COVID-19 cardiac injury: is there a common approach to nosological classification?.

The literature review showed the main scenarios of SARS-CoV-2-associated myocardial injury. On the basis of the analysis of literature it can be concluded that myocardial lesion is multi-factor at COVID-19. Possible scenarios include direct damage to myocardium, development of acute systemic inflammatory response and cytokine storm, effects of acute respiratory distress syndrome, coagulopathy and electrolyte imbalance associated with COVID-19, as well as the toxic effects of drugs used in SARS-CoV-2 treatment schemes. At the same time, a rather vague concept - <<acute damage of myocardium>> - is often used to describe symptoms and laboratory changes in literature. Given the multifactor of myocardial lesions in COVID-19, the clinician often faces a difficult situation - the need for a nosological interpretation of the clinical status of the patient. Knowledge and correct verification of the leading pathogenetic variant of a heart injury can simplify this task, narrow the scope of diagnostic monitoring and organize a personalized approach to therapy.Copyright © 2022 Sinergia Press. All rights reserved.

Cardiovascular Complications of COVID-19: Risk, Pathogenesis and Outcomes

This book discusses the evidence behind the relationship between COVID-19 and heart disease based on emerging state-of-the-art data. The rapid and unexpected global spread of the COVID-19 has revealed proportional levels of cardiovascular and metabolic complications. A myriad of pathogenetic mechanisms has come to the surface. There is still much research required to define whether cardiovascular disease causes COVID-19 complications or that cardiovascular disease appears as a result of the infection and which mechanisms are responsible. With cardiovascular and metabolic diseases already at pandemic levels and expected to increase further, this book provides readers with an urgent and thorough analysis of this association. Cardiovascular Complications of COVID-19: Risk, Pathogenesis and Outcomes provides answers to the increasing numbers of questions related to heart disease in COVID-19, highlighting the association between these pandemics and including risk factors, mechanisms and how these may impact diverse patients populations. It describes how COVID-19 impacts older patients and those with metabolic illnesses such as obesity and diabetes mellitus, while providing an overview of the observed gender dichotomy among patients. It therefore represents an essential resource not only for all cardiovascular physicians but also for any healthcare professionals managing patients with these diseases or those exploring COVID-19. © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2022.

Cardiovascular complications of COVID-19 severe acute respiratory syndrome

603,711,760 confirmed cases of COVID-19 have been reported throughout the world and 6,484,136 individuals have died from complications of COVID-19 as of September 7, 2022. Significantly, the Omicron variant has produced the largest number of COVID-19 associated hospitalizations since the beginning of the pandemic. Cardiac injury occurs in >= 20% of the hospitalized patients with COVID-19 and is associated with cardiac dysrhythmias in 17 to 44%, cardiac injury with increases in blood troponin in 22 to 40%, myocarditis in 2 to 7%, heart failure in 4 to 21%, and thromboembolic events in 15 to 39%. Risk factors for cardiac complications include age >70 years, male sex, BMI =30 kg/m(2), diabetes, pre-existing cardiovascular disease, and moderate to severe pneumonia at hospital presentation. Patients with prior cardiovascular disease who contract COVID-19 and experience a significant increase in their blood troponin concentration are at risk for mortality rates as high as 69%. This review focuses on the prevalence, the pathophysiologic mechanisms of CoV-2 injury to the cardiovascular system and the current recommended treatments in hospitalized patients with COVID-19 in order that medical personnel can decrease the morbidity and mortality of patients with COVID-19 and effectively treat patients with Covid and post Covid syndrome.

Effect of troponin I and coagulation parameters on mortality in COVID-19 patients

Objective: Our aim is to determine the levels of troponin-I and some coagulation markers (D-dimer, fibrinogen and International Normalized Ratio (INR)) in coronavirus disease 2019 (COVID-19) patients and to investigate the effects of these markers on mortality.Patients and Method: It is planned as a descriptive, cross-sectional and analytical study. The study was conducted by retrospectively scanning the files of COVID-19 patients who applied to Inonu University Turgut Ozal Medical Center between 01.03.2020 and 31.12.2020. Levels of cardiac troponin I markers and coagulation parameters (D-dimer, fibrinogen and INR) were detected.Results: The results of a total of 1858 patients were obtained. One thousand, three hundred and twenty-six patients with only troponin I and D-dimer results (Group 1), 606 patients with only troponin I and fibrinogen results (Group 2), and 1308 patients with only troponin I and INR results (Group 3) were included. Troponin I levels were significantly higher in all patients who died. 96.6% of the patients with high D-dimer levels died in Group 1, 85.5% of the patients with high fibrinogen levels died in Group 2 and 77.3 % of the patients with high INR levels died in Group 3.Conclusion: Measurements of troponin-I and coagulation markers such as D-dimer, fibrinogen and INR can help predict clinical severity and mortality in COVID-19 patients.

Characteristics of COVID-19 patients with multiorgan injury across the pandemic in a large academic health system in the Bronx, New York.

Purpose: To investigate the evolution of COVID-19 patient characteristics and multiorgan injury across the pandemic. Methods: This retrospective cohort study consisted of 40,387 individuals tested positive for SARS-CoV-2 in the Montefiore Health System in Bronx, NY, between March 2020 and February 2022, of which 11,306 were hospitalized. Creatinine, troponin, and alanine aminotransferase were used to define acute kidney injury (AKI), acute cardiac injury (ACI) and acute liver injury, respectively. Demographics, comorbidities, emergency department visits, hospitalization, intensive care utilization, and mortality were analyzed across the pandemic. Results: COVID-19 positive cases, emergency department visits, hospitalization and mortality rate showed four distinct waves with a large first wave in April 2020, two small (Alpha and Delta) waves, and a large Omicron wave in December 2021. Omicron was more infectious but less lethal (p = 0.05). Among hospitalized COVID-19 patients, age decreased (p = 0.014), female percentage increased (p = 0.023), Hispanic (p = 0.028) and non-Hispanic Black (p = 0.05) percentages decreased, and patients with pre-existing diabetes (p = 0.002) and hypertension (p = 0.04) decreased across the pandemic. More than half (53.1%) of hospitalized patients had major organ injury. Patients with AKI, ACI and its combinations were older, more likely males, had more comorbidities, and consisted more of non-Hispanic Black and Hispanic patients (p = 0.005). Patients with AKI and its combinations had 4-9 times higher adjusted risk of mortality than those without. Conclusions: There were shifts in demographics toward younger age and proportionally more females with COVID-19 across the pandemic. While the overall trend showed improved clinical outcomes, a substantial number of COVID-19 patients developed multi-organ injuries over time. These findings could bring awareness to at-risk patients for long-term organ injuries and help to better inform public policy and outreach initiatives.

Wuhan 3 years after the outbreak of the pandemic-cardiological insights and perspectives.

In November 2019, Wuhan, a city in Central China, became the center of an outbreak of pneumonia of unknown cause, which was later named "coronavirus disease 2019" (COVID-19). COVID-19 is caused by the novel severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) infection. The emergence of novel SARS-CoV­2 strains and mutations exerted a serious global public health threat. Although various vaccines have been developed, specific anti-SARS-CoV­2 drugs are limited. As cardiologists, we believe that because SARS-CoV­2 can bind to the angiotensin 2 receptor on the surface of cardiomyocytes, it may also lead to cardiac injury. COVID-19-associated cardiac injury is not rare in clinical practice, and most of these cases are mild, while a few might progress to fulminant myocarditis (FM). Overactivated immune response and inflammatory storm represent the core pathogenesis of COVID-19-associated FM. Early identification and diagnosis of COVID-19-associated FM are critical for its treatment. Recently, Wuhan was hit by the Omicron variant again. We proposed managing COVID-19-associated cardiac injury according to the severity, which has had a significant effect on outcome.

Pathophysiology of Cardiac Injury in COVID-19 Patients with Acute Ischaemic Stroke: What Do We Know So Far?-A Review of the Current Literature.

With the onset of the COVID-19 pandemic, it became apparent that, in addition to pulmonary infection, extrapulmonary manifestations such as cardiac injury and acute cerebrovascular events are frequent in patients infected with SARS-CoV-2, worsening clinical outcome. We reviewed the current literature on the pathophysiology of cardiac injury and its association with acute ischaemic stroke. Several hypotheses on heart and brain axis pathology in the context of stroke related to COVID-19 were identified. Taken together, a combination of disease-related coagulopathy and systemic inflammation might cause endothelial damage and microvascular thrombosis, which in turn leads to structural myocardial damage. Cardiac complications of this damage such as tachyarrhythmia, myocardial infarction or cardiomyopathy, together with changes in hemodynamics and the coagulation system, may play a causal role in the increased stroke risk observed in COVID-19 patients. These hypotheses are supported by a growing body of evidence, but further research is necessary to fully understand the underlying pathophysiology and allow for the design of cardioprotective and neuroprotective strategies in this at risk population.

Characteristics of cardiac injury complicating with acute kidney injury and mortality risk in coronavirus disease 2019 (COVID-19) patients

Objectives: This study aimed to identify the clinical features of cardiac injury complicating with acute kidney injury (AKI) and its risk for a fatal outcome in patients infected with coronavirus disease 2019 (COVID-19) pneumonia. Methods: Initial signs and symptoms and clinical laboratory, radiological, and treatment information were obtained from seven hospitals in China from January 23, 2020, to March 15, 2020. Results: Of 438 patients, 36 (8.22%) displayed isolated cardiac injury, 17 (3.88%) had isolated AKI, and 17 (3.88%) displayed cardiac injury complicating with AKI. Compared with patients without cardiac injury or AKI, patients with isolated cardiac injury, isolated AKI, and cardiac injury complicating with AKI were older (55, 65, 74 vs. 48 years, P < 0.0001) and critically severe. More patients displayed fatigue, dyspnea, and comorbidities in the group with cardiac injury complicating with AKI. Moreover, the indexes reflecting myocardial, renal, liver, and coagulation dysfunctions and infection-related factors were significantly different among the four groups. After adjustment for covariates, patients with cardiac injury complicating with AKI had a higher hazard ratio for mortality (6.64;95% confidence interval, 1.51–29.30). Conclusion: Cardiac injury complicating with kidney injury significantly increased the risk for in-hospital mortality in COVID-19 pneumonia patients. Therefore, early detection at admission and careful monitoring of myocardial and renal injury through biomarkers during hospitalization is recommended to reduce the harm to patients.

The molecular mechanism of cardiac injury in SARS-CoV-2 infection: Focus on mitochondrial dysfunction.

BACKGROUND: Coronavirus disease 2019(COVID-19) caused a large number of infections worldwide. Although some patients recovered from the disease, some of the other problems that accompanied it, such as cardiac injury, could affect the patient's subsequent quality of life and prognosis. OBJECTIVES: To clarify the molecular mechanism of cardiac injury in SARS-CoV-2 Infection. METHODS: The RNA-Seq dataset (GSE184715) comparing expression profiling of Mock human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and SARS-CoV-2-infected hiPSC-CMs was downloaded from Gene Expression Omnibus (GEO). Differentially expressed genes(DEGs) were performed by the R software. Degs were analyzed by enrichment analysis to clarify the affected pathways. Hub genes were screened out by a PPI network constructed from Degs. Finally, Connectivity Map was used to screen for the treatment of COVID-19 induced cardiac injury. RESULTS: 2705 differentially expressed genes were identified. Enrichment analysis confirmed that mitochondrial dysfunction was caused by SARS-CoV-2, meanwhile, cardiac muscle contraction was suppressed and NF-κB was activated. Based on the PPI network, 15 hub genes were identified. These 15 down-regulated hub genes were mainly involved in the reduced activity of complexes in the mitochondrial respiratory chain associated with mitochondrial dysfunction. Moreover, 5 candidate drugs were identified to treat cardiac injury. CONCLUSION: In conclusion, SARS-CoV-2 infection of cardiomyocytes causes mitochondrial dysfunction, including reduced mitochondrial respiratory chain complex activity and decreased ATP synthesis, leading to cardiomyocyte apoptosis, while the activated NF-κB also induced cytokine storms, ultimately resulting in cardiac injury.

How Does COVID-19 Affect the Heart?

PURPOSE OF REVIEW: Cardiac consequences occur in both acute COVID-19 and post-acute sequelae of COVID-19 (PASC). Here, we highlight the current understanding about COVID-19 cardiac effects, based upon clinical, imaging, autopsy, and molecular studies. RECENT FINDINGS: COVID-19 cardiac effects are heterogeneous. Multiple, concurrent cardiac histopathologic findings have been detected on autopsies of COVID-19 non-survivors. Microthrombi and cardiomyocyte necrosis are commonly detected. Macrophages often infiltrate the heart at high density but without fulfilling histologic criteria for myocarditis. The high prevalences of microthrombi and inflammatory infiltrates in fatal COVID-19 raise the concern that recovered COVID-19 patients may have similar but subclinical cardiac pathology. Molecular studies suggest that SARS-CoV-2 infection of cardiac pericytes, dysregulated immunothrombosis, and pro-inflammatory and anti-fibrinolytic responses underlie COVID-19 cardiac pathology. The extent and nature by which mild COVID-19 affects the heart is unknown. Imaging and epidemiologic studies of recovered COVID-19 patients suggest that even mild illness confers increased risks of cardiac inflammation, cardiovascular disorders, and cardiovascular death. The mechanistic details of COVID-19 cardiac pathophysiology remain under active investigation. The ongoing evolution of SARS-CoV-2 variants and vast numbers of recovered COVID-19 patients portend a burgeoning global cardiovascular disease burden. Our ability to prevent and treat cardiovascular disease in the future will likely depend on comprehensive understanding of COVID-19 cardiac pathophysiologic phenotypes.

Cardiac Injury in COVID-19: A Systematic Review of Relevant Meta-Analyses

Background: Cardiac injury (CI) is not a rare condition among hospitalized patients with coronavirus disease 2019 (COVID-19). Its prognostic value has been extensively reported through the literature, mainly in the context of observational studies. An impressive number of relevant meta-analyses has been conducted. These meta-analyses present similar and consistent results;yet interesting methodological issues emerge. Methods: A systematic literature search was conducted aiming to identify all relevant meta-analyses on (i) the incidence, and (ii) the prognostic value of CI among hospitalized patients with COVID-19. Results: Among 118 articles initially retrieved, 73 fulfilled the inclusion criteria and were included in the systematic review. Various criteria were used for CI definition mainly based on elevated cardiac biomarkers levels. The most frequently used biomarker was troponin. 30 meta-analyses reported the pooled incidence of CI in hospitalized patients with COVID-19 that varies from 5% to 37%. 32 meta-analyses reported on the association of CI with COVID-19 infection severity, with only 6 of them failing to show a statistically significant association. Finally, 46 meta-analyses investigated the association of CI with mortality and showed that patients with COVID-19 with CI had increased risk for worse prognosis. Four meta-analyses reported pooled adjusted hazard ratios for death in patients with COVID-19 and CI vs those without CI ranging from 1.5 to 3. Conclusions: The impact of CI on the prognosis of hospitalized patients with COVID-19 has gained great interest during the pandemic. Methodological issues such as the inclusion of not peer-reviewed studies, the inclusion of potentially overlapping populations or the inclusion of studies with unadjusted analyses for confounders should be taken into consideration. Despite these limitations, the adverse prognosis of patients with COVID-19 and CI has been consistently demonstrated.

Increasing cardiac troponin-I level as a cardiac injury index correlates with in-hospital mortality and biofactors in severe hospitalised COVID-19 patients.

BACKGROUND: Severe acute respiratory syndrome coronavirus-2 raised in 2019 (COVID-19) affects the lung tissue and other organs, specifically the heart. METHODS: The current study evaluated 120 hospitalised patients with severe COVID-19 between March 2021 and February 2022. Patients' demographics, vital signs, electrocardiogram abnormalities, clinical laboratory tests, including troponin I (TPI), mortality, and discharge type, were recorded. RESULTS: Among the 120 hospitalised patients with severe COVID-19, 54 (45.0%) patients were male, with an average age of 63.2 ± 1.4. Many patients have chronic comorbidities, including hypertension (51.6%), diabetes mellitus (34.1%), and ischemic heart disease (17.5%). The in-hospital and six months after the discharge mortality were 45.8% and 21.5%, respectively. Cardiac injury was observed in 14 (11.7%) patients with a mean TPI level of 8.386 ± 17.89 µg/L, and patients with cardiac injury had higher mortality than those without cardiac injury (P < 0.001). Furthermore, the cardiac injury was meaningfully correlated with age (ρ = 0.182, P = 0.019), history of ischemic heart disease (ρ = 0.176, P = 0.05), hospitalisation result and mortality (ρ = 0.261, P = 0.004), inpatient in ICU (ρ = 0.219, P = 0.016), and serum levels of urea (ρ = 0.244, P = 0.008) and creatinine (ρ = 0.197, P = 0.033). Additionally, the discharge results were significantly correlated with oxygen saturation with (ρ = -0.23, P = 0.02) and without (ρ = -0.3, P = 0.001) oxygen therapy, D-dimer (ρ = 0.328, P = 0.019), LDH (ρ = 0.308, P = 0.003), urea (ρ = 0.2, P = 0.03), and creatinine (ρ = 0.17, P = 0.06) levels. CONCLUSION: Elevated TPI levels are associated with increased mortality in severe COVID-19 patients. Therefore, TPI may be a beneficial biofactor for early diagnosis of cardiac injury and preventing a high mortality rate.

Cardiac Magnetic Resonance Findings in Patients Recovered from COVID-19 Pneumonia and Presenting with Persistent Cardiac Symptoms: The TRICITY-CMR Trial.

The prevalence and clinical consequences of coronavirus disease 2019 (COVID-19)-related non-ischemic cardiac injury are under investigation. The main purpose of this study was to determine the occurrence of non-ischemic cardiac injury using cardiac magnetic resonance (CMR) imaging in patients with persistent cardiac symptoms following recovery from COVID-19 pneumonia. We conducted a single-center, cross-sectional study. Between January 2021 and May 2021, we enrolled 121 patients with a recent COVID-19 infection and persistent cardiac symptoms. Study participants were divided into those who required hospitalization during the acute phase of SARS-CoV-2 infection (n = 58; 47.9%) and those non-hospitalized (n = 63; 52.1%). Non-ischemic cardiac injury (defined as the presence of late gadolinium enhancement (LGE) lesion and/or active myocarditis in CMR) was detected in over half of post-COVID-19 patients (n = 64; 52.9%). LGE lesions were present in 63 (52.1%) and active myocarditis in 10 (8.3%) post-COVID-19 study participants. The majority of LGE lesions were located in the left ventricle at inferior and inferolateral segments at the base. There were no significant differences in the occurrence of LGE lesions (35 (60.3%) vs. 28 (44.4%); p = 0.117) or active myocarditis (6 (10.3%) vs. 4 (6.3%); p = 0.517) between hospitalized and non-hospitalized post-COVID-19 patients. However, CMR imaging revealed lower right ventricular ejection fraction (RVEF; 49.5 (44; 54) vs. 53 (50; 58) %; p = 0.001) and more frequent presence of reduced RVEF (60.3% vs. 33.3%; p = 0.005) in the former subgroup. In conclusion, more than half of our patients presenting with cardiac symptoms after a recent recovery from COVID-19 pneumonia had CMR imaging abnormalities indicating non-ischemic cardiac injury. The most common finding was LGE, while active myocarditis was detected in the minority of patients. CMR imaging abnormalities were observed both in previously hospitalized and non-hospitalized post-COVID-19 patients. Further research is needed to determine the long-term cardiovascular consequences of COVID-19 infection and the optimal management of patients with suspected post-COVID-19 non-ischemic cardiac injury.

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.

Pulmonary Involvement in SARS-CoV-2 Infection Estimates Myocardial Injury Risk.

Background and Objectives: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection represents a pathology with primary pulmonary involvement and multisystemic impact, including cardiovascular injuries. The present study aimed to assess the value of clinical, biochemical, and imaging factors in COVID-19 patients in determining the severity of myocardial involvement, and to create a model that can be used toevaluate myocardial injury risk based on clinical, biochemical and imaging factors. Materials and Methods: We performed an observational cohort study on 150 consecutive patients, evaluating their age, sex, hospitalization period, peripheral oxygen saturation (SpO2) in ambient air, systolic and diastolic blood pressure, heart rate, respiratory rate, biochemical markers of cardiac dysfunction (TnI, and NT-proBNP), inflammatory markers (C reactive protein (CRP), fibrinogen, serum ferritin, interleukin-6 (IL-6), tumor necrosis factor alpha (TNFα)), D-dimers, lactate dehydrogenase (LDH), myoglobin and radio-imaging parameters. All patients underwent computerized tomography chest scan in the first two days following admission. Results: We observed elevated heart and respiratory rates, higher systolic blood pressure, and a lower diastolic blood pressure in the patients with cardiac injury; significant differences between groups were registered in TnI, NT-proBNP, LDH, CRP, and D-dimers. For the radiological parameters, we found proportional correlations with the myocardial injury for the severity of lung disease, number of pulmonary segments with alveolar consolidation, number of pulmonary lobes with pneumonia, crazy paving pattern, type of lung involvement, the extent of fibroatelectatic lesions and the mediastinal adenopathies. Conclusions: Myocardial injury occurred in 12% of patients in the study group. Ground glass opacities, interstitial interlobular septal thickening (crazy paving pattern), fibroatelectasic lesions and alveolar consolidations on CT scan were correlated with myocardial injury. Routine lung sectional imaging along with non-specific biomarkers (LDH, D-dimers, and CRP) can be further valuable in the characterization of the disease burden, thus impacting patient care.

Colchicine for the Treatment of Cardiac Injury in Hospitalized Patients With Coronavirus Disease-19.

Introduction: The impact of colchicine on hospitalized patients with Coronavirus disease-19 (COVID-19) related cardiac injury is unknown. Materials and Methods: In this multicenter randomized controlled open-label clinical trial, we randomized hospitalized adult patients with documented COVID-19 and evidence of cardiac injury in a 1:1 ratio to either colchicine 0.6 mg po twice daily for 30 days plus standard of care or standard of care alone. Cardiac injury was defined as elevated cardiac biomarkers, new arrhythmia, new/worsened left ventricular dysfunction, or new pericardial effusion. The primary endpoint was the composite of all-cause mortality, need for mechanical ventilation, or need for mechanical circulatory support (MCS) at 90 days. Key secondary endpoints included the individual components of the primary endpoint and change in and at least 2-grade reduction in the World Health Organization (WHO) Ordinal Scale at 30 days. The trial is registered with clinicaltrials.gov (NCT04355143). Results: We enrolled 93 patients, 48 patients in the colchicine arm and 45 in the control arm. There was no significant difference in the primary outcome between the colchicine and control arms (19 vs. 15%, p = 0.78), nor in the individual components of all-cause mortality (17 vs. 15%, p = 1.0) and need for mechanical ventilation (8 vs. 5%, p = 0.68); no patients in either group required MCS. The change in (-1.8 ± 2.4 vs. -1.2 ± 2.0, p = 0.12) and at least 2-grade reduction (75 vs. 75%, p = 1.0) in the WHO ordinal scale was also similar between groups. Conclusion: Patients hospitalized with COVID-19 and evidence of cardiac injury did not benefit from colchicine therapy.

Immune-inflammatory biomarkers and the risk of cardiac injury in COVID-19 patients with diabetes: a retrospective cohort study.

BACKGROUND: To determine the risk-assessment role of the immune-inflammatory biomarkers on myocardial damage in COVID-19 patients with diabetes mellitus (DM). METHODS: This retrospective study was conducted on 822 COVID-19 inpatients from 1 January to 10 March 2020 at Renmin Hospital of Wuhan University. The demographic data, clinical data, and immune-inflammatory parameters of participants were collected. The predictors of cardiac injury were assessed by Logistics regression analysis. RESULTS: A total of 246 COVID-19 inpatients were diagnosed with DM (29.9%). The incidence of cardiac injury was higher in patients with DM than in non-DM cases (28.9% vs 9.0%, p < 0.001), even grouped by age, gender, and the level of fasting plasma glucose (FPG). The mortality in diabetic COVID-19 patients with cardiac injury and without cardiac injury was 42.9% and 3.4%, respectively (p < 0.001). COVID-19 patients with DM and cardiac injury presented a decreased number of immunocyte subsets, lower C3 concentration, and a higher level of interleukin-6 (IL-6) and immunoglobulin A (IgA). The independent risk factors for cardiac injury in COVID-19 patients with DM were CD3+CD4+ T cells counts ≤ 288 cells/µl (adjusted Odds ratio (OR), 2.501; 95% confidence interval (CI) 1.282-4.877; p = 0.007) and IL-6 > 25.68mpg/ml (adjusted OR, 4.345; 95% CI 2.192-10.374; p < 0.001) (all Pinteraction < 0.05). CONCLUSIONS: For diabetic patients with COVID-19, cardiac injury not only induce severer immune-inflammatory responses, but also increase in-hospital mortality. The decreased number of CD3+CD4+ T cells and increased IL-6 are recommended to distinguish the people who refer to high risk of cardiac injury and mortality from those persons. However, it remains a testable theory whether decision-making strategies based on the risk status of cardiac injury in COVID-19 patients, especially with DM, would be expected to get better outcomes.

The Usefulness of the C2HEST Risk Score in Predicting Clinical Outcomes among Hospitalized Subjects with COVID-19 and Coronary Artery Disease.

BACKGROUND: Even though coronary artery disease (CAD) is considered an independent risk factor of an unfavorable outcome of SARS-CoV-2-infection, the clinical course of COVID-19 in subjects with CAD is heterogeneous, ranging from clinically asymptomatic to fatal cases. Since the individual C2HEST components are similar to the COVID-19 risk factors, we evaluated its predictive value in CAD subjects. MATERIALS AND METHODS: In total, 2183 patients hospitalized due to confirmed COVID-19 were enrolled onto this study consecutively. Based on past medical history, subjects were assigned to one of two of the study arms (CAD vs. non-CAD) and allocated to different risk strata, based on the C2HEST score. RESULTS: The CAD cohort included 228 subjects, while the non-CAD cohort consisted of 1956 patients. In-hospital, 3-month and 6-month mortality was highest in the high-risk C2HEST stratum in the CAD cohort, reaching 43.06%, 56.25% and 65.89%, respectively, whereas in the non-CAD cohort in the high-risk stratum, it reached: 26.92%, 50.77% and 64.55%. Significant differences in mortality between the C2HEST stratum in the CAD arm were observed in post hoc analysis only for medium- vs. high-risk strata. The C2HEST score in the CAD cohort could predict hypovolemic shock, pneumonia and acute heart failure during hospitalization, whereas in the non-CAD cohort, it could predict cardiovascular events (myocardial injury, acute heart failure, myocardial infract, carcinogenic shock), pneumonia, acute liver dysfunction and renal injury as well as bleedings. CONCLUSIONS: The C2HEST score is a simple, easy-to-apply tool which might be useful in risk stratification, preferably in non-CAD subjects admitted to hospital due to COVID-19.

Is SARS-CoV-2 Directly Responsible for Cardiac Injury? Clinical Aspects and Postmortem Histopathologic and Immunohistochemical Analysis.

Myocardial injury in patients with SARS-CoV-2 infection may be attributed to the presence of the virus at the cellular level, however, it may also be secondary to other diseases, playing an essential role in the evolution of the disease. We evaluated 16 patients who died because of SARS-CoV-2 infection and analyzed the group from both clinical and pathological points of view. All autopsies were conducted in the Sibiu County morgue, taking into consideration all the national protocols for COVID-19 patients. Of the 16 autopsies we performed, two were complete, including an extensive examination of the cranial cavity. In our study, the cardiac injury was primarily cumulative. Chronic cardiac injuries included fatty infiltration of the myocardium in five cases, fibrosis in 11 cases, and coronary atherosclerosis in two cases. Among the cases with evidence of acute cardiovascular injuries, inflammatory lymphocytic infiltrate was observed in nine cases, subepicardial or visceral pericardial neutrophil-rich vascular congestion in five cases, and venous thrombosis in three cases. Acute ischemia or myocytic distress was identified by vacuolar degeneration in four cases; areas of undulated and/or fragmented myocardial fibers, with eosinophilia and nuclear pyknosis with or without enucleation of the myocytes in nine cases; and in one case, we observed a large area of myocardial necrosis. Immunohistochemical criteria confirmed the presence of the SARS-CoV-2 antigen at the level of the myocardium in only two cases. Comorbidities existing prior to SARS-CoV-2 infection associated with systemic and local inflammatory, thrombotic, hypoxic, or immunological phenomena influence the development of cardiac lesions, leading to death.

Prognostic significance of CHADS2 and CHA2DS2-VASc scores to predict unfavorable outcomes in hospitalized patients with COVID-19.

Introduction: Owing to the imposed burden of the coronavirus disease 2019 (COVID-19),the need for stratifying the prognosis of patients has never been timelier. Hence, we aimed to ascertain the value of CHADS2, CHA2DS2-VASc, and CHA2DS2-VASc-M (one point for male instead of female) scores to predict unfavorable outcomes in COVID-19 patients. Methods: We enrolled consecutive patients above 18 years of age with confirmed COVID-19,who were admitted between February 16 and November 1, 2020. The primary endpoint of this study was three-month all-cause mortality. The secondary endpoints were considered four major in-hospital clinical features, including acute respiratory distress syndrome, cardiac injury,acute kidney injury, and mechanical ventilation. Results: A total of 1,406 hospitalized COVID-19 patients were studied, among which 301(21.40%) patients died during the follow-up period. Regarding the risk scores, CHADS 2≥1,CHA2DS2-VASc≥2, and CHA2DS2-VASc-M≥2 were significantly associated with mortality. The performance of all risk scores for predicting mortality was satisfactory (area under the curve:0.668, 0.668, and 0.681, respectively). Appraising secondary endpoints, we found that all three risk scores were associated with increased risk of acute respiratory distress syndrome, cardiac injury, acute kidney injury, and mechanical ventilation. Lastly, we revealed that all risk scores were significantly correlated with serum levels of laboratory biomarkers. Conclusion: Our analysis illustrated that the CHADS2, CHA2DS2-VASc, and CHA2DS2-VASc-Mscores could aid prognostication of unfavorable outcomes in COVID-19 patients. Therefore,these easily calculable methods could be integrated into the overall therapeutic strategy to guide the COVID-19 management more accurately.