Risultati per: Vaccinare l’adulto ai tempi del COVID-19

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 A4143186-A4143186, November 12, 2024. Introduction:Statins are lipid-lowering agents with anti-inflammatory effects. Data surrounding the benefits of statins in patients with coronavirus disease 2019 (Covid-19) are conflicting. We sought to better understand the impact of statins in the context of Covid-19-related inflammation.Methods:We leveraged the International Study of Inflammation in Covid-19, a prospective multicenter cohort study of patients hospitalized specifically for Covid-19 between February 1, 2020 and October 30, 2022. Participants underwent systematic assessment of biomarkers of inflammation. We used logistic regression modeling and inverse probability-of-treatment weighting (IPTW) to examine the association between prior statin use and the composite outcome of in-hospital death, need for mechanical ventilation, and need for renal replacement therapy.Results:A total of 4,464 patients were included in the study, of whom 1,364 (27.5%) were taking a statin prior to admission. There were 1,061 primary outcome events, including 540 deaths, 854 mechanical ventilation and 313 renal replacement therapy. Amongst biomarkers of inflammation, statin use was associated solely with lower levels of soluble urokinase plasminogen activator receptor (suPAR) after adjusting for known confounders. In multivariable logistic regression analysis, statin use was associated with lower odds of the composite outcome (adjusted odds ratio (aOR) 0.63, 95%CI[0.53-0.76]) compared to patients not on statins. Findings were consistent with IPTW (aOR 0.92, 95%CI [0.89- 0.95]). The proportion of the effect of statin on the primary outcome mediated by suPAR was estimated at 31.5%.Conclusion:Prior statin use is associated with improved outcomes and lower inflammation as measured by suPAR levels in patients hospitalized for Covid-19.

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 A4142129-A4142129, November 12, 2024. Background:The clinical impact of neutrophil to lymphocyte ratio (NLR) and right ventricular (RV) dysfunction on clinical outcomes in COVID-19 have not been studied in the often-underrepresented Indonesian population.Aim:To investigate the role of NLR and RV dysfunction in Indonesian patients hospitalized for COVID-19.Methods:A retrospective cohort study was conducted at a COVID-19 referral hospital in Indonesia. We included all adult patients hospitalized with COVID-19 between April 2020 – April 2021 who had transthoracic echocardiography (TTE) during admission. Clinical data were extracted from electronic medical records. TTE variables were defined according to the American Society of Echocardiography criteria. All statistical analyses were conducted using the SPSS software. This study was approved by the IRB at Universitas Indonesia (#2022-01-135).Results:A total of 488 patients were included – 29 with and 459 without RV dysfunction. The mean age of the population was 54.8 (SD ± 13.5), and 42% were females. Receiver operating curve analysis and Youden’s J statistics were used to determine the optimal NLR cut-off (Figure 1). An NLR > 4.79 was considered elevated, and had a sensitivity of 70.6% and a specificity of 80.6% in predicting severe – critical COVID-19. A high NLR (OR: 3.38, P = 0.02) and LV systolic dysfunction (OR: 9.76, P < 0.01) were independently associated with RV dysfunction. In multivariate cox regression analysis, older age (HR: 1.02, P = 0.01), obesity (HR: 1.85, P < 0.01), chronic kidney disease (HR: 1.69, P = 0.01), high NLR (HR: 2.75, P < 0.01), and RV dysfunction (HR: 2.07, P = 0.02) increased the risk of 30-day mortality.Conclusions:In Indonesian patients hospitalized with COVID-19, A high NLR is predictive of severe – critical COVID-19 and is associated with RV dysfunction. A high NLR at admission and RV dysfunction independently increase the risk of 30-day mortality in hospitalized Indonesian adults with COVID-19.

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 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 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 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 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 A4145299-A4145299, November 12, 2024. Background:COVID-19 can present with a wide spectrum of clinical manifestations ranging from asymptomatic to life-threatening. It is often thought of as a primarily pulmonary infection and different systemic presentations are sometimes overlooked. We present a case of COVID-19 induced myocarditis leading to hemodynamic instability and end-organ dysfunction.Case presentation:A 77-year-old male with a history of CKD, paroxysmal atrial fibrillation, and COPD was transferred to our hospital for a higher level of care due to worsening cardiogenic shock. He was cold and wet (Forrester class IV) with a High Sensitivity troponin of 331 and a BNP level of 21,503. EKG showed atrial fibrillation with RVR but no evidence of acute ischemic changes. A TTE was done which revealed an EF of 30-35% and diffuse hypokinesis with regional variation, a significant reduction from an EF of 50-55% just 4 weeks prior. The patient exhibited end-organ dysfunction, as evidenced by deranged liver function tests and a rise in creatinine from a baseline of 2 to 4.6, indicating congestive hepatopathy and cardiorenal syndrome respectively. The patient’s hemodynamics necessitated milrinone and norepinephrine infusions and efforts to wean them off were unsuccessful due to repeated failed fluid bolus challenges. Considering the patient’s clinical picture, there was a strong suspicion of viral-induced cardiomyopathy, and a COVID-19 infection was confirmed by PCR testing; his last COVID-19 booster dose was in 2021. The patient was promptly started on remdesivir and IV steroids. Unfortunately, the patient’s condition continued to deteriorate, and he succumbed to his illness.Discussion:A myriad of cardiovascular manifestations have been implicated with COVID-19, including ACS, myocarditis, and heart failure. Although the exact underlying mechanisms for each of these conditions are unclear, a complex interplay between direct viral injury, systemic inflammation, and cytokine storm has been hypothesized. Our case illustrates the quick progression of heart failure into cardiogenic shock requiring pressor support, with subsequent rapid decompensation rendering CMR, cardiac catheterization, and biopsy timely impractical. It serves as a reminder to explore COVID-19 as a potential cause of biventricular failure in individuals with no evident reason and rapid clinical deterioration, particularly as early initiation of antiviral therapy could improve prognoses.

Circulation, Volume 150, Issue Suppl_1, Page A4139661-A4139661, November 12, 2024. Introduction:Troponin-defined myocardial injury or N-terminal pro-B-type natriuretic peptide (NT-proBNP) elevation frequently coincides with coronavirus disease 2019 (COVID-19). Our prior study (COVID-MI Registry Cohort-1) confirmed that high-sensitive troponin I (HsTnI) and NT-proBNP effectively stratified mortality risk. However, variants of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) change rapidly, and it remains unclear whether these biomarkers are consistently effective in predicting prognosis of COVID-19 patients irrespective of epidemic periods.Research Questions:Can HsTnI or NT-proBNP stratify mortality risk in recent COVID-19 cohorts?Aims:To assess the potential of HsTnI and NT-proBNP levels for risk stratification in the recent COVID-19 waves.Methods:In the COVID-MI Registry Cohort-2, we enrolled 1115 consecutive COVID-19 patients admitted between October 2021 and October 2022, during the Omicron variant endemic. We collected data of HsTnI or NT-proBNP levels from hospital charts or using the samples in our hospital’s serum/plasma bank if the data were not available. The primary outcome measure was all-cause mortality.Results:On admission, more than one-third of patients were classified as having severe COVID-19. HsTnI and NT-proBNP levels were available for 427 and 414 patients, respectively. The median HsTnI and NT-proBNP levels were 16 (interquartile range [IQR]: 5-57) ng/L and 524 (IQR: 140-2056) pg/mL, respectively. We stratified the patients into three groups by HsTnI level:

Circulation, Volume 150, Issue Suppl_1, Page A4146890-A4146890, November 12, 2024. Background:COVID-19 has introduced new complexities in the management of patients undergoing the transcatheter edge-to-edge repair (TEER) procedure of the mitral valve. This study compares outcomes of mitral valve TEER in patients with and without COVID-19, utilizing data from the National Inpatient Sample (2020-2021).Methods:We conducted a retrospective cohort study on 23,465 patients without COVID-19 and 85 patients with COVID-19 undergoing mitral valve TEER. Multivariate logistic regression was employed to compare outcomes, adjusting for potential confounders. Primary outcomes included mortality and major complications, while secondary outcomes encompassed specific procedural complications.Results:Patients with COVID-19 were younger (mean age: 73.176 vs. 76.178 years, p-value

Circulation, Volume 150, Issue Suppl_1, Page A4142337-A4142337, November 12, 2024. Background:We previously demonstrated a significantly increased inpatient mortality of COVID-19 infection-induced male Takotsubo (TTS) patients during the early pandemic period. Since then, our management of COVID-19 prevention and treatment have evolved significantly, reducing both hospitalization and mortality rates. With these advancements, we have analyzed the clinical characteristics and outcomes of reported COVD-19-associated TTS patients since the initial pandemic.Research Question:What are the clinical characteristics and mortality outcomes of COVID-19-associated TTS patients especially in the context of improved prevention and treatment?Aims:To identify clinical characteristics and outcome correlates in patients with COVID-19-associated TTS.Methods:We completed a systematic review of 191 patients with TTS from 95 published case reports, 13 case series, and 4 observational cross-sectional/cohort studies published from April 1, 2020 to May 1, 2024 (PubMed). We performed clustering analysis using the clinical, imaging, and inpatient mortality data of 78 patients, which categorized groups of patients based on how closely associated or similar they are relative to other groups. Following this, we applied feature analysis to identify which features contributed the most to the clustering results.Results:Of all TTS cases, the mean age was 64.2±16.1 with 32.9% males. A total of 122 (63.9%) had COVID-19 infection, 21 (11.0%) had COVID-19 vaccination, and 50 (26.2%) patients had other triggers (2 patients had both COVID-19 infection and a non-infectious trigger). In-hospital mortality was 28.6% (16 of 56) for males and 13.2% (15 of 114) for females (p-value = 0.01). There was no association between COVID-19 vaccine administration and in-hospital mortality (0%, 0 of 21). There were notable differences in the clinical and demographic characteristics of TTS patients before and after September 2021 based on clustering analysis. Feature analysis indicated that COVID-19-induced TTS strongly correlated with in-hospital mortality and long-term adverse outcome in male patients.Conclusion:More male TTS patients were found during the pandemic than is expected of the traditional TTS archetype. A triad of “male, COVID-19 infection and TTS” appears to predict higher inpatient mortality. Compared to our prior study, inpatient mortality rates for TTS COVID patients have declined for all groups. Vaccine-induced TTS is associated with a benign clinical phenotype.

Circulation, Volume 150, Issue Suppl_1, Page A4114220-A4114220, November 12, 2024. Background:It is still not well understood whether cardiac injury observed during acute COVID-19 infection extends after recovery from the initial viral infection. The purpose of this study was to determine the incidence of left and right ventricular dysfunction in patients hospitalized with acute COVID-19 and evaluate for cardiac recovery.Methods:A multicenter, retrospective cohort study was conducted. Adult patients were identified by hospitalizations using ICD-10 code U07.1 from March 2020 to October 2021. Patients were included if they had: 1) acute COVID-19 infection confirmed by RT-PCR and 2) a transthoracic echocardiogram (TTE) performed during their hospitalization. Clinical and echocardiographic data were collected and analyzed. Longitudinal TTE parameters were obtained from follow-up studies performed after discharge.Results:A total of 750 patients (mean age 64.3 ± 15.3 years, 60.0% male) were included. The average time to follow-up TTE was 8.7± 7.4 months. 133 patients (17.7%) had new LV dysfunction seen on TTE (Figure 1). LV recovery (defined as normalization of LVEF or improvement of LVEF by >10% from baseline) was observed in 28 of 74 (37.8%) survivors. 9 of 26 patients (34.6%) who had a follow-up TTE

Circulation, Volume 150, Issue Suppl_1, Page A4137878-A4137878, November 12, 2024. Background:The COVID-19 pandemic in 2020 was marked by a sharp decrease in out-of-hospital cardiac arrest (OHCA) survival. Whether OHCA survival has recovered to pre-pandemic levels, and whether changes in OHCA survival are similar across communities of different racial and ethnic composition, is unknown.Methods:We included adult patients with non-traumatic OHCA from 2015-2022 in the Cardiac Arrest Registry to Enhance Survival registry. Using hierarchical multivariable regression, we calculated risk-adjusted rates of survival to hospital discharge during 2015-2019 (reference period) and compared this to survival rates during 2020, 2021, and 2022. We also examined whether the trajectory of survival over this period differed based on the racial/ethnic composition of the community served by the emergency medical service (EMS) agency, defined as predominantly White ( >80% White residents), majority Black or Hispanic ( >50% Black or Hispanic residents), or integrated (neither).Results:Of 485,079 patients with OHCA, mean age was 61.9 years; 64% were male, and 22% were of Black race with 7% of Hispanic ethnicity. Overall, risk-adjusted survival rates to hospital discharge for OHCA decreased from 10.1% in 2015-2019 to 8.4% in 2020 (P

Circulation, Volume 150, Issue Suppl_1, Page A4142506-A4142506, November 12, 2024. Introduction:Myocarditis has been reported after mRNA-based COVID-19 vaccination, but the immune mechanisms remain unclear. This study aimed to identify the proteome-based immunopathogenesis of post-vaccination myocarditis compared to viral myocarditis in the pre-COVID-19 era.Methods:Proteomic analysis of right ventricle (RV) biopsy specimens was performed in myocarditis patients (pre-pandemic viral myocarditis: n=3, post-vaccination myocarditis: n=3) and controls (normal endomyocardial biopsy specimens of heart transplant recipients, n=4) using mass spectrometry. Differentially expressed proteins were analyzed with CIBERSORTx, Gene Ontology (GO) analysis, and Ingenuity Pathway Analysis (IPA). To examine the relationship between the SARS-CoV-2 spike protein and post-vaccination myocarditis, immunohistochemistry (IHC), mass spectrometry analysis of spike protein, and activation-induced marker (AIM) assay in T cells from RV samples were conducted.Results:In the proteomic analysis, 6,861 proteins were identified. Post-vaccination myocarditis showed increased extracellular matrix formation and cardiac fibrosis. Both pre-pandemic and post-vaccination myocarditis had elevated pro-inflammatory cytokine activities. However, post-vaccination myocarditis exhibited higher expression of interferon-alpha (IFNα) and pattern recognition receptor activation, including TLR3 and TLR7. Pre-pandemic myocarditis showed higher activation of the complement system, neutrophils, and NK cells, whereas post-vaccination myocarditis showed increased Th2 cell activation and classical macrophage activation. Spike protein and related T-cell activation were not detected.Conclusion:The immune activation in myocarditis after COVID-19 mRNA vaccination may be triggered by the mRNA in the vaccine via an IFNα-driven immune response, leading to autoimmune-like features. Further studies are necessary to validate whether these proteins correlate with clinical characteristics.