It is common to classify patients with either acute or chronic heart failure (HF) based on their left ventricular ejection fraction (LVEF) at presentation—both in clinical practice and in research… Click to show full abstract
It is common to classify patients with either acute or chronic heart failure (HF) based on their left ventricular ejection fraction (LVEF) at presentation—both in clinical practice and in research studies, including practice-defining trials. Although this approach is rooted in the different pathophysiology of HF according to impairment of cardiac output at rest, it has some inherent limitations. First, the cutoff point to classify LVEF as reduced (HFrEF) or preserved (HFpEF) is necessarily arbitrary, ranging between 40% and 50% in the various studies. This has led the European Society of Cardiology to propose a new category of HF patients with LVEF values between 40% and 49%, termed HF with midrange ejection fraction (HFmrEF). Second, a number of echocardiographic studies, both with the standard approach and with myocardial deformation imaging, have convincingly demonstrated that preserved LVEF does not guarantee preserved systolic function of the left ventricle. In the TOPCAT trial, an echocardiographic study, 52% of patients had impaired global longitudinal strain, and this impairment was strongly associated with cardiovascular death and HF hospitalization. In addition, patients with impaired global longitudinal strain seem to have benefited more from aldosterone antagonist therapy in a post hoc analysis. Third, beyond the absolute value of LVEF at presentation, the trajectory of LVEF also has important clinical implications. In a recent large cohort study, patients who presented with preserved LVEF as a result of improvement or recovery of HFrEF had a significantly better prognosis than patients with persistently reduced or preserved LVEF. The latter is especially important for patients with HFmrEF who frequently fall under this category. Finally, in contrast to HFrEF, in which low cardiac output and the resultant neurohormonal activation dominate the pathophysiological process, HFpEF, and by extension HFmrEF, have a more diverse pathophysiology and probably cannot be treated as a single phenotype for therapeutic and management purposes. Clearly, despite the clinical utility and the prognostic significance of LVEF, especially among patients with HFrEF, the use of LVEF alone is
               
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