Abstract
BackgroundHeart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with sex-specific pathophysiology. Estrogen deficiency is believed to be responsible for the development of HFpEF in women. However, estrogen deficiency does not seem to be completely responsible for the differences in HFpEF prevalence between sexes. While diabetes mellitus (DM) frequently coexists with HFpEF in women and is associated with worse outcomes, the changes in myocardial contractility among women with HFpEF and the DM phenotype is yet unknown. Therefore, we aimed to investigate sex-related differences in left ventricular (LV) contractility dysfunction in HFpEF comorbid with DM.MethodsA total of 224 patients who underwent cardiac cine MRI were included in this study. Sex-specific differences in LV structure and function in the context of DM were determined. LV systolic strains (global longitudinal strain [GLS], circumferential strain [GCS] and radial strain [GRS]) were measured using cine MRI. The determinants of impaired myocardial strain for women and men were assessed.ResultsThe prevalence of DM did not differ between sexes (p > 0.05). Despite a similar LV ejection fraction, women with DM demonstrated a greater LV mass index than women without DM (p = 0.023). The prevalence of LV geometry patterns by sex did not differ in the non-DM subgroup, but there was a trend toward a more abnormal LV geometry in women with DM (p = 0.072). The magnitudes of systolic strains were similar between sexes in the non-DM group (p > 0.05). Nevertheless, in the DM subgroup, there was significant impairment in women in systolic strains compared with men (p < 0.05). In the multivariable analysis, DM was associated with impaired systolic strains in women (GLS [β = 0.26; p = 0.007], GCS [β = 0.31; p < 0.001], and GRS [β = −0.24; p = 0.016]), whereas obesity and coronary artery disease were associated with impaired systolic strains in men (p < 0.05).ConclusionsWomen with DM demonstrated greater LV contractile dysfunction, which indicates that women with HFpEF comorbid with DM have a high-risk phenotype of cardiac failure that may require more aggressive and personalized medical treatment.
Highlights
Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with sex-specific pathophysiology
HFpEF was defined according to the guidelines of the European Society of Cardiology (2019) [15], and patients who met the following criteria were enrolled in the HF group: (1) New York Heart Association class II–IV symptoms and signs of HF; (2) elevated plasma amino-terminal pro-B-type natriuretic peptide (NT-proBNP) levels (≥ 220 pg/mL for patients in sinus rhythm or ≥ 660 pg/mL for patients with atrial fibrillation); and (3) echocardiographic left ventricular (LV) ejection fraction (LVEF) ≥ 50% accompanied by either (a) evidence of diastolic dysfunction (ratio of peak early diastolic filling velocity (E) to early diastolic mitral annular velocity (e’) ≥ 15) or (b) structural alteration of the heart, including left atrial (LA) enlargement or LV hypertrophy (LVH)
Baseline characteristics of the study population by sex A total of 224 patients with HFpEF were included in this study
Summary
Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with sex-specific pathophysiology. How‐ ever, estrogen deficiency does not seem to be completely responsible for the differences in HFpEF prevalence between sexes. While diabetes mellitus (DM) frequently coexists with HFpEF in women and is associated with worse outcomes, the changes in myocardial contractility among women with HFpEF and the DM phenotype is yet unknown. Mounting evidence suggests that estrogen deficiency is responsible for the development of HFpEF in women [9, 10]. Estrogen deficiency does not seem to be completely responsible for the differences in HFpEF prevalence between sexes. Data from registries and multicenter studies demonstrated that DM frequently coexists with HFpEF in women and is associated with worse outcomes, regardless of ejection fraction status [3, 12, 13]. An understanding of the sex-related differences in LV contractile function and its determinants may have important implications for the development of risk stratification tools and highlight potential phenotype-specific targets
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