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Distribution of Left Ventricular Ejection Fraction in Patients With Ischemic and Hypertensive Heart Disease and Chronic Heart Failure

      The clinical manifestations and eventual outcomes of chronic heart failure (HF) are not closely related to the left ventricular ejection fraction (EF). This has contributed to the single syndrome hypothesis of HF that assumes a continuum, with the EF evolving and decreasing as the ventricle remodels and dilates. Such a continuum might be expected to be manifest as a unimodal distribution of EF in populations with chronic HF. We examined the distribution of EF in 2 populations of patients with HF (EF range 0.10 to 0.85), and we tested the hypothesis that the EF distribution is unimodal. In both populations, the distribution histogram was bimodal. This result is consonant with the 2 different patterns of cardiac structural and functional remodeling seen in patients with HF and normal and depressed EF. It is also consonant with published differences in response to the inhibition of the renin-angiotensin system in these 2 groups. In conclusion, the observed bimodal distribution of EF in patients with chronic HF is a reflection of 2 HF phenotypes with different underlying pathophysiologic features.
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      Linked Article

      • Ejection Fraction in Heart Failure
        American Journal of CardiologyVol. 105Issue 12
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          I was interested to read the report by Gaasch et al1 on the distribution of left ventricular (LV) ejection fractions (EFs) in patients with chronic heart failure (HF). Specifically, they used trial data to test whether there is a continuum of HF from patients with normal EFs (HF with normal EF [HFNEF]) to those with reduced EFs (HF with reduced EF [HFREF]). Because the investigators found that the EF distribution was suggestive of a bimodal distribution, they concluded that there is no continuum.
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