COVID-19-related subclinical myocarditis resulting in mural left ventricular thrombus

The risk of thrombosis post-COVID-19 is not insignificant during the acute phase of illness, especially in those with greater severity of infection, and can persist for several months. CMR is valuable in identifying suspected cardiac involvement and its complications in such patients. LV thrombus is a rare but potentially serious complication that may occur even with asymptomatic or mild disease and may result in embolic sequelae. A 40-year-old woman underwent an outpatient computed tomogram of the abdomen for an abdominal wall hernia. An incidental lesion was detected in the left ventricle (LV) (Figure 1A). Physical examination, serum troponin-I and chest X-ray were normal. Electrocardiogram showed normal sinus rhythm with inferolateral T wave inversion. Cardiac magnetic resonance (CMR) showed hypokinesis, edema and early gadolinium enhancement of the lateral LV wall as well as subepicardial late gadolinium enhancement (LGE), thus fulfilling Lake Louise criteria for myocarditis. A mural left ventricular thrombus (LVT) was noted adherent to the endocardium of the lateral wall (Figure 1A); LV ejection fraction was normal at 55%. Cardiac catheterization showed normal coronary arteries. (A) Left panel: contrast-enhanced CT shows a hypoattenuating lesion (arrow) adjacent to the lateral wall of the LV. Right panel: CMR in the short-axis view (short tau inversion recovery sequence) shows increased signal intensity (arrow) indicating myocardial edema along the lateral wall of the LV. First-pass perfusion sequence in four-chamber view shows hypointense thrombus (arrow) along the lateral wall endocardium and LGE sequence shows subepicardial LGE. (B) Left panel: after 3 months, repeat CMR showed significant reduction of edema, thrombus and LGE. Right panel: at 6 months, echocardiogram (with ultrasound contrast agent) shows complete resolution of LV thrombus and normal wall motion. LA: left atrium; RV: right ventricle. She recalled being diagnosed with coronavirus disease 2019 (COVID-19) 2 months ago. Her symptoms were malaise, mild cough and low-grade fever. Given normal oxygen saturation and lack of any high-risk features, she recovered at home. Two weeks later, she experienced mild left-sided sharp chest pain and palpitations—she did not seek medical care for these symptoms which resolved in a few days. Given this history and the CMR findings, she was diagnosed with subacute, subclinical myocarditis due to COVID-19, complicated by a mural LVT. Warfarin was initiated due to the embolic risk. A follow-up CMR at 3 months showed that the myocardial inflammation, edema, LGE and LVT had significantly improved. At 6-month follow-up, she reported feeling well and walking 1 mile daily. Echocardiogram showed complete resolution of the LVT and the wall motion abnormality, indicating full clinical recovery from myocarditis (Figure 1B). LVT is a rare complication of COVID-19 with intracardiac thrombosis being reported rarely (0.001–0.17%)1—arterial and venous thromboses are seen in 22–30% of critically ill patients and in 7–13% of mild COVID-19 infections. The hypercoagulable state is related to systemic inflammation, endothelial dysfunction and high levels of pro-thrombotic cytokines.1–3 LVT typically occurs in patients with underlying structural heart disorders such as post-myocardial infarction or severe LV systolic dysfunction, or in thrombophilia, but it has been described in COVID-19 patients even in the absence of underlying heart disease, especially those with severe infections requiring admission to an intensive care unit or mechanical ventilation.1 The risk of thrombosis peaks in the first 4 weeks and then declines but can persist as long as 49 weeks.4 While echocardiography is the first-line test used to diagnose LVT and has high specificity (90%), it can miss small mural thrombi due to its lower sensitivity (21–55%). Gadolinium-enhanced CMR is superior for LVT detection due to its higher sensitivity (88%) and specificity (97%).5 Myocarditis associated with COVID-19 may present with a spectrum of manifestations, ranging from an asymptomatic state to mild symptoms (palpitations, premature ventricular contractions, chest pain, shortness of breath) to severe myocarditis leading to cardiogenic shock.2 Our patient had unrecognized subclinical myocarditis which was diagnosed during the subacute phase and resolved on its own. Fortunately, she did not suffer any thromboembolic complications and made a full recovery. In non-hospitalized COVID-19 patients, the risk of thrombotic complications is low and the use of anticoagulant or antiplatelet therapy is not recommended. However, in hospitalized patients, a recent randomized trial showed that full-dose anticoagulation with enoxaparin was associated with lower rates of mortality and intubation.6 Usman Sagheer (Conceptualization [equal], Data curation [lead], Investigation [equal], Methodology [equal], Software [equal], Writing—original draft [lead], Writing—review & editing [equal]), Matthew K. Shotwell (Data curation [supporting], Project administration [supporting], Resources [equal]), Muhammad Umer (Data curation [supporting], Software [supporting]), Wilfred Furtado (Data curation [supporting], Project administration [supporting], Writing—original draft [supporting]), Jonathan Joshi (Resources [equal]), and Dinesh Kalra (Conceptualization [lead], Data curation [equal], Investigation [equal], Resources [lead], Software [lead], Supervision [lead], Visualization [equal], Writing—original draft [equal], Writing—review & editing [lead]) None declared.