Risultati per: Il significato della carica virale e l’effetto del vaccino anti-COVID-19

Circulation, Volume 150, Issue Suppl_1, Page A4142847-A4142847, November 12, 2024. Background:Clonal hematopoiesis of indeterminate potential (CHIP) can contribute to cardiovascular risk. The Interleukin-6 receptor (IL6R) polymorphism (D358A) modifies the risk of coronary artery diseases among CHIP carriers in human cohorts. However, the effects of the IL6R D358A on IL-6 pathways are discordant with the canonical expectation, that the classical IL-6 signaling pathway is anti-inflammatory while the trans-signaling pathway is pro-inflammatory.Hypothesis:DNMT3A, the most frequent driver gene for CHIP, changes the inflammatory consequence of IL-6 classical signaling from anti-inflammatory to pro-inflammatory to worsen atherosclerosis.Method:We investigated if an anti-IL6R antibody modifies atherosclerosis associated with myeloidDnmt3adeficiencyin vivo.Ldlr-/-mice were transplanted with 10% bone marrow cells fromDnmt3a-/-mice/90% of wild-type (WT) cells compared with 100% WT transfer. After engraftment, mice consumed a high-fat diet, and received an anti-IL6R antibody for 10 weeks to assess aortic root atherosclerosis vs. control antibody treatment. We also investigated the differences between IL-6 classical- vs trans-signaling pathways and whetherDnmt3adeficiency in bone marrow-derived macrophages (BMDM) modifies the IL-6 pathways. RNA-seq was performed in BMDM stimulated with IL-6, which activates the classical IL-6 pathway, or IL-6/IL6R conjugate, which activates trans-signaling. We further compared IL-6 vs control stimulation betweenDnmt3a-/-and WT BMDM using RNA-seq, and the major finding was replicated by quantitative PCR. In addition, IL-1β was quantified in the conditioned medium.Result:Anti-IL6R antibody treatment reduced atherosclerosis in the mice with myeloidDnmt3adeficiency. IL4R expression rose significantly in BMDM stimulated by IL-6 compared to IL-6/IL6R conjugate. IL4R induction by IL-6, but not the IL-6/IL6R conjugate, fell significantly inDnmt3a-/-BMDM compared to WT. IL-1β secretion declined with IL-6 stimulation and was higher in IL6R deficient BMDM, but IL-6 stimulation and deletion ofIL6Rdid not affect IL-1β secretion inDnmt3a-/-BMDMs.Conclusion:These data suggest that DNMT3A tonically limits the IL-6 classical pathway to limit atherogenesis in an IL-4 signaling-dependent manner. These findings promote understanding of the CHIP-atherosclerosis association and inform the development of management strategies for CVD risk in CHIP carriers.

Circulation, Volume 150, Issue Suppl_1, Page A4141387-A4141387, November 12, 2024. Background and Objective:To investigate the differences in Ambulatory Blood Pressure Monitoring (ABPM) parameters in patients affected by VEGFR-TKI and tumors, and to summarize the relationship between VEGFR-TKI, tumors, and blood pressure.Methods:43 patients who received VEGFR-TKI anti-tumor treatment and developed induced hypertension were selected for ABPM. Additionally, 94 cases of tumor-associated hypertension and 96 cases of primary hypertension were randomly selected for comparison. The ambulatory blood pressure-related parameters between the VEGFR-TKI-related hypertension group and the tumor-associated hypertension group, as well as between the tumor-associated hypertension group and the primary hypertension group, were analyzed.Results:Compared with the tumor-associated hypertension group, the VEGFR-TKI-related hypertension group showed higher 24-hour average diastolic blood pressure [(85.37±13.21) vs. (80.41±10.71) mmHg,t=2.332,P=0.021], daytime average diastolic blood pressure [(85.98±13.19) vs. (80.69±10.98) mmHg,t=2.452,P=0.015]. Multivariate linear regression analysis revealed that after adjusting for tumor type and BMI, the use of VEGFR-TKI remained independently associated with nighttime average diastolic blood pressure (B=5.921,P=0.021). Compared with the primary hypertension group, the tumor-associated hypertension group exhibited significantly reduced nighttime systolic blood pressure decline rate [(1.10±9.01) vs. (6.33±6.87),t=-4.508,P

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 A4143130-A4143130, November 12, 2024. Background:Chagas disease (CD), caused by Trypanosoma cruzi, leads to chronic Chagas cardiomyopathy, one of the deadliest and most debilitating cardiopathies. Benznidazole (BZN) is the medication of choice in Brazil, effective during the acute phase, but its efficacy during the chronic phase is unclear.Aims:To determine if BZN treatment reduces cardiac inflammation and fibrosis via magnetic resonance imaging (MRI) and its association with the circulating immune profile of CD patients.Methods:We collected cardiac images and plasma from a cohort of CD patients before and 6 months after BZN treatment. We performed: 1- MRI of left and right ventricle function and volumes, T1 (MAPA T1), T2 mapping (MAPA T2), and extracellular volume (ECV); 2- analysis of soluble factors including cytokines, chemokines, and growth factors using the Bio-48 Plex Human Cytokine Screening Panel kit. Changes in the variables MAPAT1, MAPAT2, and ECV were used to classify the improvement of CD patients undergoing BZN therapy. Patients with the greatest reductions in these variables post-therapy, compared to pre-therapy, were considered to have greater clinical improvement. Thus, patients were divided into two groups: greater clinical improvement (GCI; n=15) and smaller clinical improvement (SCI; n=15) (figure 1). Data were analyzed using GraphPad Prism 8 software with statistical significance set at 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 A4146209-A4146209, November 12, 2024. Background:The management of recurrent pericarditis has evolved to include colchicine and novel anti-interleukin-1 agents, given the limited efficacy of traditional NSAIDs and corticosteroids. We conducted a pairwise and network meta-analysis to evaluate the efficacy and safety of colchicine and anti-IL-1 agents in recurrent pericarditis.Methods:We conducted a comprehensive search on various databases and registries, such as MEDLINE (via PubMed), Embase, and Cochrane Central Register of Controlled Trials (CENTRAL), to retrieve relevant RCTs. We used STATA version 17 to perform meta-analyses under a random-effects model and applied the empirical Bayes (Paule and Mandel) variance estimator to dichotomous data. We performed a network meta-analysis with a placebo/standard therapy group as the comparator in MetaXL 5.3 using the Generalized Pairwise Modeling based on the Bucher method.Results:A total of 6 RCTs were included in the meta-analysis. The risk of pericarditis recurrence was significantly decreased by colchicine (RR 0.46, 95% CI 0.37-0.58) and anti-IL-1 agents (RR 0.13, 95% CI 0.03-0.54) compared to placebo or standard therapy. Colchicine significantly decreased the risk of treatment failure (RR 0.42, 95% CI 0.31-0.57) but did not have a significant impact on the risk of adverse events (RR 1.06, 95% CI 0.31-3.62). No significant risk of adverse events (RR 2.16, 95% CI 0.66-7.01) or serious adverse events (RR 1.01, 95% CI 0.23-4.41) was observed with anti-interleukin-1 agents. Colchicine was also associated with a decreased risk of pericarditis-related rehospitalization (RR 0.26, 95% CI 0.10-0.70). The network meta-analysis showed that anti-IL-1 agents (RR 0.13, 95% CI 0.05 to 0.30) were associated with a greater reduction in pericarditis recurrence than colchicine (RR 0.46, 95% CI 0.37 to 0.59). All anti-interleukin-1 agents significantly decreased the risk of pericarditis recurrence, with comparable efficacies among the different agents.Conclusion:Colchicine and anti-IL-1 agents significantly reduced the risk of pericarditis recurrence with the anti-IL-1 agents demonstrating greater efficacy. Further, high-powered, large-scale RCTs that directly compare various treatment options are needed to confirm or refute our findings.

Circulation, Volume 150, Issue Suppl_1, Page A4139928-A4139928, November 12, 2024. Background:Ketone body metabolism, known for its multifaceted effects, is gaining attention as a potential therapeutic target for cardiovascular diseases. However, the impact of ketone bodies on cardiac hypertrophy and Heart Failure with Preserved Ejection Fraction (HFpEF) remains unclear.Research Questions:To elucidate the effects of ketone bodies on cardiac hypertrophy.The aim of the present research is to investigate the impact of ketone bodies on cardiac hypertrophy induced by metabolic abnormalities using organ-specific ketone body synthesis-deficient mice.Methods:Obesity and hypertension were induced by a high-fat diet combined with NG-Nitro-L-arginine methyl ester hydrochloride (L-NAME) (Combined Stress), and the resultant cardiac hypertrophy and ketone body synthesis were evaluated. Subsequently, organ-specific knockout mice of HMG-CoA synthase 2 (Hmgcs2), a rate-limiting enzyme in ketone body synthesis, were subjected to Combined Stress to assess the impact on cardiac hypertrophy. To conduct a metabolism-focused analysis, cell type-specific nuclei were isolated and subjected to RNA sequencing (RNA-seq) and comprehensive metabolomics analysis. To evaluate the direct effects of ketone bodies, H9C2 cells, rat cardiac cells ,were treated with β-hydroxybutyrate, followed by analysis of oxygen consumption and metabolomics.Results:Combined Stress resulted in increased myocardial cross-sectional area and enhanced ketone body synthesis in the liver and heart. Hepatocyte-specific Hmgcs2 knockout mice (Hmgcs2ΔHep) subjected to Combined Stress exhibited exacerbated myocardial hypertrophy (cardiomyocyte cell size;Hmgcs2flox: 322.8 ± 88.3 μm2:Hmgcs2ΔHep: 444.0 ± 118.5 μm2; p < 0.0001). RNA-seq analysis revealed that the upregulation of glycolytic genes induced by Combined Stress did not occur inHmgcs2ΔHepmice, and a metabolic phenotype favoring fatty acid oxidation persisted. In the liver, hepatocyte destruction and increased serum fatty acid levels were observed. Additionally, H9C2 cells treated with β-hydroxybutyrate showed decreased fatty acid utilization and increased glucose utilization.Conclusion:In cardiac hypertrophy induced by obesity and hypertension, ketone body synthesis mitigates fatty acid overload and promotes glucose utilization, thereby exerting an anti-hypertrophic effect.

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 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 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 A4141163-A4141163, November 12, 2024. Background:The rising incidence of stroke among young adults is partly explained by underdiagnosis of risk factors such as hypertension. Current blood pressure cutoff values for hypertension diagnosis in adolescence are not based on cardiovascular outcomes and lack specificity for sex, even though female adolescents have lower blood pressure values.Methods:A nationwide, population-based, retrospective cohort study including data of all Israeli adolescents (16-19 years) who were evaluated prior to mandatory military service in 1985 through 2013. The medical evaluation included routine measurements of height, weight, and blood pressure. The primary outcome was the first occurrence of a stroke at a young age (≤52 years) as documented in the National Stroke Registry. Cox proportional hazard models were applied separately for males and females and adjusted for adolescent body mass index and sociodemographic variables. Diabetes status in adulthood, as documented in the National Diabetes Registry, was also accounted. Several sensitivity analyses were conducted, including the evaluation of ischemic stroke cases only as the outcome and stroke occurrence at a very young age (≤45 years).Results:The cohort comprised 1,897,048 adolescents (42.4% females). During 11,355,476 person-years of follow-up, there were 1,470 first stroke events, 1,233 (83.8%) cases were of ischemic etiology. In male adolescents, a diastolic blood pressure of ≥80 mmHg was associated with an adjusted hazard ratio (aHR) for stroke at a young age of 1.28 (95% confidence interval 1.05-1.58) (Image 1). In male adolescents with blood pressure of 70-79 mmHg, the aHR was comparable to that of the reference group (

Circulation, Volume 150, Issue Suppl_1, Page A4141859-A4141859, November 12, 2024. Background:Field activation of patients with ST-segment elevation myocardial infarction (STEMI) by Emergency Medical Services (EMS) during the COVID-19 (COVID) pandemic era involved a change in policy whereby patients underwent COVID-19 testing in the emergency department (ED) prior to Percutaneous Coronary Intervention (PCI) versus bypassing the ED to the Catheterization (Cath) Lab.Research Question:We aimed to compare In-Hospital Mortality and other performance metrics of field activated STEMI patients at a large rural health system during the COVID era to pre and post pandemic periods.Methods:Retrospective single-center (Essentia Health, Duluth, MN, USA) cohort study of consecutive patients with STEMI activation identified in the field by EMS prior to the COVID era (5/27/2018–3/26/2020), during the 22 months of the COVID testing policy (3/27/2020–1/25/2022), and post-COVID when ED bypass resumed (1/ 26/2022–11/26/2023). The main outcomes of this study were in-hospital mortality and common STEMI system performance metrics.Results:A total of 373 consecutive field activated STEMI cases were included (pre COVID [N =132], COVID [N = 104], post COVID [N = 137]). Pre COVID, 40.9% of EMS activated STEMI cases stopped in the ED prior to the Cath Lab, 97.1% during the COVID era, and 51.1% in the post-COVID era (p

Circulation, Volume 150, Issue Suppl_1, Page A4144997-A4144997, November 12, 2024. Introduction:Myocardial injury in patients hospitalized with acute on chronic heart failure concurrent with index SARS-CoV-2 (CoV-2) infection is well described, though studies incorporating pre- and post-acute COVID-19 (PAC) are lacking. We address this gap by estimating intensity of acutely decompensated heart failure (ADHF) using time-series pro-BNP levels across hospitalizations pre- vs. respectively index and initial readmission (PAC1).Hypothesis:Case time series analysis will reveal association (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.

Circulation, Volume 150, Issue Suppl_1, Page A4126581-A4126581, November 12, 2024. Background:Coronavirus Disease-19 (COVID-19) pandemic had a significant impact on emergent and elective treatment strategies in patients with cardiovascular disease. We aimed to examine the impact of COVID-19 on septal reduction therapy (SRT) in hypertrophic cardiomyopathy (HCM).Methods:National Inpatient Sample 2019-2021 was queried to identify patients with HCM and SRT using appropriate ICD codes. Temporal trends for SRT were obtained before and after COVID-19 outset.Results:There was a significant decline in the number of SRT from 2019 to 2020 (1505 vs. 1180, p

Circulation, Volume 150, Issue Suppl_1, Page ASa907-ASa907, November 12, 2024. Background:Different from the negative impact of COVID-19 pandemic on outcomes after out-of-hospital cardiac arrest (OHCA) collapsed before emergency medical service (EMS) arrival, there was a report suggested that COVID-19 pandemic did not affect outcomes after OHCA witnessed by EMS personnel. However, no large-scale studies have examined the impact of COVID-19 pandemic after EMS-witnessed OHCA, focusing on favorable neurological outcomes.Research Questions:Does COVID-19 pandemic affect favorable neurological outcomes after EMS-witnessed OHCA?Aims:To assess COVID-19’s impact on favorable neurological outcomes after EMS-witnessed OHCA.Methods:We performed an interrupted time series analysis (ITSA) with a prospective, nationwide, population-based registry in Japan to assess trends of incidence and favorable neurological outcome (Cerebral Performance Category 1 or 2) at 30 days with adult EMS-witnessed OHCA between pre-pandemic (January 2016-March 2020) and pandemic (April 2020-December 2021) periods. Subgroup analyses were performed by stratifying regions by infection spread status defined by whether a state of emergency has been declared. To assess whether there are differences in trends between areas with and without COVID-19 spread, we performed a controlled ITSA between the two areas.Results:We identified 58,315 patients with adult EMS-witnessed OHCA, 41,112 during the pre-pandemic period and 17,203 during the pandemic period. There was no significant increase in the incidence of EMS-witnessed OHCA during the pandemic period (0.03 per 100,000 person-years; 95% confidence interval [CI], –0.02 to 0.08; p = 0.21). Favorable neurological outcome significantly decreased (relative risk [RR], 0.80; 95% CI, 0.71 to 0.91; p < 0.01). In subgroup analysis, favorable neurological outcome significantly decreased in areas with COVID-19 spread (RR, 0.67; 95% CI, 0.56 to 0.81; p < 0.01), while there was no significant difference in areas without COVID-19 spread (RR, 0.91; 95% CI, 0.77 to 1.07; p = 0.24). A controlled ITSA showed that favorable neurological outcome significantly decreased in areas with COVID-19 spread compared to without COVID-19 spread (RR, 0.77; 95% CI, 0.60 to 0.98; p = 0.04).Conclusion:Unlike previous studies, our research with a nationwide, population-based registry showed that COVID-19 pandemic influenced favorable neurological outcome in EMS-witnessed OHCA. This trend appears to be more pronounced in areas with widespread infection.