STEMI associated with SARS-CoV-2 infection and the use of ECMO as a potential therapeutic approach in addition to the PCI.

A 55-year-old male presented to the emergency department with the complaints of chest pain that started 4 h before presentation. Pain was located over the anterior chest, 5 out of 10 intensity, with radiation to the left arm. Chest x-ray on admission showed severe diffuse bilateral pulmonary infiltrates concerning for COVID-19 pneumonia. Electrocardiogram showed inferior and lateral ST-segment elevation compatible with acute inferolateral myocardial infarction. Successful percutaneous coronary intervention (PCI) of the proximal and mid-right coronary artery using the balloon angioplasty and drug-eluting stent was performed. Post-PCI stenosis was 0% with a thrombolysis in myocardial infarction (TIMI) flow of 3. Five-day course of azithromycin and hydroxychloroquine was completed with no improvement overall. Patient received two doses of 400 mg of tocilizumab intravenously on hospital days 5 (HD#5) and #6. The patient was proned, on FiO2 100%, PEEP 15 cm H2O, on epoprostenol sodium and paralytics and eventually received venovenous ECMO, which improved outcome.

INTRODUCTION

Thrombosis with severe acute respiratory syndrome coronavirus infection has been reported in the past [1], which is believed to be caused from exaggerated cytokine response from the viral infection. Here, we present a case with severe acute respiratory syndrome coronavirus −2 (SARS-CoV-2) infection presenting with right coronary artery (RCA) thrombosis.

CASE REPORT

A 55-year-old male presented to the emergency department in April 2020, with the complaints of sudden-onset, left-anterior chest pain that started 4 h before presentation. Pain was 5 out of 10 in intensity, with radiation to the left arm, and no associated shortness of breath (SOB). He also reported a 2-week history of dry cough and fever. Patient is a police officer, and two of his coworkers tested positive for SARS-CoV-2 infection. Past medical history significant for hypertension, hyperlipidemia, coronary artery disease (CAD) status post-percutaneous coronary intervention (PCI) with drug-eluting stent (DES) in 2005 and coronary artery bypass graft × 4 in 2008, untreated type II diabetes mellitus and polycythemia. Differential diagnosis included acute coronary syndrome, acute pulmonary embolism, pneumonia due to corona virus disease-2019 (COVID-19), acute on chronic heart failure exacerbation, myocarditis, pericarditis, tension pneumothorax and costochondritis.

Chest X-ray (CXR) on admission showed severe diffuse bilateral pulmonary infiltrates with air bronchograms (Fig. 1), which was concerning for COVID-19 pneumonia. Electrocardiogram (ECG) showed acute inferolateral ST-segment elevation myocardial infarction (STEMI). ST-segment depression in V1 and V2 suggested posterior myocardial injury (Fig. 2). Initial cardiac troponin I (TnI) was 0.02 ng/L (reference range < 19 ng/L) at 7 h. Reverse transcription–polymerase chain reaction was positive for SARS-CoV-2.

Figure 1

CXR on admission showing diffuse bilateral infiltrates involving almost all of the lung fields.

Figure 2

ECG on admission showing marked ST-segment elevation (lead II, III, aVF and V4–V6).

On physical examination, he was diaphoretic, heart rate 100 beats/minute (bpm), elevated blood pressure at 148/100 mm hg and hypoxic on room air. Repeat TnI was elevated at 19 ng/L at 11:40 h. STEMI protocol was activated and patient was taken to the cardiac catheterization lab. Left heart catheterization with coronary angiography and graft injection showed 90% stenosis of both proximal and mid-portion of the RCA with a TIMI flow of 3. Saphenous vein grafts to mid-diagonal artery and mid-obtuse marginal artery were patent. Left ventricular ejection fraction was 55%. Successful PCI of the proximal and mid-RCA using the balloon angioplasty and DES was performed. Post-PCI stenosis was 0% with TIMI flow of 3 (Fig. 3). Severe hypoxia out of proportion to the CAD was noted during the procedure. ECG post-PCI showed near normalization of the ST-segment elevation (Fig. 4). He was given prasugrel and started on eptifibatide drip and was transferred to the medical intensive care unit. Even though his chest pain improved following the PCI, he was still complaining of SOB requiring up to 10 L of oxygen by high-flow nasal cannula (HFNC). Because of the rapid and abrupt decompensation, he was intubated on the hospital day 1 (HD#1). Five-day course of azithromycin and hydroxychloroquine was completed with no significant improvement. Patient received two doses of intravenous tocilizumab on HD#5 and #6. Refractory hypoxemia (arterial blood gases: pH 7.41, pCO2 53.4, pO2 72.4, HCO3 34) persisted despite maximal ventilator settings (proned, FiO2 100%, PEEP 15 cm H2O, epoprostenol sodium and paralytics). Therefore, given his young age and otherwise healthy status, it was decided to place him on venovenous (VV) ECMO support. He was cannulated at the bedside with 25 French inferior vena cava cannula and 25 French right internal jugular cannula. Flow of 6 L/minute was provided with FiO2 of 100% and sweep of 8. Ventilator mode was set to pressure-regulated volume control, very low tidal volume at 300 mL, 15 breaths/min, minute volume 4.5 L/min, PEEP 12 cm H2O, FiO2 60%. On HD#9, interleukin 6 (IL-6) level was 86.9 pg/ml (a 12-fold decrease), and ECMO was decannulated on the HD#13. He was extubated on the HD#16 and was breathing on 10 L oxygen by HFNC. He remained only on dexmedetomidine, was awake and followed commands. On HD#17, oxygen weaned to 4 L, and on HD#18, he was off of oxygen and breathing on room air. He was discharged to home on HD#24. Inflammatory markers trended down (Table 1) and the IL-6 level remained low at 141 pg/ml. CXR improved significantly on discharge when compared to that of admission (Fig. 5). He is doing well without any residual symptoms as we write this report.

Figure 3

(A) LHC showing 90% stenosis in the proximal and mid-RCA. (B) Guidewire insertion in the RCA. (C) Deployment of the DES in the RCA. (D) Restored perfusion with 0% stenosis in the RCA after DES deployment.

Figure 4

Normalization of the ST-segment after LHC and PCI.

Table 1

Inflammatory markers pre- and post-tocilizumab and ECMO

Inflammatory markers and cytokine	Before anti-IL-6 and ECMO	After receiving anti-IL-6 and ECMO
IL-6 (reference range (RR): 0.0–15.5 PG/ml)	1054.5	86.9
Crp (RR: 0.0–0.9 mg/dl)	42.8	16
D-dimer (RR:<0.49 mcg/ml)	2.03	1.57
Lactate dehydrogenase (LDH) (RR: 313–618 U/L)	2701	649
Ferritin (RR: 18–464 ng/ml)	680	298
Fibrinogen (RR: 180–450 mg/dl)	807	229

Figure 5

CXR on discharge showing marked improvement in pulmonary infiltrates from admission.

DISCUSSION

SARS-CoV-2 uses angiotensin-converting enzyme-2 receptor as a portal of entry into target cells, including endothelium and cardiac myocytes making heart tissue a common target for the SARS-CoV-2 [2]. Several observational studies have reported cardiovascular complications of SARS-CoV-2 infection, including myocardial injury and myocarditis, acute coronary syndrome, acute heart failure, cardiomyopathies, elevated troponins, cardiac dysrhythmias and venous thromboembolic events [3, 4]. Little is known about the pathophysiology of acute coronary syndrome (ACS) in SARS-CoV-2 infection. Multiple mechanisms have been postulated including direct myocardial injury, plaque rupture due to severe acute inflammation, aggravation of preexisting CAD, altered myocardial demand–supply ratio, coronary thrombosis. It is plausible that, the COVID-19 infection facilitated the thrombosis in the RCA by inducing a hypercoagulable state [5] in a patient already prone to ACS from preexisting CAD and polycythemia (admission hemoglobin 17.9 g/dl and hematocrit 51.1%). IL-6 plays a significant role to cause ‘cytokine storm’ in acute inflammatory settings and reported to be associated with myocardial injury [6]. In our patient, administration of tocilizumab and VV ECMO was associated with a positive outcome with significant decrease in the inflammatory markers and IL-6 possibly by slowing down the vicious inflammatory process. There is emerging evidence on the beneficial effect of ECMO in the treatment of COVID-19 including improved survival rate [7, 8], and similar mortality in patients with severe adult respiratory distress syndrome regardless of the COVID-19 status [9].

Cui et al. reported an increased incidence of venous thromboembolism (VTE) and associated mortality in their patient population with COVID-19 [10]. Our patient was discharged on apixaban in addition to clopidogrel, rosuvastatin and metoprolol due to this potential risk of developing VTE from SARS-CoV-2 infection and having a recent RCA thrombosis.