Department of Chemistry and Biochemistry, Brigham Young University, Provo, UT, USA.
Office of the Medical Examiner, Utah Department of Health and Human Services, Salt Lake City, Utah, USA.
Diagn Pathol. 2023 Oct 18;18(1):114. doi: 10.1186/s13000-023-01397-7.
Disease from Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) remains the seventh leading cause of death in the United States. Many patients infected with this virus develop later cardiovascular complications including myocardial infarctions, stroke, arrhythmia, heart failure, and sudden cardiac death (20-28%). The purpose of this study is to understand the primary mechanism of myocardial injury in patients infected with SARS-CoV-2.
We investigated a consecutive cohort of 48 medical examiner cases who died with PCR-positive SARS-CoV-2 (COVpos) infection in 2020. We compared them to a consecutive cohort of 46 age- and sex-matched controls who were PCR-negative for SARS-CoV-2 (COVneg). Clinical information available at postmortem examination was reviewed on each patient. Formalin-fixed sections were examined using antibodies directed against CD42 (platelets), CD15 (myeloid cells), CD68 (monocytes), C4d, fibrin, CD34 (stem cell antigen), CD56 (natural killer cells), and myeloperoxidase (MPO) (neutrophils and neutrophil extracellular traps(NETs)). We used a Welch 2-sample T-test to determine significance. A cluster analysis of marker distribution was also done.
We found a significant difference between COVpos and COVneg samples for CD42, CD15, CD68, C4d, fibrin, and MPO, all of which were significant at p < 0.001. The most prominent features were neutrophils (CD15, MPO) and MPO-positive debris suggestive of NETs. A similar distribution of platelets, monocytes, fibrin and C4d was seen in COVpos cases. Clinical features were similar in COVpos and COVneg cases for age, sex, and body mass index (BMI).
These findings suggest an autoinflammatory process is likely involved in cardiac damage during SARS-CoV-2 infection. No information about clinical cardiac disease was available.
由严重急性呼吸系统综合征冠状病毒 2 型（SARS-CoV-2）引起的疾病仍然是美国第七大致死原因。许多感染这种病毒的患者会出现后期心血管并发症，包括心肌梗死、中风、心律失常、心力衰竭和心源性猝死（20-28%）。本研究旨在了解 SARS-CoV-2 感染患者心肌损伤的主要机制。
我们调查了 2020 年连续 48 例尸检中 PCR 阳性 SARS-CoV-2（COVpos）感染的法医案例，并将其与连续 46 例年龄和性别匹配的 SARS-CoV-2 PCR 阴性（COVneg）对照进行比较。对每位患者的尸检时临床信息进行回顾。使用针对 CD42（血小板）、CD15（髓样细胞）、CD68（单核细胞）、C4d、纤维蛋白、CD34（干细胞抗原）、CD56（自然杀伤细胞）和髓过氧化物酶（MPO）（中性粒细胞和中性粒细胞胞外诱捕网（NETs））的抗体对福尔马林固定的切片进行检查。我们使用 Welch 2 样本 T 检验来确定显著性。还进行了标记物分布的聚类分析。
我们发现 COVpos 和 COVneg 样本之间在 CD42、CD15、CD68、C4d、纤维蛋白和 MPO 方面存在显著差异，所有这些差异在 p<0.001 时均具有统计学意义。最突出的特征是中性粒细胞（CD15、MPO）和提示 NETs 的 MPO 阳性碎片。COVpos 病例中也观察到血小板、单核细胞、纤维蛋白和 C4d 的类似分布。COVpos 和 COVneg 病例的临床特征在年龄、性别和体重指数（BMI）方面相似。
这些发现表明，在 SARS-CoV-2 感染期间，心脏损伤可能涉及自身炎症过程。没有关于临床心脏病的信息。
