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.

Scientific rationale of Indian AYUSH Ministry advisory for COVID-19 prevention, prophylaxis, and immunomodulation

The current outbreak of COVID-19 is caused by the SARS-CoV-2 virus that has affected > 210 countries. Various steps are taken by different countries to tackle the current war-like health situation. In India, the Ministry of AYUSH released a self-care advisory for immunomodulation measures during the COVID-19 and this review article discusses the detailed scientific rationale associated with this advisory. Authors have spotted and presented in-depth insight of advisory in terms of immunomodulatory, antiviral, antibacterial, co-morbidity associated actions, and their probable mechanism of action. Immunomodulatory actions of advised herbs with no significant adverse drug reaction/toxicity strongly support the extension of advisory for COVID-19 prevention, prophylaxis, mitigations, and rehabilitation capacities. This advisory also emphasized Dhyana (meditation) and Yogasanas as a holistic approach in enhancing immunity, mental health, and quality of life. The present review may open-up new meadows for research and can provide better conceptual leads for future researches in immunomodulation, antiviral-development, psychoneuroimmunology, especially for COVID-19.Copyright © 2021, Institute of Korean Medicine, Kyung Hee University.

Frequency of Supraventricular Arrhythmias in COVID.19 Patients: A Single.Center Study

Background: Cardiac arrhythias had a significant association with the increased mortality rate in COVID-19 patients in hospitals. The present study aimed to evaluate the frequency of supraventricular arrhythmias in COVID-19 patients and to assess the echocardiographic parameters and inflammatory biomarkers in COVID-19 patients who developed supraventricular arrhythmias. Method(s): This cross-sectional study enrolled 196 patients, 33 of them developed supraventricular arrhythmias during hospitalization in Zagazig University isolation hospital. Result(s): There was a statistically significant association between the occurrence of atrial fibrillation (AF) and both oxygen saturation and lymphocyte percentage, which was significantly lower in those with AF. There was a statistically significant association between the occurrence of AF and CORADS, C-reactive protein (CRP), and interleukin-6, which were significantly higher in those with AF. Younger age and higher oxygen saturation decreased the risk of supraventricular tachycardia among the studied patients. Increasing oxygen saturation decreased the risk of AF among the studied patients, while higher CRP significantly increased risk by 1.045 folds. Conclusion(s): Atrial arrhythmias, especially with AF considered prevalent in cases with COVID-19. The atrial arrhythmias were correlated with higher cardiac injury and inflammatory markers and elevated severe COVID-19 clinical manifestations. Regarding mortality in-hospital, the association between COVID-19 and atrial arrhythmias was independent. 2023 Journal of Indian College of Cardiology.Copyright © 2023 Intervention, Journal of Mental Health and Psychosocial Support in Conflict Affected Areas.

On-Site Whole-Genome Sequencing of Sars-Cov-2 Reveals C3037t Mutation in Patient with Atrioventricular Nodal Reentry Tachycardia (Avnrt)

Intro: The spike protein of the SARS-CoV-2 virus targets the human cell receptor of angiotensin-converting enzyme (ACE2), including the myocardium and heart's conduction system. Patients diagnosed with COVID-19 have also been found to exhibit cardiac arrhythmia. Here, a whole-genome sequencing analysis using long-read sequencing was proposed to evaluate the virus genome in a patient who presented with AVNRT as a main presentation of COVID-19. Method(s): The sample was recovered from nasopharyngeal and oropharyngeal swab specimens of a 46-year-old female with no comorbidities who presented with palpitation, and ECG showed typical AVNRT features. The RT-qPCR of SARS- CoV-2 was confirmed positive with a CT-value of 15.82. The total RNAs were extracted and proceeded for RT-qPCR and proceeded with Oxford Nanopore Flongle sequencing. The genomics data of the virus was deposited in GISAID (EPI_ISL_3241561) and further analysed using online bioinformatics tools such as Nextclade CLI 2.3.0. Ethical approval (IREC 2021-080) for the study was obtained from IIUM Research Ethics Committee. Finding(s): Here, we reported a total of 29,775 bp near-complete whole-genome belonging to clade 21J (Delta) of AY.79 lineage (also known as B.1.617.2.79), which formed a dominant variant in Malaysia during the time of sampling. Discussion(s): While a previous study showed an association between Delta variant infection with fulminant myocarditis, the present study reported the benign AVNRT as the main presentation of SARS-CoV-2 infection. Furthermore, we observed the presence of the C3037T mutation previously described in the endomyocardial biopsy of a patient with persistent arrhythmia. Conclusion(s): Even though SARS-CoV-2 targets the respiratory tract, the present study supports the evidence that the ACE2 receptors are present in the heart. In addition, COVID19 is causing more and more damage to heart tissue, and viral transcription has been confirmed on cardiomyocytes. Further functional studies are needed to explore the associated mutations and their relation to cardiac manifestation.Copyright © 2023

Initial High Sensitivity Troponin I Values Predict 28 Day Survival in Coronavirus-19 Patients

Objectives: To determine the 28 day survival prognostic value of the initial Emergency Department (ED) high sensitivity cardiac troponin I (hs-cTnI) measurement in coronavirus-19 disease 2019 (COVID-19) patients. Background(s): Recent reports indicate that the presence of cardiac injury [troponin level > the 99th percentile upper reference limit (99th % URL) using mostly contemporary assays] is predictive of death within 30 days during hospitalization of COVID-19 patients. Troponin values ordered in the ED or after hospitalization were used for these analyses. Method(s): Using an ED centric electronic database of COVID-19 patients (nasopharyngeal swab testing within 1 week prior to or during the ED visit) having at least 1 hs-cTnI (Beckman Coulter, Brea, CA;level of quantitation (LoQ) 4ng/L, non sex specific 99th percentile URL 18 ng/L) value reported during a visit to an urban, academic ED in the United States. All patients were followed for 28 days to determine all-cause mortality. Kaplan Meir survival curves were constructed to compare outcomes amongst predetermined initial hs-cTnI value intervals. Result(s): From March 16-November 2, 2020 1476 consecutive ED COVID-19 patients were identified with 1044 (70.7%) having at least 1 hs-cTnI value resulted in the ED. Patients' mean age and body mass index were 60.8 +/- 16.1 years and 32.4 +/- 11.3 kg/m2 respectively. 531 (50.9%) were male, 804 (77.0%) self-identified as African American and 615 (58.9%) had 2 or more comorbidities with hypertension (42.5%), diabetes (37.4%) and hyperlipidemia (27.23%) commonest. Hs-cTnI interval values were: 147 (14.1%) < 4 (LoQ), 359 (34.4%) 4-10 and 151 (14.5%) 11-18 ng/L. Hs-cTnI values were > 99th % URL in 387 (37.1%) patients with 230 (22.0%) 19-54, 63 (6.0%) 54-99 and 94 (9.0%) = 100 (laboratory reported critical value) ng/L. 145 (13.9%) patients were discharged directly home and 2 (0.2%) died in the ED. 147 (14.1%) were admitted to an ICU with 104 (70.7%) dying. Each of the interval initial ED hs-cTnI values was associated with a different (p < 0.001) 28 day survival curve (Figure). Conclusion(s): Most COVID-19 patients had a hs-cTnI value obtained with 85.9% of these > 4 ng/L. No one with an initial hs-cTnI < 4 ng/L died within 28 days while increasing presenting hs-cTnI values > 4 ng/L were associated with decreased 28 day survival. Our findings indicate that in COVID-19 patients detectable initial ED hs-cTnI values, whether reaching thresholds for cardiac injury or not, are highly prognostic of 28 day survival.Copyright © 2023

Predictors and clinical consequences of heart damage in CMR in patients after COVID-19

Methods: Out-hospital clinic patients (pts) recovered from COVID-19 were prospectively recruited and underwent cardiac magnetic resonance (CMR) examination with a protocol including: Edema, hyperemia, and necrosis or scar-derived from signal intensity assessment in T2-weighted, early gadolinium enhancement (EGE) and late gadolinium enhancement (LGE) CMR images. Result(s): A total of 702 patients (mean age 50+/-12 years, 62% female) were included. The median (IQR) time interval between COVID-19 diagnosis and CMR was 13 (8-22) weeks. In none pts signs of edema, hyperemia and necrosis derived from signal intensity assessment in T2-weighted and early gadolinium enhancement was found. LGE was found in 152 (22%). LGE+ patients had significantly lower left ventricular (LV) ejection fraction (58.5+/-7.7 vs 61.1+/-7.9%, p<0.001) and greater LV end-diastolic (117.0+/-52.2 vs 103,0+/-36.3 ml, p=0.023) and end-systolic (50.3+/-28.0 vs 41.0+/-17.5 ml, p=0.010) volumes when compared with LGE- patients. In the resting electrocardiogram (ECG) fragmented QRS was observed significantly more frequently (46% vs 25%, p<0.001) in LGE+ group, whereas in 24h Holter ECG neither single premature, nor complex ventricular extrasystole burden did not differ between groups (p>0.05). There were observed no differences between symptoms of COVD-19 and comorbidities between LGE+ and LGE- pts. In the multivariable logistic regression analysis: Fragmented QRS [OR and 95% CI: 2.85 (1.93-4.21)] and any ST-T segment deviation in resting ECG [OR: 1.93 (1.15-3.25)] were identified as independent predictors of LGE, even after adjustment for comorbidities and COVID-19 symptoms. Conclusion(s): 1. In patients with fibrosis after COVID-19 reduced left ventricular ejection fraction and greater volume of the heart was found. 2. Fragmented QRS and ST-T abnormalities were independent predictors for LGE in patients after COVID-19.

Lung damage syndromes and extra-respiratory complications at evolutionary stages of SARS-CoV- 2 infection in children

Background: Aim: Study of lung damage syndromes and extra-respiratory complications in children with CoV-2 infection. Method(s): The study included 53children with CoV-2 infection and were evaluated clinically to identify the evolutionary consequences of these diseases. Laboratory tests, pulmonary CT, brain CT, EcoCG were performed. Diagnostic tests to confirm CoV-2: RT PCR-test and/or serological tests for IgM, IgG Ab to CoV-2. Result(s): COVID-19 infection was confirmed by RT PCR test in 79.2%(CI51.7%-78.5%) children, and in 20.8%(CI 10.8%-34.1%) cases by IgM and IgG Ab to SARS-CoV- 2 virus. The mean age of the patients -6.03+/- 5.68. Respiratory manifestations at the COVID-19 stage had of 81.5% children (bronchitis -14.8%, pneumonia -62.9%), and the evolutionary stages were detected pulmonary fibrosis (30.5%), atelectasis (30.5%), bronchiectasis (11.11%). COVID-19- associated neurological syndromes were found in 39.6% of children-migraine headache (9.4%), toxic encephalopathy (7.5%), psychotic disorders (3.8%), neurotic anorexia (1.9%), but also severe neurological complications -multifocal leukoencephalitis(5.7%), acute cerebellitis (3.8%), polyradiculoneuropathy (3.8%), epilepsy (1.9%). Signs of cardiovascular damage were reported in 21.2% of cases:bouts of tachycardia (7.7%), toxic heart disease (5.7%). Children with CHDs (7.7%) had severe heart failure in the post-Covid- 19 stages. Conclusion(s): Clinical manifestations in the evolutionary stages of Covid-19 in children are dominated by impaired respiratory system with signs of pulmonary fibrosis, atelectasis, which are often associated with neurological complications and sometimes with cardiovascular signs.

Novel coronavirus disease-19:An overviwe of pathogenesis, health influences and measures

The coronavirus disease-19 (COVID-19) signs mostly include fever and respiratory symptoms (unusual viral pneumonia by SARS-Coronaviruses 2 or SARS-CoV-2). The Receptor-Binding Domain (RBD) of COVID-19 and SARS-CoV are similar, causing cross-reactivity of anti-SARSCoV antibodies with associated spike protein, exerting promising implications for rapid development of vaccines and therapeutic antibodies against COVID-19. ACE2 is the SARS TMPRSS2 for spike (S) protein receptor for initiation of infection;hence, it is a target for pharmacological intervention. Furthermore, designing novel monoclonal antibodies binding specifically to COVID-19 RBD is essential. A viral S proteins (TMPRSS2) was proposed for clinical use by blocking the viral intake by cell.Copyright © 2020, Health Biotechnology and Biopharma. All rights reserved.

High sensitivity troponin I and newly/recently diagnosed coronavirus-19 disease patients presenting to the emergency department: Values above and below the 99th percentile predict 28 day mortality

Background: Studies indicate that the presence of cardiac injury [troponin level > the 99th percentile upper reference limit (99th % URL) using mostly contemporary assays] is predictive of death within 30 days during hospitalization of coronavirus disease 2019 (COVID-19) patients. Troponin measurements in these reports were ordered and/or resulted in the Emergency Department (ED) or during various times after hospital admission and not all patients were followed for 30 days. Purpose(s): Our objective was to determine the 28 day survival prognostic value of Emergency Department (ED) resulted high sensitivity cardiac troponin I (hs-cTnI) measurements in all COVID-19 patients including those discharged after their ED visit or hospitalization. Method(s): An ED centric electronic database of COVID-19 patients (nasopharyngeal swab testing within 1 week prior to or during the ED visit) having at least 1 hs-cTnI (Beckman Coulter, Brea, CA;level of quantitation (LoQ) 4ng/L, non sex specific 99th % URL 18 ng/L) value reported during a visit to an urban, academic ED in the United States was constructed. All patients were followed for 28 days and Kaplan Meir survival curves constructed amongst predetermined initial hs-cTnI value intervals. Result(s): From March 16-November 2, 2020 1476 consecutive ED COVID- 19 patients were identified with 1044 (70.7%) having at least 1 hs-cTnI value resulted in the ED. Patients' mean age and body mass index were 60.8+/-16.1 years and 32.4+/-11.3 kg/m2 respectively. 531 (50.9%) were male, 804 (77.0%) self-identified as African American and 615 (58.9%) had 2 or more comorbidities with hypertension (42.5%), diabetes (37.4%) and hyperlipidemia (27.23%) commonest. Frequent primary presenting complaints were shortness of breath (37.7%), fever/chills (14.5%) and cough (11.9%). Hs-cTnI interval values were: 147 (14.1%) <4 (LoQ), 359 (34.4%) 4-10 and 151 (14.5%) 11-18 ng/L. Hs-cTnI values were >99th % URL in 387 (37.1%) patients with 230 (22.0%) 19-54, 63 (6.0%) 54-99 and 94 (9.0%) >=100 (laboratory reported critical value) ng/L. 145 (13.9%) patients were discharged directly home and 2 (0.2%) died in the ED. 147 (14.1%) were admitted to an ICU with 104 (70.7%) dying. Each of the interval initial ED hs-cTnI values was associated with a different (p<0.001) 28 day survival curve. Conclusion(s): Most COVID-19 patients had a hs-cTnI value obtained with 85.9% of these >4 ng/L. No one with an initial hs-cTnI <4 ng/L died within 28 days while increasing presenting hs-cTnI values >4 ng/L were associated with decreased 28 day survival. Our findings indicate that in COVID-19 patients detectable initial ED hs-cTnI values, whether reaching thresholds for cardiac injury or not, are highly prognostic of 28 day survival. Studies are needed to better define how hs-cTnI values could alter early management of COVID-19 disease to improve outcomes for these patients. (Figure Presented).

The Relationship of In-Hospital Mortality with Cardiac Injury in COVID-19 Patients: A Retrospective Cohort Study

Objective: Coronavirus disease-2019 (COVID-19) emerged in late 2019 and has caused a pandemic, resulting in significant morbidity and mortality. However, the clinical significance of cardiac injury in patients affected by COVID-19 is still unknown. Therefore, our objective was to explore the association between cardiac injury and mortality in hospitalized patients with COVID-19. Material(s) and Method(s): The study included four hundred forty-three patients with laboratory values for troponin and follow-up. The mean age was 57.3+/-16.0 years. The male to female ratio was 1.53. Fever (45.6%) and cough (42.7%) were the most frequent sign and symptom at admission. Hypertension was the most common comorbidity, identified in 140 patients (31.6%). Result(s): In 143 (32.2%) patients, we determined cardiac injury. The median length of hospital stay was ten days. The mortality rate was 14.4%. The median length of hospital stay was longer in patients with cardiac injury (14 days vs. 9 days, respectively) (p<0.001). The mortality rate was 3.7% in the patients without cardiac injury, whereas the mortality rate was significantly higher among the patients with cardiac injury (37.7%, p<0.001). The multivariable model showed that cardiac injury was the only independent risk factor for death. There was a higher risk of death in patients with cardiac injury than in those without cardiac injury [hazard ratio, 4.01 (95% confidence interval, 1.85-8.72, p<0.001)]. Conclusion(s): In conclusion, cardiac injury is a common condition among hospitalized patients with COVID-19 and is associated with an elevated risk of in-hospital mortality. In addition, it is significantly more common in patients with known heart disease, complicating the treatment process.Copyright © 2022 by Turkiye Klinikleri.

Major adverse cardiovascular events are associated with necroptosis during severe COVID-19.

BACKGROUND: The mechanisms used by SARS-CoV-2 to induce major adverse cardiac events (MACE) are unknown. Thus, we aimed to determine if SARS-CoV-2 can induce necrotic cell death to promote MACE in patients with severe COVID-19. METHODS: This observational prospective cohort study includes experiments with hamsters and human samples from patients with severe COVID-19. Cytokines and serum biomarkers were analysed in human serum. Cardiac transcriptome analyses were performed in hamsters' hearts. RESULTS: From a cohort of 70 patients, MACE was documented in 26% (18/70). Those who developed MACE had higher Log copies/mL of SARS-CoV-2, troponin-I, and pro-BNP in serum. Also, the elevation of IP-10 and a major decrease in levels of IL-17ɑ, IL-6, and IL-1rɑ were observed. No differences were found in the ability of serum antibodies to neutralise viral spike proteins in pseudoviruses from variants of concern. In hamster models, we found a stark increase in viral titters in the hearts 4 days post-infection. The cardiac transcriptome evaluation resulted in the differential expression of ~ 9% of the total transcripts. Analysis of transcriptional changes in the effectors of necroptosis (mixed lineage kinase domain-like, MLKL) and pyroptosis (gasdermin D) showed necroptosis, but not pyroptosis, to be elevated. An active form of MLKL (phosphorylated MLKL, pMLKL) was elevated in hamster hearts and, most importantly, in the serum of MACE patients. CONCLUSION: SARS-CoV-2 identification in the systemic circulation is associated with MACE and necroptosis activity. The increased pMLKL and Troponin-I indicated the occurrence of necroptosis in the heart and suggested necroptosis effectors could serve as biomarkers and/or therapeutic targets. Trial registration Not applicable.

Mesenchymal Stem Cells: A Potent Cell Source for COVID-19

Coronaviruses are enveloped positive-stranded RNA viruses that cause mild to acute respiratory illness. Coronaviruses can merge envelope proteins with the host cell membranes and de-liver their genetic material. Coronavirus disease 2019 (COVID-19) is the seventh coronavirus clos-est to the severe acute respiratory syndrome (SARS) in bats that infects humans. COVID-19 at-tacks the respiratory system and stimulates the host inflammatory responses, promotes the recruit-ment of immune cells, and enhances angiotensin-converting enzyme 2 (ACE2) activities. Patients with confirmed COVID-19 have experienced fever, dry cough, headache, dyspnea, acute kidney injury (AKI), acute respiratory distress syndrome (ARDS), and acute heart injury. Several strategies such as oxygen therapy, ventilation, antibiotic or antiviral therapy, and renal replacement therapy are commonly used to decrease COVID-19-associated mortality. Inflammation is a common and important factor in the pathogenesis of COVID-19. In recent years, stem cell-based therapies represent a promising therapeutic option against various diseases. Mesenchymal stem cells (MSCs) are multipotent stem cells that can self-renew and differentiate into various tissues of mesodermal ori-gin. MSCs can be derived from bone marrow, adipose tissue, and umbilical cord blood. MSCs, with their unique immunomodulatory properties, represent a promising therapeutic alternative against diseases associated with inflammation. Several previous studies have shown that MSCs with a strong safety profile can improve the treatment of patients with COVID-19. The information in this review provides a summary of the prevention and diagnosis of COVID-19. Also, we focus on the current clinical application of MSCs for treatments of patients with COVID-19.Copyright © 2021 Bentham Science Publishers.

Adjuvant Therapies of COVID-19-A Literature Review

Background: Coronavirus disease 2019 (COVID-19) was originated first in Wuhan, Chi-na, in December 2019, and it is known to be caused by severe acute respiratory syndrome coron-avirus-2 (SARS CoV-2). The management of COVID-19 could be achieved by means of the usage of the repurposed drugs, inhibiting the viral entry and/or viral fusion such as umifenovir, Barici-tinib, Camostat mesylate, Nafamostat mesylate, and the drugs blocking the viral replication, which include favipiravir, remdesivir, Lopinavir/ritonavir, Ribavirin, Sofosbuvir, chloroquine and Hydrox-ychloroquine. Objective(s): Along with the drugs that target the SARS-CoV-2 virus, adjunctive therapies are also employed. This review focuses on the adjuvant therapies employed to manage the COVID-19-asso-ciated complications, such as cytokine storm, acute respiratory distress syndrome (ARDS), respiratory failure, cardiac injury, coagulopathy, and multi-organ failure. Method(s): The literature was searched in databases such as Medline/PubMed Central/PubMed, Goo-gle Scholar, Science Direct, EBSCO, Scopus, EMBASE, Directory of open access journals (DOA-J), and reference lists to identify relevant articles. Result(s): Various studies have been identified for the use of corticosteroids, interferons, monoclon-al antibodies, etoposide, ruxolitinib, anticoagulants, convalescent plasma, immunoglobulins, mes-enchymal stem cells, natural killer (NK) cells, and inhaled nitric oxide (NO) as adjuvant therapy to manage the patients with COVID-19 along with the repurposed drugs targeting SARS-CoV-2. Conclusion(s): The safety and efficacy of adjuvant therapy are needed to be confirmed by various ongoing randomized controlled clinical trials.Copyright © 2021 Bentham Science Publishers.

Long Term Sequale on COVID-19

Objective In 2021, accumulated coronavirus disease 2019 (COVID-19) confirmed cases exceeded 100 million worldwide. We sought the long term sequale on COVID-19. Design and Method Although there is a hope for vaccination, continuous infection is observed with case fatality rate over 2%. Patients with cardiovascular disease are more susceptible to COVID-19 and show more severe clinical course after the infection. COVID-19 related myocardial injury evidenced by increased troponin plasma levels occur in at least 10% of hospitalized patients and 25% to 35% or more, of critically ill patients. Patients with SARS-CoV-2 infection related cardiac complications are heart failure, arrhythmia, acute thrombosis, and stress induced cardiomyopathy. Results Myocardial injury is an important entity that cause long term sequale. The extent of the local tissue damage and cytokine storm triggered by the host immune response both contribute to the severity of the myocarditis. An exaggerated inflammatory response can be extremely fatal, and immunomodulators such as corticosteroids are considered in selected cases even though the efficacy and safety is questionable. Combined with these mechanisms related to a host immune response, multiple factors are responsible for the cardiac consequence of COVID-19, such as an oxygen supply and demand imbalance (with or without coronary artery disease), increased right ventricular afterload due to respiratory acidosis, hypoxemia and positive pressure ventilation. Even though it is difficult to discriminate all the possible mechanisms related to myocarditis, accordingly the effort to identify the dominant cause is necessary for the selection of the proper target treatment. Conclusions Substantial evidence has suggested a non-negligible incidence of cardiac injury related to COVID-19. Although the clinical significance and exact mechanisms are under investigation, we should be aware of the potentially fatal cardiac manifestations when dealing with patients with COVID-19. Long-term complications are also noticed from the recent publications and need further attention.

The role of NT-proBNP in patients discharged after COVID-19 pneumonia

The aim: of study was to define the cardiac disorders in the early post-COVID-19 period. Material(s) and Method(s): 85 patients(pts) (40 (47,1%) men, age - 44,2 (39,3;47,1)) were observed on 48,3 (45,0;56,2) days after the onset of COVID-19. The main group divided into 3 subgroups: 1 - 39 pts after moderate COVID19 pneumonia, 2 - 36 pts after severe COVID-19 pneumonia, 3 - 10 pts after critical COVID-19 pneumonia. All pts before COVID-19 had no anamnestic data of previous cardiovascular disease. For all pts were performed clinical data, SpO2, echocardiography and measured NT-proBNP in serum. Result(s): All pts had normal SpO2(Me 97,5 (96,3;98,8)%) and saved left ventricular ejection fraction (LVEF) (Me 62,3(60,2;74,3)%). Level of LVEF didn't differ significantly between subgroups (p>0,05). Nevertheless the LVEF, the level of NT-proBNP was significantly higher in patients of subgroup 2 and subgroup 3 (tabl.1), whereas concentration of NT-proBNP in subgroup 1 was not differ from norm (125 pg/ml). Note: *-p<0,01 on Mann-Witney. Conclusion(s): 1) pts after severe and critical COVID-19 pneumonia have high risk for cardiac disorders developing in the early post-COVID-19 period;2) the level of NT-proBNP is the independent predictor of cardiac lesion in early post-COVID-19 period, despite ejection function;3) determination of NT-proBNP is an important element to customize the most appropriate therapeutic strategies for pts after severe and critical COVID-19 pneumonia, not just performing echocardiography.

CLINICAL PHENOTYPES OF COVID-19 PNEUMONIA: different phases of viral process or really different states?

During COVID-19 pandemic cases of severe COVID-19 demonstrate heterogeneity among group of patients (pts): some pts are severe because of more expressed respiratory failure, other - because of inflammation, another - because of cardiac and thrombotic complications. Does it different phases of viral process or really different states? Aim: to estimate most valuable categories of pts with severe COVID-19 by separating of clinical phenotypes during cluster analysis. Material(s) and Method(s): 97 pts, who were hospitalized with severe COVID-19 pneumonia (male - 43 (44,3%), age - 58,8+/-1,4yrs, SpO2 - 91,1+/-0,7%). Measurements: clinical examination, SpO2, chest CT, laboratory: CBC, Creactive protein (CRP), D-dimer, Creatine Phosphokinase-MB (CPK-MB), Troponin I, ferritin. Result(s): nevertheless that all pts were severe, cluster analysis shown two heterogeneous groups: 1) with lower saturation and higher thromboinflammation, with lower lymphocytes;2) with higher saturation and lower thromboinflammation, with normal lymphocytes (p<0,002 for all) (Fig. 1). Conclusion(s): 1. Expression of respiratory failure in pts with severe COVID-19 is not an isolated parameter;it is connected with severity of thromboinflammation and cardiac lesion. 2. The estimation of CRP, D-dimer, CPK-MB, troponin I, ferritin can be use as predictors of severity in COVID-19 pneumonia, but the first and screening pathogenetical link is lymphopenia. (Figure Presented).

Cardiac Biomarkers in 2022 - A Vital Tool for Emergency Care

The role of cardiac biomarkers in diagnosing acute myocardial infarction is undoubted. In the 2020 guidelines of the European Society of Cardiology, the measurement of cardiac peptides to gain prognostic information has a class IIa indication in all patients with ACS. In emergency care, ruling out a non-ST elevation myocardial infarction requires documentation of normal levels of cardiac biomarkers, which remain stable or have very small variations within several hours. This review aims to summarize the current knowledge and recent progresses in the field of cardiac biomarker discovery, from their routine use in emergency rooms to their prognostic roles in modern risk assessment tools. Integrated approaches combining cardiac troponin with other biomarkers of ventricular dysfunction or inflammation, or with modern cardiac imaging in emergency care are also presented, as well as the role of modern algorithms for serial troponin measurement in the modern management of emergency departments.

ASSOCIATION OF ELECTROCARDIOGRAM FINDINGS WITH MORTALITY IN COVID-19 PATIENTS

Objective: The COVID-19 virus has greatly debilitated a lot of patients in the Philippines. Baseline demographic characteristics and other parameters such as baseline electrocardiographic (ECG) findings were investigated to act as predictors for mortality among admitted patients who are RT-PCR positive for COVID. This study aims to determine the association of baseline ECG findings including both normal and abnormal variants such as those suggestive of acute cardiac injury and hypertrophy with mortality of these patients. Design and method: This is a retrospective study of patients admitted from March 2020 to May 2021 who were diagnosed to have COVID-19 thru an RT-PCR swab. Inclusion criteria include a recorded baseline ECG. Demographic characteristics were also included. Patients were divided according to their ECG findings as normal and abnormal. Among those with abnormal ECG findings, they were further subdivided into those with ischemic changes, hypertrophy, and miscellaneous (bundle branch blocks). Results: A total of one hundred thirty-six (136) patients were included in this study. Among the abnormal ECG findings obtained, the miscellaneous group particularly those with right bundle branch block was noted to be associated with mortality (OR = 4.86, 95% CI 1.04-22.7, p = 0.044). Other ECG findings such as ischemic changes and hypertrophy showed no significant association. Conclusion: Among the different classifications of ECG findings, those with baseline ECG findings of right bundle branch block showed a positive association with mortality. Other parameters such as demographic features are also noted to have no association with mortality. Further investigation and a higher population number are suggested to further conclude these findings.

COVID-19 and Cardiac Complication: what is new?

Coronavirus disease 2019 (COVID-19) has been reported to cause cardiovascular complications such as myocardial injury, thromboembolic events, arrhythmia, and heart failure. Multiple mechanisms-some overlapping, notably the role of inflammation and IL-6-potentially underlie these complications. The reported cardiac injury may be a result of direct viral invasion of cardiomyocytes with consequent unopposed effects of angiotensin II, increased metabolic demand, immune activation, or microvascular dysfunction. Thromboembolic events have been widely reported in both the venous and arterial systems that have attracted intense interest in the underlying mechanisms. These could potentially be due to endothelial dysfunction secondary to direct viral invasion or inflammation. Additionally, thromboembolic events may also be a consequence of an attempt by the immune system to contain the infection through immunothrombosis and neutrophil extracellular traps. Cardiac arrhythmias have also been reported with a wide range of implicated contributory factors, ranging from direct viral myocardial injury, as well as other factors, including at-risk individuals with underlying inherited arrhythmia syndromes. Heart failure may also occur as a progression from cardiac injury, precipitation secondary to the initiation or withdrawal of certain drugs, or the accumulation of des-Arg9-bradykinin (DABK) with excessive induction of pro-inflammatory G protein coupled receptor B1 (BK1). The presenting cardiovascular symptoms include chest pain, dyspnoea, and palpitations. There is currently intense interest in vaccine-induced thrombosis and in the treatment of Long COVID since many patients who have survived COVID-19 describe persisting health problems. This review will summarise the proposed physiological mechanisms of COVID-19-associated cardiovascular complications. Copyright © 2022, Anka Publishers. All rights reserved.

Bioinformatic-based study on genes and micrornas predisposing Covid-19-related cardiovascular injuries

Background and Aim: Apart from the direct and immediate invasion of coronavirus to vital tissues such as the heart, the virus is also capable of damaging these tissues based on the host's genetic susceptibility. The present bioinformatic- based study aimed to determine the genes and related microRNAs that most likely to be associated with susceptibility rates for virus-induced cardiovascular vulnerabilities. Method(s): A deep search was scheduled in databases including Pubmed (Medline), Google Scholar, Web of Science, and Scopus databases to assess all microRNAs and targeted genes related to cardiovascular defects induced by the coronavirus. The bioinformatic professional software systems were employed to assess gene-microRNAs interactions and mechanisms involved in cardiovascular injury. Result(s): The coronavirus can induce cardiovascular defects by the three mechanisms of inducing cardiac fibrosis (by up-regulating miR-367-3p and down-regulating hsa-miR- 5692a), inducing hypertension (by up-regulating miR-18b- 5p), and inhibiting microvascular angiogenesis (by up-regulation of miR-18b-5p and down-regulating hsa-miR-5692a). Such processes can be triggered by the effects on NFAT5, CD69, and HGF expression. Conclusion(s): Considering the central role of the revealed microRNAs and their targeted genes in cardiovascular injuries induced by coronavirus, such microRNAs can be applied for finding a way to stabilize the host against virus attacks as well as genetically based treatment for the affected host. (Figure Presented).