Risultati per: Vaccinazione anti-Covid e rischio di malattia grave

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 A4125636-A4125636, November 12, 2024. Background:Postural orthostatic tachycardia syndrome (POTS) is a prevalent cardiovascular disorder after COVID-19 infection. Although POTS is characterized by the presence of sinus tachycardia, other hemodynamic disturbances including blood pressure (BP) regulation, remain largely unexplored.Aims:We investigated BP changes using 24-hour ambulatory-BP-monitoring in patients with new-onset POTS after COVID-19 compared with pre-pandemic healthy controls.Methods:We performed a case-control study in 100 verified COVID-19 patients with new-onset POTS (mean age 40.0±12.9 years, 85% women) diagnosed by positive head-up tilt-testing versus 100 healthy controls (mean age 45.0±14.6 years, 70% women) from a population-based cohort with negative active standing test, no history of syncope, orthostatic intolerance, or endocrine disease. We analyzed 24-hour Systolic BP (SBP) and hypotensive SBP episodes (

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

Circulation, Volume 150, Issue Suppl_1, Page A4129709-A4129709, November 12, 2024. Background:The current unmet needs for aspirin usage in atherosclerosis lie in its short half-life and narrow indication for anti-platelet effects. Daily aspirin intake is mandatory, and the anti-inflammatory effects of aspirin for atherosclerosis have not successfully translated to clinical practice. Nanoparticles remain in circulation for 2-3 days, with a large portion being cleared by splenic monocytes, which are known to inherently target inflamed sites.Hypothesis:By altering the pharmacokinetics of aspirin through loading into nanoparticles, aspirin-nanoparticles can exert prolonged anti-platelet effects and target atherosclerosis sites via monocyte carriers for anti-inflammatory effects, resulting in dual therapies.Methods:Splenic monocytes were loaded with aspirin-liposomes and co-cultured with endothelial cells or platelets to examine the interactions between them using high-resolution time-series microscopy. Prolonged anti-platelet effects and targeted anti-inflammatory effects of aspirin were validated in intact mice and hindlimb ischemia models, respectively. Furthermore, the dual therapies of aspirin-liposomes were validated in an atherosclerotic mouse model created by partial carotid ligation and a western diet in apoE gene knock-out mice.Results:When splenic monocytes were loaded with aspirin-liposomes, they emitted extracellular vesicles (EVs) loaded with aspirin towards endothelial cells or platelets. As inflamed cells upregulate caveolin expression, they uptake an increased amount of transferred EVs compared to non-inflamed cells. Additionally, aspirin-liposomes showed prolonged circulation time and increased splenic accumulation compared to aspirin itself, resulting in prolonged anti-platelet effects ( >7 days) and targeted anti-inflammatory effects at inflamed sites. Compared to the daily oral aspirin group in the atherosclerosis model, the weekly intravenous aspirin-liposome group showed superior therapeutic effects, including attenuated systemic and local inflammation and patent lumen in atherosclerotic sites.Conclusion:Aspirin-nanoparticles can exert prolonged anti-platelet effects combined with targeted anti-inflammatory effects, resulting in superior therapeutic effects on atherosclerosis.

Circulation, Volume 150, Issue Suppl_1, Page A4140179-A4140179, November 12, 2024. Background:COVID-19 has led to significant global morbidity and mortality. Its impact on patients with hypertrophic cardiomyopathy (HCM) remains unclear.Aim:To evaluate the impact of COVID-19 infection on the readmission rate and associated outcomes in patients with HCM.Methods:In a retrospective study using the 2020 National Readmission Database, we collected data on patients with HCM who were admitted with the principal diagnosis of COVID-19. The primary outcome was the all-cause 30-day readmission rate. Secondary outcomes were common causes of readmission, in-hospital mortality, and resource utilization.Results:In 2020, a total of 1503 patients with HCM (mean age 67 years, 49% female) were hospitalized for COVID-19. Among them, 1216 (80.9%) were discharged alive and 180 (14.8%) were readmitted within 30 days. In-hospital mortality for readmissions remained relatively unchanged compared with index admissions (15.4% vs 19.0%, P=.34; Table 1). The most common cause of readmission was COVID-19 infection (38%), followed by other infections (11%) and acute kidney injury (4%). The most common cardiac cause for readmission was paroxysmal atrial fibrillation (2%). The mean length of stay for readmissions was relatively similar to the index admission (7.8 vs 9.9 days, P=.43). The mean hospital charge associated with readmission was $84,976 (total hospital charges were $15.2 million). The mean hospital cost associated with readmissions was $24,603 (total hospital costs were $4.4 million). A higher Charlson comorbidity index score was the main independent predictor of higher readmission rates.Conclusions:This study highlights the significant burden of COVID-19 on patients with HCM. Despite efforts to reduce readmission rates, a considerable percentage of patients experienced readmission within 30 days, largely attributed to COVID-19 infection. Close follow-up after discharge could prevent such readmission and the associated high mortality rates.

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

Circulation, Volume 150, Issue Suppl_1, Page 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 A4140218-A4140218, November 12, 2024. Background:Prior data indicated a reduction in mortality among STEMI (ST-elevation myocardial infarction) patients with COVID-19 from 2020 to 2021 in the United States.Objective:To describe national trends and determinants of outcomes among STEMI patients with COVID-19 from 2020-2021.Methods:A retrospective cohort study was conducted using the 2020-2021 Nationwide Inpatient Sample of adults diagnosed with STEMI and COVID-19, assessing in-hospital mortality and the use of percutaneous coronary intervention (PCI), mechanical ventilation, and mechanical circulatory support (MCS).Results:The study included 6,195 STEMI patients with COVID-19 and revealed stable mortality (18% in 2020 to 21% in 2021,p=0.06). Demographic shifts occurred, with White patients increasing from 52% in 2020 to 66% in 2021 (p

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

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

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

Circulation, Volume 150, Issue Suppl_1, Page 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.