Department of Cardiology Manchester University Manchester United Kingdom.
Department of Cardiology North Bristol Trust Bristol United Kingdom.
J Am Heart Assoc. 2022 Sep 20;11(18):e026399. doi: 10.1161/JAHA.122.026399. Epub 2022 Sep 14.
Background Acute COVID-19-related myocardial, pulmonary, and vascular pathology and how these relate to each other remain unclear. To our knowledge, no studies have used complementary imaging techniques, including molecular imaging, to elucidate this. We used multimodality imaging and biochemical sampling in vivo to identify the pathobiology of acute COVID-19. Specifically, we investigated the presence of myocardial inflammation and its association with coronary artery disease, systemic vasculitis, and pneumonitis. Methods and Results Consecutive patients presenting with acute COVID-19 were prospectively recruited during hospital admission in this cross-sectional study. Imaging involved computed tomography coronary angiography (identified coronary disease), cardiac 2-deoxy-2-[fluorine-18]fluoro-D-glucose positron emission tomography/computed tomography (identified vascular, cardiac, and pulmonary inflammatory cell infiltration), and cardiac magnetic resonance (identified myocardial disease) alongside biomarker sampling. Of 33 patients (median age 51 years, 94% men), 24 (73%) had respiratory symptoms, with the remainder having nonspecific viral symptoms. A total of 9 patients (35%, n=9/25) had cardiac magnetic resonance-defined myocarditis. Of these patients, 53% (n=5/8) had myocardial inflammatory cell infiltration. A total of 2 patients (5%) had elevated troponin levels. Cardiac troponin concentrations were not significantly higher in patients with and without myocarditis (8.4 ng/L [interquartile range, IQR: 4.0-55.3] versus 3.5 ng/L [IQR: 2.5-5.5]; =0.07) or myocardial cell infiltration (4.4 ng/L [IQR: 3.4-8.3] versus 3.5 ng/L [IQR: 2.8-7.2]; =0.89). No patients had obstructive coronary artery disease or vasculitis. Pulmonary inflammation and consolidation (percentage of total lung volume) was 17% (IQR: 5%-31%) and 11% (IQR: 7%-18%), respectively. Neither were associated with the presence of myocarditis. Conclusions Myocarditis was present in a third patients with acute COVID-19, and the majority had inflammatory cell infiltration. Pneumonitis was ubiquitous, but this inflammation was not associated with myocarditis. The mechanism of cardiac pathology is nonischemic and not attributable to a vasculitic process. Registration URL: https://www.isrctn.com; Unique identifier: ISRCTN12154994.
急性 COVID-19 相关的心肌、肺和血管病理学以及它们之间的关系尚不清楚。据我们所知，尚无研究使用包括分子成像在内的互补成像技术来阐明这一点。我们使用多模态成像和生化采样在体内识别急性 COVID-19 的病理生物学。具体来说，我们研究了心肌炎症的存在及其与冠状动脉疾病、全身血管炎和肺炎的关系。
本横断面研究前瞻性招募了因急性 COVID-19 住院的连续患者。影像学检查包括计算机断层扫描冠状动脉造影（识别冠状动脉疾病）、心脏 2-脱氧-2-[氟-18]氟-D-葡萄糖正电子发射断层扫描/计算机断层扫描（识别血管、心脏和肺部炎症细胞浸润）和心脏磁共振（识别心肌疾病）以及生物标志物采样。在 33 名患者（中位年龄 51 岁，94%为男性）中，24 名（73%）有呼吸道症状，其余患者有非特异性病毒症状。共有 9 名（35%，n=9/25）患者的心脏磁共振定义为心肌炎。这些患者中有 53%（n=5/8）有心肌炎症细胞浸润。共有 2 名（5%）患者肌钙蛋白水平升高。患有和不患有心肌炎的患者的肌钙蛋白浓度没有显著差异（8.4ng/L[四分位距，IQR：4.0-55.3]与 3.5ng/L[IQR：2.5-5.5]；=0.07）或心肌细胞浸润（4.4ng/L[IQR：3.4-8.3]与 3.5ng/L[IQR：2.8-7.2]；=0.89）。没有患者有阻塞性冠状动脉疾病或血管炎。肺炎症和实变（占总肺容积的百分比）分别为 17%（IQR：5%-31%）和 11%（IQR：7%-18%）。两者均与心肌炎无关。
急性 COVID-19 患者中有三分之一存在心肌炎，大多数患者有炎症细胞浸润。肺炎很普遍，但这种炎症与心肌炎无关。心脏病理学的机制是非缺血性的，不能归因于血管炎过程。
