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Update Summary
July, 2023
The following sections, tables, and figures were updated following publication of the ACC Expert Consensus Decision Pathway on Management of Heart Failure with Preserved Ejection Fraction:
Key concepts 4 and 8 were updated to reflect new guidance on the role of SGLT2 inhibitors for the treatment of HFpEF.
Pharmacologic Therapy for HFpEF section was updated to reflect new guidance on the role of SGLT2 inhibitors, ARNI, ARB, and aldosterone antagonist.
Table 36-10 was updated to include the DELIVER trial.
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CHAPTER SUMMARY FROM THE PHARMACOTHERAPY HANDBOOK
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For the Chapter in the Schwinghammer Handbook, please go to Chapter 9, Heart Failure.
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KEY CONCEPTS
Heart failure (HF) is a clinical syndrome associated with symptoms due to abnormalities in cardiac structure and/or function substantiated by the presence of increased natriuretic peptide plasma concentrations or objective evidence of pulmonary or systemic congestion of cardiogenic origin. The left ventricular ejection fraction (LVEF) is used to classify patients into four different types of HF, the two primary classifications being heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF). Patients with HFrEF or HFpEF commonly present with signs and symptoms of fluid overload.
With HFpEF, systolic function is preserved, but the heart does not relax nor fill sufficiently resulting in compromised diastolic function. Despite the activation of similar neurohormonal systems as HFrEF, patients with HFpEF are often treated differently than those with HFrEF. Most of the pharmacotherapies known to benefit patients with HFrEF have been less beneficial in HFpEF. Targeting the underlying cause, most commonly uncontrolled hypertension, has been the primary strategy for managing patient with HFpEF. However, recent trials have identified new therapies that benefit patients with HFpEF.
In HFrEF, systolic dysfunction results in a decline in cardiac output leading to the activation of a number of neurohormonal compensatory responses that attempt to maintain adequate cardiac output. These responses include activation of the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS) and other systems. These compensatory mechanisms play an important role in ventricular remodeling and contribute to the progression of HF. Importantly, pharmacotherapy targeted at antagonizing this neurohormonal activation slows the progression of HFrEF and improves survival.
Most patients with HFrEF should be routinely treated with guideline-directed medical therapy (GDMT)—medications known to reduce mortality in these patients. GDMT includes four medication classes: an angiotensin receptor II receptor blocker/neprilysin inhibitor (ARNI) or angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB), an evidence-based β-blocker, an aldosterone antagonist, and a sodium-glucose cotransporter-2 (SGLT2) inhibitor. In patients with HFrEF, GDMT dosing should be titrated to achieve target doses known to be effective in randomized clinical trials. In contrast, all patients with HFpEF benefit from a SGLT2 inhibitor and select patients with HFpEF may benefit from an ARNI, ARB, and aldosterone antagonist.
The ARNI, sacubitril/valsartan, is approved to treat patients ...