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用心血管磁共振成像技术描绘高血压危象中心肌水肿和纤维化。

Characterizing myocardial edema and fibrosis in hypertensive crisis with cardiovascular magnetic resonance imaging.

机构信息

Division of Cardiology, Department of Medicine, Faculty of Medicine, and Health Sciences, Stellenbosch University and Tygerberg Hospital, 1 Francie van Zijl Ave, Bellville, Cape Town, 7505, South Africa.

Department of Medicine, Faculty of Clinical Sciences, College of Medical Sciences, University of Maiduguri and University of Maiduguri Teaching Hospital, Maiduguri, 600004, Nigeria.

出版信息

Sci Rep. 2024 Oct 9;14(1):23509. doi: 10.1038/s41598-024-74099-9.

DOI:10.1038/s41598-024-74099-9
PMID:39379531
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11461819/
Abstract

A hypertensive crisis is associated with an increased risk of cardiovascular events. Although altered cardiac structure, function, and myocardial architecture on cardiovascular magnetic resonance (CMR) have been associated with increased adverse events in hypertensive patients, the studies did not include patients with hypertensive crisis. Our study aimed to determine myocardial tissue characteristics in patients with hypertensive crisis using CMR imaging. Participants underwent comprehensive CMR imaging at 1.5T. The imaging protocol included cine-, T2-weighted-, contrasted- and multi-parametric mapping images. Blood and imaging biomarkers were compared in hypertensive emergency and hypertensive urgency. Predictors of myocardial edema was assessed using linear regression. The predictive value of T1- and T2 mapping for identifying hypertensive emergency (from urgency) was assessed with receiver operator characteristics curves. Eighty-two patients (48.5 ± 13.4 years, 57% men) were included. Hypertensive emergency constituted 78%. Native T1 was higher in patients with LVH compared to those without (1056 ± 33 vs. 1013 ± 40, P < 0.001), and tended to be higher in hypertensive emergency than urgency (1051 ± 37 vs. 1033 ± 40, P = 0.077). T2-w signal intensity (SI) ratio and T2 mapping values were higher in hypertensive emergency (1.5 ± 0.2 vs. 1.4 ± 0.1, P = 0.044 and 48 ± 2 vs. 47 ± 2, P = 0.004), and in patients with than without LVH (1.5 ± 0.2 vs. 1.4 ± 0.1, P = 0.045 and P = 0.030). A trend for higher extracellular volume was noted in hypertensive emergency compared to urgency (25 ± 4 vs. 22 ± 3, P = 0.050). Native T1 correlated with T2 mapping (rs = 0.429, P < 0.001), indexed LV mass (rs = 0.493, P < 0.001), cardiac troponin (rs = 0.316, P < 0.001) and NT-proBNP (rs = 0.537, P < 0.001), while T2 correlated with cardiac troponin (rs = 0.390, P < 0.001), and NT-proBNP (rs = 0.348, P < 0.001). Non-ischemic LGE pattern occurred in 59% and was 21% more prevalent in the hypertensive emergency group (P = 0.005). Our findings demonstrate that hypertensive crisis is associated with distinct myocardial tissue alterations, including increased myocardial edema and fibrosis, as detected on CMR. Patients with hypertensive emergency had a higher degree of myocardial oedema than hypertensive urgency. Further research is necessary to explore the prognostic value of these findings.

摘要

高血压危象与心血管事件风险增加相关。尽管心血管磁共振(CMR)上的心脏结构、功能和心肌结构改变与高血压患者的不良事件增加有关,但这些研究并未包括高血压危象患者。我们的研究旨在使用 CMR 成像确定高血压危象患者的心肌组织特征。参与者在 1.5T 下进行全面的 CMR 成像。成像方案包括电影、T2 加权、对比和多参数映射图像。比较高血压急症和高血压亚急症的血液和成像生物标志物。使用线性回归评估心肌水肿的预测因子。使用接受者操作特征曲线评估 T1 和 T2 映射对识别高血压急症(从亚急症)的预测价值。82 名患者(48.5±13.4 岁,57%为男性)被纳入研究。高血压急症占 78%。与无左心室肥厚(LVH)患者相比,LVH 患者的原生 T1 更高(1056±33 比 1013±40,P<0.001),且在高血压急症中比在亚急症中更高(1051±37 比 1033±40,P=0.077)。高血压急症的 T2 信号强度(SI)比值和 T2 映射值较高(1.5±0.2 比 1.4±0.1,P=0.044 和 48±2 比 47±2,P=0.004),且在有和无 LVH 的患者中更高(1.5±0.2 比 1.4±0.1,P=0.045 和 P=0.030)。与高血压亚急症相比,高血压急症患者的细胞外容积有升高的趋势(25±4 比 22±3,P=0.050)。原生 T1 与 T2 映射相关(rs=0.429,P<0.001)、指数化 LV 质量(rs=0.493,P<0.001)、心脏肌钙蛋白(rs=0.316,P<0.001)和 NT-proBNP(rs=0.537,P<0.001),而 T2 与心脏肌钙蛋白(rs=0.390,P<0.001)和 NT-proBNP(rs=0.348,P<0.001)相关。非缺血性 LGE 模式发生在 59%的患者中,在高血压急症组中更为常见(21%,P=0.005)。我们的研究结果表明,高血压危象与 CMR 上检测到的心肌组织改变有关,包括心肌水肿和纤维化增加。与高血压亚急症相比,高血压急症患者的心肌水肿程度更高。需要进一步研究以探讨这些发现的预后价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb63/11461819/c34603c4a932/41598_2024_74099_Fig3_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb63/11461819/c34603c4a932/41598_2024_74099_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb63/11461819/dc2afbd5dfee/41598_2024_74099_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb63/11461819/282f71d36675/41598_2024_74099_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb63/11461819/c34603c4a932/41598_2024_74099_Fig3_HTML.jpg

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