Persistent chest pain after recovery of COVID-19: microvascu
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A 42-year-old woman, presented with fever, anosmia, and a positive polymerase chain reaction for severe acute respiratory syndrome coronavirus 2.

One month later, she complained of oppressive chest pain increasing on exertion suggestive of angina. She did not have previous symptoms or history of coronary artery disease. A 12-lead electrocardiogram demonstrated sinus rhythm with asymmetric T-wave inversion in precordial anterior leads.

A coronary computed tomography showed angiographically normal coronary arteries.

An adenosine-stress cardiac magnetic resonance (CMR) scan was performed at a state of the art 1.5 T scanner. Left and right indexed ventricular volumes and function were within normal ranges [indexed left ventricular end-diastolic volume: 79 mL/m2 (60–93 mL/m2); indexed right ventricular end-diastolic volume: 80 mL/m2 (60–87 mL/m2); left ventricular ejection fraction 69% (57–75%); right ventricular ejection fraction: 68% (53–76%)]. Native MOLLI T1 mapping was performed (at mid-ventricular level2).

Septal native T1 mapping was normal (1040 ms). Ventricular GraSE T2 mapping was 54 ms ruling out myocardial edema. A first-pass stress perfusion CMR showed a significant circumferential subendocardial perfusion defect which highly suggested microvascular dysfunction, with normal perfusion at rest. No late gadolinium enhancement was detected. During the test, the patient presented the same angina she previously reported.

Treatment with aspirin, statins, ranolazine, and nitrates was initially prescribed. Nitrates were stopped because of bad clinical tolerance. Low doses of beta-blockers and calcium antagonist could be added. She reported partial improvement of symptoms, without major cardiovascular events during follow-up.

Some patients report persistent symptoms after recovering from acute COVID-19. Chest pain is present in almost 20% of patients. Mechanisms of microvascular disease in COVID-19 include endothelial injury with endothelial dysfunction and microvascular inflammation, and thrombosis.

This case demonstrates that coronary microvascular ischaemia could be the mechanism of persistent chest pain in patients that have recovered from COVID-19. When obstructive coronary disease is excluded, functional non-invasive tests are recommended to rule out myocardial ischaemia. At present, the pattern of recovery, or the preferred management of post-COVD-19 microvascular dysfunction remains unresolved.