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无论患者的容量状态如何，固有T2均可预测心肌炎症。

Native T2 Predicts Myocardial Inflammation Irrespective of a Patient's Volume Status.

作者信息

Wolter Jan Sebastian, Treiber Julia M, Fischer Selina, Fischer-Rasokat Ulrich, Kriechbaum Steffen D, Rieth Andreas, Weferling Maren, von Jeinsen Beatrice, Hain Andreas, Hamm Christian W, Keller Till, Rolf Andreas

机构信息

Kerckhoff Heart and Thorax Center, Department of Cardiology, Benekestrasse 2-8, 61231 Bad Nauheim, Germany.

German Center for Cardiovascular Research (DZHK), Rhine-Main Partner Site, 60590 Frankfurt am Main, Germany.

出版信息

Diagnostics (Basel). 2023 Jun 30;13(13):2240. doi: 10.3390/diagnostics13132240.

DOI:10.3390/diagnostics13132240
PMID:37443634
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10340351/
Abstract

Myocardial inflammation and edema are major pathological features in myocarditis. Myocardial tissue water content and myocardial edema can be quantified via T2 mapping. Thus, cardiac magnetic resonance (CMR) is the noninvasive gold standard for diagnosing myocarditis. Several studies showed an impact of short-term volume changes on T2 relaxation time. Plasma volume status (PVS) is a good surrogate parameter to quantify a patient's volume status, and it is simple to use. The aim of this study was to determine the effect of PVS on the diagnostic value of T2 relaxation time in myocardial inflammation. Between April 2017 and December 2022, patients who were indicated for cardiac CMR were included in our prospective clinical registry. Patients with myocardial inflammation and those with unremarkable findings were analyzed in the present study. A blood sample was drawn, and PVS was calculated. Patients were separated into PVS tertiles to explore a possible nonlinear dose-response relationship. Logistic regression analysis was used to determine whether T2 is an independent predictor of myocardial inflammation. A total of 700 patients (47.43% female) were eligible for analysis. Of these, 551 patients were healthy (78.7%), while 149 (21.3%) showed signs of myocardial inflammation. The T2 relaxation time was elevated in patients with myocardial inflammation (40 ms [IQR 37-42 ms] vs. 38.0 ms [IQR 36-39 ms], < 0.001). PVS showed no difference between the groups (-12.94 [IQR -18.4--7.28] vs.-12.19 [IQR -18.93--5.87], = 0.384). T2 showed a clear dose-response relationship with PVS, with increasing T2 values along the PVS tertiles. In spite of this, T2 was found to be an independent marker of myocardial inflammation in logistic regression (OR T2 1.3 [95% CI 1.21-1.39], < 0.001), even after adjusting for PVS (OR T2 [adj. PVS] 1.31 [95% CI 1.22-1.40], < 0.001). Despite a dose-response relationship between T2 and the volume status, T2 was found to be an independent indicator of myocardial inflammation.

摘要

心肌炎症和水肿是心肌炎的主要病理特征。心肌组织含水量和心肌水肿可通过T2 mapping进行量化。因此，心脏磁共振成像（CMR）是诊断心肌炎的无创金标准。多项研究表明短期容量变化对T2弛豫时间有影响。血浆容量状态（PVS）是量化患者容量状态的一个良好替代参数，且使用简便。本研究的目的是确定PVS对心肌炎症中T2弛豫时间诊断价值的影响。2017年4月至2022年12月期间，被建议进行心脏CMR检查的患者被纳入我们的前瞻性临床登记研究。本研究分析了有心肌炎症的患者和检查结果无异常的患者。采集血样并计算PVS。将患者分为PVS三分位数组以探索可能的非线性剂量反应关系。采用逻辑回归分析来确定T2是否为心肌炎症的独立预测因子。共有700例患者（47.43%为女性）符合分析条件。其中，551例患者健康（78.7%），149例（21.3%）有心肌炎症迹象。有心肌炎症的患者T2弛豫时间升高（40 ms[四分位间距37 - 42 ms]对38.0 ms[四分位间距36 - 39 ms]，<0.001）。两组间PVS无差异（-12.94[四分位间距-18.4 - -7.28]对-12.19[四分位间距-18.93 - -5.87]，=0.384）。T2与PVS呈现明显的剂量反应关系，随着PVS三分位数升高T2值增加。尽管如此，在逻辑回归分析中发现T2是心肌炎症的独立标志物（T2的比值比为1.3[95%置信区间1.21 - 1.39]，<0.001），即使在调整PVS后（调整PVS后的T2比值比为1.31[95%置信区间1.22 - 1.40]，<0.001）。尽管T2与容量状态之间存在剂量反应关系，但T2被发现是心肌炎症的独立指标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/9dbbb005f09c/diagnostics-13-02240-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/e6182fdfd3ae/diagnostics-13-02240-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/dd762c0f1062/diagnostics-13-02240-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/dbcda6d565eb/diagnostics-13-02240-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/7efcc3f1d5bc/diagnostics-13-02240-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/9dbbb005f09c/diagnostics-13-02240-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/e6182fdfd3ae/diagnostics-13-02240-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/dd762c0f1062/diagnostics-13-02240-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/dbcda6d565eb/diagnostics-13-02240-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/7efcc3f1d5bc/diagnostics-13-02240-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef6b/10340351/9dbbb005f09c/diagnostics-13-02240-g005.jpg

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