Many patients with heart failure do not have reduced left ventricular ejection fraction, and it is not yet clear whether their treatment should be the same as that of patients who do
The syndrome of heart failure is one that is familiar to most clinicians. The cardinal symptoms of dyspnoea and fatigue when combined with signs of fluid retention — lung crackles, elevated jugular venous pressure and peripheral oedema — usually lead one to the diagnosis. Indeed, the Framingham criteria for diagnosis of heart failure are based largely on clinical findings that can be elicited at the bedside.1 When combined with what most of us have been taught in medical school, namely, that heart failure is usually caused by the loss of the pumping capacity of the left ventricle (eg, after myocardial infarction or due to cardiomyopathy), clinicians have become familiar with the concept that most cases of heart failure are associated with impaired left ventricular systolic function, shown by a reduction in the left ventricular ejection fraction (LVEF). As if to reinforce this mindset, major trials of new treatments for heart failure have historically focused on the group of patients with reduced LVEF.
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