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Key Clinical Updates in Heart Failure

Patients with HF and reduced LVEF should be treated with all four life-saving medications: beta-blockers, mineralocorticoid (aldosterone) receptor antagonists, sacubitril/valsartan, and SGLT2 inhibitors. This combination, titrated to full tolerated doses, with careful monitoring of kidney function and potassium, will provide the greatest pharmacologic benefit to the majority of patients with HF with reduced LVEF. Achieving this goal has been shown to be more effective using a systematic approach with care pathways and frequent clinic visits.

DOACs appear to be as effective as warfarin for patients with LV thrombus.

Initiating life-saving medications during hospitalization for HF with rapid titration after discharge may improve outcomes.

Heidenreich PA et al. J Am Coll Cardiol. [PMID: 35379504]

McDonagh TA et al. Eur J Heart Fail. [PMID: 35083827]


  • LV failure: Either due to systolic or diastolic dysfunction. Predominant symptoms are those of low cardiac output and congestion, including dyspnea.

  • RV failure: Symptoms of fluid overload predominate; usually RV failure is secondary to LV failure.

  • Assessment of LV function is a crucial part of diagnosis and management.

  • Optimal management of chronic HF includes combination medical therapies, such as ACE inhibitors, aldosterone antagonists, and beta-blockers.


HF is a common syndrome that is increasing in incidence and prevalence. Approximately 6 million patients in the United States have HF, with 8 million or more patients projected to have HF by 2030. Each year in the United States, 1,250,000 patients are discharged from the hospital with a diagnosis of HF. It is primarily a disease of aging, with over 75% of existing and new cases occurring in individuals over 65 years of age. Seventy-five percent of HF patients have antecedent hypertension. The prevalence of HF rises from less than 1% in individuals below 60 years to nearly 10% in those over 80 years of age.


Systolic function of the heart and resulting cardiac output is governed by four major determinants: the contractile state of the myocardium, the preload of the ventricle (the end-diastolic volume and the resultant fiber length of the ventricles prior to onset of the contraction), the afterload applied to the ventricles (the impedance to LV ejection), and the heart rate.

Cardiac function may be inadequate as a result of alterations in any of these determinants. The primary derangement is often depression of myocardial contractility caused either by loss of functional muscle (due to MI, etc) or by processes diffusely affecting the myocardium. However, the heart may fail as a pump because preload is excessively elevated, such as in valvular regurgitation, or when afterload is excessive, such as in aortic stenosis or in severe hypertension. Pump function may also be inadequate when the heart rate is too slow or too rapid. Whereas the normal heart can tolerate wide variations in preload, afterload, and heart rate, ...

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