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Editorial
Microstructure: a potential path to elucidate sex-specific pathological mechanisms in heart failure?
  1. David Belzile,
  2. Mario Sénéchal
  1. Cardiology, Institut Universitaire de Cardiologie et de Pneumologie de Québec-Université Laval, Quebec City, Quebec, Canada
  1. Correspondence to Dr Mario Sénéchal, Cardiology, Institut Universitaire de Cardiologie et de Pneumologie de Québec-Université Laval, Quebec City, G1V 4G5, Canada; mario.senechal{at}criucpq.ulaval.ca

https://doi.org/10.1136/heartjnl-2022-321250

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    Heart failure (HF) is a major public health issue affecting millions of patients worldwide. The latest report from the American Heart Association in 2022 estimated that over 2% of the American population over 20 years old was afflicted by HF, with around 1 million new cases diagnosed every year.1 Although management and treatment have improved significantly in recent decades, morbidity and mortality remain high, with more than half of those patients dying within the first 5 years after being diagnosed.1 Prevention of HF even before the disease onset is therefore one potential pathway to decrease the public health burden associated with this disease. The risk markers commonly associated with HF are numerous (figure 1) and vary according to the HF subtypes (HF with reduced ejection fraction (HFrEF) vs HF with preserved ejection fraction (HFpEF)). However, these risk factors are imperfect, and several disparities exist, among others, between men and women.2

    Figure 1

    Heart failure risk markers. Clinical and non-clinical markers associated with an increased risk of incident heart failure. AFib, atrial fibrillation; BNP, brain natriuretic protein; CAD, coronary artery disease; CKD, chronic kidney disease; COPD, chronic obstructive pulmonary disease; CRP, C reactive protein; ECHO, echocardiogram; HTN, hypertension; LBBB, left bundle branch block; LV diast D, left ventricular diastolic dysfunction; LVH, left ventricular hypertrophy; LV microstr alt, left ventricular microstructural alteration; LV syst D, left ventricular systolic dysfunction; OSA, obstructive sleep apnoea; PA, physical activity; PAI-1, plasminogen activator inhibitor-1; socioecono, socioeconomic status; sST2, soluble suppression of tumorigenesis-2; T2D, type 2 diabetes; UACR, urine albumin-to-creatinine ratio. Figure created with Biorender.com.

    Many morphological, cellular and genetic mechanisms have been proposed to explain these observations in women, such as the postmenopausal decline in oestrogen and nitric oxide, a more frequently altered autonomous nervous system balance and an increased microvascular proinflammatory state (higher proinflammatory cytokines, …

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    Footnotes

    • Twitter @DavidBelzile

    • Contributors DB drafted the first version of the manuscript. MS revised the manuscript.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; internally peer reviewed.

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