G. Michael Felker, MD, MHS, FACC

1. What is acute decompensated heart failure? Isn’t it just a worsening of chronic heart failure?

    Acute decompensated heart failure (ADHF) is a clinical syndrome of worsening signs or symptoms of heart failure requiring hospitalization or other unscheduled medical care. For many years, ADHF was viewed as simply an exacerbation of chronic heart failure as a result of volume overload, with few implications beyond a short-term need to intensify diuretic therapy (a similar paradigm to exacerbations of chronic asthma). Recent decades have seen an explosion of research into the epidemiology, pathophysiology, outcomes, and treatment of ADHF. Multiple lines of evidence now support the concept that ADHF is a unique clinical syndrome with its own epidemiology and underlying mechanisms and a need for specific therapies. ADHF is not just a worsening of chronic heart failure, any more than an acute myocardial infarction (MI) is just a worsening of chronic angina.

    Outcomes data from a variety of studies now support the concept that hospitalization for ADHF can often signal a dramatic change in the natural history of the heart failure syndrome. Rates of rehospitalization or death are as high as 50% within 6 months of the initial ADHF event, which is a much higher event rate than is seen with acute MI.

2. Are there clinically important subcategories of ADHF?

    There is great interest in developing a framework for understanding ADHF that would assist in stratifying patients, guiding therapy, and developing new treatments, similar to the basic framework developed for acute coronary syndromes (i.e., ST segment elevation myocardial infarction [STEMI], non–ST segment elevation myocardial infarction [NSTEMI], and unstable angina). Although this area is rapidly evolving, a few general clinical phenotypes of ADHF have emerged.

3. What is the role of biomarkers like B-type natriuretic peptides (BNPs) in the diagnosis of ADHF?

    Although the clinical symptoms (dyspnea, paroxysmal nocturnal dyspnea [PND], orthopnea, fatigue) and signs (elevated jugular venous pressure, pulmonary rales, edema) of ADHF are well known, the diagnosis can often be challenging in patients presenting to acute care settings. This is especially true in the elderly and patients with significant comorbid conditions such as chronic obstructive pulmonary disease (COPD). The development of natriuretic peptides as a diagnostic tool has been a major advance in ADHF diagnosis. The clinically available natriuretic peptides for ADHF diagnosis include BNP and its biologically inert amino-terminal fragment, N-terminal prohormone of B-type natriuretic peptide (NT-proBNP). Despite some subtle differences between these two biomarkers, they provide similar diagnostic information when used in patients presenting to the emergency department with unexplained dyspnea, although the range of values is significantly different (in general, NT-proBNP levels are approximately 5 to 10 times greater than BNP levels in the same patient). The landmark Breathing Not Properly Study measured BNP levels in 1586 patients presenting to the emergency department with unexplained dyspnea. In this study, treating physicians were blinded to BNP values and a panel of cardiologists adjudicated whether hospitalizations were due to ADHF or other causes (based on all clinical data other than the BNP values). As shown in Figure 22-1, a cutoff of 100 pg/mL of BNP had a positive predictive value of 79% and a negative predictive value of 89% for the diagnosis of ADHF. The area under the receiver operating characteristic (ROC) curve was 0.91, suggesting a very high degree of accuracy for establishing the diagnosis of ADHF. Subsequent studies have demonstrated similar findings for NT-proBNP, although optimal diagnostic cutoffs are different (450 pg/mL for patients younger than 50 years and 900 pg/mL for patients older than 50 years). The use of natriuretic peptide has now become the standard of care in the diagnosis of patients with dyspnea presenting to acute care settings, and has a class I indication (“should be done”) in clinical practice guidelines.

4. What features suggest patients who are particularly high risk?

    Analysis of large datasets from both clinical trials and registries of ADHF patients have identified a few features that consistently suggest a high risk of short-term morbidity and mortality in patients hospitalized with ADHF (Box 22-1). Across studies, the most consistent of these are blood urea nitrogen (BUN), serum creatinine, SBP, and hyponatremia. Interestingly, BUN has consistently proved to be a stronger predictor of outcomes than creatinine (Fig. 22-2). One potential explanation of this finding is that BUN may integrate both renal function and hemodynamic information. Unlike the situation in many other cardiovascular conditions, higher blood pressure has consistently been associated with lower

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