新发房颤是SARS-CoV-2肺炎患者急性心肌损伤的表现

Tatyana I. Makeeva, Elizaveta V. Zbyshevskaya, Mark V. Mayer, Faiz A. Talibov, Sergey A. Saiganov
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引用次数: 0

摘要

背景:在过去的3年中,房颤(AF)的患病率在全球范围内显著增加,这与SARS-CoV-2引起的大流行有关。它还伴随着缺血性中风、心肌梗死和急性心肌损伤引起的心力衰竭病例的增加。鉴于SARS-CoV-2感染(COVID-19)的高致死率,研究新发房颤的特征至关重要。 目的:探讨COVID-19肺炎患者新发房颤的预测因素,分析急性心肌损伤的临床及病理生理特征。材料与方法:36例4482岁(平均68.0岁)的COVID-19肺炎患者首次记录房颤发作。所有患者均行胸部计算机断层扫描、心电图和超声心动图检查。采用Simpson法计算左室射血分数。血氧饱和度测定为血氧饱和度。进行临床血液检查,检测c -反应蛋白(CRP)、铁蛋白、d -二聚体、纤维蛋白原和肌钙蛋白I水平。 结果:随着众所周知的房颤发展预测因子(动脉高血压、冠心病、左室心肌肥厚、左房扩张),新发房颤发作记录出现在中、老年和老年患者中。44.4%的房颤患者伴有心房和心室的扩张。随着左室射血分数的降低,房颤发作的发生率达到61.5%。在保留射血分数的情况下,房颤发作的频率要低得多(27%)。房颤患者肺损伤程度平均为62.5%(2080%),氧支持饱和度为93%(7697%)。血清肌钙蛋白I水平2000 ng/L提示急性心肌损伤。CRP和血铁蛋白值证实心肌损伤中存在明显的炎症成分。房颤合并COVID-19肺炎患者血纤维蛋白原和d -二聚体浓度高(16301 ng/mL)与高凝倾向相关。 结论:COVID-19对心肌具有直接损害作用,且可能持续时间较长,可诱发急性肺炎患者房颤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
New-onset atrial fibrillation in patients with SARS-CoV-2 pneumonia as a manifestation of acute myocardial injury
BACKGROUND: Over the past 3 years, the prevalence of atrial fibrillation (AF) has increased significantly worldwide, which was associated with the pandemic caused by SARS-CoV-2. It is accompanied by an increase in the cases of ischemic stroke, myocardial infarction, and development of heart failure due to acute myocardial injury. Given the high lethality of SARS-CoV-2 infection (COVID-19), studying the characteristics of new-onset AF is essential. AIM: The study aims at determining the predictors of new-onset AF in patients with COVID-19 pneumonia and at analyzing the clinical and pathophysiological characteristics of acute myocardial injury. MATERIALS AND METHODS: In 36 patients aged 4482 years (average 68.0) with COVID-19 pneumonia, AF paroxysms were recorded for the first time. All of them underwent computed tomography of the chest, electrocardiography, and echocardiography. The left ventricular ejection fraction was calculated using the Simpson method. Oxygen saturation was determined as blood oxygen saturation. Clinical blood tests were performed, C-reactive protein (CRP), ferritin, D-dimer, fibrinogen, and troponin I levels were measured. RESULTS: Along with the well-known predictors of AF development (arterial hypertension, coronary heart disease, left ventricular myocardial hypertrophy, and left atrial dilatation), with COVID-19 pneumonia, new-onset AF paroxysms were recorded in patients of the middle, elderly, and late-life age. In 44.4% of patients with AF, cardiomegaly occurred with dilatation of both atria and ventricles. With decreased left ventricular ejection fraction, the incidence of AF paroxysms reached 61.5%. With preserved ejection fraction, AF paroxysms occurred much less frequently (27%). In patients with AF, the extent of lung damage is on average 62.5% (2080%) with oxygen support saturation of 93% (7697%). Serum troponin I levels of 2000 ng/L indicated acute myocardial injury. CRP and blood ferritin values confirmed the presence of a pronounced inflammatory component in myocardial injury. High concentrations of blood fibrinogen and D-dimer, reaching 16,301 ng/mL, were associated with a tendency to hypercoagulation in patients with AF and COVID-19 pneumonia. CONCLUSIONS: COVID-19 has a direct damaging effect on the myocardium and probably persists for a long time, which may induce AF in patients with acute pneumonia.
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