Oslo Center for Clinical Heart Research, Department of Cardiology Ullevaal, Oslo University Hospital, Oslo, Norway
Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Open Heart. 2024 Sep 13;11(2):e002868. doi: 10.1136/openhrt-2024-002868.
In acute heart failure (HF), reduced cardiac output, vasoconstriction and congestion may damage the intestinal mucosa and disrupt its barrier function. This could facilitate the leakage of bacterial products into circulation and contribute to inflammation and adverse cardiac remodelling. We aimed to investigate gut leakage markers and their associations with inflammation, infarct size and cardiac function.
We examined 61 ST-elevation myocardial infarction (STEMI) patients who developed acute HF within 48 hours of successful percutaneous coronary intervention (PCI). Serial blood samples were taken to measure lipopolysaccharide (LPS), LPS-binding protein (LBP), soluble cluster of differentiation 14 (sCD14) and intestinal fatty acid binding protein (I-FABP). Cumulative areas under the curve (AUCs) from baseline to day 5 were calculated. Serial echocardiography was performed to assess left ventricular ejection fraction (LVEF), global longitudinal strain (GLS) and wall motion score index (WMSI). Single-photon emission CT (SPECT) was performed at 6 weeks to determine infarct size and LVEF.
I-FABP correlated positively with infarct size (r=0.45, p=0.002), GLS (r=0.32, p=0.035) and WMSI (r=0.45, p=0.002) and negatively with LVEF measured by SPECT (r=-0.40, p=0.007) and echocardiography (r=-0.33, p=0.021) at 6 weeks. LPS, LBP and sCD14 did not correlate to any cardiac function marker or infarct size. Patients, who at 6 weeks had above median GLS and WMSI, and below-median LVEF measured by SPECT, were more likely to have above median I-FABP during admission (adjusted OR (aOR) 5.22, 95% CI 1.21 to 22.44; aOR 5.05, 95% CI 1.25 to 20.43; aOR 5.67, 95% CI 1.42 to 22.59, respectively). The same was observed for patients in the lowest quartile of LVEF measured by echocardiography (aOR 9.99, 95% CI 1.79 to 55.83) and three upper quartiles of infarct size (aOR 20.34, 95% CI 1.56 to 264.65).
In primary PCI-treated STEMI patients with acute HF, I-FABP, a marker of intestinal epithelial damage, was associated with larger infarct size and worse cardiac function after 6 weeks.
在急性心力衰竭（HF）中，心输出量降低、血管收缩和充血可能会损害肠道黏膜并破坏其屏障功能。这可能会促进细菌产物漏入循环，并导致炎症和不良的心脏重构。我们旨在研究肠道渗漏标志物及其与炎症、梗死面积和心功能的关系。
我们检查了 61 例在经皮冠状动脉介入治疗（PCI）成功后 48 小时内发生急性 HF 的 ST 段抬高型心肌梗死（STEMI）患者。连续采集血样以测量脂多糖（LPS）、LPS 结合蛋白（LBP）、可溶性 CD14（sCD14）和肠脂肪酸结合蛋白（I-FABP）。计算从基线到第 5 天的累积曲线下面积（AUC）。连续进行超声心动图检查以评估左心室射血分数（LVEF）、整体纵向应变（GLS）和壁运动评分指数（WMSI）。在 6 周时进行单光子发射计算机断层扫描（SPECT）以确定梗死面积和 LVEF。
I-FABP 与梗死面积（r=0.45，p=0.002）、GLS（r=0.32，p=0.035）和 WMSI（r=0.45，p=0.002）呈正相关，与 SPECT 测量的 LVEF（r=-0.40，p=0.007）和超声心动图（r=-0.33，p=0.021）在 6 周时的 LVEF 呈负相关。LPS、LBP 和 sCD14 与任何心功能标志物或梗死面积均无相关性。在 6 周时，GLS 和 WMSI 中位数以上、SPECT 测量的 LVEF 中位数以下的患者，在住院期间更有可能出现中位数以上的 I-FABP（调整后的比值比（aOR）为 5.22，95%CI 为 1.21 至 22.44；aOR 为 5.05，95%CI 为 1.25 至 20.43；aOR 为 5.67，95%CI 为 1.42 至 22.59，分别）。在超声心动图测量的 LVEF 最低四分位数的患者（aOR 9.99，95%CI 1.79 至 55.83）和梗死面积最高四分位数的患者中也观察到了同样的情况（aOR 20.34，95%CI 1.56 至 264.65）。
在接受经皮冠状动脉介入治疗的 STEMI 合并急性 HF 的患者中，肠道上皮损伤标志物 I-FABP 与 6 周后更大的梗死面积和更差的心功能相关。
