Comments on "The management of Heart Failure with preserved ejection fraction"

Abstract

1. The use of the LV ejection fraction for diagnosing and dividing patients with heart failure is flawed. 1 EF is a poor measurement of ventricular function or mechanics, fails to correlate with functional capacity, and is more a reflection of volume and shape changes. A ventricle with reduced LV systolic function can have an increased EF if there is LV wall hypertrophy and reduction of cavity size 2 . The presumption that systolic function was normal in those with a normal LVEF led to the notion that the mechanical disorder resided in diastole and therefore drugs that might increase relaxation rate or reduced stiffness were considered to be necessary. More recent work has shown widespread abnormalities of systolic function affecting longitudinal function particularly but also twist, torsion, synchrony, radial and circumferential function which all lead to reduced recoil, suction and reduced early diastolic filling 3,4 . Thus the disordered diastolic filling begins in systole and the widespread abnormalities of ventricular mechanics will need to be addressed if overall ventricular function is to be improved. 2. The use of the word “preserved” in the labelling of these patients is irrational and misleading. 5 The definition of preserved (OED) is “maintain (something) in its original or existing state”. What evidence is there that the EF is unchanging, especially as there are usually no measurements taken before the onset of symptoms? In fact the opposite appears to be the case. Recent work by Dunlay et al has shown that in HFNEF patients on average EF decreased by 5.8% over 5 years (P<0.001) with greater declines in older individuals, and 39% of HFNEF patients had an EF<50% after 5 years i.e. they had developed HFREF 6 . Therefore there is frequently progression of disease with increasing LV remodeling, and dilatation associated with falling EF. The rate at which this occurs depends in part on the aetiology: it appears that myocardial infarction is a potent stimulus to remodeling whereas the process is slower in the older often female patient with hypertension and or diabetes. However, treatment should be directed towards preventing this progression of remodeling. It may be that the standard therapy for HFrEF, which appears to be effective in the remodeled ventricle, may be beneficial in this context and supports the notion that Coats and Shewan put forward that these treatments probably should be used despite the lack of mortality data.