Risultati per: COVID-19, nuova guida per gastroenterologi

Circulation, Volume 150, Issue Suppl_1, Page A4145209-A4145209, November 12, 2024. Background:Acute decompensated heart failure accounts for an increasing proportion of hospitalizations in the United States and is linked to high readmission and 30-day mortality rates. Prior studies suggest up to 17% mortality rate within 30 days for patients admitted with heart failure.Research Questions/Hypothesis:We present an analysis characterizing patients who experienced mortality within 30 days of admission at a large safety net hospital following the COVID-19 pandemic.Methods/Approach:A retrospective review was conducted for all heart failure admissions of patients >18 years of age admitted to the coronary care unit (CCU) at Los Angeles General Medical Center from January to December 2021 after the peak of the COVID-19 pandemic. Demographics, insurance information, drug use, medication use, heart failure etiology, and CCU interventions were indexed. The primary outcome was all-cause mortality.Results/Data:172 patients were identified during the study period. 10% of patients died within 30 days of admission, of which 94% died during the same admission. Of patients who died during index admission, 88% had heart failure with reduced EF. None of these patients were on all four pillars of guideline-directed medical therapy (GDMT), with 33% on one or no GDMT medications.There was not a statistically significant difference in mortality rate when comparing those with active stimulant use 5/60 (8%) to those without active illicit drug use 12/112 (11%) (RR 0.79, 95% CI, p= 0.64).9/17 (53%) patients died of refractory cardiogenic shock, 5/17 (29%) were found in cardiopulmonary arrest of unknown etiology while undergoing treatment for acute decompensated heart failure. Two patients (12%) died of septic shock while 1/17 (5%) died of hemorrhagic shock related to chronic liver disease.Conclusion(s)The COVID-19 pandemic exacerbated significant healthcare inequalities, especially for urban underserved populations leading to late presentations of disease and worse outcomes, however, based on our data the overall inpatient mortality rate remained largely similar to pre-pandemic values.

Circulation, Volume 150, Issue Suppl_1, Page A4137534-A4137534, November 12, 2024. Background/Aim:We previously reported that late gadolinium enhancement (LGE) on cardiac MRI (CMR) was as high as 82% in pediatric patients with COVID-19 vaccine-associated myocarditis (C-VAM) despite mild clinical symptoms and normal left ventricular function. As LGE can be a harbinger for future adverse events including arrhythmias, heart failure or sudden cardiac death, we sought to identify predictors for LGE in C-VAM, specifically assessing troponin as a screening marker for C-VAM patients at risk for myocardial scarring who could then be referred for a confirmatory CMR with LGE.Methods:In this longitudinal multicenter retrospective observational study across 38 U.S. member institutions of theMyocarditisAfterCOVIDVaccination (MACiV) study network, 333 patients with C-VAM based on CDC criteria were included from April 2021 to November 2022. Data collected included demographics, laboratory values, clinical and cardiac imaging characteristics and outcomes. Using logistic regression, troponin levels at presentation were assessed as a log transformed continuous variable and categorized into tertiles.Results:The C-VAM patients were predominantly white (67%) adolescent males (91%, 15.7± 2.8 years). There were 216/333 (65%) patients who had both a reported troponin value and had a CMR. On univariate analysis, elevated troponin increased the probability of having LGE (OR=1.29, 95% CI: 1.06, 1.58, p=0.012). Even after controlling for age, race, sex, number of vaccine doses and left ventricular ejection fraction (OR=1.32, 95% CI: 1.06, 1.65, p=0.013). Patients >15 years compared to those ≤15 years of age were 2.94 (95% CI: 1.28, 6.75, p=0.011) times more likely to have LGE at presentation. Patients with troponin levels in the highest tertile compared to lowest tertile were 2.66 times (95% CI: 1.04, 6.83, p=0.042) more likely to have LGE along with a greater involvement > 4 AHA myocardial segments with LGE (p=0.004)Conclusions:Higher troponin values are associated with presence of late gadolinium enhancement on cardiac MRI in patients with COVID-19 vaccine-associated myocarditis. Troponin levels at presentation may facilitate risk stratification and function as a screening tool to identify those C-VAM patients with the greatest likelihood of myocardial scarring, who may benefit from undergoing CMR for tissue characterization.

Circulation, Volume 150, Issue Suppl_1, Page A4141333-A4141333, November 12, 2024. Background:COVID-19 is a multiorgan disease characterized by a prothrombotic state and increased risk of venous thromboembolism (VTE), especially in hospitalized patients. Although prior studies have attempted to identify predictors of VTE, restricted sample size and use of administrative claims data have limited such analyses. We conducted a multivariable analysis to identify predictors of VTE in hospitalized patients with COVID-19 in a multicenter patient-level registry.Methods:We utilized data from the CORONA-VTE Network, a US multicenter registry of 10,420 adult (≥18 years) patients with PCR-confirmed COVID-19 of whom 3,844 were hospitalized. The primary outcome was time-to-first-event for a composite of adjudicated pulmonary embolism and deep vein thrombosis (e.g. lower extremity, mesenteric, gonadal vein, etc.) during 90-day follow-up. The candidate variables were selected by a priori clinical consensus. The variables with ≥20% missing data were excluded, whereas those with missing data

Circulation, Volume 150, Issue Suppl_1, Page A4140585-A4140585, November 12, 2024. Introduction:Stroke-related mortality poses significant challenges in the US. Increased at-home deaths since COVID-19 pandemic prompted changes in the provision of end-of-life care.Question:What were the settings of stroke deaths in the US during COVID-19 pandemic?Methods:Decedent-level mortality data from death certificates in CDC repository were obtained for the year 2020 (pandemic) and 2019 (comparison). Demographic data include age, sex, race/ethnicity, education, marital status, and place of stroke death, including inpatient, outpatient/emergency room (ER), hospice/nursing facilities (H/NF), and at-home. Multivariable logistic regression models assessed demographic impact on stroke mortality by place-of-death, yielding odds ratios (OR) with significance threshold of p65 years were more likely to die in H/NF (OR 10.05, p

Circulation, Volume 150, Issue Suppl_1, Page A4142935-A4142935, November 12, 2024. Background.Post-COVID syndrome is related to a multisystem disorder that affects in part the cardiovascular system. This disease involves symptoms, and conditions that continue or develop after acute COVID-19. SARS-CoV-2 infection of immune and endothelial cells are associated with NETosis, microthrombosis and endothelial dysfunction that could persist several weeks after acute phase of infection. Damaged endothelial cells can expose the vessel pro-coagulant area leading to platelet and neutrophil clumps. Increased levels of circulating endothelial cells (CECs) have been described as biomarkers for cardiovascular diseases. Therefore, we hypothesize that CECs and microthrombosis are potential biomarkers of vascular dysfunction in Long COVID.Methods.A cross-sectional study was conducted at the Miami VA long COVID clinic. Long COVID cases and controls were recruited according to WHO definition for long COVID. A total of 23 patients and 7 controls were included in this study. Blood samples were collected in Heparin and Sodium Citrate tubes. Cell immunophenotyping and NETosis markers (MPO) were quantified on a Cytek Aurora spectral flow cytometer system. Microclots (CD62P+PAC-1+) and platelet response were assessed by flow cytometry and response to Adenosine di-phosphate (ADP), respectively. A ttest was used for statistical analysis. Differences were considered significant when p < 0.05.Results.The age and gender were similar between cases and controls while their symptom score was significantly different. There was a significant increase in the number of CECs (CD31+CD309+CD45-CD133-) in Long COVID cases. MPO expression in neutrophils (CD11b+CD66b+CD15+) and classical monocytes (CD14+CD16-) was significantly higher in Long COVID. Microclots were significantly elevated, and the platelet aggregation response was dysregulated in Long COVID.Conclusions.CECs and microthrombosis including NETosis are present in Long COVID and may serve as potential biomarkers or causative mechanisms for vascular dysfunction.

Circulation, Volume 150, Issue Suppl_1, Page A4146592-A4146592, November 12, 2024. Introduction:Low physical activity (PA) has been identified as a risk factor for development of atrial fibrillation (AF). However, the effect of changes in PA on directly recorded AF burden has not been well studied. The COVID-19 pandemic offered an opportunity to observe whether changes in activity were correlated with changes in AF burden. To determine if reduced PA is associated with higher AF burden, we assessed daily PA and AF burden data from patients with cardiac implantable electronic devices (CIEDs) enrolled in a prospective clinical trial, Targeting Risk Interventions and Metformin for Atrial Fibrillation (TRIM-AF, NCT03603912).Methods:Daily AF burden and activity were determined from implantable cardiac devices with atrial leads. The pandemic lockdown period was analyzed for up to 1 year. Pre-pandemic periods were matched by month to pandemic periods. To test the potential confounding of aging, pre-pre-pandemic periods were matched by month to pre-pandemic periods. To reduce the confounding of study interventions, matched periods were taken on one side of the study enrollment date. For PA and AF burden, Gaussian linear mixed models and a Bayesian mixed effect model were fitted and adjusted for age, sex, and device manufacturers. A Gaussian model was used to correlate daily activity minutes and AF%. Time splines were added to adjust for non-linear time effects. Outcomes are reported as mean activity minutes and daily AF%.Results:Comparing Pandemic vs. Pre-periods (N=82 periods; 55 male, 27 female), daily activity minutes decreased by a mean of 13.16±1.06 minutes/day, and daily AF burden increased by 16% [5%-26%]. Comparing Pre vs. Pre-Pre-Pandemic periods (N=60 periods; 41 male, 19 female), mean activity decreased by 2.28±1.13 mins/day, and AF burden increased by 57% [50%-64%]. A significant negative correlation between activity and AF burden was demonstrated (coefficient -2.0, 95% CI -2.4, -1.6). A decrease in 2.0 activity minutes was associated with a 10% increase in AF burden.Conclusions:This natural history analysis of PA and AF burden demonstrated decreases in activity and increases in AF burden with time and the pandemic. Activity and AF burden were significantly negatively correlated.

Circulation, Volume 150, Issue Suppl_1, Page A4117883-A4117883, November 12, 2024. Introduction/Background:Cardiovascular symptoms appear in a high proportion of patients in the few months following a severe SARS-CoV-2 infection. Non-invasive methods to predict disease severity could help personalizing healthcare and reducing the occurrence of these symptoms.Research Questions/Hypothesis:We hypothesized that blood long noncoding RNAs (lncRNAs) and machine learning (ML) could help predict COVID-19 severity.Goals/Aims:To develop a model based on lncRNAs and ML for predicting COVID-19 severity.Methods/Approach:Expression data of 2906 lncRNAs were obtained by targeted sequencing in plasma samples collected at baseline from four independent cohorts, totaling 564 COVID-19 patients. Patients were aged 18+ and were recruited from 2020 to 2023 in the PrediCOVID cohort (n=162; Luxembourg), the COVID19_OMICS-COVIRNA cohort (n=100, Italy), the TOCOVID cohort (n=233, Spain), and the MiRCOVID cohort (n=69, Germany). The study complied with the Declaration of Helsinki. Cohorts were approved by ethics committees and patients signed an informed consent.Results/Data:After data curation and pre-processing, 463 complete datasets were included in further analysis, representing 101 severe patients (in-hospital death or ICU admission) and 362 stable patients (no hospital admission or hospital admission but not ICU). Feature selection with Boruta, a random forest-based method, identified age and five lncRNAs (LINC01088-201, FGDP-AS1, LINC01088-209, AKAP13, and a novel lncRNA) associated with disease severity, which were used to build predictive models using six ML algorithms. A naïve Bayes model based on age and five lncRNAs predicted disease severity with an AUC of 0.875 [0.868-0.881] and an accuracy of 0.783 [0.775-0.791].Conclusion:We developed a ML model including age and five lncRNAs predicting COVID-19 severity. This model could help improve patients’ management and cardiovascular outcomes.

Circulation, Volume 150, Issue Suppl_1, Page A4119613-A4119613, November 12, 2024. Introduction:Percutaneous Coronary Intervention (PCI) is recommended for reperfusion of patients presenting with ST-segment myocardial infarction (STEMI) within 90 minutes. In this study, we sought to identify differences in PCI timing based on gender, race and ethnicity in the pre- and post-COVID era.Methods:We collected retrospective data on 760 patients admitted with STEMI at our quaternary academic medical center from 2018-2022. We defined our binary outcome as time to PCI less than 90 minutes, and adjusted for transfers from outside hospitals. We utilized univariate logistic regression analysis to analyze the association of demographic, clinical, and cardiac catheterization details on our outcome. We then utilized multivariate logistic regression analysis to determine the association of our covariates of interests with time to PCI. The logistic regression model was adjusted for collinearity which were deemed not significant.Results:Among our study population, COVID did not significantly impact whether or not a patient had a diagnostic cardiac catheterization on univariate analysis (OR 2.68, 95% CI 0.61-18.40, p=0.23). However, the post-COVID era was significantly associated with a delayed time to PCI on multivariate analysis [OR 1.62, 95% CI 1.04-2.55, p=0.035) [Figure 1]. In addition, females were 1.8x more likely to have a delayed PCI than males on multivariate regression [OR 1.80, 95% CI 1.10-2.95, p= 0.019) [Figure 1]. Interestingly, on multivariate analysis, females were more likely to have delayed reperfusion in the pre-COVID era (OR 2.92, 1.29-6.77,p= 0.01) but not the post-COVID era (OR 1.54, 0.78-3.06,p=0.2134). Patients in the post-COVID era had increased risk of having their culprit coronary not revascularized on multivariate analysis (OR 2.85, 1.2-8.03, p= 0.03).Conclusions:At our center, COVID did not significantly impact cardiac catheterization rates. However, COVID was significantly associated with delayed reperfusion timing and not revascularizing culprit vessels. Females were much more likely to have a delayed PCI than males in the pre-COVID era which was not seen following COVID-19.

Circulation, Volume 150, Issue Suppl_1, Page A4140201-A4140201, November 12, 2024. Introduction:While implantable cardiac defibrillators (ICD) decrease sudden cardiac death, disparities in ICD use remain. The COVID-19 pandemic created strains on the US healthcare system that may have exacerbated these disparities.Methods:Using the US NCDR registry of primary and secondary prevention ICD implants, we compared sex, racial and ethnic disparities for 239,014 patients, aged 19-90 years, grouped into three time intervals from 2016 to 2022: Pre-COVID, COVID and Post-COVID. Centers without consistent reporting were excluded, as were patients with incomplete sex, race or ethnicity data. ICD implantation rates were compared using a Poisson regression model with interaction tests for sex, race and ethnicity by time window to see if disparities changed within this period. Implant rates by indication were also assessed.Results:Overall ICD implants decreased over the study period (Figure 1) with an average monthly rate of 3271 in the first three months of 2016 declining to 2334 in the last three months of 2022 (p=0.017). Disparities in ICD implantation for women, racial and ethnic minorities were observed pre-COVID and persisted (Table 1). Average ICD implant rates during these time periods varied by race with predominance in White patients. While gaps in ICD implant persisted, the disparities did not worsen during COVID-19 by sex, race or ethnicity (p-value for interactions were 0.79; 0.47; and 0.095, respectively). There was a more significant decrease in primary prevention ICD compared to secondary prevention ICD (p

Circulation, Volume 150, Issue Suppl_1, Page A4148010-A4148010, November 12, 2024. Background:Severe COVID-19 infection has been associated with acute respiratory distress syndrome (ARDS) and right ventricular (RV) dysfunction. In this study, we report associations between echocardiographic findings and laboratory markers that portend RV failure in patients with ARDS secondary to COVID-19 infection on ECMO.Methods:A single-center study was conducted in the cardiovascular ICU of our institute. A retrospective chart review was performed on 41 patients with COVID-19 on ECMO between March and October 2020. Twenty-two patients had transthoracic echocardiograms (TTE) completed while on ECMO (VV-ECMO = 19, VA-ECMO = 3). Echocardiograms (echo) were obtained pre-cannulation, during ECMO, and post-ECMO decannulation. RV parameters analyzed included tricuspid annular plane systolic excursion (TAPSE), basal diastolic RV diameter, right ventricular fractional area of change (RV FAC), and S’. Laboratory values including BNP, CRP, D-dimer, ferritin, fibrinogen, lactate and troponin were analyzed for correlation with echo findings.Results:TAPSE was significantly lower in deceased patients (1.9± 0.4cm vs 1.3±0.6 cm, P< 0.05). RV FAC and S’ were also lower in the deceased group. TAPSE while on ECMO showed a positive association with peak D-dimer levels in survivors and a negative association in deceased patients. Peri-ECMO fibrinogen and CRP levels were negatively associated with TAPSE in survivors while fibrinogen showed positive association in deceased patients. LDH peak, fibrinogen initial and lactate peak were higher in the deceased[ZQ1] group. There is a trend of increased RV basal diameter in the deceased group (3.9±0.9 vs 4.2±0.9 cm). Last troponin levels were negatively associated with basal diastolic RV diameter while on ECMO in deceased patients.Conclusion:Preservation of RV longitudinal contractility, as reflected by TAPSE, may play an important role in the survival of COVID-19 patients on ECMO. Laboratory markers such as LDH, D-dimer, fibrinogen and lactate may have prognostic value in predicting RV failure. Further studies are required to determine if early initiation of therapies to improve RV systolic function in COVID-19 ECMO patients with ARDS improves outcomes.

Circulation, Volume 150, Issue Suppl_1, Page A4145096-A4145096, November 12, 2024. Introduction:Postural orthostatic tachycardia syndrome (POTS) and Inappropriate sinus tachycardia (IST) are common manifestations of cardiovascular dysautonomia (CVAD) in patients with post-COVID-19 syndrome. Studies regarding differences between post-COVID-19 POTS and post-COVID-19 IST have been sparse and based on small patient series.Aims:To examine clinical differences between POTS and IST in patients with post-COVID-19 syndrome.Methods:A cross-sectional observational study based on a dataset of patients diagnosed with post-COVID-19 syndrome and POTS/IST, at Karolinska University Hospital, Stockholm in 2020-2023, was performed. Data was retrieved using patients’ medical records. ANOVA, chi-square tests and Fisher’s exact tests were used for analysis.Results:A total of 200 patients diagnosed with post-COVID POTS/IST (ICD-10 codes, I.498 + U.099) were included (female, 85%) and divided into a POTS-group (n=110) and IST-group (n=90). Sixty-one patients (31%) met the diagnostic criteria of both and were included in the IST-group. The mean ages were 38 years for the POTS-group and 42 years for the IST-group (p=0.027). Hypertension was more common within the IST-group (p

Circulation, Volume 150, Issue Suppl_1, Page A4113573-A4113573, November 12, 2024. Introduction/Background:Cardiovascular and neurological diseases develop in a significant proportion of COVID-19 patients. Minimally invasive tools to predict outcome after SARS-CoV-2 infection would enable personalized healthcare, potentially easing the disease burden. We showed that blood levels of the long noncoding RNA lymphoid enhancer-binding factor-1 antisense 1 (LEF1-AS1) predict COVID-19 in-hospital mortality.Hypothesis:LEF1-AS1 is associated with long-term clinical outcomes of COVID-19.Aim:Test the capacity of LEF1-AS1 to predict neuro-cardio-vascular outcomes post-SARS-CoV-2 infection.Methods/Approach:We enrolled 104 primo-infected COVID-19 patients aged 18+ recruited from April to December 2020 in the PrediCOVID national cohort for which 12-month follow-up data were available (Ethics Committee approvals 202003/07 and 202310/02-SU-202003/07). Whole blood samples were collected at baseline and expression levels of LEF1-AS1 were assessed by quantitative PCR.Results/Data:Of the 104 patients, 35 had at least one neurological symptom and one cardiovascular symptom at month 12. Levels of LEF1-AS1 at baseline were lower (p=0.019) in patients who developed neurological and cardiovascular symptoms as compared to patients who did not. Lower LEF1-AS1 was associated with symptoms development with an odds ratio of 0.48 (95% CI 0.28-0.83) from logistic regression model adjusted for age, sex, comorbidities and disease severity at baseline. Addition of LEF1-AS1 to a clinical model including age, sex, comorbidities and baseline severity yielded an incremental predictive value as attested by an increased AUC from 0.79 to 0.83 (likelihood ratio test p=0.005), a net reclassification index of 0.54 (p=0.007) and an integrated discrimination improvement of 0.08 (p=0.009).Conclusion:Blood levels of LEF1-AS1 predict 12-month neurological and cardiovascular outcomes of COVID-19 patients. This needs to be validated in larger populations.

Circulation, Volume 150, Issue Suppl_1, Page A4141078-A4141078, November 12, 2024. Background:Social determinants of health (SDOH),exacerbated by the COVID-19 pandemic, impact access to medical care.Research Question:Through descriptive qualitative inquiry, we explored barriers and facilitators to pediatric cardiology ambulatory care for patients with complex congenital heart disease (CCHD) during COVID-19.Methods:English- and Spanish-speaking caregivers of children with CCHD who missed at least one clinic visit during the first year of COVID-19 were recruited, with purposeful sampling of Black and Hispanic patients. Semi-structured interviews inquired about the impact of the pandemic, experience with telehealth and communication with providers, effects of SDOH, and perceived impact of their race/ethnicity on care. Content analysis summarized information and identified themes.Results:Interviews (19) were conducted: 14 in English (6 Black, 2 Hispanic, 2 White, 3 mixed race, 1 American Indian), and 5 in Spanish (5 Hispanic). Overarching themes were: Barriers to Care, Facilitators of Returning/Staying in Care, Impact of Diagnosis, and Recommendations for Improvement (Image 1). Despite challenges with finances and transportation, as well as concern for infection risk, the majority of caregivers preferred in-person care over telehealth due to physical exam, diagnostic testing, and interpersonal connection with providers. SDOH challenges including housing, transportation, and employment contributed to missing care. For some families, social vulnerability was exacerbated by their child’s CCHD diagnosis and then again by COVID-19. Universally, caregivers felt their child’s race/ethnicity did not affect the care they received. Spanish-speaking caregivers expressed their primary language as a barrier to care and their desire for more thorough explanations and teach-back from the medical team.Conclusion:While SDOH can hinder access to ambulatory cardiac care, trusting relationships with care teams facilitated engagement. Social vulnerability contributed to dynamic situations for families, especially during COVID-19, highlighting the need for routine SDOH assessment and support. English- and Spanish-speaking caregivers echoed the same challenges. Race/ethnicity was not felt to impact care received.

Circulation, Volume 150, Issue Suppl_1, Page A4143985-A4143985, November 12, 2024. Introduction:Endothelial dysfunction can trigger the development and progression of cardiovascular disease. We hypothesize that cardiovascular PASC is induced by persistent endothelial dysfunction mediated via asymmetric-dimethylarginine (ADMA, the endogenous inhibitor of endothelial nitric oxide synthase). ADMA levels rise in response to viral infections, but it is usually degraded by the enzyme DDAH1, which is inhibited by chronic inflammation and oxidative stress. This study aims to determine whether cardiovascular PASC is associated with endothelial dysfunction and to clarify the role of ADMA in this relationship.Methods:We recruited subjects who had been previously infected and developed cardiovascular symptoms (PASC+), those who had been infected but did not have PASC (PASC-), and those who had never been infected (controls) (n=20 each). Groups were matched for age, sex, and BMI and underwent blood draws and fat biopsies. Vascular function was assessedin-vivovia ultrasound imaging andex-vivoin fat-isolated arterioles.Results:Compared to PASC- and controls, PASC+ subjects exhibited 80% higher serum levels of ADMA and 40% reduced nitric oxide levels. DDAH1 activity was elevated in the PASC+, suggesting a compensatory mechanism for the elevated ADMA levels. However, PASC+ obese subjects exhibited substantially lower DDAH1 activity than non-obese subjects, which was associated with lower insulin sensitivity and higher ADMA levels. Compared to the other two groups, the PASC+ group exhibited lower brachial artery vasoreactivity, while nitroglycerin-induced dilation did not differ statistically, suggesting impaired endothelial function. In the PASC+ group, microvascular recruitment in response to reactive hyperemia was diminished, as was the ex vivo measured flow-induced arteriolar dilation and NO generation. Left ventricle (LV) dysfunction was observed in 80% of the PASC+ group, as opposed to 5% of the PASC- and controls. The LV ejection fraction and global longitudinal strain (GLS) were substantially reduced in the PASC+ group, which was correlated with higher ADMA, C-reactive protein, and troponin-1, as well as lower NO and vascular function. Obese PASC+ subjects had the highest ADMA and the lowest endothelial-dependent vasodilation and insulin sensitivity.Conclusion:Cardiovascular PASC symptoms are related to persistent endothelial dysfunction and elevated ADMA levels, which may be further exacerbated by obesity and reduced DDAH1 activity.

Circulation, Volume 150, Issue Suppl_1, Page A4145229-A4145229, November 12, 2024. Background:Stress-induced cardiomyopathy (CM) is a form of acute transient left ventricular dysfunction triggered by underlying physiological stress which often leads to increased morbidity and mortality. Coronavirus disease 2019 (COVID-19) is thought to cause stress-induced CM due to overwhelming systemic inflammation. There is paucity of data regarding the impact of COVID-19 on in-hospital outcomes of patients with stress-induced CM. The purpose of this study is to investigate in-hospital outcomes, including mortality and cardiogenic shock, of patients with concomitant COVID-19 and stress-induced CM.Methods:We queried the 2020 USA National Inpatient Sample (NIS) Database in conducting this retrospective cohort study. We identified hospitalized adult patients ≥ 18 years old with stress-induced CM and concomitant COVID-19 using ICD-10 CM codes. We used a survey multivariable logistic and linear regression analysis to calculate adjusted odds ratios (aORs) for outcomes of interest. A p value of

Circulation, Volume 150, Issue Suppl_1, Page A4145068-A4145068, November 12, 2024. Background:The COVID-19 global pandemic was the third leading cause of mortality in the US in 2020 and is associated with numerous complications, including myocarditis. Diagnosis of COVID-19 myocarditis can involve costly and invasive procedures. In addition, asymptomatic myocarditis could place people at risk for arrhythmias and sudden cardiac death.Objective:To use machine learning (ML) of serum proteomics to distinguish asymptomatic COVID-19 positive volunteers with and without myocarditis.Approach and Results:In 2020, for a cohort of 20 previously healthy 18–23-year-old individuals diagnosed with COVID-19 two weeks after the diagnosis, CMR was performed to assess for evidence of cardiac inflammation and serum samples were obtained the same day (10 were diagnosed as myocarditis positive and 10 negative) We performed proteomic analysis using the SomaScan proteomics assay from SomaLogic. The data were passed through an initial feature selection process of 1000 rounds of bootstrapped multivariate logistic regression using L1-regularization to introduce sparser feature utilization. The top 25 features (largest absolute log-odds) were utilized for a final logistic regression analysis. The feature selection step was optimized to have an average receiver operating characteristic area under the curve (ROCAUC) of 83.29% over 1000 iterations, but the final model utilizing only 25 proteins achieved an average ROCAUC of 99.58%. This method produced 22 proteins with significant odds-ratios for COVID-19 myocarditis (OR 95%CI excluding 1), of particular interest are those involved in inflammatory control and injury response mechanisms. Increases in the heat shock protein DNAJB11 (1.19 [1.10, 1.27]) and calponin-2 (1.17 [1.10, 1.25]), as well as decreases IL1RN (0.88 [0.83, 0.93]) were associated in increased likelihood of CMR diagnosed myocarditis (Fig 1A). Furthermore, a UMAP projection of the data using the 22 significant features yielded a clear visual distinction between those with and without COVID-19 myocarditis via CMR (Fig 1B).Conclusion:Utilizing ML on serum proteomic screenings of asymptomatic young COVID-19 patients, we can differentiate between those with CMR myocarditis positive and negative patients.