key: cord-267332-xc6dcb93
authors: Soltani, Marwa; Mansour, Samer
title: Biventricular thrombi associated with myocardial infarction in a patient with COVID-19: a case report
date: 2020-06-26
journal: Can J Cardiol
DOI: 10.1016/j.cjca.2020.06.016
sha: 
doc_id: 267332
cord_uid: xc6dcb93

A wide spectrum of cardiovascular manifestations has been documented in patients suffering from coronavirus disease (COVID-19). Usually associated with a poor prognosis, these manifestations include thrombo-embolic events, acute coronary syndrome, heart failure and cardiogenic shock. We describe a COVID-19 patient who presented with subacute myocardial infarction, biventricular thrombi and bilateral pulmonary emboli. Biventricular thrombi are rare, and their presence raises concern for an underlying prothrombotic condition.

Patients with coronavirus disease (COVID-19) have an increased incidence of cardiovascular comorbidities compared to the general population 1 . They can present with an acute cardiovascular event or an exacerbation of a preexisting cardiac condition. A wide spectrum of cardiovascular manifestations has been documented in patients suffering from COVID-19 such as thrombo-embolic events, acute coronary syndrome, heart failure and cardiogenic shock 1 and they are associated with poor prognosis. We describe a patient with COVID-19 who presented with subacute myocardial infarction and bilateral pulmonary emboli associated with biventricular thrombi.

A 63-year-old woman, active smoker with a known medical history of emphysema presented with a 2 weeks history of worsening of dyspnea, non-productive cough and chills. She had chest pain for 24 hours, which resolved the day prior to admission. Due to the delayed presentation and the resolution of her chest pain, she was managed conservatively with aspirin, clopidogrel and enoxaparin. A few hours later, she went into cardiac arrest with an underlying rhythm of monomorphic ventricular tachycardia. After successful cardiorespiratory resuscitation, she was transferred to our tertiary care academic center.

On presentation, the patient was tachypneic with a respiratory rate of 35 breaths/minute. Her oxygen saturation was 93% on 2L/min of oxygen via nasal prongs before cardiac arrest. She was intubated during cardiorespiratory reanimation. Blood pressure and heart rate were within normal range. Physical examination showed jugular vein distension, bibasilar crackles and lower extremity edema. Laboratory work-up revealed mild lymphopenia of 1,3 x 10 9 /L (normal range: 1,5-3,5). Platelet count, coagulation parameters and fibrinogen were normal. Troponin I (0,937 µg/L, normal value < 0,300), creatinine kinase (457 U/L, normal range: 30-185) and lactate (4,2 mmol/L, normal range: 0,6-2,4) were elevated. Lupus anticoagulant, anti-beta-2-glycoprotein and anticardiolipin antibodies were negative. PCR for SARS-CoV-2 was positive.

Electrocardiogram revealed sinus rhythm with ST-segment elevation, T-wave inversion and pathological Q waves in leads V1 to V6, I and aVL, consistent with subacute anterolateral STelevation myocardial infarction. Cardiomegaly with mild interstitial edema were demonstrated on chest X-ray. Coronary angiogram showed 99% stenosis of the proximal left anterior descending coronary artery (LAD) with organized thrombi and TIMI-1 blood flow (Fig.1a) . The circumflex and right coronary arteries had non-significant stenoses. Left ventriculography revealed severe ventricular dysfunction with extended anterolateral akinesis, apical aneurysm and thrombus (Fig. 1b) .

Cardiac tomography done to eliminate a pseudoaneurysm demonstrated severe systolic dysfunction with a left ventricular ejection fraction of 17% and complete akinesis of the LAD territory. An apical aneurysm measuring 5 cm in diameter and a left ventricular thrombus (LVT) measuring 12 mm thick extending over a 6 cm perimeter were found. Unexpectedly, a moderate right ventricular hypokinesis with a small right ventricular thrombus measuring 4 mm by 10 mm and multiple bilateral pulmonary emboli were also noted (Fig. 2) .

Given the presence of multiple thrombi in the heart and lungs, therapeutic anticoagulation with IV heparin and warfarin was initiated. The patient later deteriorated and required systemic support with vasopressors and inotropic agents. Despite treatment, she died from cardiogenic and pulmonary septic shock.

This COVID-19 patient had an extensive anterior myocardial infarction with severe systolic dysfunction. The proposed mechanisms for cardiovascular injury in COVID-19 include the release of proinflammatory cytokines leading to plaque instability, myocardial inflammation, hypercoagulable state and myocardial depression 1 .

LVT can occur as a complication of acute myocardial infarction with ejection fraction below 35% or non-ischemic cardiomyopathy 2 . It mostly occurs with anterior myocardial infarction when there is an aneurysm or apical akinesis 2 . The damage to the endocardial tissue, the hypercoagulable state and the loss of regional contractile function lead to blood stasis and thrombus formation 3 . With effective reperfusion, the incidence of LVT after myocardial infarction has decreased in the PCI era from 33% to 10% 3 . However, in patients presenting more than 12 hours after the onset of symptoms, a study showed that thrombus formation was 48% higher than in the early presentation group 4 . In contrast, the formation of biventricular thrombi following acute myocardial infarction, first reported in 1986, is even rarer. The majority of the cases subsequently reported were associated with an underlying prothrombotic condition such as nephrotic syndrome, hypereosinophilic syndrome, heparin-induced thrombocytopenia, anti-phospholipid syndrome and other coagulopathies. The presence of antiphospholipid antibodies has been associated with COVID-19 but was negative in our patient. To our knowledge, this is the first reported case of biventricular thrombi after myocardial infarction in a patient with COVID-19. Our hypothesis is that the combination of an extensive anterior myocardial infarction with delayed presentation and COVID-19 caused an important inflammatory cascade that led to thrombi formations. 

Cardiovascular manifestations and treatment considerations in covid-19

Incidence, diagnostic methods, and evolution of left ventricular thrombus in patients with anterior myocardial infarction and low left ventricular ejection fraction: a prospective multicenter study

Challenges in management of left ventricular thrombus

Left Ventricular Thrombus in Patients With Acute Anterior Wall Myocardial Infarction

Right Ventricular Infarction Complicating Left Ventricular Infarction Secondary to Coronary Heart Disease