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UPDATE SUMMARY

UPDATE SUMMARY

The following updates were made on September 29, 2020:

  • A section on Amyloid Cardiomyopathy was added to the Pathophysiology section

  • Table 35-7 was updated to include the results of the PARAGON-HF study

  • A section on Tafamidis for the treatment of amyloid cardiomyopathy was added to the Other Treatments for Heart Failure in Select Patients section

  • Updates to the Diabetes section under Special Populations reflect recent studies of sodium-glucose cotransporter 2 inhibitors in heart failure

CHAPTER SUMMARY FROM THE PHARMACOTHERAPY HANDBOOK

For the Chapter in the Schwinghammer, Handbook (not Wells Handbook anymore) please go to Chapter 9, Heart Failure.

KEY CONCEPTS

KEY CONCEPTS

  • imageHeart failure (HF) is a progressive clinical syndrome that can result from any changes in cardiac structure or function that impair the ability of the ventricle to fill with or eject blood. HF may be caused by an abnormality in systolic function, diastolic function, or both. The leading causes of HF are coronary artery disease and hypertension. The primary manifestations of the syndrome are dyspnea, fatigue, and fluid retention.

  • imageIn heart failure with reduced ejection fraction (HFrEF), there is a decrease in cardiac output resulting in the activation of a number of 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). These compensatory mechanisms are responsible for the symptoms of HFrEF and contribute to disease progression.

  • imageOur current understanding of HFrEF pathophysiology is best described by the neurohormonal model. Activation of endogenous neurohormones including norepinephrine, angiotensin II, aldosterone, vasopressin, and numerous proinflammatory cytokines play an important role in ventricular remodeling and the subsequent progression of HF. Importantly, pharmacotherapy targeted at antagonizing this neurohormonal activation slows the progression of HFrEF and improves survival.

  • imageMost patients with HFrEF should be routinely treated with guideline-directed medical therapy (GDMT) that includes an angiotensin-converting enzyme (ACE) inhibitor, angiotensin II receptor blocker (ARB), or angiotensin II blocker/neprilysin inhibitor and an evidence-based β-blocker. Selected patients should also receive aldosterone antagonists, loop diuretics, or hydralazine/nitrates. The benefits of these medications on slowing HF progression, reducing morbidity and mortality, and/or improving symptoms are clearly established.

  • imageIn patients with HFrEF, ACE inhibitors improve survival, slow disease progression, reduce hospitalizations, and improve quality of life. The doses for these agents should be targeted at those shown in clinical trials to improve survival. ARBs are recommended for patients intolerant to ACE inhibitors due to angioedema or cough. In symptomatic patients receiving an ACE inhibitor or ARB, replacement with the combination ARB/neprilysin inhibitor is recommended.

  • imageThe β-blockers carvedilol, metoprolol succinate, and bisoprolol prolong survival, decrease hospitalizations and 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 to the target dose.

  • imageAlthough chronic loop ...

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