Two Challenging Cases with COVID heart.

COVID-19 affects the heart through various pathways. It can increase thrombotic complications that ultimately lead to myocardial infarction even in patients without a history of underlying heart disease.

INTRODUCTION

COVID‐19 is an infectious disorder that converted into a pandemic dilemma. About 20%‐30% of COVID‐19 subjects suffer from cardiovascular involvement. Recently, there have been numerous descriptions of the cases with a history of cardiac disease who develop serious complications. We described two challenging COVID‐19 cases that resulted in myocardial infarction.

The “2019 coronavirus (2019‐nCoV),” known as the COVID‐19, first appeared in Wuhan, China. The first reported case encountered fever, cough, and pneumonia, accompanied by severe respiratory syndrome. The most considerable group of patients are either asymptomatic or minimally symptomatic. Nevertheless, critical manifestations, including acute respiratory distress syndrome, thrombotic event, and encephalitis, can be observed. The predominant clinical presentation is a respiratory disease, while cardiovascular manifestations are less prevalent. About 20%‐30% of subjects with COVID‐19 suffer from a kind of cardiovascular involvement. The most common type of cardiac involvement in COVID‐19 is acute heart injury, with a marked rise in cardiac biomarkers, which occur in 8%‐12% of all subjects. Additional presentations of cardiovascular disease in COVID‐19 are infrequent. In other words, it has been proved that the existence of previous CVD is a risk marker of poor outcomes in these groups of patients. While the patient's age and history of the previous CVD are considered as a risk of complications, healthy subjects, even at a young age, also have a possibility of severe disease. It is postulated that cardiac manifestations, particularly cardiac dysfunction in COVID‐19 cases with respiratory involvement, can be due to viral myocarditis, which mimics MI in clinical presentation and laboratory data. Nevertheless, thrombotic events should be kept in mind as the main cause of MI and may mimic myocarditis in the cases of COVID‐19.

According to the recent guidelines, COVID‐19 is diagnosed based on the reverse transcription‐polymerase chain reaction (RT‐PCR) test using the pharyngeal swab samples and also the evidence of respiratory involvement in chest high‐resolution computed tomography (HRCT) scan. We aim to describe two challenging cases of COVID‐19 with cardiovascular manifestations, one patient represented with a confusing diagnosis between MI and myocarditis, and another one with the thrombotic complication of this pandemic disease.

Case 1

The first case is a 39‐year‐old gentleman presented to our heart center with a complaint of pleuritic chest pain, dyspnea, and cough for 3 days. He denied previous heart disorder or any cardiac‐related risk factors. His examination was nonsignificant, except for the low‐grade fever. The oxygen level was 94%. Laboratory data, electrocardiography (ECG), and also RT‐PCR for COVID‐19 regarding disease pandemic were performed. Additionally, concerning the presence of risk markers, a chest HRCT scan was obtained. ECG showed diffuse ST‐segment elevation with pathological Q formation in inferolateral leads (Figure 1A). Elevated specific cardiac marker (cTn = 29 ng/dL), C ‐reactive protein (CRP), and erythrocyte sedimentation rate (ESR), and also leukopenia and lymphopenia, were detected. A chest HRCT examination illustrated multifocal bilateral ground‐glass opacities (GGO) (Figure 1B) along with positive RT‐PCR indicative for COVID‐19. Although the patient had a poor echo window, it revealed moderate systolic dysfunction. Regarding the lack of typical clinical signs of MI in the context of COVID‐19 in a young patient without cardiac risk factors, the referring physician had a stronger suspicion of myocarditis rather than myocardial infarction; therefore, cardiac magnetic resonance (CMR) was requested for the evaluation of associated myocarditis. CMR showed significant regional wall‐motion impairment in basal and midlateral segments in cine function sequences along with significant myocardial edema (Figure 2A) in this region on STIR (short tau inversion recovery) images. Furthermore, transmural necrosis in the base to the midposterior lateral wall was identified, surrounding a central zone of microvascular obstruction (MVO) (Figure 2B‐D).

FIGURE 1

A, ECG illustrates diffuse ST‐segment elevation with pathologic Q‐wave in inferolateral leads (II, III, aVF and V5, V5 leads). B, CT imaging displays areas of ground‐glass opacity and consolidation formation in both lung fields

FIGURE 2

CMR images demonstrate evidence of acute infarction. A, STIR (short tau inversion recovery) short‐axis image at midventricular level depicts myocardial edema of the lateral LV wall (arrow). B, 4‐chamber, (C) 2‐chamber, and (D) 3‐chamber LGE sequences indicate transmural necrosis (arrow) with a central area of MVO (arrowhead) in the base to midlateral LV wall

Interestingly, CMR findings were highly consistent with acute MI regarding the pattern of left ventricular (LV) myocardial enhancement and MVO in the specific coronary territory (probably left circumflex [LCX] region). Concerning the presence of symptoms from 3 days preceding to admission and decline in chest pain, the patient had not an indication for emergent catheterization, based on suggested guidelines in the COVID‐19 pandemic. Optimal medical treatment was administered for neglected infarction (including full‐dose anticoagulation during admission, and dual antiplatelet therapy, and also statin and beta‐blocker agents), and coronary angiography was postponed until the complete resolution of infectious disease. After recovery, the patient was a candidate for coronary angiography, but he was unwillingness to take advanced diagnostic workup including coronary angiography.

Case 2

A 33‐year‐old young man was admitted to our heart center with a chief complaint of dyspnea and severe chest discomfort for 3 hours. His examination was not remarkable for any abnormality. In ECG, there was disseminated ST elevation in all segments (Figure 3A), especially in anterior and anterolateral leads. Laboratory data revealed significant troponin elevation (cTn = 37 ng/dL). Regarding the patient's symptom, ECG data, and elevated troponin level, the subject was undertaken emergent angiography with full protection concerning the probable COVID‐19. Angiography demonstrated fresh clot at the site of the first septal branch of the left anterior descending (LAD) artery and consequent total cut of the vessel (Figure 3B). Concerning the massive clot burden, thrombus aspiration, integrilin injection in combination with LAD stenting was performed, resulting in thrombolysis in myocardial infarction (TIMI) flow 3, and significant improvement in patient's symptoms. Regarding the presence of coronary artery thrombus, thrombophilia testing was performed to evaluate inherited disorder and antiphospholipid syndrome, which was unremarkable.

FIGURE 3

A, ECG reveals disseminated ST‐segment elevation and pathologic Q‐wave in anterior and anterolateral leads. B, Angiography demonstrates the fresh clot at the site of the first septal branch of the left anterior descending (LAD) artery and consequent total cut of the vessel. C, CT finding reveals peripheral ground‐glass opacity with subpleural sparing in the left lower zone

Concerning the increased level of inflammatory parameters including CRP = 117 (mg/L) and WBC = 12 600 (cells/mm3), and evidence of lymphopenia (lymph count about 8%), in the context of COVID‐19 pandemic situation, HRCT was carried, and typical GGO in the peripheral portion of the left lung was detected (Figure 3C), and after preparation of RT‐PCR result, COVID‐19 was confirmed.

DISCUSSION

We described two cases of COVID‐19 with cardiovascular complications, hospitalized in our heart center. The first patient was a challenging case, manifested with atypical chest pain in combination with the typical respiratory presentation, which confirmed to have COVID‐19 utilizing HRCT and RT‐PCR. In hospital course, regarding significant changes in paraclinical markers, including diffuse ST‐segment elevation, enzyme level, and impaired LV function in echocardiography, the patient referred for CMR to assess possible myocarditis. Interestingly, CMR evaluation revealed the finding of significant regional wall‐motion impairment, MVO, and transmural myocardial necrosis in the base to the midportion of the inferolateral LV wall. The presence of MVO in CMR is strongly correlated with MVO in histologic examination, and although angiography has not been performed for this case, we believe that the cause of the patient's symptoms is MI, rather than myocarditis.

In this case, differentiating MI from myocarditis is a challenging issue due to a similar clinical and paraclinical presentation.

We hypothesized that considering the thrombotic complications of COVID‐19, there is a high probability of thrombotic infarction in this patient; however, myocarditis cannot be completely ruled out. It is believed that myocardial injury in patients with COVID‐19 is produced by numerous mechanism, including myocarditis , ischemic injury derived by cardiac microvascular or epicardial coronary artery damage, coronary thrombotic complications because of endothelial dysfunction, increased platelet activity, and vessel stasis, hypoxia‐induced injury, and cytokine storm. The thrombotic events can develop due to the primary effect of COVID‐19 or the secondary consequences of the viral infection, including hypoxia and critical illness. Myocardial injury in COVID‐19, as discernible by raised cardiac troponin levels or electrocardiographic and echocardiographic disturbance, is linked with a critical disease. ,

In case of presentation with acute MI, due to rupture of atherosclerotic plaques full‐dose anticoagulation and dual antiplatelet therapy (DAPT) are recommended based on suggested guidelines. , Accordingly, in this patient, and concerning the delay between symptom onset and hospital admission, invasive cardiac procedures were not conducted to reduce the risk of disease transmission for both patients and healthcare providers, and only optimal medical treatment was commenced.

In the second case, there was no prior history of underlying heart disease or other cardiac risk markers. In the illustrated case, due to the severity of the symptoms and paraclinical data, emergent invasive angiography was performed with full protection concerning the probability of COVID‐19. Catheterization findings verified the presence of fresh clot inside the coronary artery lumen, which results in vessel obstruction. Preliminary documents implicate that affected cases may suffer from hemostatic impairments. It is understood that several issues make COVID‐19 different from other conditions regarding the prevention and management of the thrombotic and thromboembolic disease. Either the direct effects of COVID‐19 itself or the indirect consequences of the disorder may eventually escalate the risk of thrombotic events.

There are several reports of COVID‐19 patients presenting with thrombotic complications. In a case report study, there is a description of a patient with brain infarction accompanied by two sided limb ischemia, in the context of antiphospholipid antibody syndrome. A study by Baldi et al designated that the incidence of out of hospital cardiac arrest (OHCA) 2 months after the first case of the COVID‐19 in 2020 was 52% higher than in 2019 at the same time. Numerous explanations have been suggested including cardiac arrest linked with respiratory failure, myocardial injury, or delayed arrival at the hospital after a heart attack. According to the results of investigations and reported cases, we believe that thrombotic events can be a cause of OHCA, especially in young patients without a history of atherosclerotic risk factors. Accordingly, particular attention should be provided to thrombotic events, especially in the context of COVID‐19 and lack of history of cardiovascular disease.

CONCLUSION

In the healthy population, COVID‐19 can affect the heart via different mechanisms. Although not clearly understood, it can increase thrombotic complications because of endothelial dysfunction, increased platelet activity, and vessel stasis that ultimately lead to MI.

CONFLICT OF INTEREST

All of the authors mention that they have no conflicts of interest.

AUTHOR CONTRIBUTIONS

Dr Mohsen Maadani and Dr Bahareh Jahanshahi: contributed to data collection. Dr Leila Hosseini and Dr Nahid Rezaeian: contributed to the writing of the manuscript. Dr Sanaz Asadian: contributed to the critical revision of the article.