Baumbach Andreas, Cui Yu-Xin, Evans Rebecca N, Culliford Lucy, Johnson Tom, Rogers Chris A, Reeves Barnaby C, Bucciarelli-Ducci Chiara, Harris Jessica, Hamilton Mark, Madeddu Paolo
Bristol Heart Institute, University of Bristol, Bristol, United Kingdom.
William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.
Front Cardiovasc Med. 2022 Nov 17;9:1011140. doi: 10.3389/fcvm.2022.1011140. eCollection 2022.
Myocardial infarction induces elevation of progenitor cells in the circulation, a reparative response inhibited by type-2 diabetes.
Determine if myocardial infarct severity and diabetes interactively influence the migratory activity of CD34+/CXCR4+ progenitor cells and if the migratory test predicts cardiac outcomes.
A longitudinal study was conducted on patients with or without diabetes with a STEMI or NSTEMI. CD34+/CXCR4+ cells were measured in the peripheral blood using flow cytometry, and migratory activity was tested on cells isolated from samples collected on days 0 and 4 post-infarct. Cardiac function was assessed at three months using cardiac MRI.
Of 1,149 patients screened, 71 (6.3%) were eligible and consented. Fifty had STEMI (16 with diabetes) and 21 NSTEMI (8 with diabetes). The proportion of CD34+/CXCR4+ cells within blood mononuclear cells was 1.96 times higher after STEMI compared with NSTEMI (GMR = 1.96, 95% CI 0.87, 4.37) and 1.55 times higher in patients with diabetes compared to patients without diabetes (GMR = 1.55, 95% CI 0.77, 3.13). In the latter, STEMI was associated with a 2.42-times higher proportion of migrated CD34 + /CXCR4 + cells compared with NSTEMI (GMR = 2.42, 95% CI 0.66, 8.81). In patients with diabetes, the association was the opposite, with a 55% reduction in the proportion of migrated CD34+/CXCR4+ cells. No statistically significant associations were observed between the frequency in peripheral blood or migration capacity of CD34+/CXCR4+ cells and MRI outcomes.
We document the interaction between infarct and diabetes on the migratory activity of CD34+/CXCR4+ cells. The test did not predict functional outcomes in the studied cohort.
心肌梗死会导致循环中祖细胞数量增加,这是一种修复反应,但会受到2型糖尿病的抑制。
确定心肌梗死严重程度和糖尿病是否会交互影响CD34+/CXCR4+祖细胞的迁移活性,以及迁移试验是否能预测心脏预后。
对患有或未患有糖尿病的ST段抬高型心肌梗死(STEMI)或非ST段抬高型心肌梗死(NSTEMI)患者进行了一项纵向研究。使用流式细胞术检测外周血中的CD34+/CXCR4+细胞,并对梗死发生后第0天和第4天采集的样本中分离出的细胞进行迁移活性测试。在三个月时使用心脏磁共振成像评估心脏功能。
在1149名接受筛查的患者中,71名(6.3%)符合条件并同意参与研究。其中50名患有STEMI(16名患有糖尿病),21名患有NSTEMI(8名患有糖尿病)。与NSTEMI相比,STEMI后血单核细胞中CD34+/CXCR4+细胞的比例高1.96倍(几何均数比[GMR]=1.96,95%可信区间[CI]0.87,4.37);与未患糖尿病的患者相比,糖尿病患者的该比例高1.55倍(GMR=1.55,95%CI0.77,3.13)。在后者中,与NSTEMI相比,STEMI患者迁移的CD34+/CXCR4+细胞比例高2.42倍(GMR=2.42,95%CI0.66,8.81)。在糖尿病患者中,情况相反,迁移的CD34+/CXCR4+细胞比例降低了55%。未观察到外周血中CD34+/CXCR4+细胞的频率或迁移能力与磁共振成像结果之间存在统计学显著关联。
我们记录了梗死与糖尿病在CD34+/CXCR4+细胞迁移活性方面的相互作用。该试验未能预测所研究队列中的功能预后。