Risultati per: Come COVID-19 influenzerà la nostra prossima generazione?

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

Circulation, Volume 150, Issue Suppl_1, Page 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 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 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 A4142935-A4142935, November 12, 2024. Background.Post-COVID syndrome is related to a multisystem disorder that affects in part the cardiovascular system. This disease involves symptoms, and conditions that continue or develop after acute COVID-19. SARS-CoV-2 infection of immune and endothelial cells are associated with NETosis, microthrombosis and endothelial dysfunction that could persist several weeks after acute phase of infection. Damaged endothelial cells can expose the vessel pro-coagulant area leading to platelet and neutrophil clumps. Increased levels of circulating endothelial cells (CECs) have been described as biomarkers for cardiovascular diseases. Therefore, we hypothesize that CECs and microthrombosis are potential biomarkers of vascular dysfunction in Long COVID.Methods.A cross-sectional study was conducted at the Miami VA long COVID clinic. Long COVID cases and controls were recruited according to WHO definition for long COVID. A total of 23 patients and 7 controls were included in this study. Blood samples were collected in Heparin and Sodium Citrate tubes. Cell immunophenotyping and NETosis markers (MPO) were quantified on a Cytek Aurora spectral flow cytometer system. Microclots (CD62P+PAC-1+) and platelet response were assessed by flow cytometry and response to Adenosine di-phosphate (ADP), respectively. A ttest was used for statistical analysis. Differences were considered significant when p < 0.05.Results.The age and gender were similar between cases and controls while their symptom score was significantly different. There was a significant increase in the number of CECs (CD31+CD309+CD45-CD133-) in Long COVID cases. MPO expression in neutrophils (CD11b+CD66b+CD15+) and classical monocytes (CD14+CD16-) was significantly higher in Long COVID. Microclots were significantly elevated, and the platelet aggregation response was dysregulated in Long COVID.Conclusions.CECs and microthrombosis including NETosis are present in Long COVID and may serve as potential biomarkers or causative mechanisms for vascular dysfunction.

Circulation, Volume 150, Issue Suppl_1, Page 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 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 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 A4139757-A4139757, November 12, 2024. Background:The COVID-19 pandemic has significantly exacerbated sleep problems. Pandemic-related lockdowns and drastic changes in daily life have disrupted sleep patterns, resulting in a marked increase in sleep disturbances.Research questions:This study aims to investigate the primary factors contributing to the increase in sleep disturbances during the COVID-19 pandemic in Korea. By utilizing nationally representative data encompassing various variables, this study seeks to identify COVID-19-related factors associated with sleep disturbances during the pandemic.Method:We analyzed data from the nationally representative Korea Community Health Survey conducted in 2020, including 216,809 adults. Changes in daily life due to COVID-19 were assessed by asking participants to score their current situation compared to their pre-pandemic situation, ranging from 100 (no change) to 0 (complete cessation of daily activities). COVID-19 concerns were assessed with five questions: 1) fear of contracting the virus; 2) fear of mortality if infected; 3) fear of blame from others; 4) concerns about the health of vulnerable family members; and 5) concerns about economic impacts. Sleep disturbances were defined as sleeping 5 hours or less per night on average. Logistic regression analyses with a complex sample design were performed to examine the relationship between COVID-19-related factors and sleep disturbances, adjusting for socioeconomic and health-related variables.Results:A high level of lifestyle changes due to COVID-19 (OR = 1.15, 95% CI = 1.11–1.19) and high COVID-19 concerns (OR = 1.04, 95% CI = 1.01–1.08) were associated with an increased likelihood of sleep disturbances. Conversely, resting during COVID-19 symptoms (OR = 0.81, 95% CI = 0.76–0.87), having support during quarantine (OR = 0.93, 95% CI = 0.89–0.97), and trust in the government and neighbors (OR = 0.92, 95% CI = 0.89–0.96) were associated with a decreased likelihood of sleep disturbances.Conclusion:These findings suggest that sleep disturbances during the COVID-19 pandemic were mediated by lifestyle disruptions and high levels of concern. Social support and trust mitigated the impact of COVID-19-related risk factors. As part of preparedness, improving the environment to facilitate adequate rest during illness, ensuring strong social support, and fostering high levels of trust in the government and neighbors may be important to protect sleep health during future public health emergencies.

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

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