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The DanGer Shock trial test the hypothesis that left ventricular (LV) mechanical circulatory support with Impella CP transvalvular microaxial flow pump improves survival in patients with ST segment elevation acute myocardial infarction complicated by cardiogenic shock (AMICS) compared to conventional guideline-driven treatment. This paper describes the rationale and design of the randomized trial, in addition to the baseline characteristics of the population screened and enrolled so far. The DanGer Shock study is a prospective, multicenter, open-label trial in patients with AMICS randomized 1:1 to Impella CP or current guideline-driven therapy with planned enrollment of 360 patients. Patients comatose after out of hospital cardiac arrest are excluded. Eligible patients are randomized immediately following shock diagnosis. Among patients randomized to receive Impella CP, the device is placed prior to angioplasty. The primary endpoint is all-cause mortality at 180 days. Baseline characteristics of patients screened and randomized in the DanGer Shock as of June 2018 are compared with 2 contemporary AMICS studies. As of end of June 2018, 314 patients were screened and 100 patients were randomized. Patients had median arterial lactate of 5.5 mmol/L (interquartile range 3.7-8.8 mmol/L), median systolic blood pressure of 76 mmHg (interquartile range 70-88 mmHg), and median LV ejection fraction of 20% (interquartile range 10%-30%). The DanGer Shock trial will be the first adequately powered randomized trial to address whether mechanical circulatory LV support with Impella CP can improve survival in AMICS. Baseline characteristics of the first 100 randomized patients indicate a population in profound cardiogenic shock.

Intercellular communication mediated by extracellular vesicles is crucial for preserving vascular integrity and in the development of cardiovascular disease. Extracellular vesicles consist of apoptotic bodies, microvesicles, and exosomes that can be found in almost every fluid compartment of the body like blood, saliva, and urine. In the recent years, a lot of reports came up suggesting that major cardiovascular and metabolic pathologies like atherogenesis, heart failure, or diabetes are highly influenced by transfer of microRNAs via extracellular vesicles leading to altered protein expression and phenotypes of recipient cells. The following review will summarize the fast developing field of intercellular signaling in cardiovascular biology by microRNA-containing extracellular vesicles.

Circulating endothelial progenitor cells are derived from the bone marrow and are believed to support the integrity of the vascular endothelium. In this study of patients with coronary artery disease, the number of such cells correlated inversely with the risk of adverse cardiovascular outcomes. The level of circulating endothelial progenitor cells thus may be a useful marker of coronary risk. In patients with coronary artery disease, the number of circulating endothelial progenitor cells correlated inversely with the risk of adverse cardiovascular outcomes. The level of these cells thus may be a useful marker of coronary risk. Coronary artery disease results from a chronic inflammatory disease of the vascular wall and leads to vessel occlusion and organ damage. 1 Despite intense efforts to determine the pathogenesis of atherosclerosis, this process remains poorly understood. Reports suggest that risk factors and a genetic predisposition together induce inflammatory processes that lead to cell damage and impair regeneration within the vessel wall. 2 , 3 Since resident endothelial cells infrequently proliferate, 4 it has been postulated that there are other sources of vascular replenishment in response to continuous damage. 5 Endothelial progenitor cells derived from bone marrow circulate in the peripheral blood and have been implicated . . .

Endothelial microparticles (EMP) are complex vesicular structures shed from activated or apoptotic endothelial cells. As endurance exercise affects the endothelium, the objective of the study was to examine levels of EMP and angiogenic growth factors following different endurance exercise protocols. 12 subjects performed 3 different endurance exercise protocols: 1. High volume training (HVT; 130 min at 55% peak power output (PPO); 2. 4 × 4 min at 95% PPO; 3. 4 × 30 sec all-out. EMPs were quantified using flow cytometry after staining platelet-poor-plasma. Events positive for Annexin-V and CD31, and negative for CD42b, were classified as EMPs. Vascular endothelial growth factor (VEGF), migratory inhibiting factor (MIF) and hepatocyte growth factor (HGF) were determined by ELISA technique. For all these measurements venous blood samples were taken pre, 0', 30', 60' and 180' after each intervention. Furthermore, in vitro experiments were performed to explore the effect of collected sera on target endothelial functions and MP uptake capacities. VEGF and HGF significantly increased after HIT interventions. All three interventions caused a significant decrease in EMP levels post exercise compared to pre values. The sera taken after exercise increased the uptake of EMP in target endothelial cells compared to sera taken under resting conditions, which was shown to be phosphatidylserin-dependent. Increased EMP uptake was associated with an improved protection of target cells against apoptosis. Sera taken prior and after exercise promoted target endothelial cell migration, which was abrogated after inhibition of VEGF. Physical exercise leads to decreased EMP levels and promotes a phosphatidylserin-dependent uptake of EMP into target endothelial cells, which is associated with a protection of target cells against apoptosis.

Aims Tricuspid regurgitation (TR) in patients with mitral valve disease is associated with poor outcome and mortality. Only limited data on the impact of TR on functional outcome and survival in patients undergoing MitraClip procedures are available. Methods and results 261 patients (mean age 76.6 ± 10, EuroScore 15.9 ± 15.1%) with symptomatic mitral regurgitation (MR) (75.2% functional MR) undergoing MitraClip procedure were included and followed for 721 ± 19.4 days. At baseline 54.7% presented with TR grade 0/I, 29.5% with grade II, 13.4% with grade III and 2.3% with grade IV. When dividing groups according to baseline TR grades, follow-up (FU)-NYHA class was significantly improved only in patients with TR ≤ II ( p  = 0.05). FU-6-min walking distance increased significantly in the overall cohort ( p  = 0.05), in patients with TR ≤ II ( p  = 0.007), but not in patients with TR > II ( p  = 0.4). Moreover, FU-NT-pro-BNP levels were higher in patients with TR > II ( p  = 0.05), compared to patients with TR ≤ II. There was a higher mortality according to baseline TR > II and multivariate Cox regression revealed TR > II as the strongest independent predictor for mortality (hazard ratio 2.04). Conclusions Concomitant TR at baseline negatively influences functional outcome and mortality in patients undergoing MitraClip procedures. Our results underline the need for dedicated interventional strategies for the treatment of TR in patients with symptomatic MR.

History of syncope is an independent predictor for sudden cardiac death. Programmed stimulation may be considered for risk stratification, but data remain sparse among different populations. Here, we analyzed the prognostic value of inducible ventricular arrhythmia (VA) regarding clinical outcome in patients with syncope undergoing defibrillator implantation. Among 4196 patients enrolled in the prospective, multi-center German Device Registry, patients with syncope and inducible VA (n = 285, 6.8%) vs. those with a secondary preventive indication (n = 1885, 45.2%), defined as previously documented sustained ventricular tachycardia or ventricular fibrillation, serving as a control group were studied regarding demographics, device implantation and post-procedural adverse events. Patients with syncope and inducible VA (64.9 ± 14.4 years, 81.1% male) presented less frequently with congestive heart failure (15.1% vs. 29.1%; p  < 0.001) and any structural heart disease (84.9% vs. 89.3%; p  = 0.030) than patients with a secondary preventive indication (65.0 ± 13.8 years, 81.0% male). Whereas dilated cardiomyopathy (16.8% vs. 23.8%; p  = 0.009) was less common, hypertrophic cardiomyopathy (5.6% vs. 2.8%; p  = 0.010) and Brugada syndrome (2.1% vs. 0.3%; p  < 0.001) were present more often. During 1-year-follow-up, mortality (5.1% vs. 8.9%; p  = 0.036) and the rate of major adverse cardiac or cerebrovascular events (5.8% vs. 10.0%; p  = 0.027) were lower in patients with syncope and inducible VA. Among patients with inducible VA, post-procedural adverse events including rehospitalization (27.6% vs. 21.7%; p  = 0.37) did not differ between those with vs. without syncope. Taken together, patients with syncope and inducible VA have better clinical outcomes than patients with a secondary preventive defibrillator indication, but comparable outcomes to patients without syncope, which underlines the relevance of VA inducibility, potentially irrespective of a syncope.

More than mild paravalvular aortic regurgitation (pAR) negatively impacts prognosis after transcatheter aortic valve implantation (TAVI). \"Newer generation\" transcatheter heart valves (THVs) including Direct Flow Medical, Medtronic Evolut R, Boston Lotus, and Edwards SAPIEN 3 valve system promise to improve outcome by reducing the rate of TAVI-related issues such as pAR. Aim was to evaluate and compare the hemodynamic performance with AR index of \"early\" vs. \"newer generation\" THVs and its impact on outcome. In 805 patients undergoing TAVI, the degree of pAR was assessed using imaging modalities (angiography, echocardiography) and hemodynamic measurements (aortic regurgitation index, ARI ratio). Severity of pAR and outcome were assessed according to the VARC-2 criteria. 805 patients underwent TAVI with use of the CoreValve (n = 400), SAPIEN XT (n = 48), Direct Flow Medical (n = 38), Evolut R (n = 114), Lotus (n = 104), or SAPIEN 3 (n = 101) prosthesis. TTE post TAVI revealed that a total of 7.3% of the patients showed moderate/severe pAR. The occurrence of greater than mild pAR occurred less frequently in patients treated with \"newer generation\" THVs (p<0.001): CoreValve (11.3%), SAPIEN XT (12.5%), Direct Flow Medical (5.3%), Evolut R (5.3%), Lotus (0.0%), and SAPIEN 3 (0.0%). The AR index was significantly higher (p<0.001) in patients receiving \"newer generation\" prostheses compared to those in whom \"earlier generation\" THVs were used. However, the ARI was only predictive of cumulative all-cause mortality at 1 and 3 years in \"early generation\", but not in \"newer generation\" THVs. In the overall cohort, 30-day and 1-year mortality was 4.8% and 20.1%, respectively. In patients treated with \"newer generation\" devices, the respective mortality rates remained substantially below those of patients treated with \"earlier generation\" THVs (30-day mortality: 2.5% vs. 6.7%, p< 0.001; 1-year mortality: 11.2% vs. 27.2%, p<0.001). TAVI with use of \"newer generation\" THVs showed significantly reduced pAR and improved outcomes compared to \"early generation\" devices that could at least in part be explained by more favorable hemodynamics.

•In this analysis of 43 propensity score-matched pairs of patients who had residual or recurrent mitral regurgitation after the first transcatheter mitral valve repair (TMVR) .•redo TMVR with the MitraClip system is feasible and safe.•MR grades reduce significantly after redo TMVR, with a significant improvement of the NYHA functional class.•Redo TMVR is associated with lower mortality as compared with medical therapy alone. There is little known about the prognostic impact of a redo transcatheter mitral valve repair (TMVR) for residual or recurrent mitral regurgitation (MR). From January 2011 to March 2019, we identified 43 consecutive patients who underwent a redo TMVR procedure with the MitraClip system. A control cohort was treated medically for MR ≥2+ after the first TMVR and was propensity score 1:1 matched using age, gender, MR severity, trans-mitral pressure gradient, and etiology of MR. To investigate the association of redo TMVR with 1-year mortality, we fitted a Cox proportional hazard model. The technical success rate of redo TMVR was 95%. A reduction in MR to ≤2+ was achieved in 79% of patients, with a significant decline of tricuspid regurgitation pressure gradient and improvement of the New York Heart Association class. After matching was performed, 43 well-matched pairs of patients were analyzed. Redo TMVR patients showed lower 1-year mortality (10.5% vs 37.6%, p = 0.01) compared with the control patients. Redo TMVR was associated with better survival (hazard ratio [HR] 0.26, 95% confidence interval [CI] 0.08 to 0.79, p = 0.02) and lower risk of the composite end point (mortality and rehospitalization due to HF: HR 0.34, 95% CI 0.15 to 0.78; p = 0.01) at 1-year follow-up. The association with the primary end point remained significant after accounting for the New York Heart Association class III/IV, TR ≥severe, the type of MR (i.e., recurrent or residual MR), or the type of previous implanted TMVR device. In conclusion, redo TMVR in selected patients with residual or recurrent MR may be associated with lower 1-year mortality than medical therapy alone.

The use of left-ventricular (LV) hemodynamic support might facilitate high-risk percutaneous coronary interventions (PCI) in patients with complex coronary artery disease. The impact on outcome is a matter of ongoing debate. We assessed the outcome of high-risk patients who underwent protected PCI in comparison to patients who underwent unprotected high-risk PCI. One hundred and thirty nine patients underwent nonemergent high-risk PCI; 24 (17%) patients underwent protected PCI. To address selection bias, we performed a propensity score matched subanalysis. The primary end point was the occurrence of a major adverse cardiac event during the first year. Patients with protected PCI had a higher logistic EuroSCORE (logES) (protected PCI: 19% vs unprotected PCI: 12%; p = 0.01), a higher SYNTAX score (45 vs 36, p = 0.07), and significantly more often reduced LV function (40% vs 55%; p < 0.001). In protected PCI patients, complete revascularization was more often achieved (87% vs 58%, p = 0.007) without the occurrence of death at 30 days of follow-up (0% vs 4%, p = 0.31). After propensity score matching, patients who underwent protected PCI had a similar 1-year major adverse cardiac event rate compared with patients who underwent unprotected PCI (21% vs 17%, p = 0.67), despite significantly higher procedural complexity for example, more often complex left main bifurcation lesions (71% vs 29%; p = 0.004). In conclusion, 1-year outcome of patients who underwent protected PCI was not different from that in patients with less complex procedures without hemodynamic support, despite more complex coronary anatomy, a higher comorbidity burden, and more often reduced LV function.

Endothelial progenitor cells (EPC) enhance endothelial cell repair, improve endothelial dysfunction and are a predictor for cardiovascular mortality. High‐density lipoprotein (HDL) cholesterol levels inversely correlate with cardiovascular events and have vasculoprotective effects. Here we postulate that HDL influences EPC biology. HDL and EPC were isolated according to standard procedures. Differentiation of mononuclear cells into DiLDL/lectin positive cells was enhanced after HDL treatment compared to vehicle. HDL was able to inhibit apoptosis (TUNEL assay, annexin V staining) while proliferation (BrdU incorporation) of early outgrowth colonies after extended cell cultivation (14 days) was increased. Flow chamber experiments revealed an improved adhesion of HDL pre‐incubated EPC on human coronary artery endothelial cells (HCAEC) compared to vehicle while HDL treatment of HCAEC prevented adhesion of inflammatory cells. Flow cytometry demonstrated an up‐regulation of β2‐ and α4‐integrins on HDL pre‐incubated EPC. Blocking experiments revealed a unique role of β2‐integrin in EPC adhesion. Treatment of wild‐type mice with recombinant HDL after endothelial denudation resulted in enhanced re‐endothelialization compared to vehicle. Finally, in patients with coronary artery disease a correlation between circulating EPC and HDL concentrations was demonstrated. We provide evidence that HDL mediates important vasculoprotective action via the improvement of function of circulating EPC.