Spontaneous coronary artery dissection in a patient with COVID-19.

A 51-year-old female with a history of hypertension and tobacco use was admitted to our unit due to recent onset of fever (38.5°C), cough, and respiratory distress. SARS-CoV-2 infection was confirmed by real-time polymerase chain reaction (RT-PCR) assays performed on nasopharyngeal swabs. We administered oxygen via a high-flow-nasal-cannula, ribavirin/interferon beta-1b, low-dose dexamethasone, and prophylactic anticoagulation (enoxaparin 40 mg subcutaneously twice daily). On day-3, the patient developed precordial chest pain after intense cough. Electrocardiography revealed normal sinus rhythm and mild ST-segment elevation/biphasic T waves in precordial leads V2 and V3. Cardiac enzymes (including troponin-I <0.01 ng/ml) and echocardiography were inconclusive for myocardial ischemia. However, coronary angiography depicted a type-two (diffuse smooth stenosis) spontaneous coronary artery dissection (SCAD) at the distal left anterior descending (LAD) artery (Fig. 1a, Supplemental Video1, Supplemental digital content 1, http://links.lww.com/MCA/A404).

Fig. 1

(a) A cranial (37°) coronary angiographic view illustrating a typical type-two coronary artery dissection at the distal left anterior descending artery (region between the two arrowheads). (b) Follow-up coronary angiography [projection approximately same to (a)] demonstrating total restoration of the patency of the affected vessel. CRA, cranial; LAO, left anterior oblique.

The patient had a single-vessel SCAD and no signs of refractory ischemia or hemodynamic instability. Hence, conservative treatment integrating dual antiplatelet, anticoagulation, and statin therapy was administered based on current recommendations [1]. Chest pain was relieved, while no ischemic or other complications occurred. RT-PCR test for COVID-19 was negative on day-18, and the patient was discharged to home isolation. Coronary angiography after 1 month (Fig. 1b, Supplemental Video2, Supplemental digital content 2, http://links.lww.com/MCA/A405) showed restored LAD anatomy and patency.

Scarce data exist regarding the pathogenesis and treatment of SCAD in COVID-19 [2]. In our patient, no conditions associated with the development of SCAD (i.e., fibromuscular dysplasia, hormonal therapy, systemic inflammatory disease, or connective tissue disorder) were identified [1]. However, COVID-19-associated thromboinflammation might have been implicated in the pathobiology of SCAD [3]. In addition, the role of intense cough as a precipitating factor in the development of SCAD was clearly highlighted in our COVID-19 patient [1].

Acknowledgements

IRB information: The study was approved by the Institutional Review Board of King Saud Medical City, Riyadh, Saudi Arabia [H-01-R-053, IORG0010374, H1RI-22-20-03]. Written informed consent was obtained from the patient.

Conflicts of interest

There are no conflicts of interest.