Search Results for: Come stress e attacchi di cuore sono collegati

Circulation, Volume 150, Issue Suppl_1, Page A4119267-A4119267, November 12, 2024. Background:Sarcoidosis, a systemic granulomatous inflammatory disorder can involve various organs, including the heart but isolated bi-atrial cardiac involvement is rare. Advanced cardiac imaging especially in atypical presentations, can aid in early diagnosis.Case:A 59 year-old man with history of biopsy-proven pulmonary sarcoidosis presented with non exertional chest pain for 2 months. EKG, cardiac enzymes, and Initial echocardiogram(TTE) was unremarkable. Stress echocardiogram ruled out myocardial ischemia. CT scan noted mediastinal lymphadenopathy consistent with known sarcidosis. In absence of other explainable etiolgies for chest pain, Cardiac MRI was done and showed preserved biventricular function, subepicardial enhancement in the basal inferior, inferolateral, and anterolateral walls. The enhancement raised suspicion for CS. However, symptoms resolved spontaneously, cardiac workup paused and he was monitored conservatively with serial Echocardiogram(TTE) until onset of dyspnea 3 years later. Repeat TTE and EKG then noted newly enlarged left atrium and atrial tachycardia. Further testing with Cardiac positron emission tomographic imaging with F-18 fluorodeoxyglucose (FDG-PET CT) showed abnormal myocardial uptake in both atrial posterior walls but no ventricular involvement, indicative of isolated bi-atrial inflammation in CS. He was treated with prednisone and methotrexate. Successful symptom and inflammation resolution on FDG-PET CT occurred in 3 monthsDiscussion:CS is rare and seen clinically in about 5% and diagnosed postmortem in 25% of sarcoidosis cases. Symptoms vary widely, with potential for severe heart complications. Left ventricle and interventricular septum are commonly involved, but isolated bi-atrial involvement is rare. Early diagnosis aided by Cardiac MRI and FDG-PET CT is crucial. Prednisone is mainstay of treatment, often combined with methotrexate. Cases of concurrent atrial CS involvement and bi-atrial fibrosis with Left ventricular hyperenhancement are documented, but this is the first known report of isolated bi-atrial hyperenhancement on FDG-PET CT for CS. This case highlights the need for symptom correlation with clinical and imaging follow-up, especially in atypical presentations.

Circulation, Volume 150, Issue Suppl_1, Page A4139715-A4139715, November 12, 2024. Background:Plaque structural stress (PSS) is the stress within the body of atherosclerotic plaques, resulting from the dilation and stretching of vessels due to arterial pressure. Plaque rupture often occurs at sites of elevated PSS, especially when the stress level exceeds the mechanical strength of the plaque. Notably, a significant difference in stiffness between the softer lipid core and the stiffer fibrous cap significantly increases PSS. By increasing the elastic modulus (a measure of material stiffness) of lipid cores and thus reducing the stiffness disparity between plaque components, it may be possible to transition vulnerable plaques from a state of instability to stability.Hypothesis:Both CSL112, a human plasma-derived apolipoprotein A-I formulation that enhances reverse cholesterol transport, and atorvastatin increase the stiffness of plaque lipid cores.Methods:Rupture-prone atherosclerotic plaques were induced in 47 ApoE knockout male mice using a carotid tandem stenosis model after a 7-week high-fat diet. After surgery, mice were treated with either CSL112 (100 mg/kg) intravenously twice weekly (n=15), saline intravenously (n=15), or atorvastatin (10 mg/kg) daily by gavage for 5 weeks (n=17). All animals were euthanized at 20 weeks of age. Multiple sections from the first proximal segment of the right common carotid artery were extracted for stiffness measurements and adjacent tissues were sliced for histological examination to identify lipid cores. Using atomic force microscopy, nano-indentation tests were conducted on the lipid-rich regions of plaque samples, and the elastic moduli were determined by fitting the Hertzian contact model to the force-indentation data. Measurements were conducted in a blinded manner with respect to treatment groups.Results:The CSL112 group had the highest lipid stiffness, with a mean elastic modulus of 5.27 kPa (95% CI [4.74, 5.80]), followed by the atorvastatin group at 3.02 kPa (95% CI [2.51, 3.53]), and the saline group at 2.11 kPa (95% CI [1.54, 2.68]). Statistical analysis indicated that CSL112 significantly increased the elastic modulus of lipid cores compared to both atorvastatin and saline (p

Circulation, Volume 150, Issue Suppl_1, Page A4146109-A4146109, November 12, 2024. Background:Although a causal relationship between diet-induced obesity (DIO) and atrial fibrillation (AF) has been established, the underlying pathophysiological mechanisms in genetic obesity remain unclear. A high-fat diet (HFD) is used to generate DIO mice, but investigating genetic models of obesity may provide mechanistic insights into atrial myopathy, a precursor state of AF and stroke that is of increasing clinical and research interest.Objective:We used a genetic (melanocortin-4 receptor knockout,Mc4r-KO) mouse model of obesity to test the hypothesis that obesity-mediated atrial myopathy creates an electrophysiologic (EP) substrate for AF.Method:MC4Rmutations are the most common monogenic form of obesity in humans. Transesophageal rapid (TE) pacing, invasive electrophysiology studies, immunohistochemistry, western blotting of plasma membrane proteins, mitoSOX staining, and whole-cell patch clamping were performed to evaluate AF burden and analyze the molecular and whole-animal EP phenotype.Results:Mc4r-KO mice were significantly heavier than wild-type lean controls (Figure A). AF burden was 257 ± 175 seconds inMc4r-KO mice vs. 14.4 ± 29 seconds in control mice (P=XX;Figure B-C). Patch-clamping and optical mapping studies showed thatMc4r-KO mice displayed a shortened atrial action potential (APD) (data&P=) and reduced conduction velocity (Figure D-F).Mc4r-KO mice also displayed significantly reduced peak cardiac sodium current (INa) and delayed rectifier potassium current (IKr), but the L-type Ca2+current (ICa,L) was unchanged, indicating that the atrial APD changes are mostly due to INamodulation (Figure G-H).Mc4r-KO atrial myocytes showed increased MitoSOX staining, indicating elevated ROS production (Figure J). Notably, fibrosis was not increased inMc4r-KO mice, suggesting AF susceptibility is primarily due to electrical remodeling (Figure K).Conclusion:Our study indicates that mice with genetic susceptibility to obesity are more prone to develop AF primarily through electrical remodeling, with minimal structural changes, differing from DIO mice. This risk is in part mediated by modulation of the cardiac Na+channel and increased oxidative stress. These findings may have important implications for the management of obesity-mediated AF in humans.

Circulation, Volume 150, Issue Suppl_1, Page A4141282-A4141282, November 12, 2024. Transcatheter valve replacement has become the preferred treatment for high-risk elderly patients considering the advantages of less invasive surgical trauma and faster postoperative recovery. Transcatheter heart valves (THVs) primarily made of glutaraldehyde-crosslinked pericardial materials pose a risk of thrombosis and calcification, and are subjected to additional stress during catheter delivery, which leads to poor durability. Herein, we constructed a novel transcatheter tissue engineered heart valve for in situ regeneration through functional modification of cystamine (CySA) and pentagalloylglucose (PGG) on decellularized porcine pericardium (DPP), referred to as CySA/PGG-PP. A dynamically reversible fiber network structure was formed by the modification of CySA and PGG, resulting in excellent resistance to enzymatic degradation and crimping stability of CySA/PGG-PP. The distinctive capability of CySA to catalyze the production of endogenous nitric oxide (NO) provided CySA/PGG-PP with a long-term NO release system that inhibited platelet adhesion and activation to improve hemocompatibility. Proteomics analysis revealed that the improvement of hemocompatibility might be mediated by protein phosphorylation and arachidonic acid metabolism-related pathways. Furthermore, we found that CySA/PGG-PP exhibited significant recellularization and tissue remodeling in a rat abdominal aortic implantation model, accompanied by a mild inflammatory response and no calcification. The positive results in vivo might be regulated by genes associated with cell adhesion and differentiation, extracellular matrix organization, and TGF-β signaling pathway, as revealed by RNA sequencing. Consequently, the instructive transcatheter tissue-engineered valve overcomes the limitations of existing THVs with the aim of significantly improving valve durability for clinical therapy.

Circulation, Volume 150, Issue Suppl_1, Page A4136700-A4136700, November 12, 2024. Hemorrhagic shock(HS) results from significant blood loss, leading to insufficient oxygen delivery, which causes metabolic changes and multi-organ dysfunction.The HS-related acute kidney injury developed by the patient are mainly due to alteration in Na/K ATPase.In previous O-GlcNAcylomic studies, we identified the Na/K ATPase as potentially O-GlcNAcylated.O-GlcNAcylation, a post-translational modification, plays a role in various cellular processes, such as cell survival and stress response.O-GlcNAcylation may have beneficial effect in shock situations.The objective of this study is to ascertain whether Na/K ATPase is O-GlcNAcylated and to elucidate its potential role during HS.Hemorrhagic shock was induced by an exsanguination of rats.They were then randomly treated or not with an O-GlcNAcase inhibitor, the NButGT(10mg/kg), to increase O-GlcNAc level.Blood pressure and heart rate were monitored throughout the experiment.Blood samples were collected for complete blood analysis, including biochemistry and gas measurements. kidneys were immediately frozen for histological and biochemical studies.To study the O-GlcNAcylation of Na/K ATPase an immunoprecipitation and Wheat Germ Agglutinin(WGA) based lectin affinity gel electrophoresis were used. HEK cells were treated with or without NButGT(100µM,6 hours) and/or ouabain(Na/K ATPase inhibitor) and a colorimetric kit was assessed to study O-GlcNAcylation impact on Na/K ATPase activity.O-GlcNAc levels increased by 2 folds in heart and kidney due to the NButGT treatment(p

Circulation, Volume 150, Issue Suppl_1, Page A4139600-A4139600, November 12, 2024. Background:Cardiac injury after subarachnoid hemorrhage (SAH) is a well-recognized phenomenon with electrocardiogram (ECG) changes, arrhythmias and myocardial dysfunction. Neurocardiac injury has been commonly reported with increased severity of SAH, however much of the evidence has focused on high grade SAH requiring hemodynamic support or mechanical ventilation. In this study we focused on neurocardiac injury with high grade World Federation of Neurological Surgeons (WFNS) grade 3-5 SAH requiring intensive care management.Methods:Patients admitted to our intensive care unit from 2009-2019 with an WFNS 3-5 aneurysmal SAH with an echocardiogram within 7 days of admission were included in our study. Electrocardiogram, cardiac biomarkers and data regarding mortality and neurological complications were collected retrospectively.Results:A total of 242 patients were included in our study analysis with 11 (5%), 89 (37%), and 142 (59%) had WFNS grade 3, 4 or 5 SAH, respectively. Of the 95 patients that underwent echocardiography in the first week, 38 (40%) had a reduced ejection fraction, which was mild (LVEF 40-52%) in 13 (14%), moderate (LVEF 30-39%) in 14 (15%), and severe (LVEF < 30%) in 11 (12%). Independent predictors of reduced ejection fraction included a lower presenting GCS score (OR 1.2 per one point reduction in (Glasgow Coma Score) GCS, 95% CI 1.0-1.5, p = 0.03), elevated troponin T concentration (OR 6.1, 95% CI 1.2-31.3, p = 0.03) and T wave inversion on ECG (OR 9.1, 95% CI 1.6-52.3, p = 0.01). In patients with reduced ejection fraction, classical apical wall motion abnormality was more prevalent in older populations (median age 64 years (apical) vs 50 years (basal wall motion abnormality) and 52 years (other) p = 0.03). In all wall motion abnormality groups, there was a female predominance. Classic Takotsubo wall motion was associated with an anterior SAH aneurysm location (p = 0.03) and highest proportion of moderate to severe LV dysfunction (p = 0.04). ICU mortality did not differ based on the pattern of wall motion abnormalities.Conclusion:Predictors of neurocardiac injury in high grade SAH include troponin elevation, T wave abnormalities and lower presenting GCS. Aneurysm location was associated with wall motion abnormalities and degree of LV dysfunction. Patients with WFNS 3-5 SAH are at increased risk of neurocardiac injury. ECG changes, cardiac biomarker elevation and aneurysm location can help identify patients who warrant echocardiography.

Circulation, Volume 150, Issue Suppl_1, Page A4134707-A4134707, November 12, 2024. Introduction:Epicardial adipose tissue (EAT) is a metabolically active tissue associated with cardiometabolic disease. EAT likely has local paracrine inflammatory and atherogenic effects on coronary vessels, but the metabolic underpinnings related to systemic metabolic pathways has not been evaluated.Hypothesis:We hypothesized that metabolic markers of lipid and fatty acid oxidation will be positively associated with volume of EAT.Methods:In a biomarker substudy of the Prospective Multicenter Imaging Study for Evaluation of Chest Pain (PROMISE) clinical trial which randomized participants to computed tomography angiography (CTA) vs. stress testing, we analyzed 1542 participants randomized to the CTA arm with available plasma at baseline. CTA phenotyping of EAT volume indexed to body surface area (cm3/m2) was determined using a validated deep-learning algorithm. Comprehensive metabolomic profiling was performed on plasma samples using mass spectrometry. Principal components analysis (PCA) was used for dimensionality reduction of 571 named metabolites. Linear regression tested the association of metabolomic factors with EAT. Univariate models were adjusted for multiple comparisons and multivariate models were adjusted for age, race and ethnicity, sex, diabetes, BMI, LDL-C, HDL-C and metabolic syndrome.Results:Of 82 PCA-derived metabolomic factors, 16 were associated with EAT in univariate models and nine were associated with EAT in multivariate models (p=0.001-0.046); 116 individual metabolites heavily loaded within these factors were significantly associated with EAT volume in multivariate models (Figure 1). This included three linoleic acid derivatives, six cholesterol esters, and glycine that were inversely associated with EAT volume (p

Circulation, Volume 150, Issue Suppl_1, Page A4134837-A4134837, November 12, 2024. Background:Mitochondrial dysfunction is linked to myocardial ischemia-reperfusion (I/R) injury. Checkpoint kinase 1 (CHK1) could facilitate cardiomyocyte proliferation and cardiac repair post myocardial infarction, however, its role on mitochondrial function in I/R injury remains unknown.Research Questions:The purpose of this study is to explore the potential effects and mechanisms of CHK1 on mitochondrial homeostasis during myocardial I/R injury.Methods:To investigate the role of CHK1 on mitochondrial function following I/R injury, cardiomyocyte-specific knockout/knock-in mouse models were generated. Mass spectrometry-proteomics analysis and protein co-immunoprecipitation assays were conducted to dissect the molecular mechanism of CHK1. The interaction between CHK1 and SIRT1 was explored using truncated plasmids.Results:CHK1 was downregulated in myocardium post I/R and neonatal mouse cardiomyocytes (NMCMs) post oxygen-glucose deprivation/re-oxygenation (OGD/R).In vivo, CHK1 overexpression protected against myocardial I/R injury, while heterogenous CHK1 knockout exacerbated cardiomyopathy.In vitro, CHK1 inhibited OGD/R-induced cardiomyocyte apoptosis and bolstered cardiomyocyte survival. Mechanistically, CHK1 attenuated oxidative stress and preserved mitochondrial metabolism in cardiomyocytes under I/R. Moreover, disrupted mitochondrial homeostasis in I/R myocardium was restored by CHK1 through the promotion of mitochondrial biogenesis and mitophagy. Through mass spectrometry analysis following co-immunoprecipitation, SIRT1 was identified as a direct target of CHK1. The 266-390 domain of CHK1 interacted with the 160-583 domain of SIRT1. Importantly, CHK1 phosphorylated SIRT1 at Thr530 residue, thereby inhibiting SMURF2-mediated degradation of SIRT1. CHK1 Δ390 amino acids (aa) mutant functioned similarly to full-length CHK1 in scavenging ROS and maintaining mitochondrial dynamics. Consistently, cardiac-specific SIRT1 knockdown partially attenuated the protective role of CHK1 in I/R injury.Conclusions:Our findings revealed that CHK1 mitigates I/R injury and restores mitochondrial dynamics in cardiomyocytes through a SIRT1-dependent mechanism.

Circulation, Volume 150, Issue Suppl_1, Page A4142510-A4142510, November 12, 2024. Background:An acute hyperglycemic status is reportedly associated with poor prognosis in patients with acute cardiovascular diseases. Although the stress hyperglycemia ratio (SHR) is a novel index to accurately represent the hyperglycemic condition on admission, relations between SHR and clinical outcomes are not fully evaluated in a setting of acute myocardial infarction (MI).Methods:This retrospective, multicenter registry study included 2,386 patients with acute MI undergoing percutaneous coronary intervention. SHR was calculated as a blood glucose level on admission divided by the estimated average glucose derived from a glycated hemoglobin level. The co-primary endpoints of this study included heart failure (HF)-related events (a composite of all-cause death and worsening and hospitalized HF) and major atherosclerotic cardiovascular events (MACE) (a composite of all-cause death, recurrent MI, and ischemic stroke), during the index hospitalization and after discharge.Results:Of the 2,386 patients, 890 (37.3%) had diabetes, and the median SHR was 1.17 [0.99, 1.45]. HF events and MACE occurred in 680 (28.5%) and 233 (9.8%) during hospitalization. SHR was identified as a factor significantly associated with both in-hospital HF events (adjusted odds ratio 1.65, 95% confidence interval 1.18-2.29, p=0.003) and MACE (adjusted odds ratio 1.50, 95% confidence interval 1.10-2.03, p=0.009). Among 2,017 patients who survived to discharge and had follow-up information, 195 (9.7%) and 214 (10.6%) experienced HF events and MACE during the median of 536 days after discharge. Patients with the high SHR ( >1.45, 4th quartile) had an increased risk of HF events than those with SHR ≤1.45, while the incidence of MACE after discharge did not differ significantly between the two groups (Figure). The multivariable analysis confirmed the association of SHR with long-term HF events.Conclusions:In patients with acute MI, SHR was predictive of in-hospital outcomes including HF events and MACE, while after discharge, the higher SHR was associated with a higher HF risk but not with MACE. Further studies are needed to elucidate the underlying mechanisms and potential incremental benefit of SHR in stratifying patient risks after MI.

Circulation, Volume 150, Issue Suppl_1, Page A4117594-A4117594, November 12, 2024. The “theory of developmental origins of health and disease” posits that stress in critical developmental periods will program life-course health and may affect cardiovascular (CV) health. Mothers at risk for premature delivery receive synthetic glucocorticoids (sGC) to enhance fetal lung maturation and manage fetal respiratory distress, but sGC exposure is linked to long-term CV dysfunction in offspring. Four groups of male baboons were studied: sGC exposedin uteroat middle age (sGC-MA, 13.8±0.2Y), older sGC exposedin utero(sGC-O, 17.1±0.4Y), middle age unexposed (CTR-MA, 13.5±0.6Y), and older, unexposed baboons (CTR-O, 17.4±0.4Y). Gated, breath-hold, cine cardiac magnetic resonance imaging was performed at 3 Tesla (Siemens TIM Trio) to assess left ventricular (LV) function and myocardial strain, analyzed using cvi42® software. Mitochondrial electron transport chain (ETC) complex activity was analyzed using LV tissue from sGC-O and CTR-O euthanized baboons. Protein quantification was used to measure mitochondrial function and RNA-seq assessed differential gene expression and gene ontology (GO) enrichment. Unpaired t-tests were used. Data are reported as mean ± SD. Stroke volume and ejection fraction were similar in the elderly groups (4 sGC-O, 8 CTR-O). However, higher end-systolic and end-diastolic sphericity indexes (SI) and shorter LV axis lengths indicated remodeling. Also, global longitudinal and radial strains were reduced (both p

Circulation, Volume 150, Issue Suppl_1, Page A4139708-A4139708, November 12, 2024. Background:Racial and ethnic disparities exist in cardiovascular health (CVH) in pregnancy. While social determinants of health (SDOH) affect CVH, the extent to which SDOH assessed in early pregnancy explain racial and ethnic differences in CVH postpartum remains to be defined.Objective:This study examines the relative contribution of SDOH in early pregnancy to racial and ethnic differences in maternal CVH 2-7 years after delivery.Methods:This is a secondary analysis of the prospective nulliparous pregnancy outcomes study: Monitoring Mothers-to-be Heart Health Study (nuMoM2b-HHS) cohort. The outcome was maternal CVH defined using the American Heart Association’s Life’s Essential 8 (LE8) framework, which included body mass index, blood pressure, lipids, fasting glucose, diet, physical activity, sleep health, and smoking status, and calculated as a score of 0-100. We used the Blinder-Oaxaca decomposition to quantify the statistical contributions of differences in demographic (age and nativity), socioeconomic status ([SES], education, income, insurance, and health literacy), and psychosocial (resilience, social support, anxiety, depression, and stress) factors in early pregnancy to differences in mean postpartum CVH between the two largest self-identified minoritized racial and ethnic groups (non-Hispanic [NH] Black and Hispanic) and NH White individuals.Results:Of 4,161 assessed pregnant individuals, 17.7% identified as Hispanic, 15% as Black, and 67.3% as White. After adjusting for demographic, SES, and psychosocial factors, the average CVH score in White individuals was 12.2 (SE 1.2) points higher (better) than in Black individuals and 3.3 (SE 0.8) points higher than in Hispanic individuals (Figure, all p

Circulation, Volume 150, Issue Suppl_1, Page A4146993-A4146993, November 12, 2024. Introduction:Anthracyclines (AC), a class of chemotherapeutic drugs, are used to treat various cancers, including breast cancer (BC). However, AC cause dose-dependent cardiac toxicity. Practice guidelines list pre-existing cardiomyopathy as a risk factor for cancer therapy-related cardiac dysfunction (CTRCD), but there is a lack of data on cardiotoxicity risk in patients with left ventricular (LV) hypertrabeculation without LV hypertrophy/dilation. We present a patient with LV hypertrabeculation who developed LV dysfunction after AC chemotherapy for BC.Description of Case:A 55-year-old woman diagnosed with multicentric invasive ductal carcinoma (IDC) of the right breast, stage IIA (cT3 cN1 cM0), grade 2, ER+/PR+/HER2-, was treated with neoadjuvant Paclitaxel for 3 months. Before AC-based chemotherapy, stress cardiac MRI due to residual post-COVID-19 dyspnea showed LV hypertrabeculation with a non-compacted/compacted ratio of 2.3, LVEF 56%, and no delayed enhancement. Transthoracic echocardiography (TTE) reported an LVEF of 52% with GLS of -17%. The patient’s electrocardiogram (ECG) showed normal sinus rhythm, and NT-pro BNP levels were

Circulation, Volume 150, Issue Suppl_1, Page A4147433-A4147433, November 12, 2024. Background:In adults with hypertrophic cardiomyopathy (HCM), left ventricular outflow tract (LVOT) obstruction and reduced left atrial strain (LAS) predict heart failure and cardiac event risk. However, data in children are limited.Hypothesis:LVOT gradient and LAS together determine cardiac outcome risk in children and young adults with HCM.Methods:All HCM patients with exercise stress echocardiography (ESE) from 2014-2022 at a single center were included. Patients were stratified by LVOT gradients: Group 1 (n=44, rest/exercise gradients < 30mmHg); Group 2 (n=41, rest < 30mmHg; exercise ≥ 30mmHg); Group 3 (n=29, rest/exercise ≥ 30mmHg). Composite cardiac outcome included cardiac syncope, non-sustained/sustained ventricular tachycardia, cardiac arrest, NYHA heart failure class ≥ II, heart transplantation, and HCM-related death. LA reservoir (LASr) and conduit (LAScd) strain were analyzed with TOMTEC AutoStrain LA. Cumulative incidence of composite outcome by LVOT group was estimated by Kaplan-Meier method. Multivariable Cox regression was used to evaluate the effect of adding LAS to a model containing only LVOT group. Model discrimination was assessed using the concordance (c) index.Results:114 patients (32%F, median age 17 years) formed the cohort. At median 2.1 years follow-up [IQR: 1.0, 3.4] composite cardiac outcome risk was higher in Group 3 vs. 2 (HR=4.97, p=0.013, Figure 1). Composite cardiac outcome risk was lower in Group 1 vs. 2, but not significant (HR=0.70, p=0.66). Adjusting for LVOT group, lower LASr and LAScd were associated with greater cardiac outcome risk (per 5% LAS decrease: LASr HR=1.56, p=0.008; LAScd HR=1.77, p=0.002, Table 1). C index increased with inclusion of LASr or LAScd in the model (Table 1).Conclusion:In one of the largest young HCM cohorts evaluated with ESE, cardiac outcome risk increased with resting LVOT obstruction and reduced LA strain. LA strain demonstrated additive value for prediction of cardiac outcomes in children.

Circulation, Volume 150, Issue Suppl_1, Page A4141135-A4141135, November 12, 2024. BACKGROUND:Right atrial (RA) dysfunction related to right ventricular (RV) function has been reported in patients with repaired TOF. Increased liver stiffness in these patients has also been reported. Whether RA function worsens under exercise stress, and its relationship with worsened liver stiffness is unknown.HYPOTHESIS:In patients after TOF repair, RA functional reserve during exercise stress is reduced and correlated with raised liver stiffness and RV dysfunction.METHODS:19 patients (8 male) aged 17.92 ± 3.81 at 16.06 ± 3.98 years after repair and 25 controls (16 male, aged 19.99 ± 1.67 years) were studied. RA mechanics was assessed by speckle-tracking echocardiography (STE) at rest and during bicycle exercise, with quantification of positive, negative, and total strain, and strain rates at ventricular systole (aSRs), early diastole (aSRed), and atrial contraction (aSRac). RAFR is calculated as (Change in RA total strain x [1-1/ baseline RA total strain]). Biventricular (RV, LV) function were quantified using Doppler interrogation and STE. Hepatic shear wave velocity (c) and tissue elasticity (E) were measured using shear wave elastography.RESULTS:At rest, patients had lower RA positive, negative and total strain, aSRs and aSRed than control subjects (all p

Circulation, Volume 150, Issue Suppl_1, Page A4146119-A4146119, November 12, 2024. Introduction:Refractory angina (RA) is a challenging and debilitating condition in the presence of myocardial ischemia regardless of a combination of antianginal drugs and revascularization procedures. Among the phenotypes of RA, there is angina in the absence of obstructive coronary disease (ANOCA). Coronary artery fistulas (CAF) are rare connections between coronary arteries and heart chambers or vessels. 3% of CAF drain into the left ventricle (LV), which can lead to the coronary steal phenomenon and angina in the form of ANOCA. We report here under a case of symptomatic chronic coronary syndrome (CCS) and CAF.Case Report:An 85-year-old woman with CCS had angina progression, reaching functional class 3 and frequent need of nitrate use, despite the use of three antianginal drugs. Stress myocardial perfusion scintigraphy showed reversible hypoperfusion in the lateral, inferolateral and inferior LV walls. A coronary angiogram was performed, revealing the absence of obstructions. However, CAF for the LV was identified around the ischemic territory. It was decided to start our Alopurinol protocol for RA. A treadmill test was done before and after the treatment to assess time to angina occurrence and ST segment change. After 3 months, there were an improvement in the threshold and intensity of angina (class 2) and reduction in nitrate need. In a new scintigraphy, normalization of perfusion was observed, and a new treadmill test showed reduction of 4.1 minutes for angina occurrence with an increase of 1.7 mets and no difference in ST change.Discussion:CAF are rare, identified in up to 0.2% of angiograms. They can lead to heart failure (HF), myocardial ischemia and arrhythmias. Treatment is based on the clinic, the patient’s age and the hemodynamic significance of the CAF. For adults, one of the indications for CAF occlusion is the presence of myocardial ischemia. However, the association between RA and CAF is rarely described in the literature. In the present report, we illustrate the case of an octogenarian with RA, ANOCA and FAC who, before considering interventional treatment, underwent medical optimization with excellent response and improvement in cardiac perfusion and exercise tolerance.Conclusion:In the scenario of RA and ANOCA, a combination of different antianginal drugs can promote symptoms control and improvement of myocardial perfusion and exercise performance, even in the face of uncommon causes such as the one here reported.

Circulation, Volume 150, Issue Suppl_1, Page A4144270-A4144270, November 12, 2024. Background:Air pollution is a leading cause of cardiovascular diseases including ischemic heart disease and stroke contributing to millions of deaths, with elevated blood pressure, endothelial dysfunction, and systemic inflammation being some of the most important underlying mechanisms. Various studies showed a promising beneficial effect of indoor air purification on various health outcomes, including blood pressure. We aimed to assess the effect of indoor air purification on systolic blood pressure (SBP) and Diastolic blood pressure (DBP) and provide a rationale for home use of these filters.Methods:We searched PubMed, Web of Science, Cochrane and Scopus for published literature up to May 2024. We included studies that assessed air purification, including HEPA filters or electrostatic air filters, as an intervention compared to no intervention. The primary outcome of interest was mean changes in blood pressure both systolic and diastolic. Secondary outcomes were biomarkers of inflammation and oxidative stress. Mean difference (MD) and 95% CI was used in a fixed-effect model to analyze the data.Results:A total of 21 studies were included in our meta-analysis with a total of 1955 participants. Air purification was associated with a significant reduction in systolic blood pressure (SBP) (MD: -2.42, 95% CI: -3.42, -1.41), and diastolic blood pressure (DBP) (MD: -1.11, 95% CI: -1.76, -0.46). However, there was no significant changes in levels of inflammatory biomarkers or oxidative stress.Conclusion: Indoor air purification was associated with significant reductions in systolic and diastolic blood pressure levels, but questions arise whether these reductions are clinically relevant or not. Further studies should assess these findings.Conclusion:Indoor air purification was associated with significant reductions in systolic and diastolic blood pressure levels, but questions arise whether these reductions are clinically relevant or not. Further studies should assess these findings.