Circulation. Heart failure
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Randomized Controlled Trial Multicenter Study Comparative Study
Cardio-renal effects of the A1 adenosine receptor antagonist SLV320 in patients with heart failure.
Blocking the tubuloglomerular feedback mechanism with adenosine A1 receptor antagonists seems to improve diuresis and sodium excretion without compromising the glomerular filtration rate in patients with heart failure. However, the direct cardiac effects of this compound class have not been investigated to date. ⋯ SLV320 infusion shows no immediate effects on cardiac hemodynamics. SLV320 might improve glomerular filtration rate while simultaneously promoting natriuresis and diuresis. Clinical Trial Registration- clinicaltrials.gov Indentifier: NCT00160134.
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Multicenter Study
Factors associated with neurologically intact survival for patients with acute heart failure and in-hospital cardiac arrest.
Hospitalized patients with heart failure are at risk for cardiac arrest. The ability to predict who may survive such an event with or without neurological deficit would enhance the information on which patients and providers establish resuscitative preferences. ⋯ A number of prearrest factors seem to be associated with NIS, the majority inversely. Consideration of these before cardiac arrest could enhance the resuscitative decision-making process for patients with acute heart failure.
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Autonomic dysfunction, characterized by sympathetic activation and vagal withdrawal, contributes to the progression of heart failure (HF). Although the therapeutic benefits of sympathetic inhibition with beta-blockers in HF are clear, the role of increased vagal tone in this setting has been less studied. We have investigated the impact of enhancing vagal tone (achieved through chronic cervical vagus nerve stimulation, [VNS]) on HF development in a canine high-rate ventricular pacing model. ⋯ Chronic VNS improves cardiac autonomic control and significantly attenuates HF development in the canine high-rate ventricular pacing model. The therapeutic benefit of VNS is associated with pronounced anti-inflammatory effects. VNS is a novel and potentially useful therapy for treating HF.
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Urocortin 2 (Ucn2), a novel peptide with therapeutic potential in heart failure, and diuretics have opposing effects on renal function and the renin-angiotensin-aldosterone system. Because any prospective new treatment is likely to be used in conjunction with standard diuretic therapy, it is necessary to investigate the combined effects of these agents. ⋯ Ucn2 cotreatment with furosemide enhanced hemodynamic and renal function and diuretic responsiveness (without additional potassium depletion) in experimental heart failure. Furthermore, Ucn2 reversed furosemide-induced increases in plasma renin activity and induced greater decreases in plasma aldosterone and vasopressin. These data indicate that adjunct Ucn2 therapy with diuretics in heart failure is beneficial.
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Inflammation has been implicated in the pathogenesis of heart failure (HF), but knowledge about the production and role of inflammatory actors remains incomplete. On the basis of its role in vascular inflammation, vascular proliferation, and matrix degradation, we hypothesized a role for the chemokine CXCL16 in the pathogenesis of myocardial remodeling and development of HF. ⋯ We show enhanced myocardial CXCL16 expression in experimental and clinical HF. The effect of CXCL16 on cardiomyocytes and fibroblasts suggests a role for CXCL16 in matrix remodeling and ultimately in the development of HF.