Cardiac injury in children with COVID-19.

BACKGROUND: There is little known about the spectrum of cardiac injury in acute COVID-19 infection in children. METHODS: A single-centre, retrospective chart analysis was performed. The protocol was deemed IRB exempt. All patients under the age of 21 years admitted from 20 March, 2020 to 22 June, 2021 for acute symptomatic COVID-19 infection or clinical suspicion of multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19 were included. Past medical history, lab findings, echocardiogram and electrocardiogram/telemetry findings, and clinical outcomes were reviewed. RESULTS: Sixty-six patients with MIS-C and 178 with acute COVID-19 were reviewed. Patients with MIS-C had more cardiac testing than those with acute COVID-19. Inflammatory markers were more likely elevated, and function was more likely abnormal on echocardiogram in those with MIS-C with testing performed. Among patients with MIS-C, 17% had evidence of coronary dilation versus 0% in the acute COVID-19 group. One (0.6%) patient with acute COVID-19 had clinically significant electrocardiogram or telemetry findings, and this was in the setting of prior arrhythmias and CHD. Four (6%) patients with MIS-C had clinically significant findings on electrocardiogram or telemetry. Among patients with acute COVID-19, extracorporeal membrane oxygenation support was required in 0.6% of patients with acute COVID-19, and there was a 2.8% mortality. There were no deaths in the setting of MIS-C. CONCLUSIONS: Patients with acute COVID-19 and clinical suspicion of cardiac injury had a lower incidence of abnormal laboratory findings, ventricular dysfunction, or significant arrhythmia than those with MIS-C.

Multifaceted role of cardiovascular biomarkers.

Cardiovascular diseases, a global health issue, claim the lives of many every year. Lifestyle changes and genetic predisposition are the key drivers for the development of CVDs. In many of the patients, the disease is detected at the end stage making heart transplantation the only treatment option. Hence every attempt should be made to identify the risk at an early stage and initiate preventive measures to improve the quality of their life. Biomarkers are one of the critical factors that aid in the early diagnosis of CVDs. More specific and highly sensitive biomarkers have been discovered lately and have been employed for prognosis and diagnosis of CVDs. The present review briefs about the various categories of cardiovascular biomarkers with emphasis on novel biomarkers and discusses the biomarkers employed for different purposes in CVDs. The biomarkers have also helped in identifying COVID-19 patients with increased risk for developing cardiovascular complications. Being non-invasive makes biomarkers advantageous over other methods for evaluating the pathophysiological status of CVDs.

Describing our experience with the effects of multisystem inflammatory syndrome in children with COVID-19 on the cardiovascular system.

Cardiac involvement with multisystem inflammatory syndrome in children can include coronary artery abnormalities, ventricular dysfunction, conduction abnormalities, arrhythmias, pericarditis, and myocarditis. We report the cardiac findings in 34 patients with multisystem inflammatory syndrome in children admitted to a single institution. We looked at patient age, sex, brain natriuretic peptide levels, troponin levels, ejection fraction, presence of pericardial effusion, valvular changes, need for inotropic agents, and electrocardiogram findings. Our data showed that elevated brain natriuretic peptide did not predict troponin elevation and vice versa. Additionally, troponin rise was not a reliable marker for decreased left ventricular ejection fraction. All changes tracked were proven to be transient and resolved after initiating steroids, Intravenous immune globulin (IVIG), and occasionally anakinra.

Inflammatory biomarkers and cardiac injury in COVID-19 patients.

Introduction: Cardiac injury has received considerable attention due to the higher risk of morbidity and mortality associated with coronavirus disease. However, in a developing country, there is a scarcity of data on cardiac injury in COVID-19 patients related to inflammatory biomarkers. Methods: Therefore, the present research retrospectively analyzes data from three territorial hospitals in Pakistan's Punjab province to investigate the potential impact of the cardiac injury on the mortality and severity of COVID-19-infected patients. We evaluated 2,051 patients between January 16 and April 18, 2022, with confirmed COVID-19. The in-hospital mortality recorded for the selected sample size was about 16.28%. Results: The majority of the participants were identified as male (64%) with a median age of 65 years. Also, fever, fatigue, and dyspnea were reported as common symptoms. An aggregate of 623 patients (30.38%) had a cardiac injury, and when these patients are compared to those without cardiac injury, the participants were significantly older and had more comorbidities with higher leukocyte counts, elevated levels of C-reactive protein, interleukin-6, procalcitonin, myohemoglobin, creatinine kinase-myocardial band, serum creatinine, high-sensitivity troponin-I, N-terminal pro-B-type natriuretic peptide had a significant amount of multiple ground-glass opacity and bilateral pulmonary infiltration in radiographic results. Participants with heart injury required more non-invasive or invasive mechanical respiration than those who did not have a cardiac injury. Individuals with cardiac injury had higher rates of sepsis, acute respiratory distress syndrome (ARDS), d-dimer concentration, and respiratory failure than those without cardiac injury. Patients who had had a cardiac injury died at a higher rate than those who had not suffered cardiac damage. In the multivariable logistic regression analysis, participants with cardiac injury showed greater odds of COVID-19 mortality and were found associated with older age (OR = 1.99, 95% CI = 0.04-3.19), elevated cardiac troponin I (OR = 18.64, 95% CI = 13.16-23.01), the complication of sepsis (OR = 10.39, 95% CI = 7.41-13.39) and ARDS (OR = 6.65, 95% CI = 4.04-8.91). Conclusion: Cardiac injury is a frequent complication among patients with coronavirus-induced infection in Punjab, Pakistan, and it is significantly linked to a greater risk of in-hospital mortality.

Evaluation of Cardiac Biomarkers and Expression Analysis of IL-1, IL-6, IL-10, IL-17, and IL-25 among COVID-19 Patients from Pakistan.

Coronavirus disease 19 (COVID-19) is caused by viral infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Where upregulation of several important biomarkers and multiple organ dysfunction occurs, this study aimed to evaluate the association of cardiac biomarkers and CS induced acute lung damage with disease severity and mortality in survival of COVID-19 patients. A total of 500 COVID-19 patients with elevated cardiac biomarkers were studied for the analysis of myocardial abnormality through cardiac enzymes, inflammatory biomarkers, and the expression analysis of various cytokines, including IL-1, IL-6, IL-10, IL-17, and IL-25 genes. The elevation of various cardiac enzymes including LDH (87%), CK (78.4%), TNI (80.4%), CK-MB (83%), and D-dimer (80.8%) were found correlated (p < 0.001) with COVID-19 infection. Cardiac enzyme elevation was highly associated with an increased level of inflammatory biomarkers such as CRP (14.2%), SAA (11.4%) and erythrocyte sedimentation rate (ESR) (7.8%) (p = 0.001 for all). The quantitative expression analysis of IL-10, 1L-17, and 1L-25 were found to be high, while those of IL-1 and IL-6 were moderately elevated. The death-to-live ratio of COVID-19 patients was 457:43 indicating that the patients having elevated levels of both CKMB, D-dimer, CK and IL-1, IL-6, IL-10 and D-dimer, Troponin, CK and IL-1, IL-10 had high fatality rate (73% and 12% respectively). The current finding concludes that the evaluation of cardiac biomarkers with cytokine storm plays a significant role in COVID-19-associated anatomical organ damage, myocardial injury, and mortality. Physicians should pay special attention to cardiac biomarkers in patients with old age, inflammation, and comorbidities among COVID-19 infections.

Elucidating the Role of Cardiac Biomarkers in COVID-19: A Narrative Evaluation with Clinical Standpoints and a Pragmatic Approach for Therapeutics.

With the incidence of the unabated spreading of the COVID-19 (coronavirus disease 2019) pandemic with an increase in heart-related complications in COVID-19 patients, laboratory investigations on general health and diseases of heart have greater importance. The production of a higher level of clots in the blood in COVID-19 individuals carries a high risk of severe lethal pneumonia, pulmonary embolism, or widespread thromboembolism. The COVID-19 pandemic has raised awareness regarding the severe consequences for the cardiac system that might cause due to severe acute respiratory distress syndrome (SARS-CoV-2). COVID-19 causes acute respiratory distress syndrome (ARDS), acute myocardial infarction, venous thromboembolism, and acute heart failure in people with preexisting cardiac illness. However, as COVID-19 is primarily a respiratory infectious disease, there is still a lot of debate on whether and how cardiac biomarkers should be used in COVID-19 patients. Considering the most practical elucidation of cardiac biomarkers in COVID-19, it is important to note that recent findings on the prognostic role of cardiac biomarkers in COVID-19 patients are similar to those found in pneumonia and ARDS studies. The use of natriuretic peptides and cardiac troponin concentrations as quantitative variables should help with COVID-19/pneumonia risk classification and ensure that these biomarkers sustain their high diagnostic precision for acute myocardial infarction and heart failure. Serial assessment of D-dimers will possibly aid clinicians in the assortment of patients for venous thromboembolism imaging in addition to the increase of anticoagulation from preventive to marginally higher or even therapeutic dosages because of the central involvement of endothelitis and thromboembolism in COVID-19. Therefore, cardiac biomarkers are produced in this phase because of some pathological processes; this review will focus on major cardiac biomarkers and their significant role in COVID-19.

An overview of prognostic value of neurologic and cardiac biomarkers in patients with COVID-19 sequelae.

Many studies conducted after the pandemic period revealed that, while COVID-19 primarily injured the lungs, it also affects other organs in the form of cardiovascular complications, metabolic derangements, renal damage, and so on. Although we know that inflammatory cascades, complement activation, and pro-inflammatory cytokines are all involved in vasculitic processes that cause organ damage, we do not know the exact mechanism of complications such as acute respiratory distress syndrome (ARDS), cardiovascular ischemia, deep vein thrombosis, pulmonary thromboembolism, and brain injuries (embolism) that are frequently observed in COVID 19. The currently available biomarkers do not predict the severity of the aforementioned complications. As a result, more specific biomarkers such as serum calcium binding protein (S100B), glial fibrillary acid protein (GFAP), myelin basic protein (MBP), neuron-specific enolase (NSE), hs-TNI, (highly sensitive cardiac troponin) - HBDH, (Hydroxybutyrate Dehydrogenase), CK-MB (creatine kinase myocardial band), ST2 (suppression of tumorigenicity 2) are in need for early detection & improved clinical outcome.

Takotsubo Syndrome in the Emergency Room - Diagnostic Challenges and Suggested Algorithm

Takotsubo syndrome is an important condition to consider among patients with acute chest pain in the emergency room. It often mimics acute coronary syndrome since chest pain and ECG changes are key features in both conditions. The hallmark of takotsubo syndrome is transient left ventricular dysfunction (characterized by apical ballooning) followed by complete echocardiographic recovery in most cases. Although most patients exhibit a benign course, lethal complications may occur. The use of hand-held point-of-care focused cardiac ultrasound may be helpful for early identification of takotsubo syndrome and distinguishing it from acute coronary syndrome and other cardiovascular emergencies. Emergency room physicians should be familiar with typical and atypical presentations of takotsubo syndrome and its key electrocardiographic changes. The approach in the emergency room should be based on a combination the clinical presentation, ECG, and handheld echocardiography device findings, rather than a single electrocardiographic algorithm.

Cardiac biomarkers in COVID-19: a narrative review

The diagnosis and risk stratification of coronavirus disease 2019 (COVID-19) is primarily based on discretionary use of laboratory resources. Several lines of evidence now attest that cardiovascular disease not only is a frequent complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, but its pre-existence may increase the risk of morbidity, disability, and death in patients with COVID-19. To this end, routine assessment of biomarkers of cardiac injury (i.e., cardiac troponin I or T) and dysfunction (e.g., natriuretic peptides) has emerged as an almost essential practice in patients with moderate, severe, and critical COVID-19 illness. Therefore, this narrative review aims to provide an overview of cardiac involvement in patients with SARS-CoV-2 infection as well as the clinical background for including cardiac biomarkers within specific panels of laboratory tests for managing COVID-19 patients. © 2021 International Federation of Clinical Chemistry and Laboratory Medicine. All rights reserved.

Biomarkers Associated with Cardiovascular Disease in COVID-19.

Coronavirus disease-19 (COVID-19) emerged late December 2019 in the city of Wuhan, China and has since spread rapidly all over the world causing a global pandemic. While the respiratory system is the primary target of disease manifestation, COVID-19 has been shown to also affect several other organs, making it a rather complex, multi-system disease. As such, cardiovascular involvement has been a topic of discussion since the beginning of the COVID-19 pandemic, primarily due to early reports of excessive myocardial injury in these patients. Treating physicians are faced with multiple challenges in the management and early triage of patients with COVID-19, as disease severity is highly variable ranging from an asymptomatic infection to critical cases rapidly deteriorating to intensive care treatment or even fatality. Laboratory biomarkers provide important prognostic information which can guide decision making in the emergency department, especially in patients with atypical presentations. Several cardiac biomarkers, most notably high-sensitive cardiac troponin (hs-cTn) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), have emerged as valuable predictors of prognosis in patients with COVID-19. The purpose of this review was to offer a concise summary on prognostic cardiac biomarkers in COVID-19 and discuss whether routine measurements of these biomarkers are warranted upon hospital admission.

Cardiovascular Spectrum and Cardiac Biomarkers in Pediatric Inflammatory Multisystem Syndrome with Kawasaki-Like Disease-Our Experience During the COVID-19 Pandemic in the West Part of Romania

Aim. In COVID-19 Pandemic, a new hyperinflammatory syndrome was reported with clinical features of Kawasaki disease, named PIMS-TS. We want to present a single center experience where the patients were diagnosed with Kawasaki-like in PIMS-TS with cardiac affliction. Material and method: The study was observational and retrospective, enrolled 14 patients fulfilling the criteria of PIMS-TS with the median age of 9 (IQR, 1.6-11), 9 male (64.2 %) and 5 female (35.8 %). Results: ECG revealed tachycardia and ST-T changes in 60% of patients. In evolution, ECG modified in 20% and consisted of long QT in 7% of cases, bradycardia in 7%, 3% transitory sick sinus syndrome and 3% grade I/II Atrio-Ventricular block. Cardiac disfunction was evidenced in 4 patients (28%), with reduced ejection fraction under 50%, mitral insufficiency in 6 (42.8%), pericardial fluid in 8 (57.1%) and perivascular brightness in 8 (57.1%). The cardiac biomarkers: NT-proBNP (increased in 9), cTroponin T (increased in 7) and cTroponin I (increased in 5) confirmed heart dysfunction. During the hospitalization and under medical treatment, all the modifications recover. Evolution was good for 12 children. Conclusions: Cardiac dysfunction and myocardial injury were confirmed by elevated cardiac biomarkers. Rapid recognition allows prompt treatment for a good outcome. NT-proBNP, cTroponin T and I are of capital significance in monitoring the myocardial injury, the treatment and evolution of these patients. © 2021, MediaMed Publicis. All rights reserved.

Cardiac dysfunction and mortality in critically ill patients with COVID-19: A Swedish multicentre observational study.

BACKGROUND: The prevalence and importance of cardiac dysfunction in critically ill patients with COVID-19 in Sweden is not yet established. The aim of the study was to assess the prevalence of cardiac dysfunction and elevated pulmonary artery pressure (PAP), and its influence on mortality in patients with COVID-19 in intensive care in Sweden. METHODS: This was a multicentre observational study performed in five intensive care units (ICUs) in Sweden. Patients admitted to participating ICU with COVID-19 were examined with echocardiography within 72 h from admission and again after 4 to 7 days. Cardiac dysfunction was defined as left ventricular (LV) dysfunction (ejection fraction <50% and/or regional hypokinesia) or right ventricular (RV) dysfunction (defined as TAPSE <17 mm or visually assessed moderate/severe RV dysfunction). RESULTS: We included 132 patients, of whom 127 (96%) were intubated. Cardiac dysfunction was found in 42 (32%) patients. Most patients had cardiac dysfunction at the first assessment (n = 35) while a few developed cardiac dysfunction later (n = 7) and some changed type of dysfunction (n = 3). LV dysfunction was found in 21 and RV dysfunction in 19 patients, while 5 patients had combined dysfunction. Elevated PAP was found in 34 patients (26%) and was more common in patients with RV dysfunction. RV dysfunction and elevated PAP were independently associated with an increased risk of death (OR 3.98, p = .013 and OR 3.88, p = .007, respectively). CONCLUSIONS: Cardiac dysfunction occurs commonly in critically ill patients with COVID-19 in Sweden. RV dysfunction and elevated PAP are associated with an increased risk of death.

Improving risk prediction for pulmonary embolism in COVID-19 patients using echocardiography.

SARS-CoV-2 infection is associated with increased risk for pulmonary embolism (PE), a fatal complication that can cause right ventricular (RV) dysfunction. Serum D-dimer levels are a sensitive test to suggest PE, however lacks specificity in COVID-19 patients. The goal of this study was to identify a model that better predicts PE diagnosis in hospitalized COVID-19 patients using clinical, laboratory, and echocardiographic imaging predictors. We performed a cross-sectional study of 302 adult patients admitted to the Johns Hopkins Hospital (March 2020-February 2021) for COVID-19 infection who underwent transthoracic echocardiography and D-dimer testing; 204 patients had CT angiography. Clinical, laboratory and imaging predictors including, but not limited to, D-dimer and RV dysfunction were used to build prediction models for PE using logistic regression. Model discrimination was assessed using area under the receiver operator curve (AUC) and calibration using Hosmer-Lemeshow χ 2 statistic. Internal validation was performed. The prevalence of PE was 7.6%. The model with positive D-dimer above 5 mg/L, RV dysfunction on echocardiography, and troponin had an AUC of 0.77, and cross-validated AUC of 0.74. D-dimer (>5 mg/L) had a positive association with PE (adj odds ratio = 4.40; 95% confidence interval: [1.80, 10.78]). We identified a model including clinical, imaging and laboratory variables that predicted PE in hospitalized COVID-19 patients. Positive D-dimer >5, RV dysfunction on echocardiography, and troponin were important predictors for calculating likelihood of PE diagnosis. This approach may be useful to aid in clinical decision-making related to diagnostic imaging and treatment. Prospective studies are needed to evaluate impact on patient outcomes.

A close-up view of dynamic biomarkers in the setting of COVID-19: Striking focus on cardiovascular system.

Based on the recent reports, cardiovascular events encompass a large portion of the mortality caused by the COVID-19 pandemic, which drawn cardiologists into the management of the admitted ill patients. Given that common laboratory values may provide key insights into the illness caused by the life-threatening SARS-CoV-2 virus, it would be more helpful for screening, clinical management and on-time therapeutic strategies. Commensurate with these issues, this review article aimed to discuss the dynamic changes of the common laboratory parameters during COVID-19 and their association with cardiovascular diseases. Besides, the values that changed in the early stage of the disease were considered and monitored during the recovery process. The time required for returning biomarkers to basal levels was also discussed. Finally, of particular interest, we tended to abridge the latest updates regarding the cardiovascular biomarkers as prognostic and diagnostic criteria to determine the severity of COVID-19.

Prevalence and Outcomes Associated with Hyperuricemia in Hospitalized Patients with COVID-19.

INTRODUCTION: Coronavirus 2019 (COVID-19) can increase catabolism and result in hyperuricemia. Uric acid (UA) potentially causes kidney damage by alteration of renal autoregulation, inhibition of endothelial cell proliferation, cell apoptosis, activation of the pro-inflammatory cascade, and crystal deposition. Hyperuricemia in patients with COVID-19 may contribute to acute kidney injury (AKI) and poor outcomes. METHODS: We included 834 patients with COVID-19 who were >18 years old and hospitalized for >24 h in the Mount Sinai Health System and had at least 1 measurement of serum UA. We examined the association between the first serum UA level and development of acute kidney injury (AKI, defined by KDIGO criteria), major adverse kidney events (MAKE, defined by a composite of all-cause in-hospital mortality or dialysis or 100% increase in serum creatinine from baseline), as well as markers of inflammation and cardiac injury. RESULTS: Among the 834 patients, the median age was 66 years, 42% were women, and the median first serum UA was 5.9 mg/dL (interquartile range 4.5-8.8). Overall, 60% experienced AKI, 52% experienced MAKE, and 32% died during hospitalization. After adjusting for demographics, comorbidities, and laboratory values, a doubling in serum UA was associated with increased AKI (odds ratio [OR] 2.8, 95% confidence interval [CI] 1.9-4.1), MAKE (OR 2.5, 95% CI 1.7-3.5), and in-hospital mortality (OR 1.7, 95% CI 1.3-2.3). Higher serum UA levels were independently associated with a higher level of procalcitonin (ß, 0.6; SE 0.2) and troponin I (ß, 1.2; SE 0.2) but were not associated with serum ferritin, C-reactive protein, and interleukin-6. CONCLUSION: In patients admitted to the hospital for COVID-19, higher serum UA levels were independently associated with AKI, MAKE, and in-hospital mortality in a dose-dependent manner. In addition, hyperuricemia was associated with higher procalcitonin and troponin I levels.

A Novel Paradigm Based on ST2 and Its Contribution towards a Multimarker Approach in the Diagnosis and Prognosis of Heart Failure: A Prospective Study during the Pandemic Storm.

BACKGROUND: Acute heart failure (HF) represents an increasingly common and challenging presentation in the emergency room, also inducing a great socio-economic burden. Extensive research was conducted toward finding an ideal biomarker of acute HF, both in terms of sensitivity and specificity, but today practicians' interest has shifted towards a more realistic multimarker approach. Natriuretic peptides (NPs) currently represent the gold standard for diagnosing HF in routine clinical practice, but novel molecules, such as sST2, emerge as potentially useful biomarkers, providing additional diagnostic and prognostic value. METHODS: We conducted a prospective, single-center study that included 120 patients with acute HF and 53 controls with chronic HF. Of these, 13 patients (eight with acute HF, five from the control group) associated the coronavirus-19 disease (COVID-19). The diagnosis of HF was confirmed by a complete clinical, biological and echocardiographic approach. RESULTS: The serum levels of all studied biomarkers (sST2, NT-proBNP, cardiac troponin) were significantly higher in the group with acute HF. By area under the curve (AUC) analysis, we noticed that NT-proBNP (AUC: 0.976) still had the best diagnostic performance, closely followed by sST2 (AUC: 0.889). However, sST2 was a significantly better predictor of fatal events, showing positive correlations for both in-hospital and at 1-month mortality rates. Moreover, sST2 was also associated with other markers of poor prognosis, such as the use of inotropes or high lactate levels, but not with left ventricle ejection fraction, age, body mass index or mean arterial pressure. sST2 levels were higher in patients with a positive history of COVID-19 as compared with non-COVID-19 patients, but the differences were statistically significant only within the control group. Bivariate regression showed a positive and linear relationship between NT-proBNP and sST2 (r(120) = 0.20, p < 0.002). CONCLUSIONS: we consider that sST2 has certain qualities worth integrating in a future multimarker test kit alongside traditional biomarkers, as it provides similar diagnostic value as NT-proBNP, but is emerging as a more valuable prognostic factor, with a better predictive value of fatal events in patients with acute HF.

COVID-19 and Heart: From Clinical Features to Pharmacological Implications.

A highly pathogenic human coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been recently recognized in Wuhan, China, as the cause of the coronavirus disease 2019 (COVID-19) outbreak which has spread rapidly from China to other countries in the world, causing a pandemic with alarming morbidity and mortality. The emerging epidemiological data about COVID-19 patients suggest an association between cardiovascular diseases (CVD) and SARS-CoV-2 infection, in term of clinical features at hospital admission and prognosis for disease severity. The aim of our review is to describe the cardiological features of COVID-19 patients at admission, the acute cardiac presentation, the clinical outcome for patients with underlying CVD and the pharmacological implications for disease management.

Cardiac biomarkers, cardiac injury, and comorbidities associated with severe illness and mortality in coronavirus disease 2019 (COVID-19): A systematic review and meta-analysis.

AIMS: To explore the correlation between cardiac-related comorbidities, cardiac biomarkers, acute myocardial injury, and severity level, outcomes in COVID-19 patients. METHOD: Pubmed, Web of Science, Embase, CNKI, VIP, Wanfang, Cochrane Library databases, medRxiv, and Sinomed were reviewed systemically. Various types of clinical research reporting cardiac-related comorbidities, cardiac biomarkers including lactate dehydrogenase (LDH), troponin I (TnI), high sensitivity troponin I (hs-TnI), creatine kinase (CK), creatine kinase-MB (CK-MB), myoglobin (Myo), N-terminal pro-b-type natriuretic peptide (NT-proBNP) and acute cardiac injury grouped by severity of COVID-19 were included. Outcome measures were events and total sample size for comorbidities, acute cardiac injury, and laboratory parameters of these biomarkers. The study was performed with Stata version 15.1. RESULTS: Seventy studies, with a total of 15,354 cases were identified. The results showed that COVID-19's severity was related to cardiovascular disease. Similar odds ratios (ORs) were achieved in hypertension except for severe versus critical group (OR = 1.406; 95% CI, 0.942-2.097; p = .095). The relative risk (RR) of acute cardiac injury is 7.01 (95% CI, 5.64-8.71) in non-survivor cases. When compared with the different severity of cardiac biomarkers, the pool OR of CK, CK-MB, TnI, Myo and LDH were 2.683 (95% CI, 0.83-8.671; p = .106; I2 = 0%), 2.263 (95% CI, 0.939-5.457; p = .069), 1.242 (95% CI, 0.628-2.457; p = .534), 1.756 (95% CI, 0.608-5.071; p = .298; I2 = 42.3%), 1.387 (95% CI, 0.707-2.721;  p = .341; I2 = 0%) in the critical versus severe group, whose trends were not similar to other groups. The standard mean differences (SMD) of CK and TnI in the critical versus severe group were 0.09 (95% CI, -0.33 to 0.50; p = .685; I2 = 65.2%), 0.478 (95% CI, -0.183 to 1.138; p = .156; I2 = 76.7%), which means no difference was observed in the serum level of these indicators. CONCLUSION: Most of the findings clearly indicate that hypertension, cardiovascular disease, acute cardiac injury, and related laboratory indicators are associated with the severity of COVID-19. What is now needed are cross-national prospectively designed observational or clinical trials that will help improve the certainty of the available evidence and treatment decisions for patients.

Cardiac biomarkers and COVID-19: A systematic review and meta-analysis.

OBJECTIVE: To systematically investigate the relationship between cardiac biomarkers and COVID-19 severity and mortality. METHODS: We performed a literature search using PubMed, Web of Science, and Google Scholar. The standardized mean difference (SMD) and 95% confidence interval (CI) were applied to estimate the combined results of 67 studies. A meta-analysis of cardiac biomarkers was used to evaluate disease mortality and severity in COVID-19 patients. RESULTS: A meta-analysis of 7812 patients revealed that patients with high levels of cardiac troponin I (SMD = 0.81 U/L, 95% CI = 0.14-1.48, P = 0.017), cardiac troponin T (SMD = 0.78 U/L, 95% CI = 0.07-1.49, P = 0.032), high-sensitive cardiac troponin I (SMD = 0.66 pg/mL, 95% CI = 0.51-0.81, P < 0.001), high-sensitive cardiac troponin T (SMD = 0.93 U/L, 95% CI = 0.21-1.65, P = 0.012), creatine kinase-MB (SMD = 0.54 U/L, 95% CI = 0.39-0.69, P < 0.001), and myoglobin (SMD = 0.80 U/L, 95% CI = 0.57-1.03, P < 0.001) were associated with prominent disease severity in COVID-19 infection. Moreover, 9532 patients with a higher serum level of cardiac troponin I (SMD = 0.51 U/L, 95% CI = 0.37-0.64, P < 0.001), high-sensitive cardiac troponin (SMD = 0.51 ng/L, 95% CI = 0.29-0.73, P < 0.001), high-sensitive cardiac troponin I (SMD = 0.51 pg/mL, 95% CI = 0.38-0.63, P < 0.001), high-sensitive cardiac troponin T (SMD = 0.85 U/L, 95% CI = 0.63-1.07, P < 0.001), creatine kinase-MB (SMD = 0.48 U/L, 95% CI = 0.32-0.65, P < 0.001), and myoglobin (SMD = 0.55 U/L, 95% CI = 0.45-0.65, P < 0.001) exhibited a prominent level of mortality from COVID-19 infection. CONCLUSION: Cardiac biomarkers (cardiac troponin I, cardiac troponin T, high-sensitive cardiac troponin, high-sensitive cardiac troponin I, high-sensitive cardiac troponin T, creatine kinase-MB, and myoglobin) should be more frequently applied in identifying high-risk COVID-19 patients so that timely treatment can be implemented to reduce severity and mortality in COVID-19 patients.

Biomarkers of Cardiac Stress and Cytokine Release Syndrome in COVID-19: A Review.

PURPOSE OF REVIEW: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resulted in the coronavirus 2019 (COVID-19) global pandemic. While primarily a respiratory virus, SARS-CoV-2 can cause myocardial injury. The pattern of injury, referred to as acute COVID-19 cardiovascular syndrome (ACovCS), is defined by cardiac troponin leak in the absence of obstructive coronary artery disease. Although the etiology of the injury is unknown, many speculate that a cytokine release syndrome (CRS) may be an important factor. We aim to review recent data concerning markers of cardiac injury in ACovCS and its relation to the CRS. RECENT FINDINGS: Cardiac injury was common in patients hospitalized for COVID-19, with both cardiac troponin and B-type natriuretic peptide (BNP) being elevated in this population. Biomarkers were correlated with illness severity and increased mortality. Cytokines such as IL-6 were more often elevated in patients with ACovCS. Myocarditis evident on cardiac MR following COVID-19 may be associated with cardiac troponin levels. The impact of dexamethasone and remdesivir, two therapies shown to have clinical benefit in COVID-19, on myocardial injury is unknown. Biomarkers of cardiac stress and injury in COVID-19 may be used to stratify risk in the future. Currently, there is no evidence that inhibition of cytokine release will reduce myocardial injury in patients with COVID-19.