The Year in Cardiology 2013: heart failure

Heart failure has become a worldwide epidemic of the 21st century with increasing impact on healthcare systems. The 2012 ESC and 2013 ACCF/AHA guidelines have set the stage for current therapy to reduce mortality and morbidity. There is a dawn of hope for therapy of acute and diastolic heart failure; it has become clearer that patients benefit from mitral reconstruction and which patients benefit from heart failure management programmes; genetics and proteomics advance in great strides; competing concepts of cell therapy seem to spiral, hopefully upwards; and we can further nurture our hope for evidence-based individualized diagnostic and therap

The year in cardiology: heart failure 2014

The year 2014 has become a remarkable year for heart failure. A bad start was caused by the publication of TOPCAT, showing that spironolactone did not prove to be beneficial for the treatment of patients with heart failure and preserved ejection fraction (HFpEF). Nevertheless, further insights in the study yields a few bright spots, and treatment with spironolactone might still be considered in patients with HFpEF. In acute heart failure, additional data were published on the effects of serelaxin. Serelaxin reduced wedge pressures, had similar effects in acute heart failure patients with and without a reduced ejection fraction, and had a neutral effect on diuretic response. But the most important news was related to the results of PARADIGM, where LCZ696, the first-in-class angiotensin-receptor neprilysin inhibitor, proved to be superior to enalapril in reducing mortality and morbidity in patients with heart failure and reduced ejection fraction (HFrEF

Preventive strategies in endothelin-induced renal failure

Preventive strategies in endothelin-induced renal failure. The endothelial vasoconstrictor endothelin (ET) can induce acute renal failure when fibrinolysis and vasodilatory prostanoids (PGs) are inhibited. This study compares therapeutic agents preventing ET-induced acute renal failure in anesthetized female pigs. We investigated the effect of four ET boli (1.5 μg/kg, i.v.) after pretreatment with indomethacin (2mg/kg) and ε-aminocaproicacid (100 + 50mg/kg) alone (controls, group 1) or during additional nifedipine (10 μg/kg/h; group 2), hirudin (0.5mg/kg; group 3), or enalapril (2 × 0.15mg; group 4) on coagulation, PGs, and renal function. The ET-induced blood pressure increase was lower in groups 2 to 4 (lowest in group 3, P < 0.05). PG synthesis was blocked in all groups. The initial hypercoagulability (controls) resulted in disseminated intravascular coagulation that was prevented by hirudin and was attenuated in groups 2 and 4. At the end of the experiment, creatinine clearance was significantly (P < 0.05) decreased. The recovery of renal function two hours after the last ET bolus was most pronounced in the hirudin group. All therapeutic drugs attenuated ET-induced impairment of renal function. Hirudin seems to be the most potent protective drug. Prevention of further ET release evoked by ET-mediated secretion of thrombin might explain this. These results suggest three important pathways for ET's hemodynamic and renal effects