Journal Logo

Research Communication

SARS-CoV-2 in coronary blood from thrombus aspiration in a patient with myocardial infarction

Hauguel-Moreau, Mariea; Mansencal, Nicolasa; Gault, Elyanneb; Prati, Giulioa; Dubourg, Oliviera; Annane, Djillalic

Author Information
doi: 10.1097/MCA.0000000000001107
  • Free

To The Editors

Coronavirus disease 2019 (COVID-19) is characterized by endothelial dysfunction, hypercoagulability and increased risk of micro- and macrothrombosis including cerebral and coronary arteries. While the exact underlying mechanisms for arterial thrombosis remain unelucidated, the role of the upregulation of proinflammatory mediators and of disrupted endothelial integrity as amplifying factors of coagulation disorders prevails.

A 53-year-old man with hypertension and diabetes mellitus was admitted to ICU with respiratory distress. He had been complaining of cough for 7 days. A nasopharyngeal swab was positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by reverse transcription-polymerase chain reaction (RT-PCR) assays. Laboratory tests found increased levels of fibrinogen [6.4 g/L (N <3.5 g/L) and C-reactive protein (CRP) [78 mg/L (N <6 mg/L)]. D-dimer was normal [647 ng/mL (N <650 ng/mL)]. Treatment with nasal high flow oxygen supplementation, prone position, dexamethasone (intravenous bolus of 6 mg per day), tocilizumab (intravenous 600 mg as a single dose), prophylactic enoxaparin, azithromycin and cefotaxime was started in ICU with a rapid clinical and biologic improvement.

At day 8 from hospitalization in ICU, he complained of sudden-onset chest pain. An ECG documented an ST-elevation myocardial infarction (STEMI) in inferior leads. Coronary angiography found an acute occlusion with high thrombus burden in the mid and distal right coronary artery (RCA) (Fig. 1) Primary percutaneous coronary intervention (PCI) partially restored a flow in the RCA after multiple manual thrombus aspirations, performed as recommended in the current guidelines because of a large residual thrombus burden after opening the vessel with a guidewire [1], balloon angioplasty, aspirin, ticagrelor, adjunctive tirofiban (glycoprotein IIb/IIIa inhibitor) infusion and heparin. The final result was thrombolysis in myocardial infarctiongrade 2 flow in the posterior descending artery and in the right posterolateral artery branch with residual thrombus, with a resolution of chest pain but a persistent ST-segment elevation. At the time of myocardial infarction, laboratory tests indicated a normalization of inflammatory markers fibrinogen: 3.2 g/L, CRP: 1.9 mg/L, whereas an increased platelet count [483 g/L versus 229 g/L at admission (N <400 g/L)] and D-dimer (5742 ng/mL) were observed. A per PCI intra-coronary blood sample obtained at the site of occlusion during thrombus aspiration was positive for SARS CoV-2 infection by RT-PCR, whereas aspired thrombus analysis revealed platelet-rich thrombus without virus. Systemic blood was also tested for SARS-CoV-2, but negative echocardiography showed large inferior akinesia with a reduced left ventricular ejection fraction of 35%. The patient experimented with transient Mobitz type 1 second-degree atrioventricular block without any further complications. He was treated with tirofiban for 24 h post-PCI and heparin for 5 days because of high thrombus burden. At discharge, the antithrombotic regimen was aspirin 75 mg, ticagrelor 90 mg twice daily. Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

Fig. 1.:
Coronary angiography. (a) Acute thrombosis with high thrombus burden (white arrows) in the mid and distal right coronary artery. (b) Right coronary artery after percutaneous coronary intervention with residual thrombus (white arrows).

Sustained hypercoagulability with a high risk of both venous and arterial thrombotic events has been reported with COVID-19 [2,3]. However, pathologic mechanisms underlying STEMI events remain unknown. STEMI is uncommon in the setting of COVID-19 (<1%) [4], with a special angiographic pattern in the form of a high thrombus burden. This cardiovascular complication may be related to cytokines triggered coagulopathy

The first noticeable point of this study is that STEMI occurred in a COVID-19 patient treated with tocilizumab, an interleukin-6 receptor inhibitor. To our knowledge, this is the first report of STEMI occurring in a patient treated with tocilizumab. Interleukin-6 activates coagulation by inducing tissue factor expression. It increases the expression of fibrinogen, factor VIII, von Willebrand factor, activation of endothelial cells, platelet production. Thus, one would expect that interleukin-6 blockade with tocilizumab by reducing inflammation would decrease the prothrombotic state. The patient had resolution of overt inflammation (normal fibrinogen and CRP) arguing against a prevailing role of upregulated cytokines in the onset of the acute coronary syndrome.

In this case, SARS CoV-2 was found in coronary blood from thrombus aspiration at day 15 from COVID-19 onset. If SARS-CoV-2 viremia is well-described, the demonstrable presence of viral replication in the coronary blood may support direct viral activation of the endothelium. Postmortem reports variably found [5] or did not find [6] evidence for infection of cardiac endothelial cells by SARS CoV-2. SARS-CoV-2 enters into host cells by binding to the angiotensin-converting enzyme 2 receptors which is widely expressed on endothelial cells surface [7]. The endothelial dysfunction that follows endothelial cells infection by SARS-CoV-2 contributes to vasoconstriction, tissue ischemia, aggravating inflammation and coagulopathy.

The present case challenges the hypothesis that overwhelming systemic inflammation is the prevailing mechanism of coronary thrombosis in the setting of COVID-19. The presence of SARS-CoV-2 in coronary artery blood after resolution of inflammation suggests that direct activation of cardiac endothelium is a plausible mechanism of coronary artery thrombus, resulting in STEMI.


The authors received no financial support for the research, authorship and/or publication of this article. Written informed consent was obtained from the patient for publication of this case report and any accompanying images. Data may be obtained from a third party and are not publicly available.

M.H.M., N.M., E.G., G.P. and D.A. contributed to the acquisition and interpretation of the work. M.H.M. drafted the manuscript. N.M., O.D. and D.A. critically revised the manuscript. All authors had full access to the data. All authors gave final approval of the article and agree to be accountable for all aspects of work ensuring integrity and accuracy.

Conflicts of interest

There are no conflicts of interest.


1. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al.; ESC Scientific Document Group. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018; 39:119–177.
2. Hauguel-Moreau M, Hajjam ME, De Baynast Q, Vieillard-Baron A, Lot A-S, Chinet T, et al. Occurrence of pulmonary embolism related to COVID-19. J Thromb Thrombolysis 2020; 6:1–7.
3. Stefanini GG, Montorfano M, Trabattoni D, Andreini D, Ferrante G, Ancona M, et al. ST-elevation myocardial infarction in patients with COVID-19: clinical and angiographic outcomes. Circulation 2020; 141:2113–2116.
4. Cammann VL, Szawan KA, D’Ascenzo F, Gili S, Dreiding S, Würdinger M, et al. Outcomes of acute coronary syndromes in coronavirus disease 2019. Clin Res Cardiol 2020; 109:1601–1604.
5. Varga Z, Flammer AJ, Steiger P, Haberecker M, Andermatt R, Zinkernagel AS, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet 2020; 395:1417–1418.
6. Pellegrini D, Kawakami R, Guagliumi G, Sakamoto A, Kawai K, Gianatti A, et al. Microthrombi as a major cause of cardiac injury in COVID-19: a pathologic study. Circulation 2021; 143:1031–1042.
7. Ferrario CM, Jessup J, Chappell MC, Averill DB, Brosnihan KB, Tallant EA, et al. Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2. Circulation 2005; 111:2605–2610.
Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.