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

Circulation, Volume 150, Issue Suppl_1, Page A4119262-A4119262, November 12, 2024. Background:Impediment in the excretion of lipid deposits within SMC-derived foam cells (SMC-FCs) is one of the reasons for the continuous expansion of the plaque necrotic core. This study aims to explore the effect and underlying mechanimsm of exosomes secreted by M2 macrophage (M2-exos) on SMC-FCs lipid metabolism and plaque stability.Methods:First, immunofluorescence was used to detect the expression levels of CD45 (a recognized differentially expressed molecule of myeloid and SMC-FCs) and the key proteins of cholesterol efflux pathway, ABCA1 and ABCG1, in human early and late plaques. Exosomes derived from M0 and M2 macrophages were purified by sucrose density gradient centrifugation, and characterized based on specific morphology and surface markers. Western blot, Oil red O staining and cell total cholesterol assay were used to assess the effects of M2-exos on the lipid mechanism of SMC-FCs. RNA-seq was used to detect the miRNA profiles of M2-exos. Quantitative real-time PCR was used to identify candidate miRNAs. The dual-luciferase reporting system was utilized to assess the regulatory effect of candidate miRNA on target gene. Then, the effect of M2-exos on the progression and stability of plaques in ApoE-/-mice was evaluated using Oil red O, H&E, Masson, Movat and immunohistochemistry.Results:Immunofluorescence revealed that compared with early plaques, VSMC-FCs (CD45-) were significantly increased in late plaques, and the expression levels of ABCG1 and ABCA1 were marked lower than those in macrophage-derived foam cells (CD45+). Purified M2-exos treatment significantly promoted the cholesterol efflux of SMC-FCs in vitro. In high-fat-fed ApoE-/-mice, M2-exos significantly reduced the VSMC-FCs, delayed the progression of plaques, decreased necrotic core area and enhanced plaque stability. MiRNA profiling and comprehensive analysis of signaling pathways showed that M2-exos were rich in miR-7683-3p, which played a key role in regulating SMC-FCs lipid metabolism through PPARγ-LXRα-ABCA1/ABCG1 pathway. Dual-luciferase reporting assay showed that miR-7683-3p can specifically bind to the promoter region of homeobox genes A1(HoxA1), an inhibitor of PPARγ-LXRα-ABCA1/ABCG1 pathway.Conclusion:M2-exos exerted an obvious atherosclerotic protective effect, and the underlying mechanism was closely related to MiR-7683-3p, which targeted the 3’UTR of HoxA1 mRNA and activated the PPARγ-LXRα-ABCA1/ABCG1 mediated cholesterol efflux in SMC-FCs.

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 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

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 A4138339-A4138339, November 12, 2024. Introduction:Immune checkpoint inhibitors (ICI), such as anti-PD-1 monoclonal antibodies are increasingly used in anti-cancer therapy. However, several cardiovascular adverse effects can occur with the use of ICIs, including new-onset heart failure.Hypothesis:We hypothesized that prior myocardial ischemic injury could exacerbate cardiac dysfunction and inflammation caused by anti-PD-1 treatment. Moreover, we investigated whether abatacept, a T-cell co-stimulation blocker, can prevent ICI-induced cardiac effects.Methods:To induce reversible cardiac ischemia, C57Bl/6J mice were treated with isoprenaline (ISOP group) or with PBS (CON group), followed by 16 weeks of recovery period. Following this, mice from both groups were divided into three further treatment groups: isotype control, anti-PD-1, or anti-PD-1 combined with abatacept, and were treated for two weeks, with three weekly intraperitoneal injections. Echocardiography was performed to evaluate cardiac function while myocardial inflammation was assessed by qRT-PCR and immunohistochemistry. Flow cytometry and Western blot were used to investigate changes occurring in the thymus.Results:Mice with normal heart function but with prior ischemic injury and anti-PD-1 treatment (ISOP + anti-PD-1) showed significantly decreased fractional shortening and cardiac index on echocardiography, while in animals with abatacept co-treatment (ISOP+anti-PD-1+abatacept) cardiac function was not altered. Increased immune cell infiltration was seen in the myocardium of the ISOP+anti-PD-1 treated group compared to CON animals, including T-cells and macrophages, with increased expression of pro-inflammatory cytokines, while co-treatment with abatacept ameliorated the inflammatory response. In the thymus, increased expression of PD-1 was found after abatacept co-treatment.Conclusion:Prior myocardial ischemic injury was associated with cardiac dysfunction and inflammation after anti-PD-1 treatment, which was ameliorated by abatacept co-treatment. Patients with prior cardiac ischemic events may be at greater risk for developing ICI-induced cardiotoxicity, including new-onset HF.

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 A4147456-A4147456, November 12, 2024. Background:Cardiac fibrosis is a condition characterized by deposition of extracellular matrix proteins and myofibroblasts, leading to scar formation, cardiac dysfunction and arrhythmogenesis. Various cardiometabolic stressors can promote fibrosis and scarring, including MI, hypertension, diabetes and obesity. Targeted therapy to prevent cardiac fibrosis is therefore an important unmet medical need. In a mouse model of obesity-related atrial fibrillation (AF), inhibition of SGK1 reduced markers of inflammation and fibrosis, suggesting SGK1 as a novel target. Several SGK1 inhibitors are being evaluated in clinical studies for the treatment of long QT syndrome, paroxysmal AF, and heart failure.Hypothesis:SGK1 activation is a significant driver of inflammation and fibrosis, and its inhibition may offer a new therapeutic strategy for treating fibrotic diseases, including those of the cardiovascular system.Methods:Primary hepatic stellate cells, lung fibroblasts, and proximal tubule cells were treated with TGFβ for 24-48 hours to induce fibrosis and measure the effects of SGK1 inhibition on markers of fibrosis (alpha SMA and collagen 1). Three, selective and potent, SGK1 inhibitors (SGK1-I 1,2,3) were tested in a BioMAP fibrosis panel at concentrations ranging from 0.3 to 10 µM. The fibrosis panel includes three systems that model TGFβ and TNFα driven myofibroblast differentiation during chronic inflammation and wound healing. Markers of fibrosis, tissue remodeling, myofibroblast activation, and inflammation were measured quantitatively. IC50s were determined using GraphPad Prism.Results:In primary human stellate cells, SGK1-I,1,2,3 inhibited αSMA and collagen 1 mRNAs with IC50s ranging from 0.1- 0.8 µM and 1.0-3.0 µM, respectively. In primary lung fibroblasts, treatment with SGK1-I reduced the mRNA and protein expression of αSMA. Treatment of cells from different tissues with TGFβ resulted in a 1.5-to-3.0-fold increase in SGK1 mRNA and protein and this was blocked by the TGFβ receptor inhibitor SB525334. SGK1 inhibitors displayed anti-inflammatory and anti-fibrotic properties in the BioMAP panel, with inhibition of IL-6, IL-8, MCP-1, and αSMA, collagen 1, and TIMP1 respectively.Conclusion:SGK1 is an important effector of TGFβ signaling. The development of SGK1 inhibitors may represent a new therapeutic strategy for treating fibrotic diseases. Additional studies are warranted to further evaluate novel SGK1 inhibitors in cardiac fibrosis

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 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 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

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 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 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 A4137045-A4137045, November 12, 2024. The formation of occlusive thrombi resulting in myocardial infarction or stroke present a significant challenge for the healthcare community. Activation of the prostacyclin (IP) receptor has been shown to decrease platelet reactivity, however current IP agonists lack a sustained effect in the blood. We have developed CS585, an IP receptor agonist with sustained anti-thrombotic effects in the blood, which could represent a novel prevention strategy in targeting thrombosis. We sought to assess the anti-thrombotic efficacy and pharmacodynamic stability of IP agonists CS585, iloprost and selexipag, in bothex vivoandin vivomodels.We evaluated the timeframe of effect of CS585, iloprost, and selexipag in mice following a single IV dose. Inhibition of thrombus formation was measuredex vivoin whole blood under arterial shear rates.In vivo, CS585, iloprost, or selexipag, were administered prior to labeling of platelets and fibrin. Thrombus formation at the site of injury was measured using the cremaster arteriole injury thrombosis assay.CS585 administered to mice prior to blood draw decreases platelet adhesion and blood clot formation under arterial shear conditions. These effects are observed up to 24 hours post-administration; however, the effects of iloprost and selexipag return to pre-treatment levels by 24 hours.In vivo, mice administered iloprost or selexipag demonstrated a decrease in platelet accumulation and fibrin formation, however the effects were abrogated post-administration by 10 minutes and 4 hours, respectively. Administration of CS585, however, demonstrated sustained inhibition of thrombus formation at the site of injury, with inhibitory effects observed at 18 hours post-administration.We have used bothin vivoandex vivomodels to demonstrate the anti-thrombotic efficacy of IP receptor agonists. Our results suggest that CS585, a novel IP receptor agonist, sustainably inhibits platelet activation and clot formation for extended periods, in contrast to existing alternatives. This demonstrates a significant improvement in the pharmacodynamic effects of IP receptor agonists in the blood, highlighting CS585 as a novel anti-platelet therapeutic with the potential to treat thrombotic diseases.

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: