Wang Jingyao, Li Yachao, Lei Mengjie, Guan Zeyong, Zhao Zhigang, Wang Xiao, Xue Zengming
Department of Cardiology, Langfang People's Hospital, Hebei Medical University, Langfang Core Laboratory of Precision Treatment of CAD, Langfang, China.
Cardiometabolic Medicine Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Medicine (Baltimore). 2025 Jul 18;104(29):e43412. doi: 10.1097/MD.0000000000043412.
Although the global impact of coronavirus disease 2019 (COVID-19) has diminished, cardiovascular complications, such as acute myocardial infarction, remain a critical concern. This case highlights the potential role of COVID-19 in destabilizing preexisting coronary plaques through systemic inflammation and hypercoagulability, offering insights into diagnostic and therapeutic strategies for similar patients.
A 41-year-old woman with no prior cardiovascular risk factors presented with sudden-onset chest pain 5 days after a confirmed COVID-19 diagnosis. Initial electrocardiography showed ST-segment changes and troponin I levels were mildly elevated.
Emergency coronary angiography revealed 90% stenosis in the middle segment of left anterior descending artery with thrombus, confirming acute anterior myocardial infarction. Optical coherence tomography identified vulnerable plaque features, including macrophages and cholesterol crystals, without plaque rupture.
Thrombus aspiration and optical coherence tomography-guided drug-eluted balloon angioplasty were performed. Post-procedural multimodal imaging (coronary computed tomography angiogram, cardiac magnetic resonance) demonstrated residual plaque burden and mid-myocardial late gadolinium enhancement, suggesting dual ischemic and inflammatory injuries. Intensive lipid-lowering therapy (alirocumab and rosuvastatin) and dual antiplatelet therapy were also administered.
The disease course of the patient suggests that COVID-19 could play a role in the destabilization of atherosclerotic plaques through a high inflammatory status in the blood vessels, leading to a hypercoagulable state and acute myocardial infarction induction. Therefore, monitoring inflammatory markers and administering adequate anti-inflammatory treatments may be necessary for such patients.
尽管2019冠状病毒病（COVID-19）的全球影响已有所减弱，但心血管并发症，如急性心肌梗死，仍然是一个关键问题。本病例突出了COVID-19通过全身炎症和高凝状态使先前存在的冠状动脉斑块不稳定的潜在作用，为类似患者的诊断和治疗策略提供了见解。
一名41岁无既往心血管危险因素的女性在确诊COVID-19后5天出现突发胸痛。初始心电图显示ST段改变，肌钙蛋白I水平轻度升高。
急诊冠状动脉造影显示左前降支中段90%狭窄并伴有血栓，确诊为急性前壁心肌梗死。光学相干断层扫描识别出易损斑块特征，包括巨噬细胞和胆固醇结晶，但无斑块破裂。
进行了血栓抽吸和光学相干断层扫描引导下的药物洗脱球囊血管成形术。术后多模态成像（冠状动脉计算机断层扫描血管造影、心脏磁共振成像）显示有残余斑块负荷和心肌中层延迟钆增强，提示存在缺血和炎症双重损伤。还给予了强化降脂治疗（阿利西尤单抗和瑞舒伐他汀）和双联抗血小板治疗。
该患者的病程表明，COVID-19可能通过血管内的高炎症状态导致动脉粥样硬化斑块不稳定，从而引发高凝状态并诱发急性心肌梗死。因此，对此类患者监测炎症标志物并给予充分的抗炎治疗可能是必要的。
