背景:糖尿病患者发生射血分数保留心力衰竭(HFpEF)的风险增加。本研究旨在比较有和无HFpEF的2型糖尿病(T2DM)患者的心肌变形和灌注指标,并探讨心肌应变与灌注储备之间的关系。
方法:本研究纳入156例无阻塞性冠状动脉疾病(CAD)的T2DM患者和50例健康志愿者,他们在我们中心接受了心脏磁共振(CMR)检查。T2DM患者分为T2DM-HFpEF组(n=74)和T2DM-非HFpEF组(n=82)。比较了左心室(LV)和左心房(LA)应变以及压力心肌灌注的参数。还评估了心肌变形与灌注参数之间的相关性。中介分析用于评估T2DM对LA菌株的直接和间接影响。
结果:T2DM和HFpEF患者的LV径向收缩期峰值应变率(PSSR)降低,左心室周向峰值舒张应变率(PDSR),LA储层应变,全局心肌灌注储备指数(MPRI)与无HFpEF的T2DM患者相比,LA加强应变增加(均P<0.05)。此外,LV纵向PSSR,洛杉矶水库,与对照组相比,无HFpEF的T2DM患者的LA导管应变明显受损(均P<0.05),但LV扭转,低压径向PSSR,LA增强应变补偿了这些变化(所有P<0.05)。多元线性回归分析表明,LA储层和LA升压应变与整体MPRI独立相关(β=0.259,P<0.001;β=-0.326,P<0.001)。Further,有和没有HFpEF的T2DM患者之间LA储库和LA加强应变的差异完全由整体MPRI介导。全球压力PI,洛杉矶助推器,全局RESTPI,和全局MPRI在诊断T2DM患者的HFpEF方面显示出较高的准确性(曲线下面积[AUC]分别为0.803、0.790、0.740、0.740).
结论:T2DM和HFpEF患者表现出明显的LV收缩和舒张变形,降低LA储层应变,心肌灌注严重受损,和升高的LA加强菌株,这是HFpEF的代偿反应。全球MPRI被确定为LA储层和LA助推器菌株的独立影响因素。有和没有HFpEF的T2DM患者之间LA储库和LA升压应变的差异完全由全局MPRI介导,提示糖尿病患者微循环损伤与心功能障碍之间可能存在的机制联系。心肌灌注和LA应变可能对将来诊断和管理HFpEF很有价值。
BACKGROUND: Patients with diabetes have an increased risk of developing heart failure with preserved ejection fraction (HFpEF). This study aimed to compare indices of myocardial deformation and perfusion between patients with type 2 diabetes mellitus (T2DM) with and without HFpEF and to investigate the relationship between myocardial strain and perfusion reserve.
METHODS: This study included 156 patients with T2DM without obstructive coronary artery disease (CAD) and 50 healthy volunteers who underwent cardiac magnetic resonance (CMR) examination at our center. Patients with T2DM were subdivided into the T2DM-HFpEF (n = 74) and the T2DM-non-HFpEF (n = 82) groups. The parameters of left ventricular (LV) and left atrial (LA) strain as well as stress myocardial perfusion were compared. The correlation between myocardial deformation and perfusion parameters was also assessed. Mediation analyses were used to evaluate the direct and indirect effects of T2DM on LA strain.
RESULTS: Patients with T2DM and HFpEF had reduced LV radial peak systolic strain rate (PSSR), LV circumferential peak diastolic strain rate (PDSR), LA reservoir strain, global myocardial perfusion reserve index (MPRI), and increased LA booster strain compared to patients with T2DM without HFpEF (all P < 0.05). Furthermore, LV longitudinal PSSR, LA reservoir, and LA conduit strain were notably impaired in patients with T2DM without HFpEF compared to controls (all P < 0.05), but LV torsion, LV radial PSSR, and LA booster strain compensated for these alterations (all P < 0.05). Multivariate linear regression analysis demonstrated that LA reservoir and LA booster strain were independently associated with global MPRI (β = 0.259, P < 0.001; β = - 0.326, P < 0.001, respectively). Further, the difference in LA reservoir and LA booster strain between patients with T2DM with and without HFpEF was totally mediated by global MPRI. Global stress PI, LA booster, global rest PI, and global MPRI showed high accuracy in diagnosing HFpEF among patients with T2DM (areas under the curve [AUC]: 0.803, 0.790, 0.740, 0.740, respectively).
CONCLUSIONS: Patients with T2DM and HFpEF exhibited significant LV systolic and diastolic deformation, decreased LA reservoir strain, severe impairment of myocardial perfusion, and elevated LA booster strain that is a compensatory response in HFpEF. Global MPRI was identified as an independent influencing factor on LA reservoir and LA booster strain. The difference in LA reservoir and LA booster strain between patients with T2DM with and without HFpEF was totally mediated by global MPRI, suggesting a possible mechanistic link between microcirculation impairment and cardiac dysfunction in diabetes. Myocardial perfusion and LA strain may prove valuable for diagnosing and managing HFpEF in the future.