Increased Angio-Derived Index of Microcirculatory Resistance Within a Timeframe of 30–60 days After COVID-19 Infection

IF 1.9 4区医学 Q3 HEMATOLOGY

Microcirculation Pub Date : 2024-03-18 DOI:10.1111/micc.12851

Lei Dong, Ritai Na, Lang Peng, Xinye Xu

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引用次数: 0

Abstract

Background and Objectives

Chest pain is a relatively long-term symptom that commonly occurs in patients who have contracted COVID-19. The reasons for these symptoms remain unclear, with coronary microvascular dysfunction (CMD) emerging as a potential factor. This study aimed to assess the presence of CMD in these patients by measuring the angio-derived index of microcirculatory resistance (AMR).

Methods

In this cross-sectional case–control study, patients who had chest pain and a history of COVID-19 infection within the preceding 30 to 60 days were included. The control subjects were patients without COVID-19. Demographic, clinical, and echocardiographic data were recorded. Angiographic images were collected for AMR analysis through an angioplus quantitative flow ratio measurement system. Propensity score matching (PSM) was performed to match the two groups. Multivariate logistic regression was used to examine the association between COVID-19 incidence and the increase in AMR (AMR > 285 mmHg*s/m) after correction for other confounders.

Results

After PSM, there were 58 patients in each group (the mean age was 66.3 ± 9.04 years, and 55.2% were men). The average time between the onset of COVID-19 infection and patient presentation at the hospital for coronary angiography was 41 ± 9.5 days. Moreover, there was no significant difference in the quantitative flow ratio between the two groups. Patients with COVID-19 had a greater mean AMR (295 vs. 266, p = 0.002). Multivariate logistic regression analysis revealed that COVID-19 (OR = 3.32, 95% CI = 1.50–7.60, p = 0.004) was significantly associated with an increase in AMR.

Conclusions

Long-term COVID-19 patients who experience chest pain without evidence of myocardial ischemia exhibit an increase in AMR, and CMD may be one of the reasons for this increase. COVID-19 is an independent risk factor for an increase in AMR.

查看原文本刊更多论文

在 COVID-19 感染后 30-60 天内，血管衍生的微循环阻力指数增加。

背景和目的：胸痛是一种相对长期的症状，常见于感染 COVID-19 的患者。出现这些症状的原因尚不清楚，冠状动脉微血管功能障碍（CMD）是一个潜在因素。本研究旨在通过测量血管衍生的微循环阻力指数（AMR）来评估这些患者是否存在CMD：在这项横断面病例对照研究中，纳入了在之前 30 到 60 天内有胸痛和 COVID-19 感染史的患者。对照组为未感染 COVID-19 的患者。研究人员记录了人口统计学、临床和超声心动图数据。收集血管造影图像，通过血管造影定量流量比测量系统进行 AMR 分析。进行倾向得分匹配（PSM）以匹配两组患者。在校正其他混杂因素后，采用多变量逻辑回归法检测 COVID-19 发病率与 AMR（AMR > 285 mmHg*s/m）增加之间的关联：PSM 后，每组有 58 名患者（平均年龄为 66.3 ± 9.04 岁，55.2% 为男性）。从感染 COVID-19 到患者到医院接受冠状动脉造影术的平均时间为 41 ± 9.5 天。此外，两组患者的定量血流比率没有明显差异。COVID-19 患者的平均 AMR 更大（295 对 266，P = 0.002）。多变量逻辑回归分析显示，COVID-19（OR = 3.32，95% CI = 1.50-7.60，p = 0.004）与 AMR 的增加显著相关：结论：长期患有 COVID-19 的胸痛但无心肌缺血证据的患者会出现 AMR 增高，而 CMD 可能是导致 AMR 增高的原因之一。COVID-19是导致AMR增加的一个独立风险因素。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Microcirculation 医学-外周血管病

CiteScore

5.00

自引率

4.20%

发文量

审稿时长

6-12 weeks

期刊介绍： The journal features original contributions that are the result of investigations contributing significant new information relating to the vascular and lymphatic microcirculation addressed at the intact animal, organ, cellular, or molecular level. Papers describe applications of the methods of physiology, biophysics, bioengineering, genetics, cell biology, biochemistry, and molecular biology to problems in microcirculation. Microcirculation also publishes state-of-the-art reviews that address frontier areas or new advances in technology in the fields of microcirculatory disease and function. Specific areas of interest include: Angiogenesis, growth and remodeling; Transport and exchange of gasses and solutes; Rheology and biorheology; Endothelial cell biology and metabolism; Interactions between endothelium, smooth muscle, parenchymal cells, leukocytes and platelets; Regulation of vasomotor tone; and Microvascular structures, imaging and morphometry. Papers also describe innovations in experimental techniques and instrumentation for studying all aspects of microcirculatory structure and function.