Risultati per: Gestione dell’infarto del miocardio acuto durante COVID-19

Circulation, Volume 150, Issue Suppl_1, Page A4126987-A4126987, November 12, 2024. Background:COVID-19 infection has been associated with a broad range of clinical manifestations. There are very few reported cases of COVID-19 patients presenting with syncope as an initial symptom. We present an extraordinary case of recurrent neurocardiogenic syncope in a COVID-19 patient.Case:A 66-year-old male presented after experiencing two episodes of syncope. He denied any prodromal or anginal symptoms. His medications included propranolol 10 mg twice daily for essential tremors. He had no family history of unexplained syncope or sudden cardiac death. He was hemodynamically stable and had one episode of fever at 102°F. Telemetry recording showed vagal-mediated sinus arrest and pauses without escape. Blood work showed normal cell counts, electrolytes, thyroid-stimulating hormone, and erythrocyte sedimentation rate, with a slightly elevated C-reactive protein of 22.2 mg/L. He tested positive for COVID-19 and had negative Lyme and Ehrlichia serologies.Decision Making:Due to symptomatic long sinus pauses, propranolol was discontinued, and he received a temporary pacemaker set at 50 beats per minute (bpm). He had another syncopal episode while being paced at 50 bpm, suggesting a neurocardiogenic mechanism, so the pacing rate was increased to 70 bpm. An echocardiogram showed a normal ejection fraction without any significant valvular disease. The syncope was determined to be vasovagal due to autonomic dysfunction in the setting of COVID-19. After 72 hours without further syncope, the temporary pacemaker was removed, and he was discharged home with an implantable loop recorder (ILR). A one-month follow-up showed no syncope, and ILR interrogation showed no bradycardia or pauses.Conclusion:Neurocardiogenic syncope with prolonged asystole and sinus pauses is an uncommon presentation of COVID-19 infection. The clinical course of autonomic dysfunction following COVID-19 is not very clear, and monitoring with an ILR is reasonable before considering permanent pacemaker implantation.

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.

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 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 A4144056-A4144056, November 12, 2024. Background:COVID-19 infections have been associated with cardiovascular autonomic dysfunction (AD). Clinical findings include fatigue, cognitive impairment, and postural intolerance. However, quantitative post-COVID AD assessments are lacking.Objective:Compare autonomic testing measures of post-COVID-19 subjects to controls and those with pure autonomic failure (PAF).Methods:Autonomic testing included 1) change in heart rate (HR) and blood pressure (BP) with active standing (AS) and tilt table testing (TT), 2) time to BP nadir and recovery during AS and TT, 3) Valsalva ratio (VR), and 4) respiratory sinus arrhythmia (RSA). Comparisons between two groups were made using t-tests, Kruskal-Wallis, or chi-square tests. Multivariable linear regression was used to adjust findings for age and sex. A p-value of

Circulation, Volume 150, Issue Suppl_1, Page ASa807-ASa807, November 12, 2024. Background:Despite the lack of evidence supporting the use of chest compression-only cardiopulmonary resuscitation (CO-CPR) emphasizing the importance of rescue breathing for pediatric out-of-hospital cardiac arrest (OHCA), prehospital CO-CPR is increasing. The COVID-19 pandemic may have led more bystanders to perform CO-CPR, even for pediatric OHCA. However, studies on the dissemination of CO-CPR and outcomes in pediatric OHCA are limited.Hypothesis:Spread of CO-CPR led to increased mortality in pediatric OHCA.Aims:Investigate the mortality of nationwide pediatric OHCA patients with the dissemination of CO-CPR pre- and post-COVID-19.Methods:We conducted a retrospective study using a Utstein-Style population cohort database (Japanese National Registry). Pediatric OHCA patients (≤17 years old) with bystander resuscitation attempts registered between the pre-COVID-19 era (2017-2019) and the post-COVID-19 era (2020-2021) were included. The primary outcome was 30-day mortality after OHCA. The secondary outcome was 30-day poor neurological outcomes, defined as Cerebral Performance Category scores of 3, 4, or 5. We used Poisson regression with robust variance to estimate adjusted risk ratio (aRR) with 95% confidence interval (CI) and the population attributable fraction (PAF, %) with a focus on the post-COVID-19 period.Results:A total of 3,352 pediatric OHCA, 2,023 pre-COVID-19, and 1,329 post-COVID-19 patients received bystander CPR and were registered in the database. CO-CPR was more common than CPR with rescue breathing (RB-CPR) during the pre- and post-COVID-19 periods [pre-COVID-19: 1,356 (67.0%) vs. 667 (33.0%), post-COVID-19: 1,048 (78.9%) vs. 281 (21.1%)]. Comparison of CO-CPR vs. RB-CPR showed increased 30-day mortality in both periods [pre-COVID-19: 1,081/1,356 (79.7%) vs. 420/667 (63.0%), post-COVID-19: 841/1,048 (80.2%) vs. 181/281 (64.4%)]. In the overall cohort, mortality increased with CO-CPR (aRR: 1.16, 95% CI: 1.09-1.23, PAF:1.60%). Due to the increased number of patients receiving CO-CPR, we estimated 21.2 excess deaths over the two-year post-COVID-19 period. Similar results were observed for poor neurological outcome (aRR: 1.10, 95% CI: 1.05-1.16, PAF: 1.10%, excess poor outcome: 14.6]).Conclusion:With the spread of CO-CPR for pediatric OHCA, an estimated 10.6 excess deaths per year attributed to CO-CPR may have occurred in the post-COVID-19 period compared to the pre-COVID-19 period in Japan.

Circulation, Volume 150, Issue Suppl_1, Page A4140703-A4140703, November 12, 2024. Background:The mRNA vaccines against COVID-19 are highly effective but have been associated with a rare non-infective form of myocarditis, particularly in young males after receiving the second dose. Understanding the mediators of this adverse effect is crucial to enhance the safety of future mRNA vaccines.Hypothesis:Myocardial injury following COVID-19 mRNA vaccination is mediated by overproduced cytokines, and estrogens have a protective effect on this adverse effect.Approach:Candidate cytokine mediators were identified through analysis of proteomics data from plasma samples of vaccinated individuals. Human iPSC-derived macrophages and cardiomyocytes were used to model cytokine-induced effects. An in vivo mouse model of cytokine-induced myocardial injury was employed to assess the impact of the cytokine cocktail and estrogens.Results:CXCL10 and IFN-γ were consistently upregulated in vaccinated individuals on day 1 and further elevated in patients with myocarditis following mRNA vaccination. Consistently, iPSC-derived macrophages exposed to COVID-19 mRNA vaccines produced these cytokines. Next, iPSC-derived cardiomyocytes exposed to these cytokines showed impaired contractility, arrhythmogenicity, and pro-inflammatory gene expression. The phytoestrogen genistein mitigated these effects in vitro, reducing cytokine-induced proteasomal degradation of cardiac proteins and preserving contractile function. In vivo, genistein significantly decreased cardiac injury markers and immune cell infiltration in a mouse model of cytokine-induced myocardial injury.Conclusion:CXCL10 and IFN-γ are key mediators of myocardial injury post-mRNA vaccination. Genistein shows potential as a therapeutic agent to mitigate associated cardiovascular risks.

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 A4143094-A4143094, November 12, 2024. Background:Peripartum cardiomyopathy (PPCM) is defined as a dilated form of cardiomyopathy that occurs within the last month of pregnancy and up to 5 months postpartum. The etiology is likely multifactorial and viral infections may account for up to a third of PPCM cases. We aimed to examine the impact of concurrent COVID-19 infection on in-hospital outcomes of women with PPCM.Methods:National Inpatient Sample was queried to identify women admitted with PPCM with COVID-19 (group A) between the years 2020-2021 and without (group B) concurrent COVID-19 infection between the years 2016-2019.Results:A total of 19135 women were admitted with PPCM between the years 2016-2021, of whom 420 (2%) had concurrent COVID-19 infection. Group A PPCM followed a seasonal pattern with peak incidence in fall (43%) followed by winter (31%), spring (13%) and summer (13%) [p=0.002]. Group A was more often Hispanic (20.3% -vs- 10.8%, 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.

Circulation, Volume 150, Issue Suppl_1, Page A4138301-A4138301, November 12, 2024. Background:Hyperlipidemia (HLD) is a major risk factor for cardiovascular disease (CVD). Little is known regarding temporal variation in CVD mortality related to HLD. The COVID-19 pandemic added complexity to factors influencing CVD mortality.Question:What are the yearly trends and impact of the COVID-19 pandemic on HLD-related CVD mortality in the United States?Methods:Mortality and demographic data for adults were obtained from CDC repository from 1999-2020, using ICD-10 codes HLD (E78.0-E78.5) and CVD (I00-I99). Age adjusted mortality rates (AAMR) per 1,000,000 population was standardized to the 2000 US population. Log-linear regression models evaluated mortality shifts. Average annual percentage change (AAPC) from 1999-2019 was used to calculate projected AAMR in 2020, subsequently compared to actual 2020 death rates to estimate pandemic-attributed excess deaths.Results:A total of 483,155 HLD-related CVD deaths were recorded between 1999-2020. Despite the CVD mortality decline in general population, HLD-related CVD AAMR rose from 36.33 [95% CI, 35.52-37.13] in 1999 to 99.77 [98.67-100.87] in 2019. Ischemic heart diseases (AAMR 49.39) were the most common causes of death while hypertension had the highest annual mortality increase (AAPC +10.23%) in populations with HLD. Higher HLD-related CVD mortality was observed in males (AAMR 104.87) than females (AAMR 61.93), in those ≥75 years (AAMR 646.45) than 35-75 years (AAMR 54.11), in non-Hispanic (NH) (AAMR 82.49) than Hispanic (AAMR 58.98) populations, and in rural (AAMR 89.98) than urban (AAMR 78.94) regions. NH Black populations (AAMR 84.35) and Western US regions (AAMR 96.88) had the highest HLD-related CVD. The first year of COVID-19 pandemic resulted in 10.55% excess HLD-related CVD death, with the most prominent increase in the 35-75 years age group (14.23%), Hispanic (17.96%), Black (14.82%), and urban (11.68%) populations.Conclusions:Our study revealed an increase in HLD-related CVD mortality which was exacerbated by the COVID-19 pandemic. Higher CVD mortality disproportionately affected males, Black, elderly (≥75 years), and rural populations with HLD. Further research is needed to validate our findings and identify contributing factors.

Circulation, Volume 150, Issue Suppl_1, Page A4141946-A4141946, November 12, 2024. INTRODUCTION:Mechanisms contributing to the post-acute sequelae of SARS-CoV-2 (PASC, aka Long COVID) and associated functional limitations are unclear.RESEARCH QUESTION:Determine cardiovascular, autonomic and exercise physiology among patients with Long COVID.METHODS:Twenty-one Long COVID patients (16 females, 41±12yrs) underwent cardiovascular assessment during head-up tilt at supine, 30oand 60o, a 10-minute upright standing orthostatic challenge and cardiopulmonary exercise testing (CPET). Baroreceptor sensitivity was determined with Valsalva maneuver. Heart rate (HR) and blood pressure (BP) were monitored continuously. Plasma norepinephrine (NE) was monitored during tilt.RESULTS:During tilt, HR increased with transition from supine to 30oand 60o(72±12 v. 80±14 v. 90±15bpm, P

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 A4146939-A4146939, November 12, 2024. Background:New onset AF during acute illness has a high rate of AF recurrence within 5-yr. However, little is known about AF progression in patients with new onset AF during COVID illness. It is also unknown whether the time of COVID diagnosis (early vs late) impacts AF progression. More specifically, did the potentially different immune and inflammatory responses during early vs late COVID produce structural and electrical cardiac remodeling that would increase the likelihood of AF progression.Objective:We sought to compare AF progression in patients with new onset AF during early vs late COVID and hypothesized that early COVID was associated with increased AF progression compared to late COVID.Methods:From Apr 2020 to Feb 2024, patients receiving a SARS-2-CoV test without a history of AF with new onset AF and at least 3-mo of follow up were included (N=11,767). Patients were subdivided based on pos vs neg SARS-2-CoV test and time of diagnosis. Early COVID diagnosis (n=3052) included Apr 2020-Aug 2021 and late COVID (n=8715) included Sep 2021-Feb 2024. AF progression endpoints at 3-, 6- and 12-mo included AF hospitalization, AF emergency department (ED) visit, cardioversion and AF ablation.Results:Patients with late COVID were more likely females with hypertension, coronary artery disease and hyperlipidemia compared to early COVID patients. At 3- and 6-mo follow-up there was no difference in AF progression between the early and late COVID groups for any endpoint. In contrast, at 12-mo follow up there was in increase in late diagnosis group AF ED visits (11% vs 7.6%,p

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