A Systematic Review of COVID-19 and Myocarditis.

BACKGROUND: The COVID-19 infection which emerged in December 2019, is caused by the virus SARS-CoV-2. Infection with this virus can lead to severe respiratory illness, however, myocarditis has also been reported. The purpose of this study is to identify the clinical features of myocarditis in COVID-19 patients. METHODS: A systematic review was conducted to investigate characteristics of myocarditis in patients infected with COVID-19 using the search term "Coronavirus" or "COVID" and "myocarditis," "heart," or "retrospective." Case reports and retrospective studies were gathered by searching Medline/Pubmed, Google Scholar, CINAHL, Cochrane CENTRAL, and Web of Science databases. 11 articles were selected for review. RESULTS: COVID-19 myocarditis affected patients over the age of 50 and incidences among both genders were equally reported. Patients presented with dyspnea, cough, fever with hypotension and chest pain. Laboratory tests revealed leukocytosis with increased C-reactive protein, while arterial blood gas analysis demonstrated respiratory acidosis. All cardiac markers were elevated. Radiographic imaging of the chest showed bilateral ground glass opacities or bilateral infiltrates, while cardiac magnetic resonance imaging produced late gadolinium enhancements. Electrocardiography demonstrated ST-segment elevation or inverted T waves, while echocardiography revealed reduced left ventricular ejection fraction with cardiomegaly or increased wall thickness. Management with corticosteroids was favored in most cases, followed by antiviral medication. The majority of studies reported either recovery or no further clinical deterioration. CONCLUSION: Current available data on COVID-19 myocarditis is limited. Further research is needed to advance our understanding of COVID-19 myocarditis.

A Systematic Review of COVID-19 and Pericarditis

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was first identified in Wuhan, China in December 2019. Since then, the disease has spread globally, leading to the ongoing pandemic. It can cause severe respiratory illness;however, many cases of pericarditis have also been reported. This systematic review aims to recognize the clinical features of pericarditis and myopericarditis in COVID-19 patients. Google Scholar, Medline/PubMed, CINAHL, Cochrane Central, and Web of Science databases were searched for studies reporting “Coronavirus” or “COVID” and “Peri-myocarditis,” “heart,” or “retrospective.” Case reports and retrospective studies published from May 2020 to February 2021 were reviewed. In total, 33 studies on pericarditis, myopericarditis, and pericardial infusion were included in this review. COVID-19 pericarditis affected adult patients at any age. The incidence is more common in males, with a male-to-female ratio of 2:1. Chest pain (60%), fever (51%), and shortness of breath (51%) were the most reported symptoms, followed by cough (39%), fatigue (15%), myalgia (12%), and diarrhea (12%). Laboratory tests revealed leukocytosis with neutrophil predominance, elevated D-dimer, erythrocyte rate, and C-reactive protein. Cardiac markers including troponin-1, troponin-T, and brain natriuretic peptide were elevated in most cases. Radiographic imaging of the chest were mostly normal, and only 31% of chest X-rays showed cardiomegaly and or bilateral infiltration. Electrocardiography (ECG) demonstrated normal sinus rhythm with around 59% ST elevation and rarely PR depression or T wave inversion, while the predominant echocardiographic feature was pericardial effusion. Management with colchicine was favored in most cases, followed by non-steroidal anti-inflammatory drugs (NSAIDs), and interventional therapy was only needed when patient developed cardiac tamponade. The majority of the reviewed studies reported either recovery or no continued clinical deterioration. The prevalence of COVID-19-related cardiac diseases is high, and pericarditis is a known extrapulmonary manifestation. However, pericardial effusion and cardiac tamponade are less prevalent and may require urgent intervention to prevent mortality. Pericarditis should be considered in patients with chest pain, ST elevation on ECG, a normal coronary angiogram, and COVID-19. We emphasize the importance of clinical examination, ECG, and echocardiogram for decision-making, and NSAIDs, colchicine, and corticosteroids are considered to be safe in the treatment of pericarditis/myopericarditis associated with COVID-19.

Thrombus in Transit and Impending Pulmonary Embolism Detected on POCUS in a Patient with COVID-19 Pneumonia.

Coronavirus disease 2019 (COVID-19) is a pandemic that started in China in December 2019 and carries a high risk of morbidity and mortality. To-date (4-22-2020) it affected over 2.6 million people and resulted in nearly 200,000 death worldwide mainly due to severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2). Among the major underlying pathophysiologic mechanisms in COVID 19 is hypercoagulability, leading to increased risk for deep vein thrombosis and pulmonary embolism that contribute to increased morbidity and mortality. In this report, we present the case of a 55-year-old man who presented with COVID-19 pneumonia, and was found to have a thrombus in transit by routine point of care ultrasound (POCUS). While computer tomography (CT) angiography is the test of choice, the utilization of point of care ultrasound (POCUS) has gained traction as an adjunctive means of surveillance for the development of VTE in patients with COVID-19. In this report, we discuss the clinical utility of POCUS in diagnosing thrombus in transit in COVID 19 populations.

Apical Takotsubo Cardiomyopathy in a COVID-19 Patient Presenting with Stroke: A Case Report and Pathophysiologic Insights.

COVID-19 is a pandemic that started in Wuhan city, Hubei province in China in December 2019 and is associated with high morbidity and mortality. It is characterized by a heightened inflammatory and prothrombotic state that are known to cause various cardiovascular manifestations such as thromboembolism, acute coronary syndrome and stroke. We here present a 72-year-old woman with multiple cardiovascular risk factors and COVI 19 pneumonia who presented with acute ischemic stroke. She was also noted to have ST segment elevation myocardial infarction (STEMI) on the electrocardiogram however the imaging and clinical presentation was consistent with apical takotsubo cardiomyopathy. We here discuss the various pathophysiologic mechanisms by which COVID-19 can result in acute stroke. The patient likely developed takotsubo cardiomyopathy because of stroke and acute COVID-19 induced sympathetic stimulation and catecholamine surge. To the best of our knowledge this is the first case of apical variant of takotsubo cardiomyopathy in a COVID-19 report.

Utility of D-dimer as a Prognostic Factor in SARS CoV2 Infection: A Review.

Coronavirus Disease-2019 (COVID-19) is currently a public health emergency and has been listed by the World Health Organization (WHO) as a pandemic. It has commonly been associated with pulmonary manifestations and there is a growing body of evidence of multisystem involvement of the virus. As evidenced by various case reports and cohort studies, COVID-19-associated coagulopathy has been a common manifestation amongst the critically ill and has been associated with increased mortality. The presence of venous thromboembolic events in patients who are critically ill due to COVID-19 has prompted the adoption of anticoagulation regimens aimed at preventing thromboembolic phenomena. Coagulation abnormalities have also been implicated in the progression and the severity of COVID-19 related acute respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC). There is strong evidence that D-dimer levels help predict which patients are at risk of thromboembolic events, progression to ARDS, DIC, immune dysregulation and mortality. We will review the utility of D-dimer as screening tool and in the risk stratification of COVID-19 patients prone to developing thromboembolic events, DIC, immune dysregulation and death. To date, the studies that have been published show the presence of elevated D-dimer levels in both the adult and pediatric populations and the measured level correlates with disease severity. Studies have also shown the relative increase of D-dimer levels in non-survivors compared to survivors. The elevation of D-dimer levels has shown to guide clinical decision making, namely the initiation of therapeutic anticoagulation and mortality benefit in patients with severe COVID-19 pneumonia compared to severe non COVID-19 pneumonia. Although the current body of literature suggested the use of D-dimer as a risk stratification tool and as a test to augment clinical judgement regarding the initiation of anticoagulation, randomized control trials are needed to fully understand the relationship between COVID-19 infection and the efficacy of D-dimer assays in clinical decision making.

Observational Study of Thrombotic Events in a Random Cohort of Hospitalized COVID-19 Patients at a Community-Based Hospital of New York City During the Beginning of the 2020 Pandemic.

Coronavirus disease 2019 (COVID-19) continues to pose an unprecedented challenge for the entire world and the healthcare system. Different theories have been proposed elucidating the pathophysiological mechanisms attributing to high mortality and morbidity in COVID-19 infection. Out of them, thrombosis and procoagulant state have managed to earn the maximum limelight. We conducted an observational study based on data from randomly selected 349 hospitalized patients with COVID-19 infection in a community-based hospital in New York City during the first wave of the COVID-19 viral surge in March 2020. The main objective of our study was to assess the risk and occurrence of thrombotic events (both venous and arterial) among the hospitalized patients including the intensive care unit (ICU) and non-ICU admissions with confirmed COVID-19 infection. The primary outcome in our study was defined as the thrombotic events that included myocardial infarction (MI), deep venous thrombosis (DVT), cerebrovascular accidents (CVA), and pulmonary embolism (PE). The study correlated the association of thrombotic events with the level of biomarkers of interest: D-dimer >1000 ng/ml, troponin-I >1 ng/ml, or both. The association of D-dimers and troponin-I with thrombotic events was measured using both univariate and multivariate Cox proportional hazard (PH) regression analysis. Out of a total of 349 patients, 78 patients (22.35%) were found to have elevated biomarkers (D-dimer >1000 ng/ml and/or troponin-I >1 ng/ml) and were categorized as a high-risk group. Eighty-nine patients developed thrombotic complications (evidence of more than one thrombotic event was found in several patients). Two-hundred seventy-one (77.65%) patients had no documentation of thrombosis. The incidence of thrombotic events included myocardial infarction (MI; N=45; 12.8%), cerebrovascular accidents (CVA; N=16; 4.5%), deep venous thrombosis (DVT; N=16; 4.5%), and pulmonary embolism (PE; N=9; 2.57%).

Incidental Asymptomatic Splenic Infarct in a COVID-19 Patient.

A high incidence of thromboembolic events and coagulation parameter abnormalities are seen in cases of coronavirus disease 2019 (COVID-19). Both venous and arterial thrombosis, including arterial thrombosis in unusual sites, have been reported in COVID patients in recent literature. Herein, we report a case of a 67-year-old female patient with non-critical COVID-19 disease with an incidental finding of an asymptomatic splenic infarct. In the absence of a cardio-embolic source, we believe this was an arterial thromboembolic event in the splenic circulation. The duration and modality of anticoagulation of inpatient and ambulatory COVID patients remains a dynamic discussion. Our case adds the evidence of a clinically silent arterial thrombotic event in a non-critical COVID-19 patient which further emphasizes the need to address the strategies for diagnosis and management of thrombo-embolism to prevent potentially fatal complications.

Left gonadal vein thrombosis in a patient with COVID-19-associated coagulopathy.

COVID-19 disease is a viral illness that predominantly causes pneumonia and severe acute respiratory distress syndrome. The endothelial injury and hypercoagulability secondary to the inflammatory response predisposes severely ill patients to venous thromboembolism. The exact mechanism of hypercoagulability is still under investigation, but it is known to be associated with poor prognosis. The most common thrombotic complication reported among these patients is pulmonary embolism. To our knowledge, gonadal vein thrombosis is an uncommon phenomenon that has not been reported in the setting of COVID-19-associated coagulopathy. We report an unusual case of ovarian vein thrombosis and pulmonary embolism associated with COVID-19 presenting with abdominal pain. To our knowledge, this is the first reported case of COVID-19 with absent respiratory symptoms and presentation with venous thrombosis in an unusual location.

COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response.

Since the onset of the global pandemic in early 2020, coronavirus disease 2019 (COVID-19) has posed a multitude of challenges to health care systems worldwide. In order to combat these challenges and devise appropriate therapeutic strategies, it becomes of paramount importance to elucidate the pathophysiology of this illness. Coronavirus disease 2019, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), is characterized by a dysregulated immune system and hypercoagulability. COVID-associated coagulopathy (CAC) was recognized based on profound d-dimer elevations and evidence of microthrombi and macrothrombi, both in venous and arterial systems. The underlying mechanisms associated with CAC have been suggested, but not clearly defined. The model of immunothrombosis illustrates the elaborate crosstalk between the innate immune system and coagulation. The rendering of a procoagulant state in COVID-19 involves the interplay of many innate immune pathways. The SARS-CoV2 virus can directly infect immune and endothelial cells, leading to endothelial injury and dysregulation of the immune system. Activated leukocytes potentiate a procoagulant state via release of intravascular tissue factor, platelet activation, NETosis, and inhibition of anticoagulant mechanisms. Additional pathways of specific relevance in CAC include cytokine release and complement activation. All these mechanisms have recently been reported in COVID-19. Immunothrombosis provides a comprehensive perspective of the several synergistic pathways pertinent to the pathogenesis of CAC.

A Systematic Review of COVID-19 and Myocarditis

BACKGROUND: The COVID-19 infection which emerged in December 2019, is caused by the virus SARS-CoV-2. Infection with this virus can lead to severe respiratory illness, however, myocarditis has also been reported. The purpose of this study is to identify the clinical features of myocarditis in COVID-19 patients. METHODS: A systematic review was conducted to investigate characteristics of myocarditis in patients infected with COVID-19 using the search term "Coronavirus" or "COVID" and "myocarditis," "heart," or "retrospective." Case reports and retrospective studies were gathered by searching Medline/Pubmed, Google Scholar, CINAHL, Cochrane CENTRAL, and Web of Science databases. 11 articles were selected for review. RESULTS: COVID-19 myocarditis affected patients over the age of 50 and incidences among both genders were equally reported. Patients presented with dyspnea, cough, fever with hypotension and chest pain. Laboratory tests revealed leukocytosis with increased C-reactive protein, while arterial blood gas analysis demonstrated respiratory acidosis. All cardiac markers were elevated. Radiographic imaging of the chest showed bilateral ground glass opacities or bilateral infiltrates, while cardiac magnetic resonance imaging produced late gadolinium enhancements. Electrocardiography demonstrated ST-segment elevation or inverted T waves, while echocardiography revealed reduced left ventricular ejection fraction with cardiomegaly or increased wall thickness. Management with corticosteroids was favored in most cases, followed by antiviral medication. The majority of studies reported either recovery or no further clinical deterioration. CONCLUSION: Current available data on COVID-19 myocarditis is limited. Further research is needed to advance our understanding of COVID-19 myocarditis.