duration of 12 months. QRS duration (QRSd) increased from 139.3 ± 28.0 ms at baseline to 176.2 ± 21.4 ms (P less then 0.001) with right ventricular pacing (RVP) and was shortened to 120.9 ± 15.2 ms after LBBP (P less then 0.001). The mean LBBP threshold was 0.7 ± 0.3 V at 0.4 ms at implant and remained stable during follow-up. The left ventricular ejection fraction (LVEF) increased from 36.3% ± 6.5% to 51.9% ± 13.0% (P less then 0.001) with left ventricular end-systolic volume (LVESV) reduced from 180.1 ± 43.5 to 136.8 ± 36.7 ml (P less then 0.001) during last follow-up. LBBP paced beyond the site of block, which results in a low pacing threshold with a high success rate in infranodal AVB patients. LBBP improved LV function with stable parameters over the 12 months, making it a reasonable alternative to cardiac resynchronization pacing via a coronary sinus lead in infranodal AVB and PICM patients.Introduction Donation after circulatory death (DCD) could substantially improve donor heart availability. In DCD, the heart is not only exposed to a period of warm ischemia, but also to a damaging pre-ischemic phase. We hypothesized that the DCD-relevant pre-ischemic lactate levels negatively affect the post-ischemic functional and mitochondrial recovery in an isolated rat heart model of DCD. Methods Isolated, working rat hearts underwent 28.5' of global ischemia and 60' of reperfusion. Prior to ischemia, hearts were perfused with one of three pre-ischemic lactate levels no lactate (0 Lac), physiologic lactate (0.5 mM; 0.5 Lac), or DCD-relevant lactate (1 mM; 1 Lac). In a fourth group, an inhibitor of the mitochondrial calcium uniporter was added in reperfusion to 1 Lac hearts (1 Lac + Ru360). Results During reperfusion, left ventricular work (heart rate-developed pressure product) was significantly greater in 0.5 Lac hearts compared to 0 Lac or 1 Lac. In 1 vs. 0.5 Lac hearts, in parallel with a decreased function, cellular and mitochondrial damage was greater, tissue calcium content tended to increase, while oxidative stress damage tended to decrease. The addition of Ru360 to 1 Lac hearts partially abrogated the negative effects of the DCD-relevant pre-ischemic lactate levels (greater post-ischemic left ventricular work and less cytochrome c release in 1 Lac+Ru360 vs. 1 Lac). Conclusion DCD-relevant levels of pre-ischemic lactate (1 mM) reduce contractile, cellular, and mitochondrial recovery during reperfusion compared to physiologic lactate levels. Inhibition of mitochondrial calcium uptake during early reperfusion improves the post-ischemic recovery of 1 Lac hearts, indicating calcium overload as a potential therapeutic reperfusion target for DCD hearts.Background Although troponin elevation is common in COVID-19, the extent of myocardial dysfunction and its contributors to dysfunction are less well-characterized. We aimed to determine the prevalence of subclinical myocardial dysfunction and its association with mortality using speckle tracking echocardiography (STE), specifically global longitudinal strain (GLS) and myocardial work efficiency (MWE). We also tested the hypothesis that reduced myocardial function was associated with increased systemic inflammation in COVID-19. Methods and Results We conducted a retrospective study of hospitalized COVID-19 patients undergoing echocardiography (n = 136), of whom 83 and 75 had GLS (abnormal >-16%) and MWE (abnormal less then 95%) assessed, respectively. We performed adjusted logistic regression to examine associations of GLS and MWE with in-hospital mortality. Patients were mean 62 ± 14 years old (58% men). While 81% had normal left ventricular ejection fraction (LVEF), prevalence of myocardial dysfunction was high by STE; [39/83 (47%) had abnormal GLS; 59/75 (79%) had abnormal MWE]. Higher MWE was associated with lower in-hospital mortality in unadjusted [OR 0.92 (95% CI 0.85-0.99); p = 0.048] and adjusted models [aOR 0.87 (95% CI 0.78-0.97); p = 0.009]. In addition, increased systemic inflammation measured by interleukin-6 level was associated with reduced MWE. Conclusions Subclinical myocardial dysfunction is common in COVID-19 patients with clinical echocardiograms, even in those with normal LVEF. Reduced MWE is associated with higher interleukin-6 levels and increased in-hospital mortality. Non-invasive STE represents a readily available method to rapidly evaluate myocardial dysfunction in COVID-19 patients and can play an important role in risk stratification.Introduction Right ventricular failure (RVF) after cardiac surgery is an important risk factor for morbidity and mortality. Its diagnosis is challenging, and thus, its incidence and predictors are not well-established. We investigated the incidence, complications, and variables associated with clinically relevant post-operative RVF. Methods We included all patients who underwent cardiac surgery with cardiopulmonary bypass between 2016 and 2019 in a cardiac surgery center with standardized diagnostic and therapeutic management of RVF. RVF was considered only if clinically relevant associated with hemodynamic instability requiring catecholamine support and inhaled nitric oxide relayed by sildenafil. Results Overall, 3,826 patients were included, of whom, 110 (2.9%) developed post-operative RVF. Mortality was not different among patients who developed post-operative RVF, compared with the rest of the cohort (1.8 vs. 0.7%, p = 0.17). Using a composite outcome that combined death, reintubation, stroke, and prolonged intensive care unit stay (more than 14 days) yielded an incidence of 6.