What is actually preserved in HFpEF? Focus on myocyte calcium handling remodelling

Johnson, Daniel and Pavlovic, Davor (2022). What is actually preserved in HFpEF? Focus on myocyte calcium handling remodelling. Journal of Molecular and Cellular Cardiology, 170 pp. 115–116.

DOI: https://doi.org/10.1016/j.yjmcc.2022.06.002


One of the hallmarks of heart failure with reduced ejection fraction (HFrEF) is ultrastructural remodelling of the t-tubular system and of the dyadic structure found in ventricular cardiomyocytes which would normally ensure tight control and regulation of excitation-contraction coupling. Remodelling of these specific microdomains, and more specifically Ca2+ cycling in these areas, are thought to contribute to the arrhythmogenic phenotype seen in many HFrEF patients. However, we note that according to recent epidemiological studies, more than half of patients suffering with HF in the community have heart failure with preserved ejection fraction (HFpEF). Treatment options for HFpEF remain limited with standard therapy used in HFrEF, such as β-blockers and angiotensin-converting enzyme having minimal effects on prolongation of life in these patients. Sudden death is the most common cause of death in this population, for example in the recently published EMPEROR-Preserved trial, between 3.3 and 3.8% of participants died from sudden cardiac death. Although speculative, it is more than likely that at least some, if not the majority, of these deaths were due to sudden cardiac arrhythmias.

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