John Sealy School of Medicine, University of Texas Medical Branch, 301 University Blvd., Galveston, TX, USA.
Department of Pathology, University of Texas Medical Branch, 301 University Blvd., Galveston, TX, USA.
Cardiovasc Pathol. 2024 Sep-Oct;72:107661. doi: 10.1016/j.carpath.2024.107661. Epub 2024 May 25.
The epidemic caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has had a significant global impact, especially on immunosuppressed populations such as heart transplant recipients. While SARS-CoV-2 initially infects the respiratory system, cardiovascular complications induced by coronavirus disease 2019 (COVID-19) include cardiac arrest, myocardial infarction, heart failure, myocarditis, arrhythmia, acute myocyte injury, thrombotic events, and cardiogenic shock. Here, we present a case of a 45-year-old African American male who tested positive for COVID-19 infection six months after receiving a heart transplant. The patient was asymptomatic initially, but two weeks later he developed dyspnea, early satiety, and abdominal bloating. The patient was admitted to the hospital for acute renal failure and subsequently diagnosed with moderate acute T cell-mediated allograft rejection (Grade 2R) by endomyocardial biopsy. Three months after testing positive for COVID-19, the patient suffered a sudden cardiac death. At autopsy, the epicardium was diffusely edematous and showed vascular congestion. The coronary arteries showed a striking concentric narrowing of lumens and diffusely thickened arterial walls of all major extramural arteries deemed consistent with a rapidly progressive form of cardiac allograft vasculopathy (CAV). SARS-CoV-2 nucleocapsid protein was localized by immunohistochemistry (IHC) in endothelial cells of venules and capillaries within the epicardium. Our localization of SARS-CoV-2 in coronary vessel endothelial cells by IHC suggests that endothelial cell infection, endotheliitis, and immune-related inflammation may be a primary mechanism of vascular injury. The present case represents an early onset rapidly progressive form of CAV. This case may be the first case of post-transplant arteriopathy occurring in such a short time that includes corresponding autopsy, surgical pathology, and IHC data.
严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）引起的疫情对全球产生了重大影响，特别是对心脏移植受者等免疫抑制人群。虽然 SARS-CoV-2 最初感染呼吸系统，但由 2019 年冠状病毒病（COVID-19）引起的心血管并发症包括心脏骤停、心肌梗死、心力衰竭、心肌炎、心律失常、急性心肌损伤、血栓事件和心源性休克。在这里，我们报告了一例 45 岁的非裔美国男性，他在心脏移植后六个月检测出 COVID-19 感染呈阳性。患者最初无症状，但两周后出现呼吸困难、早饱和腹胀。患者因急性肾衰竭入院，随后通过心内膜心肌活检诊断为中度急性 T 细胞介导的同种异体移植排斥反应（2R 级）。COVID-19 检测呈阳性三个月后，患者发生心源性猝死。尸检时，心外膜弥漫性水肿，并显示血管充血。冠状动脉显示出明显的同心性管腔狭窄和所有主要外膜动脉弥漫性增厚的动脉壁，与快速进展型心脏同种异体移植血管病（CAV）一致。免疫组织化学（IHC）显示 SARS-CoV-2 核衣壳蛋白定位于心外膜静脉和毛细血管的内皮细胞内。我们通过 IHC 在冠状动脉内皮细胞中定位 SARS-CoV-2 表明内皮细胞感染、血管内皮炎和免疫相关炎症可能是血管损伤的主要机制。本病例代表一种早期发生的快速进展型 CAV。这种情况可能是首例在如此短的时间内发生的移植后动脉病，包括相应的尸检、外科病理学和 IHC 数据。
