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Heart failure (HF) is the inability of the heart to pump an adequate supply of blood to meet the demands of the body. It is an epidemic and is associated with significant morbidity, mortality, and healthcare expenditure. Heart failure has an estimated prevalence of 5.8 million in the United States, and affects over 23 million people worldwide.1 The cost of HF in the United States was around $30 billion in 2012, a number that is projected to increase to around $70 billion by the year 2030.2 Acute decompensated HF (ADHF) is the clinical syndrome of new onset or worsening HF symptoms and signs requiring urgent treatment.3 In the United States, ADHF exacerbations result in about 1 million hospitalizations yearly and contribute largely to the overall HF healthcare expenditure.2 Hospitalization for ADHF serves as a poor prognostic indicator with an approximate 30% and 50% readmission rate at 1 month and 6 months, respectively, and a 1-year all-cause mortality as high as 30%.4,5


Patients with HF can either present to the hospital with symptoms for the first time or present with ADHF in the setting of having a diagnosis of chronic HF. Heart failure is classified based on the left ventricular ejection fraction (LVEF), as usually determined by echocardiography, into HF with reduced ejection fraction (EF) (HFrEF) with an LVEF less than 40%, or HF with preserved EF (HFpEF) with an LVEF 50% or greater.6 An EF between 40% and 49% is considered a gray zone. Epidemiological data indicates that HFpEF and HFrEF contribute equally to the total HF population.6 Patients with HFpEF have a similar postdischarge mortality risk and equally high rates of rehospitalization as patients with HFrEF.7 The pathophysiology of HF is complex and involves intricate interactions between neurohormonal systems and hemodynamic abnormalities, resulting in abnormal myocardial remodeling and progressive myocardial, endothelial, valvular, and vascular dysfunction.8

Heart failure with reduced EF results from systolic dysfunction, which limits the ability of the contracting myocardium to effectively eject the preload of the failing myocardium. This results in backward failure, elevated end-diastolic pressure, and an inability to produce an adequate cardiac output. Heart failure with preserved EF results from abnormal or impaired myocardial diastolic relaxation, which causes elevated end-diastolic pressures and prevents an appropriate increase in the ejection fraction under conditions of stress. Regardless of the type of HF, symptoms of acute decompensation are from elevated left ventricular end-diastolic pressure (filling pressure) with resultant alveolar and interstitial edema causing pulmonary congestion and dyspnea. The backward transmission of elevated filling pressures and subsequent pulmonary venous hypertension increase pulmonary arterial and right heart pressures, causing systemic congestive symptoms.

Irrespective of the type of HF, the symptoms and signs of HF are due to either congestion or decreased cardiac output and tissue perfusion. The spectrum of presentation ...

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