Acute Cardiac Injury Research Articles

Clinical characteristics and outcomes of COVID-19 critically ill patients

Background Medical information regarding critically ill coronavirus disease 2019 (COVID-19) patient course of disease and outcomes are fundamental to providing the best medical care and avoiding possible complications. Objective To evaluate the clinical characters, outcomes, and mortality risk factors in COVID-19 critically ill patients Patients and methods In our study, 31 adult ICU patients admitted to Sohag General Hospital and Health Insurance Hospital in Sohag Governorate were included from September 2020 to October 2020. Coronavirus was affirmed by an reverse transcriptase-PCR of a nasopharyngeal swab. Clinical information was separated from clinical sheets. Results The mean age of the patients was 60 years, 61.3% were males, 64.5% had comorbidities, which were more in improved than dead cases (P<0.04). The dead cases had a significantly longer symptom duration till ICU admission than the improved (P<0.0001). The improved cases had considerably higher oxygen saturation on admission than dead cases (P<0.02). Mechanical ventilation was indicated in eight out of 31 patients with a mean duration of 4±2.56 days and all of them died. Mortality rate was 41.9%. The dead cases needed a vasopressor therapy more than the improved (P<0.001). Acute respiratory distress syndrome was higher in the dead cases (P<0.003). Acute cardiac injury was higher in the dead cases (P<0.02). Conclusion Several predictors influence survival in COVID-19 critically ill patients including comorbidities, duration of symptoms till ICU admission, O2 saturation on admission, development of complication, and laboratory findings including ferritin, C-reactive protein, D-dimer, and thrombocytopenia on ICU admission.

Research advance in lipid nanoparticle-mRNA delivery system and its application in CAR-T cell therapy.

Chimeric antigen receptor (CAR) T cell therapy has shown significant efficacy for hematological malignancies, however, it needs to be further optimized. Recently, the lipid nanoparticle (LNP)-mRNA delivery system as a nonviral gene transfer vector has gained rapid progress in CAR-T cell therapy. The claudin-6 (CLDN6) mRNA is delivered to antigen presenting cells (APCs) through LNP system, thereby enhancing the function of CLDN6 CAR-T cells for the clearance of solid tumor cells. For treatment of acute cardiac injury, the fibroblast activation protein (FAP) CAR mRNA can be delivered to T cells through LNP system for the in vivo production of FAP CAR-T cells, thereby blocking the process of myocardial fibrosis. The LNP-mRNA delivery system has advantages including having no integration in host genome, inexpensiveness, low toxicity and modifiability; on the other hand, it has certain disadvantages such as limited cell persistence caused by transient protein expression and limitations in preparation techniques. This article reviews the research advance in LNP-mRNA in vivo delivery system and its application in CAR-T cell therapy.

THE ROLE OF PROSTHODONTICS IN VARIOUS CLINICAL SCENARIOS OF MUCORMYCOSIS: A REVIEW ARTICLE

Coronavirus disease 2019 (COVID-19) is a new disease thing caused by a unique coronavirus (SARS-CoV-2) first documented in China in December 2019 and subsequently causing a worldwide pandemic. COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been sweeping across the globe. During the current pandemic of COVID-19, acountless of manifestations and complications have emerged and are being reported on. There is anincidence of patients with COVID-19 who are at increased risk of acute cardiac injury, arrhythmias, thromboembolic complications like pulmonary embolism and acute stroke), and secondary infection to name a few.The frequency of fungal infections is increasing due to immunodeficiency viruses and immunosuppressive drugs. Candidiasis is the most common fungal infection of the oral cavity.Mucormycosis is an invasive fungal infection, often acute and extremely severe, occurring in patients with an underlying condition. Mucormycosis isproduced by saprophytic fungi of the order Mucorales. The estimated prevalence of mucormycosis is about70 times greater in India than that in global data. Diabetes mellitus is the most common risk factor, followed by hematological malignancy and solid-organ transplant.

Genetic alteration of human MYH6 is mimicked by SARS-CoV-2 polyprotein: mapping viral variants of cardiac interest

Acute cardiac injury has been observed in a subset of COVID-19 patients, but the molecular basis for this clinical phenotype is unknown. It has been hypothesized that molecular mimicry may play a role in triggering an autoimmune inflammatory reaction in some individuals after SARS-CoV-2 infection. Here we investigate if linear peptides contained in proteins that are primarily expressed in the heart also occur in the SARS-CoV-2 proteome. Specifically, we compared the library of 136,704 8-mer peptides from 144 human proteins (including splicing variants) to 9926 8-mers from all the viral proteins in the reference SARS-CoV-2 proteome. No 8-mers were exactly identical between the reference human proteome and the reference SARS-CoV-2 proteome. However, there were 45 8-mers that differed by only one amino acid when compared to the reference SARS-CoV-2 proteome. Interestingly, analysis of protein-coding mutations from 141,456 individuals showed that one of these 8-mers from the SARS-CoV-2 Replicase polyprotein 1a/1ab (KIALKGGK) is identical to an MYH6 peptide encoded by the c.5410 C > A (Q1804K) genetic variation, which has been observed at low prevalence in Africans/African Americans (0.08%), East Asians (0.3%), South Asians (0.06%), and Latino/Admixed Americans (0.003%). Furthermore, analysis of 4.85 million SARS-CoV-2 genomes from over 200 countries shows that viral evolution has already resulted in 20 additional 8-mer peptides that are identical to human heart-enriched proteins encoded by reference sequences or genetic variants. Whether such mimicry contributes to cardiac inflammation during or after COVID-19 illness warrants further experimental evaluation. We suggest that SARS-CoV-2 variants harboring peptides identical to human cardiac proteins should be investigated as “viral variants of cardiac interest”.

Persistent cardiac injury - An important component of long COVID-19 syndrome.

Persistent cardiac injury - An important component of long COVID-19 syndrome.

Sleep-Disordered Breathing Is Associated With Reduced Left Atrial Strain Measured by Cardiac Magnetic Resonance Imaging in Patients After Acute Myocardial Infarction.

AimsSleep disordered breathing (SDB) is known to cause left atrial (LA) remodeling. However, the relationship between SDB severity and LA dysfunction is insufficiently understood and may be elucidated by detailed feature tracking (FT) strain analysis of cardiac magnetic resonance images (CMR). After myocardial infarction (MI), both the left ventricle and atrium are subjected to increased stress which may be substantially worsened by concomitant SDB that could impair consequential healing. We therefore analyzed atrial strain in patients at the time of acute MI and 3 months after.Methods and Results40 patients with acute MI underwent CMR and polysomnography (PSG) within 3–5 days after MI. Follow-up was performed 3 months after acute MI. CMR cine data were analyzed using a dedicated FT software. Atrial strain (ε) and strain rate (SR) for atrial reservoir ([εs]; [SRs]), conduit ([εe]; [SRe]) and booster function ([εa]; [SRa]) were measured in two long-axis views. SDB was defined by an apnea-hypopnea-index (AHI) ≥15/h. Interestingly, LA εs and εe were significantly reduced in patients with SDB and correlated negative with AHI as a measure of SDB severity at both baseline and follow-up. Intriguingly, patients that exhibited a reduced AHI at follow-up were more likely to have developed improved atrial reservoir and conduit strain (linear regression, p=0.08 for εs and εe). Patients with improved SDB (ΔAHI < −5/h) exhibited a mean improvement of LA reservoir strain of +7.2 ± 8.4% whereas patients with SDB deterioration (ΔAHI> + 5/h) showed a mean decrease of −5.3 ± 11.0% (p = 0.0131). Similarly, the difference for LA conduit function was +4.8 ± 5.9% (ΔAHI < −5/h) vs −3.6 ± 8.8% (ΔAHI> +5/h). Importantly, conventional volumetric parameters for atrial function (LA area, LA volume index) did not correlate with AHI at baseline or follow-up.ConclusionOur results show that LA function measured by CMR strain but not by volumetry is impaired in patients with SDB during acute cardiac injury. Consistent with a mechanistic association, improvement of SBD at follow-up resulted in improved LA strain. LA strain measurement might thus provide insight into atrial function in patients with SDB.

Outcomes of Hospitalized Patients With COVID-19 With Acute Kidney Injury and Acute Cardiac Injury.

PurposeThis study investigated the incidence, disease course, risk factors, and mortality in COVID-19 patients who developed both acute kidney injury (AKI) and acute cardiac injury (ACI), and compared to those with AKI only, ACI only, and no injury (NI).MethodsThis retrospective study consisted of hospitalized COVID-19 patients at Montefiore Health System in Bronx, New York between March 11, 2020 and January 29, 2021. Demographics, comorbidities, vitals, and laboratory tests were collected during hospitalization. Predictive models were used to predict AKI, ACI, and AKI-ACI onset. Longitudinal laboratory tests were analyzed with time-lock to discharge alive or death.ResultsOf the 5,896 hospitalized COVID-19 patients, 44, 19, 9, and 28% had NI, AKI, ACI, and AKI-ACI, respectively. Most ACI presented very early (within a day or two) during hospitalization in contrast to AKI (p < 0.05). Patients with combined AKI-ACI were significantly older, more often men and had more comorbidities, and higher levels of cardiac, kidney, liver, inflammatory, and immunological markers compared to those of the AKI, ACI, and NI groups. The adjusted hospital-mortality odds ratios were 17.1 [95% CI = 13.6–21.7, p < 0.001], 7.2 [95% CI = 5.4–9.6, p < 0.001], and 4.7 [95% CI = 3.7–6.1, p < 0.001] for AKI-ACI, ACI, and AKI, respectively, relative to NI. A predictive model of AKI-ACI onset using top predictors yielded 97% accuracy. Longitudinal laboratory data predicted mortality of AKI-ACI patients up to 5 days prior to outcome, with an area-under-the-curve, ranging from 0.68 to 0.89.ConclusionsCOVID-19 patients with AKI-ACI had markedly worse outcomes compared to those only AKI, ACI and NI. Common laboratory variables accurately predicted AKI-ACI. The ability to identify patients at risk for AKI-ACI could lead to earlier intervention and improvement in clinical outcomes.

Identification of Crucial Genes and Key Functions in Type 2 Diabetic Hearts by Bioinformatic Analysis.

Type 2 diabetes (T2D) patients with SARS-CoV-2 infection hospitalized develop an acute cardiovascular syndrome. It is urgent to elucidate underlying mechanisms associated with the acute cardiac injury in T2D hearts. We performed bioinformatic analysis on the expression profiles of public datasets to identify the pathogenic and prognostic genes in T2D hearts. Cardiac RNA-sequencing datasets from db/db or BKS mice (GSE161931) were updated to NCBI-Gene Expression Omnibus (NCBI-GEO), and used for the transcriptomics analyses with public datasets from NCBI-GEO of autopsy heart specimens with COVID-19 (5/6 with T2D, GSE150316), or dead healthy persons (GSE133054). Differentially expressed genes (DEGs) and overlapping homologous DEGs among the three datasets were identified using DESeq2. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses were conducted for event enrichment through clusterProfile. The protein-protein interaction (PPI) network of DEGs was established and visualized by Cytoscape. The transcriptions and functions of crucial genes were further validated in db/db hearts. In total, 542 up-regulated and 485 down-regulated DEGs in mice, and 811 up-regulated and 1399 down-regulated DEGs in human were identified, respectively. There were 74 overlapping homologous DEGs among all datasets. Mitochondria inner membrane and serine-type endopeptidase activity were further identified as the top-10 GO events for overlapping DEGs. Cardiac CAPNS1 (calpain small subunit 1) was the unique crucial gene shared by both enriched events. Its transcriptional level significantly increased in T2D mice, but surprisingly decreased in T2D patients with SARS-CoV-2 infection. PPI network was constructed with 30 interactions in overlapping DEGs, including CAPNS1. The substrates Junctophilin2 (Jp2), Tnni3, and Mybpc3 in cardiac calpain/CAPNS1 pathway showed less transcriptional change, although Capns1 increased in transcription in db/db mice. Instead, cytoplasmic JP2 significantly reduced and its hydrolyzed product JP2NT exhibited nuclear translocation in myocardium. This study suggests CAPNS1 is a crucial gene in T2D hearts. Its transcriptional upregulation leads to calpain/CAPNS1-associated JP2 hydrolysis and JP2NT nuclear translocation. Therefore, attenuated cardiac CAPNS1 transcription in T2D patients with SARS-CoV-2 infection highlights a novel target in adverse prognostics and comprehensive therapy. CAPNS1 can also be explored for the molecular signaling involving the onset, progression and prognostic in T2D patients with SARS-CoV-2 infection.

Emerging Role of Platelet-Endothelium Interactions in the Pathogenesis of Severe SARS-CoV-2 Infection-Associated Myocardial Injury.

Cardiovascular dysfunction and disease are common and frequently fatal complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, from early on during the SARS-CoV-2 virus pandemic it was recognized that cardiac complications may occur, even in patients with no underlying cardiac disorders, as part of the acute infection, and that these were associated with more severe disease and increased morbidity and mortality. The most common cardiac complication is acute cardiac injury, defined by significant elevation of cardiac troponins. The potential mechanisms of cardiovascular complications include direct viral myocardial injury, systemic inflammation induced by the virus, sepsis, arrhythmia, myocardial oxygen supply-demand mismatch, electrolyte abnormalities, and hypercoagulability. This review is focused on the prevalence, risk factors and clinical course of COVID-19-related myocardial injury, as well as on current data with regard to disease pathogenesis, specifically the interaction of platelets with the vascular endothelium. The latter section includes consideration of the role of SARS-CoV-2 proteins in triggering development of a generalized endotheliitis that, in turn, drives intense activation of platelets. Most prominently, SARS-CoV-2–induced endotheliitis involves interaction of the viral spike protein with endothelial angiotensin-converting enzyme 2 (ACE2) together with alternative mechanisms that involve the nucleocapsid and viroporin. In addition, the mechanisms by which activated platelets intensify endothelial activation and dysfunction, seemingly driven by release of the platelet-derived calcium-binding proteins, SA100A8 and SA100A9, are described. These events create a SARS-CoV-2–driven cycle of intravascular inflammation and coagulation, which contributes significantly to a poor clinical outcome in patients with severe disease.

Clinical predictors of acute cardiac injury and normalization of troponin after hospital discharge from COVID-19.

SummaryBackgroundAlthough acute cardiac injury (ACI) is a known COVID-19 complication, whether ACI acquired during COVID-19 recovers is unknown. This study investigated the incidence of persistent ACI and identified clinical predictors of ACI recovery in hospitalized patients with COVID-19 2.5 months post-discharge.MethodsThis retrospective study consisted of 10,696 hospitalized COVID-19 patients from March 11, 2020 to June 3, 2021. Demographics, comorbidities, and laboratory tests were collected at ACI onset, hospital discharge, and 2.5 months post-discharge. ACI was defined as serum troponin-T (TNT) level >99th-percentile upper reference limit (0.014ng/mL) during hospitalization, and recovery was defined as TNT below this threshold 2.5 months post-discharge. Four models were used to predict ACI recovery status.ResultsThere were 4,248 (39.7%) COVID-19 patients with ACI, with most (93%) developed ACI on or within a day after admission. In-hospital mortality odds ratio of ACI patients was 4.45 [95%CI: 3.92, 5.05, p<0.001] compared to non-ACI patients. Of the 2,880 ACI survivors, 1,114 (38.7%) returned to our hospitals 2.5 months on average post-discharge, of which only 302 (44.9%) out of 673 patients recovered from ACI. There were no significant differences in demographics, race, ethnicity, major commodities, and length of hospital stay between groups. Prediction of ACI recovery post-discharge using the top predictors (troponin, creatinine, lymphocyte, sodium, lactate dehydrogenase, lymphocytes and hematocrit) at discharge yielded 63.73%-75.73% accuracy.InterpretationPersistent cardiac injury is common among COVID-19 survivors. Readily available patient data accurately predict ACI recovery post-discharge. Early identification of at-risk patients could help prevent long-term cardiovascular complications.FundingNone

COVID-19, hipertensión y enfermedad cardiovascular: una revisión narrativa

El SARS-CoV-2 ha provocado una pandemia emergente, que ha dominado el panorama de la salud pública. Al cuadro clínico característico de la COVID-19, se suman en determinados casos manifestaciones cardiovasculares, como lesión cardíaca aguda, insuficiencia cardíaca (IC), shock, arritmias, entre otras. El objetivo de la presente revisión es explorar el vínculo entre la COVID-19, la hipertensión y la enfermedad cardiovascular. Se realizó una búsqueda bibliográfica utilizando las bases de datos PubMed, Embase, China National Knowledge Infrastructure (CNKI), Chinese Scientific Journals Full-text Database (CQVIP). En términos generales se ha descrito que el SARS-CoV-2 consigue penetrar en las células por medio de la enzima convertidora de angiotensina 2, un participante significativo en el sistema renina angiotensina aldosterona y la modulación del sistema cardiovascular. En efecto, el uso de fármacos inhibidores de la enzima convertidora de angiotensina y antagonistas de los receptores de angiotensina II podría ocasionar un aumento de ACE2 y facilitar la entrada del virus. Por ello, resulta fundamental identificar a las personas con mayor riesgo para instaurar un tratamiento adecuado.

Cardiovascular System during SARS-CoV-2 Infection.

SARS-CoV-2 virus can not only damage the respiratory system but may also pose a threat to other organs, such as the heart or vessels. This review focuses on cardiovascular complications of COVID-19, including acute cardiac injury, arrhythmias, biomarkers, accompanying comorbidities and outcomes in patients diagnosed with SARS-CoV-2 infection. The research was conducted on the databases: PubMed, Springer, ScienceDirect, UpToDate, Oxford Academic, Wiley Online Library, ClinicalKey. Fifty-six publications from 1 November 2020 till 15 August 2021 were included in this study. The results show that cardiac injury is present in about 1 in 4 patients with COVID-19 disease, and it is an independent risk factor, which multiplies the death rate several times in comparison to infected patients without myocardial injury. New-onset cardiac injury occurs in nearly every 10th patient of the COVID-19-suffering population. Comorbidities (such as hypertension, cardiovascular disease and diabetes) severely deteriorate the outcome. Therefore, patients with SARS-CoV-2 infection should be carefully assessed in terms of cardiac medical history and possible cardiological complications.

Cardiac Manifestations in Patients with COVID-19: A Scoping Review.

Background:Coronavirus disease 2019 (COVID-19), commonly affects the lungs, but the involvement of other organs, particularly the heart, is highly prevalent as has been reported in several studies. The overall aim of this review was to provide an in-depth description of the available literature related to the cardiac system and COVID-19 infection. It focuses on type and the frequency of cardiac manifestations, clinical parameters and cardiac biomarkers that support the prognosis of COVID-19 patients, and the cardiac adverse events and outcomes related to pharmacotherapy.Methods:A scoping review was conducted searching Embase, PubMed, Epistomonikos, Medrxiv, BioRxiv databases, up to November 2020, for systematic reviews relevant to cardiac manifestations in adult COVID-19 patients. Relevant articles were screened and extracted to summarize key outcomes and findings.Results:A total of 63 systematic reviews met the inclusion criteria. The overall frequency of acute cardiac injury ranged from 15% to 33% in the reporting studies. The main cardiac complications were arrhythmias (3.1% to 6.9% in non-severe patients, 33.0% to 48.0% in severe disease), acute coronary syndromes (6% to 33% in severe disease), and myocarditis. Most studies found no association with the use of Renin-angiotensin-aldosterone system inhibitors (RAASI) with COVID-19 outcomes such as susceptibility to infection, hospitalization, severity, and mortality.Conclusion:This study provided an overview of the several cardiac complications associated with Covid-19. Cardiac injury, arrhythmias, myocarditis, cardiac failure, and acute coronary syndrome, are prevalent and clinically significant and associated with COVID-19 disease severity and mortality. Other studies are needed to clearly identify what is the part of viral heart infection and what is the part of cardiac injury secondary to acute respiratory failure and inflammation. In the therapeutic field, these systematic reviews gave heterogenous results. This underlines the importance of randomized trials to determine the right therapeutic approach.

Acute Myocardial Injury Assessed by High-Sensitive Cardiac Troponin Predicting Severe Outcomes and Death in Hospitalized Patients with COVID-19 Infection.

BackgroundCardiac injury has been linked to a poor prognosis during COVID-19 disease. Nevertheless, the risk factors associated are yet to be thoroughly investigated.ObjectivesWe sought to compare demographical characteristics and in-hospital outcomes in patients infected by the SARS-CoV-2 with and without cardiac injury, to further investigate the prevalence of acute cardiac injury as well as its impact on their outcomes in COVID-19-patients.MethodsWe included in a retrospective analysis, all COVID-19 patients admitted between October first and December first, 2020, at the University Hospital Center of Oujda (Morocco) who underwent a troponin assay which was systematically measured on admission. The study population was divided into two groups: cardiac-injured patients and those without cardiac injury. Clinical, biological data and in-hospital outcomes were compared between the two groups.Results298 confirmed COVID-19 cases were included. Our study found that compared to non-cardiac-injured, cardiac-injured patients are older, with higher possibilities of existing comorbidities including hypertension (68 [42.2%] vs 40 [29.2%], P = 0.02), diabetes (81 [50.3%] vs 53 [38.7%] P = 0.044), the need for mechanical ventilation, ICU admission and mortality. A Cox proportional hazards regression analysis shows a significantly increased risk of death among cardiac-injured COVID-19-patients as compared to non-cardiac injured. (HR, 1.620 [CI 95%: 2.562-1.024])ConclusionOur retrospective cohort found that old age, comorbidities, a previous history of CAD, were significantly associated with acute cardiac injury. COVID-19 patients with acute cardiac injury are at a higher risk of ICU admission, and death.

Mortality in patients with Coronavirus disease 2019 (COVID- 19) and its clinicoradiological and laboratory correlates: A retrospective study.

To delineate and analyze the mortality from COVID -19 in our institute during the devastating second wave of pandemic. A retrospective cohort analysis. A comprehensive mortality analysis of 142 laboratory-confirmed severe acute respiratory syndrome coronavirus 2-infected deceased patients from our hospital's medical records was done. These patients presented with severe disease at the time of admission and were managed in intensive care units. Statistical Package for Social Sciences software, IBM manufacturer, Chicago, USA, version 21.0 was used. The number of deceased males (82, 62.6%) was higher than females (53, 37.3%). Median age of deceased patient was 57 (44.25-69.75) years. Most frequent comorbidities were diabetes mellitus (42, 29.6%) and hypertension (41, 28.9%). Most common symptoms being shortness of breath (137, 96.5%), fever (94, 66.2%) and cough (73, 51.4%). Median peripheral capillary oxygen saturation (SpO2) at time of admission was 86% (77.25-90). Median time interval from symptom onset to admission in hospital was 3 (2.25-5) days. Neutrophil lymphocyte ratio was more than 5 in 117 (90.7%) patients. Complications seen were acute respiratory distress syndrome in 82.3%, acute liver injury in 58.4%, acute kidney injury in 26.7%, sepsis in 13.3% and acute cardiac injury in 12% patients. The median high-resolution computed tomography score was 20 (17-22). Male and elderly patients with underlying comorbidities had poorer outcome and involvement of multiple organ systems was common. A short time interval between symptom onset and admission/mortality, particularly encountered was worrisome.

Wnt4 is crucial for cardiac repair by regulating mesenchymal-endothelial transition via the phospho-JNK/JNK.

Rational: Wnt4 plays a critical role in development and is reactivated during fibrotic injury; however, the role of Wnt4 in cardiac repair remains unclear. In this study, our aim was to clarify the pathophysiological role and mechanisms of Wnt4 following acute cardiac ischemic reperfusion injury.Methods and results: We investigated the spatio-temporal expression of Wnt4 following acute cardiac ischemic reperfusion injury and found that Wnt4 was upregulated as an early injury response gene in cardiac fibroblasts near the injury border zone and associated with mesenchymal-endothelial transition (MEndoT), a beneficial process for revascularizing the damaged myocardium in cardiac repair. Using ChIP assay and in vitro and in vivo loss- and gain-of-function, we demonstrated that Wnt4 served as a crucial downstream target gene of p53 during MEndoT. Wnt4 knockdown in cardiac fibroblasts led to decreased MEndoT and worsened cardiac function. Conversely, Wnt4 overexpression in cardiac fibroblasts induced MEndoT in these cells via the phospho-JNK/JNK signaling pathway; however, both the p53 and Wnt4 protein levels were dependent on the β-catenin signaling pathway. JNK activation plays a critical role in the induction of MEndoT and is crucial for Wnt4 regulated MEndoT. Moreover, Wnt4 overexpression specifically in cardiac fibroblasts rescued the cardiac function worsening due to genetic p53 deletion by decreasing fibrosis and increasing MEndoT and vascular density.Conclusion: Our study revealed that Wnt4 plays a pivotal role in cardiac repair with involvement of phospho-JNK mediated MEndoT and is a crucial gene for cardiac fibroblast-targeted therapy in heart disease.

Troponin levels in COVID-19 patients and its correlation with the severity of disease and clinical outcomes

Introduction: The epidemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2) has become a major health problem globally. The most common cardiac manifestation of COVID-19 infection is acute cardiac injury observed in patients even without any prior cardiac comorbidities. It is seen that several patients positive for COVID-19 showed increased concentrations of cardiac troponin, which lead to confusion in clinical interpretation. Our study was performed to observe the correlation between elevated troponin levels with clinical outcomes and the severity of COVID-19 disease. Aim: To observe the correlation between elevated troponin levels with clinical outcomes and severity of COVID-19 disease. Materials and Methods: This was a cross-sectional study among 100 reverse transcription–polymerase chain reaction positive COVID-19 patients with measurement of troponin-I on the 1st and 5th days of admission. Results: The greatest number of deaths were reported in patients with troponin-I ≥ 0.39 ng/ml. Higher Troponin levels were seen in the elderly population. Higher Troponin Levels were also seen in severe diseases. Conclusion: The present study showed that higher troponin levels were associated with increased mortality in COVID-19 patients and higher values were observed with severe disease.

Persistent Troponin Elevation: Macrotoponin and Diagnostic Pathways for the Unexplainable Positive Troponin Result

Cardiac troponins are very sensitive biomarkers of myocardial injury and have a central role in the diagnosis of acute ischemic and inflammatory cardiac disease. It is increasingly recognized that the specificity of serum troponin assays for clinically important cardiac injury is affected by non-cardiac illnesses including sepsis and systemic inflammation, or by factors that can spuriously elevate the cardiac troponin assay. A less recognised cause of serum troponin elevation occurring in the absence of acute cardiac injury is macrotroponin.

Relationship between lung injury extent and phenotype manifested in non-contrast CT and cardiac injury during acute stage of COVID-19.

PurposeThis study evaluated the diagnostic values of the extent of lung injury manifested in non-contrast enhanced CT (NCCT) images, the inflammatory and immunological biomarkers C-reactive protein (CRP) and lymphocyte for detecting acute cardiac injury (ACI) in patients with COVID-19. The correlations between the NCCT-derived parameters and arterial blood oxygen level were also investigated.MethodsNCCT lung images and blood tests were obtained in 143 patients with COVID-19 in approximately two weeks after symptom onset, and arterial blood gas measurement was also acquired in 113 (79%) patients. The diagnostic values of normal, moderately and severely abnormal lung parenchyma volume relative to the whole lungs (RVNP, RVMAP, RVSAP, respectively) measured from NCCT images for detecting the heart injury confirmed with high-sensitivity troponin I assay was determined.ResultsRVNP, RVMAP and RVSAP exhibited similar accuracy for detecting ACI in COVID-19 patients. RVNP was significantly lower while both RVMAP and RVSAP were significantly higher in the patients with ACI. All of the NCCT-derived parameters exhibited poor linear and non-linear correlations with PaO2 and SaO2. The patients with ACI had a significantly higher CRP level but a lower lymphocyte level compared to the patients without ACI. Combining one of these two biomarkers with any of the three NCCT-derived parameter further improved the accuracy for predicting ACI in patients with COVID-19.ConclusionThe NCCT-delineated normal and abnormal lung parenchmyma tissues were statistically significant predictors of ACI in patients with COVID-19, but both exhibited poor correlations with the arterial blood oxygen level. The incremental diagnostic values of lymphocyte and CRP suggested viral infection and inflammation were closely related to the heart injury during the acute stage of COVID-19.

353 SARS-CoV-2 pulmonary vasculitis and Takotsubo myocarditis syndrome. Hypoxia, endothelial dysfunction, and inflammation are the trigger?

353 SARS-CoV-2 pulmonary vasculitis and Takotsubo myocarditis syndrome. Hypoxia, endothelial dysfunction, and inflammation are the trigger?