title: Optimizing outcomes in the patient with acute decompensated heart failure.
abstract: Heart failure (HF) and episodes of acute decompensated HF (ADHF) continue to pose a substantial clinical challenge in the United States and represent a significant source of morbidity, mortality, and health care resource use. Recent therapeutic advances have shifted ADHF treatment paradigms from diuretic management with or without inotrope use to therapy where intravenous vasodilators are the central component, above a background of diuretics. This shift in treatment has resulted in more rapid symptomatic improvements as well as in decreases in overall morbidity and mortality. Elevated left ventricular filling pressure has become an important clinical target for resolution during ADHF, as this parameter most closely correlates with degree of symptoms, extent of ischemic complications, and the deleterious neurohormonal activation in response to ADHF. Therapies that lead to rapid improvements in left ventricular filling pressure, including the use of nesiritide, a recombinant analog of B-type natriuretic peptide, have been shown to provide rapid symptomatic relief, but effects on long-term morbidity and mortality are as yet unclear. In addition to new treatments, new technologies--including assays based on cardiac biomarkers and techniques such as impedance cardiography for noninvasive monitoring of hemodynamic parameters--are contributing to improvements in care that will ultimately reduce the sizeable clinical and economic burden that HF represents.
authors.affiliation: Division of Cardiology, Department of Medicine, University of Maryland, Baltimore, MD, USA. mmehra@medicine.umaryland.edu
authors.forename: Mandeep R
authors.initials: MR
authors.lastname: Mehra
mesh_terms: D015415:Biomarkers / Q000097:blood; D002316:Cardiotonic Agents / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy*; D006439:Hemodynamics; D006801:Humans; D006835:Hydrazones / Q000627:therapeutic use; D020105:Milrinone / Q000627:therapeutic use; D045283:Natriuretic Agents / Q000627:therapeutic use; D020097:Natriuretic Peptide, Brain / Q000097:blood / Q000627:therapeutic use; D005996:Nitroglycerin / Q000627:therapeutic use; D011724:Pyridazines / Q000627:therapeutic use; D011725:Pyridines / Q000627:therapeutic use; D018570:Risk Assessment; D000077464:Simendan; D013777:Tetrazoles / Q000627:therapeutic use; D013812:Therapeutics; D014336:Troponin / Q000097:blood; D014665:Vasodilator Agents / Q000627:therapeutic use; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D015415:Biomarkers; D002316:Cardiotonic Agents; D004232:Diuretics; D006835:Hydrazones; D045283:Natriuretic Agents; D011724:Pyridazines; D011725:Pyridines; D013777:Tetrazoles; D014336:Troponin; D014665:Vasodilator Agents; D020097:Natriuretic Peptide, Brain; D000077464:Simendan; C120582:tezosentan; D005996:Nitroglycerin; D020105:Milrinone