Novel Strategies for the Management of Acute Decompensated Heart Failure

Abstract

Acute decompensated heart failure (ADHF) is the primary diagnosis for approximately one million hospital admissions in the United States, with an estimated $13.6 billion dollars of direct hospital cost in 2003. Until recently, diagnosis and management of ADHF has largely been "tradition-based" rather than evidence-based. Diuretic therapy has been the mainstay of symptom relief for pulmonary congestion and fluid retention. The introduction of nesiritide has revived the emphasis on vasodilator therapy for preload and afterload reduction in ADHF. Newer intravenous vasodilator drugs such as tezosentan, an endothelin antagonist, and carperitide, a natriuretic peptide, currently are being tested in multicenter clinical trials. New inotropic agents, such as levosimendan, appear to have an improved safety and efficacy profile. Vasopressin receptor antagonists and adenosine receptor antagonists may offer improved renal preservation during aggressive diuresis. Mechanical unloading with ultrafiltration devices and extracorporeal circulatory support devices have been developed to supplement pharmacological therapies and are undergoing clinical trials.

Who is managing acute decompensated heart failure? The need for a multidisciplinary approach

“…without inducing arrhythmogenicity or increasing mortality risk [48][49][50][51][52][53][54][55][56][57][58][59] (Table 1). Finally, although major advancements in the medical therapy of heart failure patients have substantially improved outcomes, 60 technological advances in mechanical devices, 61 including automatic implantable cardioverter defibrillators, cardiac resynchronization therapy, and ventricular assist devices, as well as advances in the surgical treatment of heart failure, 62 have also been used to support the failing heart.…”

“…These new therapies represent an attempt to improve on existing therapies, and consequently, they fall into the same 3 general categories as current therapies: diuretics, vasodilators, and inotropic agents. 48,49 Vasopressin receptor antagonists and adenosine receptor antagonists represent an attempt to stimulate aquaresis without inducing hyponatremia, hypokalemia, diminished glomerular filtration, or adverse neurohormonal activation; [48][49][50][51][52][53][54] endothelin receptor antagonists and newer natriuretic peptides represent an attempt to stimulate vasodilation and improve cardiac output without diminishing renal function; 49,55 and myosin activators and sodiumpotassium adenosine triphosphatase inhibitors represent an attempt to enhance contractility …”