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

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 A4143772-A4143772, November 12, 2024. Introduction:Mitral valve prolapse (MVP) is the most common cause of primary mitral regurgitation and is estimated to affect between 1-3% of the general population. A subset of individuals with MVP develop malignant arrhythmias, often in the context of myocardial fibrosis. The genetics of MVP, and genetic factors explaining why only some individuals with MVP have adverse outcomes, remains poorly understood.Methods:We defined MVP using a combination of claims data and echocardiographic diagnosis across 15 cohorts spanning 5 countries and performed a meta-analysis of genome-wide association studies (GWAS) for MVP including 19,487 MVP cases among 2,247,054 individuals. Causal genes were prioritized using a combination of methods including the identification of variants in active promoters/enhancers using mitral valve ATAC-seq data from an external dataset. To determine whether prioritized genes may be differentially expressed in myocardial fibrosis, we compared single-cell RNA sequencing between fibrosed papillary muscles and normal left ventricular among two individuals with severe MVP.Results:There were 67 unique genome-wide significant (GWS; 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 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 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 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 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 A4127513-A4127513, November 12, 2024. Background:SARS-CoV-2 infection affects the cardiopulmonary system in both the acute and long-term phase. This study aimed to comprehensively assess symptoms and potential long-term impairments 6, 18 and 30 months in patients previously hospitalized for severe Covid-19 infection.Methods:This prospective registry included patients hospitalized for PCR-confirmed Covid-19 infection. Approximately 6 months post-discharge, follow-up examination included patient history, clinical examination, echocardiography, electrocardiogram, cardiac magnetic resonance imaging (cMRI), chest computed tomography (CT) scan, pulmonary function test (PFT), six-minute walk test (6MWT) and a comprehensive laboratory panel. Patients with pathologic findings during the first visit underwent a second (at 18 months) and third (at 30 months) follow-up examination. Those without pathologic findings or who refused further medical examinations were contacted via phone to inquire about symptoms.Results:Between July 2020 and April 2022, 200 patients (91% general ward, 9% intensive care unit) were recruited. Due to dropouts, the second visit was conducted in 170 patients, and the third visit in 139 (74 in person, 65 via telephone). Long Covid criteria were fulfilled by 73% at 6 months, 52% at 18 months and 49% at 30 months post-discharge, with fatigue being the most common symptom (Figure 1). Echocardiography at 6 months showed impaired left ventricular function in 15 patients, with normalization in 80% at 18 months and further 66% at 30 months (Figure 2). cMRI revealed pericardial effusions in 28 patients at 6 months, which resolved in 47% at 18 months and in further 60% at 30 months. Signs of peri- or myocarditis were present in 7 patients at 6 months and were resolved in all 4 patients who attended control studies at 18 months. Chest CT scans at 6 months identified post-infectious residues in 41 patients, with full recovery in 20% at 18 months without further normalization after 30 months.The length of in-hospital stay was identified as a significant predictor for persisting Long Covid 6 months after discharge (95% CI: 1.005 – 1.12, p=0.03).Conclusion:While the prevalence of Long Covid decreased over time, a significant symptom burden persisted at 6, 18 and even 30 months after severe Covid-19 infection. Structural and functional abnormalities were less frequent compared to reported symptoms, posing a challenge in substantiating the causes of these symptoms.

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 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 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 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 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 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 A4143723-A4143723, November 12, 2024. Introduction:Thrombocytosis, sometimes extreme, after acute Kawasaki disease (KD) is common and felt to be pathognomonic of this diagnosis, although has also been reported after multisystem inflammatory syndrome in children (MIS-C), a clinically similar condition. We sought to determine differences in factors associated with thrombocytosis for each condition.Methods:From 01/2020 to 10/2023 across 41 sites in 8 countries from the International KD Registry, 1674 MIS-C and 1290 contemporaneous KD patients with adequate laboratory data were included in the analysis. Age-related cutpoints (derived from the CALIPER Study of normal children/adolescents; AJCP 2020; 154:342) were applied to peak platelet counts to define thrombocytosis (age 647 x109/L; age 1 to 434; age 12 to 371). Associations of demographic, clinical, laboratory and outcome factors with thrombocytosis were determined for each diagnosis group.Results:Thrombocytosis was more prevalent after KD (57%) than MIS-C (49%; p