1,721,146 research outputs found
Percutaneous mechanical circulatory support. Options and importance
No full textIn cases of low cardiac output and chronic cardiac failure despite conventional therapy, mechanical circulatory support may be the only option to ensure adequate organ perfusion and to save the life of the patient. In recent years, several conceptionally different methods of circulatory support have been developed for percutaneous application in interventional cardiology and intensive care. Indications range from elective use in complex cardiac interventions to long-term support as a bridge to recovery. As intra-aortic balloon pump support can no longer be considered for routine use in ischemic cardiogenic shock, micro-axial pumps for extracorporeal membrane oxygenation and extracorporeal life support systems (ECMO/ECLS) gain attractiveness due to a more convincing impact on the hemodynamics. However, an increasing level of support is paralleled by greater invasiveness and complexity of the systems. Due to a lack of larger comparative trials, the benefits and risks of adverse events must be balanced against those of conventional therapy with inotropes and largely on an individual basis. This review summarizes the options for percutaneous circulatory support with special consideration to applications in the catheter laboratory and intensive care units in internal medicine
Coronary interventions. Current developments for improved long-term results
No full textBased on solid scientific evidence, new generation drug-eluting stents (DES) have become established as the standard of care in interventional cardiology. With at least similar safety and superior efficacy over uncoated bare metal stents (BMS) in various scenarios and including patients with increased bleeding risk, there are probably no remaining indications favoring the use of BMS. Additional developments regarding the platform, drug elution characteristics and polymer design were aimed at optimizing DES with even better outcomes. Although there is no lack of new variations, none has proven to be superior and several non-inferiority trials lacked statistical power, which precludes the label third generation (over second generation or new generation DES). While it is recognized that potential long-term advantages of bioresorbable scaffolds cannot be expected at this stage from the current ABSORB III trial, the safety and efficacy are encouraging. Beyond procedural aspects, such as intracoronary imaging, variations in duration of antiplatelet therapy should help to improve outcomes but still require careful individual weighting of ischemic vs. bleeding risk
B-RAF and its novel negative regulator reticulocalbin 1 (RCN1) modulates cardiomyocyte hypertrophy
No full textAim Activation of the kinase RAF and its downstream targets leads to cardiomyocyte hypertrophy. It has been hypothesized that B-RAF might be the main activator of MEK in various cell types. Therefore, the aim of this study was to investigate the role of B-RAF and its modulating factors in cardiomyocyte hypertrophy. Methods and results Neonatal rat cardiomyocytes were pre-treated with and without the specific B-RAF inhibitor SB590885 and then stimulated with phenylephrine to induce hypertrophy. Inhibition of B-RAF completely impeded the hypertrophic response and led to a significant reduction of MEK1/2 phosphorylation. By applying a eukaryotic cDNA expression screen, based on a dual-luciferase reporter assay for B-RAF activity measurement, we identified RCN1 as a new negative modulator of B-RAF activity. Adenovirus-mediated overexpression of reticulocalbin 1 (RCN1) completely impeded phenylephrine-induced hypertrophy and led to significantly reduced MEK1/2 phosphorylation. Conversely, adenoviral knockdown of RCN1 with a specific synthetic miRNA induced cardiomyocyte hypertrophy and significantly increased MEK1/2 phosphorylation. Conclusions In summary, our results show that the inhibition of B-RAF abolishes cardiomyocyte hypertrophy and we identified RCN1 as novel negative modulator of cardiomyocyte hypertrophy by inhibition of the mitogen-activated protein kinase signalling cascade. Our results show that B-RAF kinase activity is essential for cardiac hypertrophy and RCN1, its newly identified negative regulator, abolishes hypertrophic response of cardiomyocytes in vitro
Na+/Ca2+ exchanger overexpression increases sensitivity to hydroxyl radical-induced injury
No full textThe effects of over-expressing an FKBP12.6 mutant that prevents calcineurin binding, on Ca sparks in permeabilised adult rabbit ventricular cardiomyocytes.
No full textFeasibility and outcomes of interventional treatment for vascular access site complications following transfemoral aortic valve implantation
No full textAdenoviral expression of short interfering RNA effectively silences gene expression in adult rabbit cardiac myocytes
No full textFkbp9: An alternative splice variant of the FK506-binding protein FKBP12.6 expressed in the human heart.
No full textNa+/Ca2+ exchanger overexpression increases sensitivity to hydroxyl radical-induced injury
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