2 型糖尿病对射血分数保留型心力衰竭的影响取决于是否存在心房颤动

N. Kulaiets, V.M. Kulaiets, O.O. Tkachuk-Hryhorchuk, N. Nyshchuk-Oliinyk
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引用次数: 0

摘要

背景。心血管疾病,包括心力衰竭(HF)和射血分数保留型心力衰竭(HFpEF),对全球健康构成了挑战。射血分数保留型心力衰竭呈上升趋势,尤其是在老年人和患有糖尿病、肥胖症和高血压等疾病的人群中。2 型糖尿病(T2DM)通常与 HFpEF 同时存在,而心房颤动(AF)由于具有共同的风险因素,使问题进一步复杂化。本研究旨在全面调查 2 型糖尿病对存在或不存在心房颤动的射血分数保留型心力衰竭患者的心脏功能和生物标志物特征的影响。材料和方法。这是一项队列单中心研究。共有 448 名射血分数保留型心力衰竭患者接受了研究。他们被分为 4 组:第 1 组--189 名仅患有高频心衰的患者;第 2 组--39 名患有高频心衰和 T2DM 的患者;第 3 组--176 名患有高频心衰和心房颤动的患者;第 4 组--44 名患有高频心衰、心房颤动和 T2DM 的患者。结果。T2DM可能导致HFpEF患者年龄稍大,但年龄本身并不是主要的判别因素。T2DM 本身不会对左心室质量指数产生重大影响,但如果合并房颤,则会产生重大影响。T2DM 与左心房容积指数增加有关,而房颤会加剧这种影响。T2DM 影响舒张功能,而房颤会加剧这种影响。T2DM 会影响左心室充盈压,而房颤会加重高房颤患者的左心室充盈压。T2DM 还影响左心室收缩功能,如果合并房颤,HFpEF 患者的左心室收缩功能会进一步受损。患有 T2DM 的 HFpEF 患者的 Galectin-3 水平升高,房颤会进一步加剧这一情况。NT-proBNP 水平受 T2DM 的影响,在 HFpEF 患者合并房颤时会进一步恶化。患有 T2DM 的 HFpEF 患者的 SST2 水平升高,房颤时进一步升高,表明心肌纤维化和不良重塑。结论T2DM和房颤在高频低氧血症患者中的相互作用产生了协同效应,导致心脏结构和功能发生显著改变。新的生物标记物,如 galectin-3、NT-proBNP 和 sST2 成为有价值的诊断工具,反映了 HFpEF 复杂的病理生理过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Impact of type 2 diabetes mellitus on heart failure with preserved ejection fraction depending on the presence of atrial fibrillation
Background. Cardiovascular diseases, including heart failure (HF) and heart failure with preserved ejection fraction (HFpEF), pose a global health challenge. HFpEF is on the rise, especially among the elderly and those with conditions like diabetes, obesity, and hypertension. Type 2 diabetes mellitus (T2DM) often coexists with HFpEF, and atrial fibrillation (AF) further complicates matters due to shared risk factors. The purpose of this study is to comprehensively investigate the influence of type 2 diabetes mellitus on cardiac function and biomarker profiles in patients with heart failure with preserved ejection fraction in the presence or absence of atrial fibrillation. Mate­rials and methods. This was a cohort, single-center study. Four hundred and forty-eight patients with HFpEF were examined. They were divided into 4 groups: group 1 — 189 patients with HFpEF alone; group 2 — 39 patients with HFpEF and T2DM; group 3 — 176 patients with HFpEF and atrial fibrillation; group 4 — 44 patients with HFpEF, AF, T2DM. Results. T2DM may contribute to a slightly older patient population in HFpEF, but age alone is not a primary discriminator. T2DM alone does not substantially impact left ventricular mass index but, when combined with AF, it does. T2DM is associated with an increased left atrial volume index, and AF intensifies this effect. T2DM influences diastolic function, with AF exacerbating it. T2DM affects left ventricular filling pressure, and AF worsens this in HFpEF. T2DM also influences left ventricular systolic function, further compromised when combined with AF in HFpEF patients. Galectin-3 levels are elevated in HFpEF patients with T2DM, further exacerba­ted with AF. NT-proBNP levels are influenced by T2DM and worsened with the combination of AF in HFpEF. SST2 levels are elevated in HFpEF patients with T2DM, further increased with AF, indicating myocardial fibrosis and adverse remodeling. Conclusions. The interaction between T2DM and AF in HFpEF patients creates a synergistic effect, resulting in significant cardiac structural and functional alterations. Novel biomarkers such as galectin-3, NT-proBNP, and sST2 emerge as valuable diagnostic tools, reflecting the complex pathophysiological processes in HFpEF.
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