A 45-year-old woman presented with chest pain and ECG showed ST-elevation in antero-lateral leads. She did not have connective tissue disease, risk factors for coronary artery disease and was not pregnant. She experienced classical symptoms of COVID-19 eight weeks previously including anosmia, hypogeusia, and an influenza-like illness but was not tested for severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2) as, at the time, testing was not routinely available in the community in the U.K. Coronary angiography showed an extensive type 2 spontaneous coronary artery dissection (SCAD) involving the entire left anterior descending artery (LAD) but with thrombolysis in myocardial infarction (TIMI) III flow (Panel A). The remainder of the coronary tree was normal and since her symptoms and ECG improved, a conservative approach was adopted. The peak hsTroponinT was 468 ng/dL, and transthoracic echocardiography confirmed moderate left ventricular systolic impairment with anterior wall hypokinesia. The nasopharyngeal swab was negative for SARS-CoV-2, but she was positive for COVID-19 IgG antibodies, confirming previous exposure. The patient was discharged on dual anti-platelet therapy, beta-blockade, and an angiotensin converting enzyme (ACE) inhibitor. Cardiovascular magnetic resonance performed 3 weeks later showed resolution of left ventricular function with evidence of infarction and elevated T2 in the mid- to apical septum and anterior walls (Panel B; arrows).
It is established that active COVID-19 infection can trigger vascular endothelial dysfunction but whether this persists remains unclear. The development of severe SCAD in the aftermath of COVID-19 infection raises the possibility that exposure to SARS-CoV-2 might lead to a chronic predisposition to endothelial dysfunction in susceptible patients.
Funding
This work was part funded by King’s College Hospital R&D Grant and was supported by the Department of Health via a National Institute for Health Research Biomedical Research Centre award to Guy’s & St Thomas’ NHS Foundation Trust in partnership with King’s College London and King’s College Hospital NHS Foundation Trust. This study was also part funded by a Science and Technology Facilities Council grant.
Conflict of interest: The authors have submitted their declaration which can be found in the article Supplementary Material online.
