May 2026 Br J Cardiol 2026;33:77–8 doi:10.5837/bjc.2026.024
Andrew Chisom Madu, Brian Li, Daniela Toumazi, Muhammad Asad, Aryan Sabir, Duncan Coles, Anthony Dimarco, Henry Oluwasefunmi Savage
Introduction Heart failure (HF) remains a leading cause of hospital admissions and healthcare expenditure worldwide, and is associated with substantial morbidity and mortality.1 HF is commonly classified into three subtypes based on left ventricular ejection fraction (LVEF)1 as heart failure with preserved ejection fraction (HFpEF), LVEF ≥50%; mildly reduced ejection fraction (HFmrEF), LVEF 41–49%; or with a reduced ejection fraction (HFrEF), LVEF ≤40%. Patients with HF are at risk of decompensation due to the inability of the heart to sustain a functional cardiac output. Compensatory mechanisms, such as neurohormonal activation and sa
January 2024 Br J Cardiol 2024;31:17–22 doi:10.5837/bjc.2024.002
Hayley Birrell, Omar Fersia, Mohamed Anwar, Catherine Mondoa, Angus McFadyen, Christopher Isles
Introduction In recent years heart failure with preserved ejection fraction (HFpEF) has become a research priority, since despite having a preserved ejection fraction (EF), it is still associated with mortality and survival rates similar to heart failure with a reduced ejection fraction (HFrEF).1 Historically, the interest in HFpEF stems from the collaboration of two areas of research. Studies found that diastolic left ventricular (LV) dysfunction contributed to myocardial hypertrophy.2,3 Shortly after, HFpEF was found to be an adjunct in heart failure (HF) trials, examining the usefulness of angiotensin-converting enzyme (ACE) inhibitors in
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