Medical Department I (L.T.W., S.B., A.K., J.B., C.S., S.K., M.O., S. Massberg, J.H., U.G.), Ludwig-Maximilians-University, Munich, Germany.
Institute of Cardiovascular Physiology and Pathophysiology, Biomedical Center, Ludwig-Maximilians-University, Planegg-Martinsried, Germany (L.T.W.).
Circ Cardiovasc Imaging. 2021 Jan;14(1):e012220. doi: 10.1161/CIRCIMAGING.120.011713. Epub 2021 Jan 19.
Myocardial injury, defined by elevated troponin levels, is associated with adverse outcome in patients with coronavirus disease 2019 (COVID-19). The frequency of cardiac injury remains highly uncertain and confounded in current publications; myocarditis is one of several mechanisms that have been proposed.
We prospectively assessed patients with myocardial injury hospitalized for COVID-19 using transthoracic echocardiography, cardiac magnetic resonance imaging, and endomyocardial biopsy.
Eighteen patients with COVID-19 and myocardial injury were included in this study. Echocardiography revealed normal to mildly reduced left ventricular ejection fraction of 52.5% (46.5%-60.5%) but moderately to severely reduced left ventricular global longitudinal strain of -11.2% (-7.6% to -15.1%). Cardiac magnetic resonance showed any myocardial tissue injury defined by elevated T1, extracellular volume, or late gadolinium enhancement with a nonischemic pattern in 16 patients (83.3%). Seven patients (38.9%) demonstrated myocardial edema in addition to tissue injury fulfilling the Lake-Louise criteria for myocarditis. Combining cardiac magnetic resonance with speckle tracking echocardiography demonstrated functional or morphological cardiac changes in 100% of investigated patients. Endomyocardial biopsy was conducted in 5 patients and revealed enhanced macrophage numbers in all 5 patients in addition to lymphocytic myocarditis in 1 patient. SARS-CoV-2 RNA was not detected in any biopsy by quantitative real-time polymerase chain reaction. Finally, follow-up measurements of left ventricular global longitudinal strain revealed significant improvement after a median of 52.0 days (-11.2% [-9.2% to -14.7%] versus -15.6% [-12.5% to -19.6%] at follow-up; =0.041).
In this small cohort of COVID-19 patients with elevated troponin levels, myocardial injury was evidenced by reduced echocardiographic left ventricular strain, myocarditis patterns on cardiac magnetic resonance, and enhanced macrophage numbers but not predominantly lymphocytic myocarditis in endomyocardial biopsies.
肌钙蛋白水平升高定义的心肌损伤与 2019 年冠状病毒病(COVID-19)患者的不良预后相关。目前发表的文献中,心肌损伤的发生率仍然高度不确定且混杂;心肌炎是提出的几种机制之一。
我们前瞻性评估了因 COVID-19 住院并伴有心肌损伤的患者,采用经胸超声心动图、心脏磁共振成像和心内膜心肌活检进行评估。
本研究共纳入 18 例 COVID-19 合并心肌损伤患者。超声心动图显示左心室射血分数正常至轻度降低,为 52.5%(46.5%至 60.5%),但左心室整体纵向应变中度至重度降低,为-11.2%(-7.6%至-15.1%)。心脏磁共振显示 16 例患者(83.3%)存在任何心肌组织损伤,表现为 T1 升高、细胞外容积增加或晚期钆增强呈非缺血模式。7 例(38.9%)患者除组织损伤外,还表现为符合心肌炎 Lake-Louise 标准的心肌水肿。心脏磁共振结合斑点追踪超声心动图显示 100%的研究患者存在心脏功能或形态学改变。5 例行心内膜心肌活检,所有 5 例患者均显示巨噬细胞数量增加,1 例患者表现为淋巴细胞性心肌炎。实时定量聚合酶链反应检测未在任何活检标本中检测到 SARS-CoV-2 RNA。最后,中位随访 52.0 天后,左心室整体纵向应变的随访测量值显著改善(-11.2%[-9.2%至-14.7%]与随访时-15.6%[-12.5%至-19.6%];=0.041)。
在这项肌钙蛋白水平升高的 COVID-19 小队列患者中,心肌损伤的证据为超声心动图左心室应变降低、心脏磁共振显示心肌炎模式和巨噬细胞数量增加,但心内膜心肌活检中主要不是淋巴细胞性心肌炎。