Torrens University Australia
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Preserved ejection fraction and structural heart disease in 446 848 patients investigated with echocardiography

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journal contribution
posted on 2021-03-24, 06:56 authored by David Playford, Geoffrey Strange, Simon StewartSimon Stewart, NEDA Investigators
Background Sex-specific differences in left ventricular ejection fraction (LVEF) and responses to neurohormonal modulating therapies are relevant to clinical trials of treatment for heart failure with preserved ejection fraction (HFpEF).
Aims This study aimed to identify the proportion and characteristics of patients presenting with possible or confirmed HFpEF within the National Echo Database of Australia.
Results A total of 237 046 women (48.1%) and 256 019 men (aged 61.0 ± 18.3 vs. 60.6 ± 17.1 years, respectively) had sex-specific distributions of LVEF: 94.3% of women had LVEF ≥ 45% (mean LVEF 66.0 ± 8.6%), compared with 87.2% of men (mean LVEF 63.4 ± 8.7%). The presence of structural heart disease (SHD) according to the PARAGON-HF criteria could be calculated in 93.8% of women and 93.4% of men with an LVEF ≥ 45%. Of these, 64 502 (30.8%) women and 104 344 (50.0%) of men had left ventricular hypertrophy, and 78 948 (35.3%) and 95 846 (42.9%), respectively, had left atrial enlargement. As a result, the proportion of women vs. men fulfilling echocardiographic criteria for HFpEF was very different: 111 497 (53.2%) vs. 146 359 (70.1%). SHD markedly increased with age, associated with a greater increase in women than men. The same signal was observed in those referred for suspected or previously confirmed HFpEF.
Conclusions Double the number of men than women had LVEF < 45%, and the distribution of SHD had was highly sex specific. Left ventricular hypertrophy and left atrial enlargement were more common in men and becoming more frequent in women with advancing age. The echocardiographic SHD distribution was similar in those referred with suspected or confirmed HFpEF. The findings are relevant to sex-specific recruitment criteria for future clinical trials.

Funding

This work has been funded by Novartis. S.S. is supported by the National Health and Medical Research Council of Australia (GNT1135894).

History

Year of publication

2020

Publisher doi

10.1002/ehf2.13149

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