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Fig. 3 | Cardiovascular Diabetology

Fig. 3

From: Sodium-glucose cotransporter-2 inhibition for heart failure with preserved ejection fraction and chronic kidney disease with or without type 2 diabetes mellitus: a narrative review

Fig. 3

Reproduced from Heart 2022, volume 108, pages 1342–1350, Gevaert AB, Kataria R, Zannad F, Sauer AJ, Damman K, Sharma K, et al. Heart failure with preserved ejection fraction: recent concepts in diagnosis, mechanisms and management, Copyright 2022, with permission from BMJ Publishing Group Ltd

Evolution of pathophysiological understanding of HFpEF [84]. A Prevailing concept of HFpEF and HFrEF as separate diseases, HFpEF is caused by microvascular inflammation and HFrEF is caused by cardiomyocyte loss. B Emerging concept of heart failure as phenotypes overlapping across the spectrum of LV systolic function. There is a gradual change in underlying pathophysiology, mode of death, and response to HF therapies across the LVEF spectrum, with influences from genetics, sex, comorbidities, and lifestyle. C Personalized treatment of HFpEF. Different phenotypes (based on clinical, imaging, biomarker and/or transcriptomic data) are represented by red, green and blue colors. Personalized treatment: considering the phenotype-specific response to medical therapy, a targeted approach using specific drugs in specific phenotypes could lead to net clinical benefit for all patients. CV cardiovascular, GLS global longitudinal strain, HF heart failure, HFpEF heart failure with preserved ejection fraction, HFrEF heart failure with reduced ejection fraction, LV left ventricle, LVEF left ventricular ejection fraction, NO nitric oxide, ROS reactive oxygen species, SV stroke volume.

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