Utah Cardiac Recovery (UCAR) Program (University of Utah Health & School of Medicine, Intermountain Medical Center, and George E. Wahlen Department of Veterans Affairs Medical Center) Salt Lake City UT USA.
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah Salt Lake City UT USA.
J Am Heart Assoc. 2024 Jul 16;13(14):e032936. doi: 10.1161/JAHA.123.032936. Epub 2024 Jul 11.
Type 2 diabetes is prevalent in cardiovascular disease and contributes to excess morbidity and mortality. We sought to investigate the effect of glycemia on functional cardiac improvement, morbidity, and mortality in durable left ventricular assist device (LVAD) recipients.
Consecutive patients with an LVAD were prospectively evaluated (n=531). After excluding patients missing pre-LVAD glycated hemoglobin (HbA1c) measurements or having inadequate post-LVAD follow-up, 375 patients were studied. To assess functional cardiac improvement, we used absolute left ventricular ejection fraction change (ΔLVEF: LVEF post-LVAD-LVEF pre-LVAD). We quantified the association of pre-LVAD HbA1c with ΔLVEF as the primary outcome, and all-cause mortality and LVAD-related adverse event rates (ischemic stroke/transient ischemic attack, intracerebral hemorrhage, gastrointestinal bleeding, LVAD-related infection, device thrombosis) as secondary outcomes. Last, we assessed HbA1c differences pre- and post-LVAD. Patients with type 2 diabetes were older, more likely men suffering ischemic cardiomyopathy, and had longer heart failure duration. Pre-LVAD HbA1c was inversely associated with ΔLVEF in patients with nonischemic cardiomyopathy but not in those with ischemic cardiomyopathy, after adjusting for age, sex, heart failure duration, and left ventricular end-diastolic diameter. Pre-LVAD HbA1c was not associated with all-cause mortality, but higher pre-LVAD HbA1c was shown to increase the risk of intracerebral hemorrhage, LVAD-related infection, and device thrombosis by 3 years on LVAD support (<0.05 for all). HbA1c decreased from 6.68±1.52% pre-LVAD to 6.11±1.33% post-LVAD (<0.001).
Type 2 diabetes and pre-LVAD glycemia modify the potential for functional cardiac improvement and the risk for adverse events on LVAD support. The degree and duration of pre-LVAD glycemic control optimization to favorably affect these outcomes warrants further investigation.
2 型糖尿病在心血管疾病中较为普遍,会导致发病率和死亡率过高。我们试图研究血糖对长期接受左心室辅助装置(LVAD)治疗的患者的心脏功能改善、发病率和死亡率的影响。
连续前瞻性评估了接受 LVAD 的患者(n=531)。排除了缺少 LVAD 前糖化血红蛋白(HbA1c)测量值或 LVAD 后随访不足的患者后,对 375 名患者进行了研究。为了评估心脏功能改善,我们使用绝对左心室射血分数变化(ΔLVEF:LVAD 后 LVEF-LVED 前 LVEF)。我们将 LVAD 前 HbA1c 与ΔLVEF 的关联作为主要结果进行量化,并将全因死亡率和 LVAD 相关不良事件发生率(缺血性卒中/短暂性脑缺血发作、脑出血、胃肠道出血、LVAD 相关感染、装置血栓形成)作为次要结果。最后,我们评估了 LVAD 前后的 HbA1c 差异。2 型糖尿病患者年龄较大,更可能为男性,患有缺血性心肌病,且心力衰竭持续时间更长。在调整年龄、性别、心力衰竭持续时间和左心室舒张末期直径后,LVAD 前 HbA1c 与非缺血性心肌病患者的ΔLVEF 呈负相关,但与缺血性心肌病患者的ΔLVEF 无关。LVAD 前 HbA1c 与全因死亡率无关,但较高的 LVAD 前 HbA1c 使 3 年内接受 LVAD 支持的患者脑出血、LVAD 相关感染和装置血栓形成的风险增加(<0.05)。LVAD 前 HbA1c 从 6.68±1.52%降至 LVAD 后 6.11±1.33%(<0.001)。
2 型糖尿病和 LVAD 前血糖改变了心脏功能改善的潜力和 LVAD 支持的不良事件风险。为了有利于这些结果,进一步优化 LVAD 前血糖控制的程度和持续时间值得进一步研究。