Literature DB >> 35793859

Minimally invasive treatment of left main coronary artery thrombosis in a young patient with COVID-19.

Jacob Johnsen1,2, Steen Dalby Kristensen3,2, Nicolaj Brejnholt Støttrup3,2.   

Abstract

COVID-19 has been associated with cardiovascular events. This case demonstrates severe left main coronary artery thrombosis with distal embolisation in a young male patient admitted with COVID-19 who developed ST-elevation myocardial infarction. The patient was treated with thrombus aspiration combined with aggressive anticoagulant treatment, which yielded complete resolution of the thrombus. Left main thrombus represents a life-threatening coronary event and is most often associated with atherosclerotic plaque rupture. In this case, however, we suspect that COVID-19-related intimal inflammation and hypercoagulopathy might be the causal mechanism of thrombus formation. Revascularisation with coronary artery bypass grafting or percutaneous coronary intervention is the standard treatment of left main thrombosis. However, due to the patient's young age and lack of significant atherosclerotic disease burden, we used a conservative medical treatment strategy using potent antithrombotic therapy. © BMJ Publishing Group Limited 2022. No commercial re-use. See rights and permissions. Published by BMJ.

Entities:  

Keywords:  COVID-19; Interventional cardiology; Ischaemic heart disease

Mesh:

Year:  2022        PMID: 35793859      PMCID: PMC9260788          DOI: 10.1136/bcr-2022-250011

Source DB:  PubMed          Journal:  BMJ Case Rep        ISSN: 1757-790X


Background

Acute coronary thrombus formation is associated with high mortality and morbidity. Thrombus formation in the left main coronary artery is the most threatening thrombus localisation which most often occurs in elderly patients with significant arteriosclerotic disease. Revascularisation by coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) is the standard of care therapy.1 The current SARS-CoV-2 (COVID-19) global pandemic has been demonstrated to be associated with an increased incidence of thrombotic disease in infected patients.2

Case presentation

A young man in his early 30s, with a family predisposition to ischaemic heart disease, was admitted to the department of infectious diseases due to breathlessness, fever and severe coughing. The patient tested positive for SARS-CoV-2 RNA 3 days prior to admission. At admission, the patient was treated with oxygen, dexamethasone, remdesivir and subcutaneous dalteparin 5000 IU×1. A CT chest scan showed diffuse infiltrative ground-glass opacification with consolidation. Piperacillin/tazobactam treatment was commenced on suspicion of bacterial superinfection. After 7 days of admission, the patient no longer required oxygen treatment and discharge was planned. However, the patient developed sudden onset of chest pain.

Investigations

ECG showed ST-segment elevation in the anterior leads (figure 1A) and echocardiography showed anteroapical akinesia and a left ventricular ejection fraction of approximately 50%.
Figure 1

(A) ECG prior to coronary angiography showing ST-segment elevation myocardial infarction. (B) Acute coronary angiography showed thrombus formation in the left main coronary artery. (C) Repeat coronary angiography on day 2 showing resolution of thrombus in the left main coronary artery after antithrombotic and anticoagulant treatment. (D) Coronary angiography with optical coherence tomography at 1 month with complete resolution of the left main coronary thrombus and (E) no signs of plaque rupture, plaque ulceration, thin cap plaque morphology or extensive plaque burden. (F) Cardiac MRI after 1 month was consistent with transmural acute myocardial infarction and no evidence of myocarditis.

(A) ECG prior to coronary angiography showing ST-segment elevation myocardial infarction. (B) Acute coronary angiography showed thrombus formation in the left main coronary artery. (C) Repeat coronary angiography on day 2 showing resolution of thrombus in the left main coronary artery after antithrombotic and anticoagulant treatment. (D) Coronary angiography with optical coherence tomography at 1 month with complete resolution of the left main coronary thrombus and (E) no signs of plaque rupture, plaque ulceration, thin cap plaque morphology or extensive plaque burden. (F) Cardiac MRI after 1 month was consistent with transmural acute myocardial infarction and no evidence of myocarditis. The patient was transferred to the catheterisation laboratory for acute coronary angiography. Coronary angiography revealed a large ostial thrombus in the left main coronary artery (figure 1B) with embolisation to the distal left anterior descending artery. The circumflex and right coronary artery appeared normal.

Treatment

An intravenous bolus of unfractionated heparin and oral loading dose of aspirin was administered prior to transportation to the catheterisation laboratory. PCI with thrombus aspiration from the left anterior descending artery followed by balloon angioplasty without stenting resulted in acceptable flow (Thrombolysis In Myocardial Infarction (TIMI) flow grade 2) to the apical region. The left main coronary thrombus did not cause significant flow obstruction and was left untreated. Unfractionated heparin was administered in order to keep an Activated Clotting Time (ACT) of >250 s. The medical therapy after PCI consisted of an intravenous infusion of eptifibatide for 4 hours together with an oral loading dose of ticagrelor in combination with subcutaneous dalteparin 10 000 IU. The following days, aspirin 75 mg, ticagrelor 90 mg two times per day and dalteparin 10 000 IU two times per day were administered, and the patient was closely monitored in the acute coronary care unit.

Outcome and follow-up

A repeat coronary angiography after 2 days showed attenuated thrombus formation (figure 1C). Dual antiplatelet therapy was continued and dalteparin was reduced to a single subcutaneous dose of 15 000 IU for the following 2 weeks, after which it was reduced to 10 000 IU/day. The patient was discharged after 48 hours in the acute coronary care unit as he remained stable without cardiac symptoms or arrhythmias during admission. Echocardiography with agitated saline contrast in the outpatient clinic at 2 weeks showed no signs of interatrial shunting. After 1 month, repeat coronary angiography showed complete thrombus resolution and no angiographic signs of coronary atherosclerosis (figure 1D). Optical coherence tomography, however, revealed signs of atherosclerosis with some intimal thickening and lipid accumulation in the left main coronary artery but no intimal disruption, plaque ulceration or thin cap plaque morphology (figure 1E). Dalteparin treatment was stopped and dual antiplatelet treatment was planned for a total of 12 months. Cardiac MRI with gadolinium contrast was consistent with a recent myocardial infarction with oedema in the anteroapical regions and a slightly reduced left ventricular ejection fraction of 53%. No myocarditis-like changes were observed (figure 1F). The patient reported no chest discomfort or other cardiac symptoms. Due to familial predisposition to ischaemic heart disease and elevated total cholesterol of 286 mg/dL (7.4 mmol/L) and low-density lipoprotein (LDL) cholesterol of 182 mg/dL (4.7 mmol/L), a follow-up examination with evaluation of cholesterol levels in first-degree relatives and genetic testing was performed. The tests did not meet the diagnostic criteria for familial hypercholesterolaemia. However, an elevated Lp(a) level was noted and atorvastatin was supplemented with ezetimibe. Standard examination for thrombophilia (including tests for protein C, protein S, antiphospholipid syndrome, antithrombin, prothrombin, beta2-glycoprotein and factor V Leiden mutation) was negative. The patient was followed up in the outpatient clinic after 12 months. He was feeling well with no symptoms. LDL cholesterol level was reduced to 34.8 mg/dL (0.9 mmol/L).

Discussion

An increased incidence of both venous and arterial thrombotic events has been reported in patients with ongoing COVID-19 infection.2 3 Proinflammatory cytokines and endothelial dysfunction caused by COVID-19 may in part explain the increased incidence of acute myocardial infarction, and patients with high cholesterol levels may in particular be at risk.2 4, Our patient did not suffer from significant atherosclerotic disease in the index coronary angiogram, and follow-up examination with optical coherence tomography did not show evidence of high-risk plaque morphology or rupture as the causal mechanism of left main thrombus formation. Left main coronary artery thrombosis is an uncommon condition usually associated with a poor outcome.1 The therapeutic options are mainly CABG or PCI. Our patient was in his early 30s and angiography did not reveal a large atherosclerotic disease burden. We therefore chose an alternative and more conservative treatment approach using balloon angioplasty with thrombus aspiration of the embolic occlusion distal in the left anterior descending artery combined with an aggressive antithrombotic treatment without PCI treatment of the left main coronary artery with angiographic follow-up, thus avoiding the potential risks related to CABG and left main coronary artery interventions. I am grateful for the treatment I received when I suffered from a blood clot in my heart. I feel well again without chest pain or shortness of breath. However, I am worried that it could happen again. I am pleased that I did not have to undergo a large surgical procedure and I am happy to share my story if it could be helpful to others. Systemic inflammation with COVID-19 may lead to an increased risk of acute myocardial infarction. COVID-19 may be associated with a large coronary thrombus burden. Antithrombotic treatment with potent antiplatelet therapy and high therapeutic doses of low-molecular-weight heparin may constitute an alternative to percutaneous coronary intervention or coronary artery bypass grafting in left main coronary thrombosis in selected patients.
  4 in total

1.  2018 ESC/EACTS Guidelines on myocardial revascularization.

Authors:  Franz-Josef Neumann; Miguel Sousa-Uva; Anders Ahlsson; Fernando Alfonso; Adrian P Banning; Umberto Benedetto; Robert A Byrne; Jean-Philippe Collet; Volkmar Falk; Stuart J Head; Peter Jüni; Adnan Kastrati; Akos Koller; Steen D Kristensen; Josef Niebauer; Dimitrios J Richter; Petar M Seferovic; Dirk Sibbing; Giulio G Stefanini; Stephan Windecker; Rashmi Yadav; Michael O Zembala
Journal:  Eur Heart J       Date:  2019-01-07       Impact factor: 29.983

2.  Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection.

Authors:  Jeffrey C Kwong; Kevin L Schwartz; Michael A Campitelli; Hannah Chung; Natasha S Crowcroft; Timothy Karnauchow; Kevin Katz; Dennis T Ko; Allison J McGeer; Dayre McNally; David C Richardson; Laura C Rosella; Andrew Simor; Marek Smieja; George Zahariadis; Jonathan B Gubbay
Journal:  N Engl J Med       Date:  2018-01-25       Impact factor: 91.245

3.  Post COVID-19 Arterial Thromboembolism: A Clear and Present Danger.

Authors:  Bingwen Eugene Fan; Christine Cheung
Journal:  Semin Thromb Hemost       Date:  2021-04-15       Impact factor: 4.180

  4 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.