Key result
Ejection fraction may be preserved despite impaired long-axis shortening in left ventricular hypertrophy, suggesting it alone may be an insufficient descriptor of systolic function.
Ejection fraction alone may be an insufficient descriptor of systolic function, highlighting the need for more comprehensive measures like tissue Doppler velocity, strain, and strain rate.
Ejection fraction is the most widely used measure of left ventricular systolic function, but why? It was initially adopted before the introduction of echocardiography, when ventricular function was assessed by ventriculography at cardiac catheterisation. To avoid the huge effort of calibrating ventriculographic volumes, ejection fraction was born as a quick way of quantifying function. In this edition of Heart , MacIver and Townsend report their findings from a mathematical model that investigates the separated effects of changes to left ventricular (LV) mass and to longitudinal shortening, on ejection fraction ( see article on page 446 ).1 They show that the increased radial wall thickness in LV hypertrophy means that ejection fraction may be preserved despite impaired long-axis shortening. This supports the growing evidence that ejection fraction alone may be an insufficient descriptor of systolic function. As cardiology is no longer bereft of rapid, calibrated measures of systolic function with the availability of tissue Doppler velocity, strain and strain rate, perhaps we can progress from limiting our assessment to ejection fraction. Assessment of LV systolic function is used to predict morbidity and mortality,2 in the diagnosis of heart failure, and also to enable or preclude patients from receiving a variety of potentially beneficial procedures including chemotherapy,3 cardioverter-defibrillator …
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Manisty et al. (2008) conducted an editorial in Left ventricular systolic function / Left ventricular hypertrophy. Ejection fraction assessment was evaluated. Ejection fraction may be preserved despite impaired long-axis shortening in left ventricular hypertrophy, suggesting it alone may be an insufficient descriptor of systolic function.
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