1,720,974 research outputs found
Herzinsuffizienz, Antikoagulation, Dyslipidämien
No full textThree innovative pharmaceuticals which might play an important role in the field of cardiology in the near future were recently tested in large clinical studies. Serelaxin, a vasoactive hormone peptide that is produced during pregnancy, reduces vessel resistance, increases cardiac output, and improves renal function. Lately, it was demonstrated that serelaxin significantly reduces congestion symptoms in patients with acute heart failure. As a secondary endpoint the mortality at day 180 was reduced. Therefore, serelaxin seems to be a promising new drug for the treatment of acute heart failure which might have a prognostic impact. Edoxaban is a selective factor Xa inhibitor, which inhibits thrombin production and thrombus formation. Two recently published studies reported that edoxaban is at least as effective as the vitamin K antagonist warfarin in prevention and treatment of venous thromboembolism and in the prevention of stroke and systemic embolism due to nonvalvular atrial fibrillation. Compared to warfarin, edoxaban significantly exhibited less frequent severe bleeding complications. Edoxaban will probably soon be the fourth new oral anticoagulant available for patients. The serine protease proprotein convertase subtilisin/kexin 9 (PCSK9) reduces the ability of the liver to bind low-density lipoprotein cholesterol (LDL-C) and to remove it from the circulation. Recently, a monoclonal antibody for PCSK9 was developed which induces a LDL-C plasma level reduction up to 73 % and also decreases lipoprotein(a) and apolipoprotein B. PCSK9 inhibition is a promising new mechanism for LDL-C reduction and the corresponding drug will be presumably approved soon by the regulatory authorities
Genetic determinants of heart failure: facts and numbers
No full textThe relevance of gene mutations leading to heart diseases and hence heart failure has become evident. The risk for and the course of heart failure depends on genomic variants and mutations underlying the so‐called genetic predisposition. Genetic contribution to heart failure is highly heterogenous and complex. For any patient with a likely inherited heart failure syndrome, genetic counselling is recommended and important. In the last few years, novel sequencing technologies (named next‐generation sequencing – NGS) have dramatically improved the availability of molecular testing, the efficiency of genetic analyses, and moreover reduced the cost for genetic testing. Due to this development, genetic testing has become increasingly accessible and NGS‐based sequencing is now applied in clinical routine diagnostics. One of the most common reasons of heart failure are cardiomyopathies such as the dilated or the hypertrophic cardiomyopathy. Nearly 100 disease‐associated genes have been identified for cardiomyopathies. The knowledge of a pathogenic mutation can be used for genetic counselling, risk and prognosis determination, therapy guidance and hence for a more effective treatment. Besides, family cascade screening for a known familial, pathogenic mutation can lead to an early diagnosis in affected individuals. At that timepoint, a preventative intervention could be used to avoid or delay disease onset or delay disease progression. Understanding the cellular basis of genetic heart failure syndromes in more detail may provide new insights into the molecular biology of physiological and impaired cardiac (cell) function. As our understanding of the molecular and genetic pathophysiology of heart failure will increase, this might help to identify novel therapeutic targets and may lead to the development of new and specific treatment options in patients with heart failure
Predictors of High Post-Procedural Gradients after Catheter-Based Aortic Valve Implantation Using Direct Flow Medical Bioprostheses
No full textThe Direct Flow Medical (DFM) valve is a new non-metallic and repositionable bioprosthesis used for transcatheter aortic valve implantation (TAVI). The study aim was to investigate procedural and post-implant valve data in patients receiving differently sized DFM bioprostheses
The transfemoral Implantation of a 29 mm metal-free Aortic Valve Bioprosthesis in the elderly is associated with longer Procedure times and post interventional higher Flaps-Gradient
No full textIncreased proatherogenic monocyte-platelet cross-talk in monocyte subpopulations of patients with stable coronary artery disease
No full textBackgroundMonocytes and platelets are important cellular mediators of atherosclerosis. Human monocytes can be divided into CD14(++)CD16(-), CD14(++)CD16(+) and CD14(+)CD16(++) cells, which differ in their functional properties. The aim of this study was to examine monocyte subset distribution, monocyte-platelet aggregate (MPA) formation and expression of CCR5, the receptor of the platelet-derived chemokine CCL5, and to determine whether these parameters are altered in individuals with coronary atherosclerosis. MethodsPeripheral blood cells from 64 healthy blood donors (HBDs) and 60 patients with stable coronary artery disease (CAD) were stained with antibodies against CD14, CD16, CD42b and CCR5 and analysed by flow cytometry. Circulating CCL5 levels were determined using an enzyme-linked immunosorbent assay. ResultsIn patients with CAD, the relative proportion of the CD14(++)CD16(-) monocyte subset was elevated (P<0.05) and of the CD14(+)CD16(++) subset was reduced (P<0.001) compared with the HBD group. Furthermore, MPA formation significantly increased in patients with CAD in all three monocyte subsets. In both study groups, the majority of CCR5(+) cells was detected in CD14(++)CD16(+) monocytes (P<0.001 versus CD14(++)CD16(-) and CD14(+)CD16(++)), although the CCR5(+) monocyte number was reduced in patients with CAD (CD14(++)CD16(-)/CD14(+)CD16(++), P<0.001; CD14(++)CD16(+), P<0.05) compared with the HBD group, particularly in those who were not taking statins. Ex vivo incubation of monocytes from HBDs with plasma from patients with CAD also decreased CCR5(+) expression (P<0.05 versus plasma from HBDs). Serum CCL5 levels were similar in both groups. ConclusionsThe increased monocyte-platelet cross-talk in patients with CAD might have contributed to atherosclerosis progression. The decreased CCR5(+) monocyte numbers in patients with CAD could have resulted from CCR5(+) cell recruitment into atherosclerotic lesions or CCR5 downregulation in response to circulating factors
Atheroprotective Kruppel-like factor 4 is downregulated in monocyte subsets of patients with coronary artery disease
No full textStage-dependent detection of CD14+ and CD16+ immune cells in human heart tissue after myocardial infarction: A post-mortem analysis
No full textThe transfemoral Implantation of a 29 mm metal-free Aortic Valve Bioprosthesis in the elderly is associated with longer Procedure times and post interventional higher Flaps-Gradient
No full textStage-dependent detection of CD14+ and CD16+ immune cells in human heart tissue after myocardial infarction: A post-mortem analysis
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