Intestinal fatty acid binding protein is associated with infarct size and cardiac function in acute heart failure following myocardial infarction

IF 2.8 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Open Heart Pub Date : 2024-09-01 DOI:10.1136/openhrt-2024-002868
Andraž Nendl, Geir Øystein Andersen, Ingebjørg Seljeflot, Marius Trøseid, Ayodeji Awoyemi
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Abstract

Background 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. Methods 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. Results I-FABPAUC correlated positively with infarct size (rs=0.45, p=0.002), GLS (rs=0.32, p=0.035) and WMSI (rs=0.45, p=0.002) and negatively with LVEF measured by SPECT (rs=−0.40, p=0.007) and echocardiography (rs=−0.33, p=0.021) at 6 weeks. LPSAUC, LBPAUC and sCD14AUC 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-FABPAUC 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). Conclusions 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. Data are available on reasonable request. The data are available on request from the corresponding author, following the establishment of a material and data transfer agreement between the institutions and the approval of an amendment application to the Regional Committees for Medical Research Ethics to ensure that the aim of the planned research is covered by the participant consent forms.
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肠脂肪酸结合蛋白与心肌梗死后急性心力衰竭的梗死面积和心脏功能有关
背景 急性心力衰竭(HF)时,心输出量减少、血管收缩和充血可能会损伤肠粘膜并破坏其屏障功能。这可能会促进细菌产物渗漏到血液循环中,导致炎症和不良心脏重塑。我们旨在研究肠道渗漏标志物及其与炎症、梗死面积和心脏功能的关系。方法 我们研究了 61 名 ST 段抬高型心肌梗死(STEMI)患者,这些患者在经皮冠状动脉介入治疗(PCI)成功后 48 小时内出现急性心房颤动。我们采集了连续血液样本,以测量脂多糖(LPS)、LPS 结合蛋白(LBP)、可溶性分化簇 14(sCD14)和肠道脂肪酸结合蛋白(I-FABP)。计算了从基线到第 5 天的累积曲线下面积(AUC)。进行连续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)和室壁运动评分指数(WMSI)。6 周后进行单光子发射 CT (SPECT),以确定梗塞大小和 LVEF。结果 I-FABPAUC与6周时的梗塞大小(rs=0.45,p=0.002)、GLS(rs=0.32,p=0.035)和WMSI(rs=0.45,p=0.002)呈正相关,而与SPECT(rs=-0.40,p=0.007)和超声心动图(rs=-0.33,p=0.021)测量的LVEF呈负相关。LPSAUC、LBPAUC 和 sCD14AUC 与任何心功能指标或梗塞大小均无相关性。6周时GLS和WMSI高于中位数、SPECT测量的LVEF低于中位数的患者更有可能在入院时I-FABPAUC高于中位数(调整OR(aOR)分别为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)。在超声心动图测量的 LVEF 最低四分位数(aOR 9.99,95% CI 1.79 至 55.83)和梗死面积较高的三个四分位数(aOR 20.34,95% CI 1.56 至 264.65)的患者中也观察到同样的情况。结论 在初级 PCI 治疗的 STEMI 急性 HF 患者中,肠上皮损伤标志物 I-FABP 与 6 周后梗死面积增大和心功能恶化有关。如有合理要求,可提供相关数据。在机构间达成材料和数据传输协议,并向地区医学研究伦理委员会提交修订申请以确保参与者同意书涵盖计划研究的目的后,可向通讯作者索取数据。
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来源期刊
Open Heart
Open Heart CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
4.60
自引率
3.70%
发文量
145
审稿时长
20 weeks
期刊介绍: Open Heart is an online-only, open access cardiology journal that aims to be “open” in many ways: open access (free access for all readers), open peer review (unblinded peer review) and open data (data sharing is encouraged). The goal is to ensure maximum transparency and maximum impact on research progress and patient care. The journal is dedicated to publishing high quality, peer reviewed medical research in all disciplines and therapeutic areas of cardiovascular medicine. Research is published across all study phases and designs, from study protocols to phase I trials to meta-analyses, including small or specialist studies. Opinionated discussions on controversial topics are welcomed. Open Heart aims to operate a fast submission and review process with continuous publication online, to ensure timely, up-to-date research is available worldwide. The journal adheres to a rigorous and transparent peer review process, and all articles go through a statistical assessment to ensure robustness of the analyses. Open Heart is an official journal of the British Cardiovascular Society.
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