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  • image Heart failure (HF) is a clinical syndrome associated with symptoms and/or signs 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.

  • imageWith HFpEF, systolic function is preserved. In contrast, 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.

  • imageIn 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.

  • image 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. Patients with HFpEF may benefit from an ARNI and SGLT2 inhibitor.

  • image The ARNI, sacubitril/valsartan, is the only therapy approved to treat patients with HFrEF and many with HFpEF. In patients with HFrEF, ARNI is preferred over either ACE inhibitors or ARBs to improve survival, slow disease progression, reduce hospitalizations, and improve quality of life. Patients receiving ACE inhibitors or ARBs can be switched to ARNI or ARNI can be used as initial treatment in patients with newly detected HFrEF without previous exposure to ACE inhibitors or ARBs. The doses for these agents should be targeted at those shown in clinical trials to improve survival.

  • image The β-blockers carvedilol, metoprolol succinate, and bisoprolol prolong survival, decrease hospitalizations, reduce the need for transplantation, and promote “reverse remodeling” of the left ventricle. These agents are recommended for all patients with HFrEF unless contraindicated. Therapy must be instituted at low doses, with slow upward titration ...

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