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There are four main myocarditis presentations identified in the context of severe acute respiratory coronavirus 2 (SARS-CoV-2): myocarditis associated with acute coronavirus disease 2019 (COVID-19) infection, post-acute COVID-19 syndrome, multisystem inflammatory syndrome, and vaccination-associated myocarditis. This article reviews the clinical fe...
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The coronavirus disease 2019 (COVID-19), instigated by the zoonotic Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), rapidly transformed from an outbreak in Wuhan, China, into a widespread global pandemic. A significant post-infection condition, known as ‘long- COVID’, emerges in a substantial subset of patients, manifesting with a con...
Citations
... Signs and symptoms of possible myocardial injury after COVID-19 may include severe fatigue, palpitations, chest pain, shortness of breath, postural orthostatic tachycardia syndrome (POTS) due to neurologic disturbances, post-exertional fatigue, and higher troponin levels [7][8][9][10]. ...
... In addition, COVID-19 appears to cause severe myocarditis. It can affect the myocardium and pericardium, causing severe fatigue without other apparent symptoms [7]. Diagnosis of myocarditis is relatively inaccurate because both tests and diagnostic protocols lack accuracy. ...
Background
Two years after the COVID-19 pandemic, it became known that one of the complications of this disease is myocardial injury. Electrocardiography (ECG) and cardiac biomarkers play a vital role in the early detection of cardiovascular complications and risk stratification. The study aimed to investigate the value of a new electrocardiographic metric for detecting subtle myocardial injury in patients during COVID-19 treatment.
Methods
The study was conducted in 2021. A group of 26 patients with verified COVID-19 diagnosis admitted to the intensive care unit for infectious diseases was examined. The severity of a patient's condition was calculated using the NEWS score. The digital ECGs were repeatedly recorded (at the beginning and 2 to 4 times during the treatment). 240 primary and composite ECG parameters were analyzed for each electrocardiogram. Among these patients, 6 patients died during treatment. Cluster analysis was used to identify subgroups of patients that differed significantly in terms of disease severity (NEWS), SрО2and integral ECG index (an indicator of the state of the cardiovascular system).
Results
Using analysis of variance (ANOVA repeated measures), a statistical assessment of changes of indicators in subgroups at the end of treatment was given. These subgroup differences persisted at the end of the treatment. To identify potential predictors of mortality, critical clinical and ECG parameters of surviving(S) and non-surviving patients (D) were compared using parametric and non-parametric statistical tests. A decision tree model to classify survival in patients with COVID-19 was constructed based on partial ECG parameters and NEWS score.
Conclusions
A comparison of potential mortality predictors showed no significant differences in vital signs between survivors and non-survivors at the beginning of treatment. A set of ECG parameters was identified that were significantly associated with treatment outcomes and may be predictors of COVID-19 mortality: T-wave morphology (SVD), Q-wave amplitude, and R-wave amplitude (lead I).
... However, direct myocardial injury by the coronavirus (virus-induced toxicity) and dysregulated immune response, cytokine-mediated organ damage, ischemia, endothelial injury, edema, inflammation in the arterial wall, subintimal bleeding, coagulopathy and microthrombus have been suggested as possible pathophysiological mechanisms. 17 Regarding the mechanism of COVID-19-induced myocarditis in the early phase of the pandemic, Hoffman et al., provided useful insights into the first step of SARS-CoV-2 infection and viral entry into cells defining potential targets for antiviral intervention. 9,18 The diagnosis of COVID-19 related myocarditis is based on the clinical presentation, results of blood tests, myocardial biopsy, electrocardiogram and imaging modalities, i.e. echocardiography and CMR. ...
The clinical spectrum of Coronavirus disease 2019 (COVID-19) varies from asymptomatic infection to severe disease with multiorgan dysfunction. Cardiovascular involvement is common and in rare cases can lead to serious complications, such as fulminant myocarditis. The clinical course of COVID-19 myocarditis varies from complete recovery to death in rare cases. The pathophysiology of COVID-19-related myocarditis is still unclear but is believed to involve direct viral injury and cardiac damage due to the host’s immune response. Guidelines on the management of COVID-19-related myocarditis are yet to be established. We present here the case of a male patient in his early fifties admitted with life-threatening myocarditis in the course of COVID-19 infection who was successfully treated and recovered without any sequelae.
... An increase in hs-troponin alone cannot describe the incidence of myocarditis; therefore, its increase can also result from microangiopathy and myocardial infarction [39]. Biopsy examinations show diffuse monocular infiltration or high viral loads by the SARS-CoV-2 virus [40,41]. However, limited infrastructure does not allow biopsies or CMR examinations to be carried out. ...
... In our study, myocardial injury assessment was performed based on CDC criteria. This statement is supported by various studies that show hs-troponin as a biomarker that is very useful in assessing myocardial injury, as well as studies that show hs-troponin as a gold standard for the early diagnosis of cardiac complications with good clinical relevance [40,41]. Hs-troponin is even able to assess subclinical myocardial inflammation, which helps determine early treatment and assess the prognostics of cardiac complications in patients with COVID-19 [40]. ...
... Subclinical myocardial dysfunction was reported in 79% of COVID-19 patients who underwent a strainimaging examination using speckle-tracking echocardiography (GLS). Therefore, the use of these two parameters simultaneously needs to be analyzed in diagnosing myocarditis [41]. ...
Background. Myocardial involvement among critically ill patients with coronavirus disease 2019 (COVID-19) often has worse outcomes. An imbalance in the oxygen supply causes the excessive release of pro-inflammatory cytokines, which results in increased ventilation requirements and the risk of death in COVID-19 patients.
Purpose. We evaluated the association between the hs-troponin I levels and global longitudinal strain (GLS) as evidence of myocardial involvement among critical COVID-19 patients.
Methods. We conducted a prospective cohort study from 1 February to 31 July 2021 at RSUD Dr. Soetomo, Surabaya, as a COVID-19 referral center. Of the 65 critical COVID-19 patients included, 41 (63.1%) were men, with a median age (interquar-tile range) of 51.0 years (20.0-75.0). Subjects were recruited based on WHO criteria for severe COVID-19, and myocardial involvement in the form of myocarditis was assessed using CDC criteria. Subjects were examined using echocardiography to measure the GLS, and blood samples were taken to measure the hs-troponin. Subjects were then followed for their need for mechanical ventilation and in-hospital mortality.
Results. Severe COVID-19 patients with cardiac injury were associated with an increased need for intubation (78.5%) and an increased incidence of myocarditis (50.8%). There was a relationship between the use of intubation and the risk of death in patients (66.7% vs. 33.3%, p-value < 0.001). Decreased GLS and increased hs-troponin were associated with increased myocarditis (p values < 0.001 and 0.004, respectively). Decreased GLS was associated with a higher need for mechanical ventilation (12.17 + 4.79 vs. 15.65 + 4.90, p-value = 0.02) and higher mortality (11.36 + 4.64 vs. 14.74 + 4.82; p-value = 0.005). Elevated hs-troponin was associated with a higher need for mechanical ventilation (25.33% vs. 3.56%, p-value = 0.002) and higher mortality (34.57% vs. 5.76%, p-value = 0.002).
Conclusions. Critically ill COVID-19 patients with myocardial involvement and elevated cardiac troponin levels are associated with a higher need for mechanical ventilation and higher mortality.
... An increase in hs-Troponin alone cannot describe the incidence of myocarditis, therefore its increase can also result from microangiopathy and myocardial infarction [34]. Biopsy examinations show diffuse monocular infiltration or high viral load by the SARS-CoV-2 virus [35,36]. However, limited infrastructure does not allow biopsy or CMR examinations to be carried out. ...
... In our study, myocardial injury assessment is performed based on CDC criteria. This statement is supported by various literature that showed hs-Troponin as biomarker that is very useful in assessing myocardial injury as well as studies by researchers that showed hs-Troponin as a gold standard for early diagnosis of cardiac complications with good clinical relevance [35,36]. Hs-Troponin is even able to assess subclinical myocardial inflammation which is helpful in determining early treatment and assessing the prognostics of cardiac complications in patient with COVID-19 [35]. ...
... Besides that, subclinical myocardial dysfunction was reported in 79% of COVID-19 patients who underwent strain imaging examination using speckletracking echocardiography (GLS). Therefore, the use of these two parameters simultaneously needs to be analyzed in diagnosing myocarditis [36]. ...
Myocardial involvement among critical patients with coronavirus disease 2019 (COVID-19) has a worse outcome. The occurrence of an imbalance in oxygen supply results in the release of pro-inflammatory cytokines which leads to increased ventilation support requirement and increase risk of mortality. Our aim was to evaluate the association between hs-Troponin I level and global longitudinal strain as evidence of myocardial involvement among critical COVID-19 patients. Methods. We performed prospective cohort study from February 1st – July 31st, 2021 at Dr. Soetomo General Hospital, Surabaya as referral center for COVID-19 care. Of the 65 critical COVID-19 included, 41 (63.1%) were men, with a median (interquartile range) age of 51.0 years (20.0-75.0).Subjects were recruited according to WHO criteria for severe COVID-19 and CDC criteria for myocarditis. All subjects recruited were examined using echocardiography to measure global longitudinal strain (GLS) and blood samples were taken to measure hs-Troponin. Subjects were then followed to assess their needs for mechanical ventilation and in-hospital mortality. Severe COVID-19 subjects with cardiac injury were associated with an increased need for intubation (78.5%) and an increased incidence of myocarditis (50.8%). There was an association between the use of intubation and the risk of mortality in patients (66.7% vs. 33.3%, p-value <0.001). Both reduced GLS and increased hs-troponin are associated with increased myocarditis (p-value <0.001 and 0.004 respectively). Reduced GLS is associated with higher mechanical ventilation needs (12.17 + 4.79 vs.15.65 + 4.90, p-value 0.02) and a higher mortality rate (11.36 + 4.64 vs. 14.74 + 4.82; p-value 0.005). Increased hs-troponin is associated with higher mechanical ventilation needs (25.33% vs. 3.56%, p-value 0.002) and a higher mortality rate (34.57% vs. 5.76%, p-value 0.002). Compared with contemporary controls, critical COVID-19 patients with myocardial involvement and elevated cardiac troponin level are associated with higher mechanical ventilation needs and a higher mortality rate.
... In COVID-19, the determinants of disease severity and extrapulmonary complications (EPCs) are incompletely understood. Viremia, however, may predict the severity of COVID-19 and EPCs [8,9], i.e., the possible spread of virus to multiple tissues, including vascular endothelia [10,11], heart [12], kidneys [13], brain [14], and the endocrine system [15]. Some of these targets may act as virus reservoirs that consent the protracted replication of SARS-CoV-2 [16][17][18]. ...
Purpose
SARS-CoV-2 infection may be limited to the respiratory tract or may spread to multiple organs. Besides disease severity, factors associated with virus spread within the host are elusive. Here, we tried to identify features associated with SARS-CoV-2 spread to endocrine organs.
Methods
In a retrospective autoptic cohort of 51 subjects who died because of COVID-19, we analyzed the severity and type of lung pathology, patients’ features and the detection of virus in thyroid, testis, adrenal gland, pancreas, anterior pituitary, and the white adipose tissue (WAT).
Results
The SARS-CoV-2 genome was detected in endocrine organs of 30/51 cases. The anterior pituitary and WAT were most frequently positive for virus. While pathological features of lung were not associated with the presence of virus in endocrine organs, obesity (BMI > 30) was significantly associated to virus detection in pancreas (p = 0.01) and thyroid (p = 0.04). WAT infection was detected more frequently in males (p = 0.03).
Conclusion
In subject with obesity dying of COVID-19, the virus frequently spreads to endocrine organs. The findings emphasize the need for optimal treatment of patients with obesity at the very onset of COVID-19. Since post-COVID conditions remain a major issue worldwide, a rigorous follow-up of endocrine function—especially of thyroid and pancreas—is advocated in subjects with obesity.
... Accelerated viral replication, more severe inflammation, and cellular death are thought to be the causes of this dysfunction. Being an athlete was probably a contributing aspect as well [62,63]. ...
The repercussions of coronavirus disease 2019 (COVID-19) have been devastating on a global scale. Long COVID, which affects patients for weeks or even months after their initial infection, is not limited to individuals with severe symptoms and can affect people of all ages. The condition can impact various physiological systems, leading to chronic health conditions and long-term disabilities that present significant challenges for healthcare systems worldwide. This review explores the link between long COVID and cardiovascular complications such as myocardial injury and myocarditis. It also highlights the prevalence of these complications and identifies risk factors for their development in long COVID patients. Myocardial injury occurs due to direct cellular damage and T-cell-mediated cytotoxicity resulting in elevated cardiac biomarkers. Diagnostic techniques like electrocardiogram, troponin level testing, and magnetic
resonance imaging can help identify myocarditis, but endomyocardial biopsy is considered the gold-standard diagnostic technique. Guideline-directed medical therapy is recommended for COVID-19 myocarditis patients for better prognosis while being monitored under comprehensive care management approaches. Therefore, it's critical to develop effective screening techniques specifically for vulnerable populations while conducting further research that addresses the effects of long COVID on society's physical health.
... COVID-19 myocarditis and COVID-19 mRNA vaccine myocarditis can present with a variety of clinical symptoms including chest pain (97.34%), dyspnea (21.26%), body ache, myalgia, headache (15.61%) fever (37.54%), cough, chills, nausea, vomiting, lightheadedness and syncope. 8,33,34 COVID-19 mRNA vaccine myocarditis should be suspected in any young patient presenting with chest complaints within 48e96 h of vaccination. 4 Most cases of myocarditis (COVID-19 and mRNA vaccine) subside spontaneously and resolve without any sequelae. ...
According to recent epidemiological analysis, the percentage of world population infected with COVID-19 by end of December 2020 is approximately 12.56%1. COVID induced acute care and ICU hospitalization rates are around 9.22 (95% CI: 18.73-19.51), and 4.14 (95% CI: 4.10-4.18) per 1000 population1. Although therapeutic strategies such as antivirals, intravenous immunoglobulins and corticosteroids have shown modest efficacy in reducing the disease progression, they are not disease specific and only temper the immune mediated attack on the systemic tissues. Therefore, clinicians started to rely on mRNA COVID-19 vaccines, which are clinically efficacious in reducing the incidence, disease severity and systemic complications of COVID-19 infections. Nevertheless, usage of COVID-19 mRNA vaccines is also associated with cardiovascular complications such as myocarditis and pericarditis. On the other hand, COVID-19 infections itself are associated with cardiovascular complications such as myocarditis. The underlying signaling pathways for occurrence of COVID-19 and mRNA COVID-19 vaccine induced myocarditis are quite different although there is some overlap in autoimmunity and cross reactivity mechanisms. With media reports highlighting the cardiovascular complications of COVID-19 vaccines such as myocarditis, general population have become more hesitant and uncertain regarding the safety and efficacy of these mRNA vaccines. We plan to review the current literature and provide insights into their pathophysiological mechanisms for myocarditis and offer recommendations for further research studies in this regard. This will hopefully dispel some doubts and encourage more people to be vaccinated for preventing the risk of COVID-19 induced myocarditis and other associated cardiovascular complications.
... Risk factors associated with developing this condition were male sex and ever smoking, as well as low transfer capacity of the lung for carbon monoxide (T LCO ). A review focusing on post-COVID-19 myocarditis found that between 8% and 30% of patients showed myocarditis on cardiac MRI following infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [15]. The differences in disease severity, as well as whether the patients were hospitalised or not, and the criteria to define myocarditis on MRI, could explain the prevalence discrepancies. ...
It is a challenge to keep abreast of all the clinical and scientific advances in the field of respiratory medicine. This article contains an overview of laboratory-based science, clinical trials and qualitative research that were presented during the 2022 European Respiratory Society International Congress within the sessions from the five groups of the Assembly 1 – Respiratory clinical care and physiology. Selected presentations are summarised from a wide range of topics: clinical problems, rehabilitation and chronic care, general practice and primary care, electronic/mobile health (e-health/m-health), clinical respiratory physiology, exercise and functional imaging.
... Clinicians typically assess myocardial damage (ie, necrosis) by examining serum cardiac troponins. 30,31 However, myocarditis often occurs without necrosis so that the absence of elevated troponin does not rule out the presence of myocarditis, even severe myocarditis. 32,33 Potentially low SARS-CoV-2 infection may damage cardiomyocytes leading to cardiac myosin release and activation of resident APCs like mast cells and macrophages to recruit inflammation to the heart. ...
... Myocarditis and pericarditis/myopericarditis from COVID-19 present similarly to other forms of viral myocarditis and pericarditis, with symptoms including fever, cough, chest pain/pressure, dyspnea, palpitations, and syncope. 2,31 As for other causes of myocarditis, probable cases of COVID-19 myocarditis are diagnosed as ≥1 new or worsening clinical symptoms, as well as ≥1 of the following: arrhythmias on electrocardiogram, cardiac dysfunction using echocardiography, or cardiac magnetic resonance imaging (cMRI) indicative of myocarditis. 31,75 Confirmed diagnosis of myocarditis requires an endomyocardial biopsy (EMB), which was typically not conducted during the pandemic due to heightened concerns for viral transmission to staff. ...
... 2,31 As for other causes of myocarditis, probable cases of COVID-19 myocarditis are diagnosed as ≥1 new or worsening clinical symptoms, as well as ≥1 of the following: arrhythmias on electrocardiogram, cardiac dysfunction using echocardiography, or cardiac magnetic resonance imaging (cMRI) indicative of myocarditis. 31,75 Confirmed diagnosis of myocarditis requires an endomyocardial biopsy (EMB), which was typically not conducted during the pandemic due to heightened concerns for viral transmission to staff. 68,76 The diagnosis of myocarditis in patients with COVID-19, in general, relied more heavily on clinical symptoms and the presence of elevated troponins without evidence of coronary artery disease, especially in the United States where EMB is not typically acquired for lymphocytic myocarditis cases. ...
Viral infections are a leading cause of myocarditis and pericarditis worldwide, conditions that frequently coexist. Myocarditis and pericarditis were some of the early comorbidities associated with SARS-CoV-2 infection and COVID-19. Many epidemiologic studies have been conducted since that time concluding that SARS-CoV-2 increased the incidence of myocarditis/pericarditis at least 15× over pre-COVID levels although the condition remains rare. The incidence of myocarditis pre-COVID was reported at 1 to 10 cases/100 000 individuals and with COVID ranging from 150 to 4000 cases/100 000 individuals. Before COVID-19, some vaccines were reported to cause myocarditis and pericarditis in rare cases, but the use of novel mRNA platforms led to a higher number of reported cases than with previous platforms providing new insight into potential pathogenic mechanisms. The incidence of COVID-19 vaccine-associated myocarditis/pericarditis covers a large range depending on the vaccine platform, age, and sex examined. Importantly, the findings highlight that myocarditis occurs predominantly in male patients aged 12 to 40 years regardless of whether the cause was due to a virus-like SARS-CoV-2 or associated with a vaccine-a demographic that has been reported before COVID-19. This review discusses findings from COVID-19 and COVID-19 vaccine-associated myocarditis and pericarditis considering the known symptoms, diagnosis, management, treatment, and pathogenesis of disease that has been gleaned from clinical research and animal models. Sex differences in the immune response to COVID-19 are discussed, and theories for how mRNA vaccines could lead to myocarditis/pericarditis are proposed. Additionally, gaps in our understanding that need further research are raised.
... The mechanism of COVID-19 myocarditis is still not well understood [9,10]. Both direct myocyte injury during the cytokine storm as well as the binding of angiotensin-converting enzyme 2 (ACE2) spike protein on cardiomyocytes to induce myocyte injury, have been proposed as possible mechanisms of COVID-19 myocarditis [9,10]. ...
... The mechanism of COVID-19 myocarditis is still not well understood [9,10]. Both direct myocyte injury during the cytokine storm as well as the binding of angiotensin-converting enzyme 2 (ACE2) spike protein on cardiomyocytes to induce myocyte injury, have been proposed as possible mechanisms of COVID-19 myocarditis [9,10]. ...
... Clinical features of COVID-19 myocarditis include fever, chest pain, shortness of breath, palpitations, syncope, and arrhythmias. The symptoms of COVID-19 myocarditis are known to overlap with those of COVID-19-induced ARDS [9]. COVID-19 myocarditis is differentiated from ARDS primarily by characteristic features of acute heart failure, cardiogenic shock, or clinically significant ventricular arrhythmias [7,9]. ...
Coronavirus disease 2019 (COVID-19) myocarditis is a rare but serious complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and has been associated with high-case fatality. For a very long time, since the beginning of the pandemic, there were no definitive guidelines to diagnose and manage this condition, probably secondary to the gaps in understanding the exact pathophysiology of the disease. We present the case of a young, unvaccinated female, with no comorbidities, who had an aggressively progressive COVID-19 myocarditis that was fatal. The patient presented with exertional dyspnea of two days duration and was found to be tachycardic with a heart rate ranging between 130-150 beats per minute. A nasopharyngeal swab for SARS CoV-2 was positive and a bedside echocardiogram showed a low ejection fraction of 20%. Within hours of presenting, she experienced a rapid decompensation requiring intubation. Due to fulminant myocarditis with cardiogenic shock, the patient was planned for cardiac catheterization, Impella placement, and extracorporeal membrane oxygenation (ECMO) support. The cardiac catheterization revealed non-obstructive coronary arteries and the hemodynamics suggested biventricular failure. However, around the time of the cardiac catheterization procedure, she had two events of cardiac arrest with pulseless electrical activity and unfortunately could not be revived after the second arrest despite all resuscitative efforts.
