■甲状腺激素(TH)似乎对梗死后心肌具有修复作用。这个新颖的动作最近在飞行员身上进行了测试,随机化,双盲,安慰剂对照试验(ThyRepair)。本研究对ThyRepair研究的数据进行了事后分析,以进一步了解TH对人类缺血后心肌的新作用。
■来自参与ThyRepair研究的41名患者(n=20安慰剂和n=21LT3)的数据包括在分析中。LT3治疗在支架置入后开始,持续静脉48小时。所有患者在出院时进行心脏磁共振(CMR);左心室(LV)射血分数(LVEF%),左心室舒张末期容积指数(LVEDVi;mL/m2),左心室收缩末期容积指数(LVESVi;mL/m2),梗死体积(IV),左心室质量指数(LVMi)作为水肿指数,评估微血管阻塞(MVO)。根据IV的中位数将患者分为两组:IV≤LV的20%的患者(A组)和IV>20%的患者(B组)。放电时的CMR测量值表示为平均值±SD。
■在A组中,安慰剂组和T3治疗组的LVEF%相似(56.8±10.2vs.52.2±10.5),LVEDVi(90.9±19.8vs.92.8±14.5),和LVESVi(40.8±18.2vs.放电时44.9±14.1)。B组,安慰剂与安慰剂的LVEDVi和LVESVi分别为112±23.8和68.3±21.5。T3治疗组91.8±18.6和49.0±14.0,分别,p<0.05。与T3治疗组相比,LVEF%显着增加安慰剂,47.3±6.5vs.39.9±8.7,p<0.05。B组,CMRLVMi在T3治疗的患者中低于安慰剂,但没有达到统计学意义(p=0.1)。安慰剂的MVO为1.95±2.2LT3治疗组的0.84±0.9,p=0.15。
■本研究表明,急性LT3治疗可能对梗死面积较大的患者的心功能恢复产生更有利的影响。此外,它预示着LT3对心肌水肿和微血管阻塞的潜在影响。这些新发现值得在大型试验中进一步研究。
UNASSIGNED: Thyroid hormone (TH) appears to have a reparative action on the postinfarcted myocardium. This novel action was recently tested in a pilot, randomized, double-blind, placebo-controlled trial (ThyRepair). The present study performed a post-hoc analysis of data from the ThyRepair study to provide further insights into the novel actions of TH on the human postischemic myocardium.
UNASSIGNED: Data from 41 patients participating in the ThyRepair study (n = 20 placebo and n = 21 LT3) were included in the analysis. LT3 treatment started after stenting and continued intravenously for 48 h. All patients had cardiac magnetic resonance (CMR) at hospital discharge; left ventricular (LV) ejection fraction (LVEF%), LV end-diastolic volume index (LVEDVi; mL/m2), LV end-systolic volume index (LVESVi; mL/m2), infarct volume (IV), left ventricular mass index (LVMi) as edema index, and microvascular obstruction (MVO) were assessed. Patients were divided into two groups based on the median value of the IV: patients with IV ≤ 20% of the LV (group A) and patients with IV > 20% (group B). CMR measurements at discharge are expressed as mean ± SD.
UNASSIGNED: In group A, the placebo and T3-treated groups had similar LVEF% (56.8 ± 10.2 vs. 52.2 ± 10.5), LVEDVi (90.9 ± 19.8 vs. 92.8 ± 14.5), and LVESVi (40.8 ± 18.2 vs. 44.9 ± 14.1) at discharge. In group B, LVEDVi and LVESVi were 112 ± 23.8 and 68.3 ± 21.5 for placebo vs. 91.8 ± 18.6 and 49.0 ± 14.0 for the T3-treated group, respectively, p < 0.05. LVEF% was significantly increased in the T3-treated group vs. placebo, 47.3 ± 6.5 vs. 39.9 ± 8.7, p < 0.05. In group B, CMR LVMi was lower in T3-treated patients vs. placebo but did not reach statistical significance (p = 0.1). MVO was 1.95 ± 2.2 in placebo vs. 0.84 ± 0.9 in the LT3-treated group, p = 0.15.
UNASSIGNED: The present study suggests that acute LT3 treatment may exert more favorable effects on the recovery of cardiac function in patients with large infarct size. Furthermore, it signals a potential effect of LT3 on myocardial edema and microvascular obstruction. These novel findings merit further investigation in large trials.