Search Results for: Nelle donne lo stress danneggia la salute dell’intestino

Circulation, Volume 150, Issue Suppl_1, Page A4143744-A4143744, November 12, 2024. Introduction/Background:Hypertension and hypercholesterolemia are important risk factors of endothelial dysfunction and atherosclerosis. Previous studies suggested a crosstalk between an activated renin-angiotensin-aldosterone system (RAAS), reactive oxygen species (ROS) and oxidized low-density lipoproteins (oxLDL) in atherosclerosis, but the underlying molecular mechanisms are not well understood.Research Question/Hypothesis:Can we identify novel signaling pathways controlling the molecular crosstalk of the RAAS with ROS and oxLDL in endothelial dysfunction and atherosclerosis?Methods/Approach:The impact of AT1R blockade on oxLDL-induced superoxide anion formation and endothelial dysfunction was studied in human umbilical artery endothelial cells and aortic rings of wild-type mice by chemiluminescence and Mulvany myograph. We cloned 5’-terminal deletions of the AT1R promoter and assessed the luciferase activity in human endothelial cells. Oct-1 binding to the human AT1R promoter region was studied by EMSA. Further assays included real-time PCR, confocal microscopy, Western blotting, G protein reporter assays, phospho-ERK1/2 antibodies and specific siRNAs. The data were validated in heart of obese C57BL/6 mice and cardiac and aortic tissue of AT1a/AT1bdouble knockout micein vivo.Results/Data:AT1R promoter activation studies upon Ang II- and oxLDL-stimulation in endothelial cells revealed that Ang II and oxLDL activate AT1R signaling through G protein Gα12/13, followed by activation of ERK1/2 MAP kinases, and transcription and translation of Oct-1, resulting in up-regulation of AT1R, LOX-1 and NOX2 expression, which could be antagonized by specific inhibitors at each step of the identified signaling cascade. AT1R blockade improved oxLDL-induced endothelial dysfunction in aortic rings of wild-type mice. Male C57BL/6 mice fed a high-fat diet exhibited upregulation of Oct-1 levels in cardiac tissues, compared to normal controls, while AT1a/AT1bdouble knockout mice demonstrated downregulation of Oct-1, AT1R, LOX-1, and NOX2 on mRNA and protein level in cardiac and aorta tissue, thus confirming the identified signaling cascadein vivo.Conclusions:Oct-1 is an essential transcription factor for Ang II- and oxLDL-induced upregulation of AT1R and LOX-1 expression in endothelium, thus identifying a novel molecular cross-talk of oxLDL with ROS signaling and the RAAS contributing to development of endothelial dysfunction and atherosclerosis.

Circulation, Volume 150, Issue Suppl_1, Page A4146686-A4146686, November 12, 2024. Carvedilol (CAR) is an FDA-approved adrenergic blocker commonly given to cardiovascular disease patients. Interestingly, CAR also shows anti-cancer potential in reducing cancer-specific mortality in breast cancer patients. To advance CAR usage in cardio-oncology, we hypothesize that elucidating the molecular mechanism of the energy sensing and homeostasis pathways underlying CAR’s cardioprotective capabilities can enhance its clinical translation.Canine cardiac slices were generated from 3 euthanized pet dogs free of cardiovascular disease. CAR pretreatment (1μM, 4 hrs) with or without a 24-hr exposure to 5μM of cardiotoxic doxorubicin (DOX) was performed. Murine slices from 5 C57Bl6 mice with the same treatments as above was also performed. Direct tissue imaging on IVIS Spectrum was carried out to assess apoptosis by Annexin V staining, autophagy with autophagy detecting nanoparticle (ADN) developed in-house, and DOX retention in tissue by the inherent DOX fluorescence. Tissue was analyzed by histological staining of apoptosis and Western blot of autophagy and energy sensing pathways. Energetics quantified by Seahorse assay was performed in isolated mitochondria from cardiac slices in rat cardiomyoblasts (H9C2 cells) and human iPSC-induced cardiomyocytes (iCells).In both canine and murine cardiac slices, autophagy was significantly reduced (p

Circulation, Volume 150, Issue Suppl_1, Page A4141191-A4141191, November 12, 2024. Introduction:Regular physical exercise is widely recognized for its beneficial effects on overall health. Despite emerging evidence that early-life experiences profoundly impact adult and aged health, the long-term effects of early-life exercise remain uncertain.Hypothesis:We hypothesized that early-life exercise extends healthspan and attenuates cardiovascular aging in aged mice.Methods:Male and female C57BL/6J mice were subjected to a 3-month swimming exercise regimen starting from 1 month of age (1.5 hour per day, 5 days per week), while no exercise intervention was conducted at other times. The sedentary group was raised under similar conditions. The healthspan of aged male and female mice was assessed, including overall metabolic function, cardiovascular function, frailty index and other relevant measurements. Transcriptional profiling of young and old mice was performed to gain insights into the mechanisms underlying the effects of early-life exercise on aging.Results:Early-life exercise improved metabolic health in aged mice. Assessment of body composition showed increased lean mass in the exercise group. When subjected to food deprivation stress in metabolic chambers, aged mice with early-life exercise exhibited increased energy expenditure, carbohydrate oxidation, and fat oxidation levels in both males and females. Evaluation of frailty index at 24 months of age, involving 31 frailty phenotypes, indicated lower frailty index score in the early-life exercise group, suggesting an attenuation of age-related phenotypes. While no significant differences were observed in blood pressure and cardiac systolic function, early-life exercise was associated with improved cardiac diastolic function at 19 months of age. Furthermore, early-life exercise resulted in decreased heart-carotid pulse wave velocity and improved endothelial-dependent vascular relaxation in aged mice, indicating better vascular function in elderly mice with early-life exercise.Conclusions:The findings demonstrate that early-life exercise contributes to an increased healthspan, as evidenced by enhanced metabolic health and reduced frailty. Both male and female aged mice exposed to early-life exercise exhibit improved cardiovascular function.

Circulation, Volume 150, Issue Suppl_1, Page A4141959-A4141959, November 12, 2024. Blood pressure (BP) control among older adults may differ by neighborhood due to differences in access to healthy foods, safe places to exercise, and stress. Neighborhood disadvantage may also influence clinician behaviors for hypertension management.This retrospective observational study utilized electronic health data from 52,750 primary care visits among 8,434 adults age ≥ 65 years with hypertension between January 1, 2017, and March 10, 2020 to examine the association of Area Deprivation Index (ADI) with odds of uncontrolled BP during a clinic visit and with therapeutic inertia (TI). Higher ADI values indicate higher deprivation. TI was defined as the absence of a prescription for or escalation of a new BP lowering medication during clinic visits with systolic BP ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg. Binary generalized linear mixed models were used to determine the association of ADI quartiles with uncontrolled BP and with TI during a clinic visit while adjusting for demographics, comorbidities, insurance status, and the intra-patient correlation. Among the 8,434 patients, the mean age at the first visit was 74.3 years (standard deviation 7.8), 57.7% were female, and race/ethnicity was self-reported as non-Hispanic (NH) White in 69.1%, NH Black in 15.9%, NH Other in 5.0%, and Hispanic in 8.2%. The median ADI was 41 (interquartile range: 26-53). The percentage of clinic visits with uncontrolled BP ranged from 39.1% in the first to 44.1% in the fourth ADI quartile.Figure 1 shows the unadjusted and adjusted odds of uncontrolled BP and TI by ADI quartiles. Adjusted odds of uncontrolled BP during a clinic visit was 1.17 (95% confidence interval (CI) 1.06, 1.28) in the fourth vs. first ADI quartile. Among the 21,928 clinic visits with uncontrolled BP, TI occurred in 79.5%, 82.2%, 83.0%, and 81.6% of visits in ADI quartiles one, two, three, and four, respectively. Adjusted odds of TI during a clinic visit was 1.16 (95% CI 1.01, 1.33) in the fourth vs. first ADI quartile.Our findings of higher odds of uncontrolled BP and TI during clinic visits with patients residing in neighborhoods with higher vs. lower ADI suggest that neighborhood disadvantage is associated with both uncontrolled BP and TI in older adults.

Circulation, Volume 150, Issue Suppl_1, Page A4137913-A4137913, November 12, 2024. Background:Cardiac sarcoidosis (CS) was characterized by formation of granulomas in the heart. Enhancement in myocardial inflammatory activity and oxidative stress is a crucial cause of major cardiovascular adverse events (MACE). Although immunosuppressive therapy is recommended for active CS, there is no established markers for treatment and prognosis.Hypothesis:We hypothesized that the inflammation and oxidative stress in heart were associated with MACE after steroid therapy.Aims:We identified prognostic markers for MACE in patients with CS after steroid therapy.Methods:This study was a prospective observational cohort study. Patients with CS diagnosed according to Japanese criteria were enrolled in this study. Patients with abnormal accumulation of18F-FDG in heart were treated with steroids with standard guideline-recommended protocol.18F-FDG PET were performed after more than 6 months of induction. Urinary 8-hydroxy-2′-deoxyguanosine (U-8-OHdG), a marker of oxidative DNA damage, and indices of cardiac and renal function were measured. The major outcome was a composite of the first sustained ventricular tachycardia (sVT) /sudden cardiac death (SCD), hospitalization for heart failure, and radiological relapse with exacerbation of clinical manifestation.Results:Fifty consecutive patients with CS underwent steroid therapy and followed up (median follow-up period of 58 months). 39 of 50 patients underwent 18F-FDG PET/CT more than 6 months after steroid therapy. During the follow-up period, 17 of 39 patients showed MACE, consisting of sVT/SCD (N= 11), hospitalization (N= 2) and radiological relapse (N= 4). A Cox proportional-hazard model showed that the U-8-OHdG and SUV max value of FDG-PET were independent predictors of MACE. ROC analysis revealed that the cut-off values of U-8-OHdG and SUV max for predicting the MACE were 11.6 ng/mg Cr (AUC 0.913, sensitivity 86.7%, specificity 90.0%) and 4.64 (AUC 0.878, sensitivity 76.5%, specificity 91.0%), respectively (Fig.1). Patients with a U-8-OHdG ≧11.6 ng/mg Cr or SUV max ≧4.64 had a significantly higher MACE risk (P values for U-8-OHdG and SUV max were both 0.001 by Log Rank analysis) (Fig.2). It is noted that U-8-OHdG

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 A4114198-A4114198, November 12, 2024. Background:Mitochondrial dysfunction contributes to heart failure (HF) progression via diminished energy supply, release of reactive oxygen species, and increased cell death. However, there has yet to be clinically relevant biomarkers that address mitochondrial-mediated cardiac injury in patients. Humanin (HN) is a mitochondria-derived peptide that protects cells through the interference of apoptosis and reduction of oxidative stress. The objectives of our study were to measure circulating plasma HN levels in patients with HF with reduced ejection fraction and describe the relationship of HN to validated, clinically relevant measures of HF.Methods:We conducted a prospective cohort study. To be included in the study, patients must have: 1) left ventricular ejection fraction

Circulation, Volume 150, Issue Suppl_1, Page A4135229-A4135229, November 12, 2024. Background:Endothelial glycocalyx (eGC) is a layer of glycosaminoglycans adhered to proteoglycans that cover the inner surface of the vessels. The integrity of this structure sustains some vascular properties such as shear stress-induced nitric oxide release and the prevention of platelets and neutrophils adhesion on the vessel surface. eGC shedding could contribute to atherosclerotic plaque vulnerability and acute myocardial infarction (AMI) installation. This research investigated whether acute eGC damage and microvascular dysfunction occurred during AMI.Methods:Sublingual microcirculation was assessed through Capiscope HCVS Handheld Video Capillaroscopy System (KK Technology, Honiton, UK) during the first 72h of hospital admission because of ST-elevation AMI (before) and repeated around six months later (after). All images were automatically analyzed using the GlycoCheck (Alpine, UT, USA), which estimated the perfused vascular density (PVD), the red blood cell (RBC) filling of the vessels, the perfused boundary region (PBR) in µm, an inverse parameter of the eGC thickness; and the microvascular health score (MVHS). This score ranges from 0-10; the lower its numerical value, the greater the microvascular impairment.Results:Twenty patients were included (61±10 years old, 85% males, 55% anterior AMI, 70% hypertension, 25% diabetes, 45% current smoker, all underwent primary PCI). The time between the two sublingual assessments was 188±31 days. The PBR [1.96±0.22µm vs. 1.84±0.19µm]; p=0.047 and flow-adjusted PBR [1.40±0.25µm vs. 1.24±0.16µm]; p=0.045 decreased statistically significant over time. The RBC filling [71.56±4.33% vs. 74.02±3.88%]; p=0.016 and the MVHS [4.28 (interquartile range (IRQ) 3.38-4.90) vs. 5.04 (IQR 4.37-6.00)]; p=0.044 increased statistically significant over time. The PVD [500±86 x10-2µm/mm vs. 522±84×10-2µm/mm]; p=0.255 did not modify over time.Conclusion:This finding was compatible with eGC shedding and microvascular dysfunction during AMI and later reconstitution of this structure after six months.

Circulation, Volume 150, Issue Suppl_1, Page A4119210-A4119210, November 12, 2024. Introduction:Insulin growth factor (IGF) binding protein-1 and 2 (IGFBP-1 and 2) are implicated in acute myocardial infarction (AMI) and have been suggested as predictors of mortality and development of heart failure. The IGF axis has been shown to play roles in cell proliferation and apoptosis. We analysed the serum IGFBP-1 and 2 levels in AMI before and after percutaneous coronary intervention (PCI) and correlated this with cardiac magnetic resonance (CMR) imaging to better establish their significance as biomarkers in AMI.Methods:Patients with AMI who presented to Royal Free Hospital, London, were recruited for proteomic analysis (O link Proximity Extension Immunoassay) at presentation, 24h and 72h following primary PCI. All underwent both admission and follow-up CMR at 6 months to assess for myocardial oedema, left ventricular volumes and function, and assessment of scar.Results:Proteomic evaluation in 20 AMI patients (male 95%; median age 59) revealed significant reduction in the average IGFBP-1 values at discharge compared with presentation, from 5.93 to 4.52 (24% reduction, p=0.003). Conversely, the average IGFBP-2 values at discharge significantly increased from 7.66 to 8.29 (8% increase, p=0.001). Higher discharge IGFBP-2 value was also correlated with increased indexed left ventricle end diastolic volume (LVEDV) at 6-month follow-up (R=0.54, p=0.032).Discussion:IGFBP-1 and 2 showed significant change following intervention for AMI. IGFBP-1 is a stress hormone, which is directly and indirectly activated by cytokines, dysglycaemia and vasopressin activation. Its subsequent reduction following PCI in AMI indicates relative resolution of inflammation, but this was not correlated with changes in infarct size or LV function at follow-up. IGFBP-2 showed significant upregulation, and higher values at discharge were significantly correlated with increased LDEDV at follow-up, suggesting adverse clinical outcomes within this setting. This data suggests differential roles of IGFBP-1 and 2 in the pathogenesis of AMI.

Circulation, Volume 150, Issue Suppl_1, Page A4144377-A4144377, November 12, 2024. Mammalian cells have several adaptive mechanisms to counteract the adverse effects of metabolic and redox stress induced by ischemia. Hypoxia, a hallmark of ischemia, results in the selective reduction of the tricarboxylic acid cycle metabolite, α-ketoglutarate, to theL-(S)-enantiomer of 2-hydroxyglutarate (L2HG) in several cell types. L2HG protects hypoxic cells by buffering increases in the NADH/NAD+redox couple and inhibiting mitochondrial electron transport. In addition, the accumulation of L2HG induced by genetic knockout of L2HG dehydrogenase (L2HGDH), the only known enzyme capable of oxidizing L2HG back to α-ketoglutarate, protects mice against myocardial injury during ischemia. This protection by L2HG manifests as decreased myocardial infarct size and improved cardiac function, owing partly to a metabolic shift in carbon flux from glycolysis towards the pentose phosphate pathway. However, myocardial ischemia also leads to perturbations in fatty acid metabolism as manifest by accumulation of acylcarnitines and acyl-CoA’s. It remains unclear as to whether or not L2HG accumulation affects fatty acid metabolic homeostasis during myocardial ischemia. Here, we induced L2HG accumulation by homozygous deletion of thel2hgdhgene in male mice (l2hgdh-/-; n=12). Hearts isolated from these mice and their wild-type littermates (l2hgdh+/+; n=13) were subjected toex vivoLangendorff perfusion at coronary perfusion pressure of 80 mmHg for 30 min with (ischemic group) or without (control group) subsequent perfusion at ~10% pressure for 90 min. Using liquid chromatography tandem mass spectrometry (LC-MS/MS)-based nontargeted lipidomics, we identified several species of long chain acylcarnitines that accumulated by ischemia in hearts obtained fromL2HGDH+/+mice [linoleoyl carnitine, palmitoyl carnitine, and hydroxy-linoleoyl carnitine increased by 13.2-fold (p=4.2 x 10-6), 10.7-fold (p=1.7 x 10-6), and 10.0-fold (p=5.8 x 10-6), respectively]. Interestingly, however, this accumulation was attenuated substantially in ischemic hearts obtained fromL2HGDH-/-mice [hydroxy-linoleoyl carnitine, palmitoyl carnitine, and linoleoyl carnitine were downregulated by 62.6% (p=0.034), 54.2% (p=0.018), and 35.4% (p=0.054) in ischemic hearts fromL2HGDH-/-mice when compared toL2HGD+/+littermates]. Overall, these findings highlight a novel and potentially important role for L2HG in restoring the perturbations in fatty acid metabolism induced by myocardial ischemia.

Circulation, Volume 150, Issue Suppl_1, Page A4119195-A4119195, November 12, 2024. Introduction:Acute myocardial infarction (AMI) is a leading global cause of mortality. Following primary percutaneous coronary intervention (PCI), 25% require hospitalisation for symptomatic heart failure. Further understanding of the molecular pathogenesis and the temporal relationship of the protein profile associated with ischaemic insult and subsequent cardiac remodelling is required to improve risk stratification following AMI.Methods:20 patients with AMI presenting to Royal Free Hospital in London were recruited for proteomic analysis (O link Proximity Extension Immunoassay) at presentation and at 24 and 72 hours following primary PCI. All underwent initial CMR on admission and at 6 month follow up to assess for myocardial oedema, left ventricular volumes and function and assessment of scar.Results:Proteomic biomarkers that increased on discharge following AMI were: IGFBP2 (8% increase, p=0.001), MMP-10 (5% increase, p=0.001), TIMP4 (14.4% increase, p

Circulation, Volume 150, Issue Suppl_1, Page A4138546-A4138546, November 12, 2024. Introduction:Takotsubo cardiomyopathy (TCM) is a reversible cardiac condition often precipitated by emotional or physical stress. Certain medications have also been implicated. While prognosis is generally favorable, associated QTc prolongation and ventricular arrhythmias can be life threatening, necessitating identification of potential triggers. This report highlights TCM in a patient using high-dose berberine, a plant alkaloid known for its hypoglycemic properties.Case description:A 69-year-old female with a history of type 2 diabetes mellitus, and hyperlipidemia presented after a syncopal event. It was preceded by sudden onset of dizziness, nausea, and vomiting. She had been using berberine for a year to lower her blood sugar and had recently switched to a higher dose of a more potent formulation. Vitals were unremarkable. Initial evaluation revealed a prolonged QTc interval of 659 ms (Figure 1A) and elevated troponin-I levels. She was treated with intravenous magnesium, which improved her QTc to 540 ms and revealed new T-wave inversions in the precordial leads. Echocardiogram showed an ejection fraction (EF) of 35%, with LV apical akinesia and hypercontractile basal segments. Cardiac catheterization ruled out significant coronary artery disease, leading to a diagnosis of TCM. Berberine was discontinued, and guideline-directed medical therapy was initiated. Given the presentation with syncope and high suspicion of aborted sudden cardiac death (SCD), she was discharged with a wearable cardioverter-defibrillator (WCD) as a precaution due to the risk of ventricular arrhythmias during recovery. At her 8-week follow-up, QTc and EF had normalized (Figure 1B), prompting WCD removal.Conclusion:The pathophysiology of berberine-induced cardiomyopathy remains uncertain and requires further research. This case underscores the importance of recognizing the potential cardiotoxic effects of berberine, particularly when used in high doses. A thorough medication and supplement history is crucial in patients presenting with unexplained cardiac symptoms. The reversible nature of TCM, when promptly recognized and treated, highlights the need for comprehensive follow-up to ensure recovery of cardiac function.

Circulation, Volume 150, Issue Suppl_1, Page A4138552-A4138552, November 12, 2024. Background:Cardiovascular disease and cancer are the leading causes of mortality in developed countries. Recent evidence suggests that these conditions share common underlying factors, such as inflammation and oxidative stress. However, there is a lack of data on the association between cardiogenic shock and cancer.Purpose:Our study aimed to investigate the prevalence and outcomes of cardiogenic shock in patients with a history of breast cancer.Methods:We conducted a retrospective analysis of data from the National Inpatient Sample Database (2018-2020) to identify patients with a primary diagnosis of breast cancer. We employed the International Classification of Diseases (ICD-10) diagnostic criteria. Our analysis focused on the impact of cardiogenic shock on mortality, morbidity, and resource utilization. We used chi-square tests for categorical variables and t-tests for continuous variables.Results:Our analysis identified 516,125 breast cancer patients admitted between 2018 and 2020, with 11.3% experiencing cardiogenic shock. The mean age of these patients was 64 years, with 1.2% males and 98.8% females. The mortality rate among patients with cardiogenic shock was 11.8%, which was significantly higher than the 4.1% mortality rate in those without cardiogenic shock (OR 1.9, CI 1.5-2.4, p-value

Circulation, Volume 150, Issue Suppl_1, Page A4137907-A4137907, November 12, 2024. Background:Takotsubo cardiomyopathy (TC) is characterized by left ventricular apical ballooning and intact coronary arteries. The pathogenesis of this disorder is likely to be catecholamine-mediated myocyte damage, microvascular dysfunction and subsequent oxidative stress; however, a number of possible alternative theories have been suggested. Neopterin is produced by activated macrophages following stimulation by interferon-g produced by T-lymphocytes and is capable of enhancing the oxidative potential of reactive oxygen species. The aim of this study was to compare plasma neopterin levels between TC patients and patients with coronary artery disease.Methods:Plasma neopterin levels were measured on admission in patients with TC (n=37), stable angina pectoris (SAP, n=66), unstable angina pectoris (UAP, n=72) and acute myocardial infarction (AMI, n=67) using HPLC. A frozen myocardium specimen was obtained by biopsy from a patient with TC and stained for neopterin, macrophages, and microvessels using immunohistochemistry.Results:Plasma neopterin levels were significantly higher in TC patients compared with SAP patients (P

Circulation, Volume 150, Issue Suppl_1, Page A4140682-A4140682, November 12, 2024. Introduction:Dextrocardia is a rare congenital condition where the heart’s apex points to the right, with an incidence of about 0.01%. Patients usually have a normal life expectancy unless other structural heart diseases are present. The prevalence of atherosclerotic coronary artery disease (CAD) in these individuals is believed to be similar to that of the general population.Due to its rarity, data on coronary interventions in this subset are scarce, with available literature mostly limited to case reports. Patients with dextrocardia present a diagnostic challenge, particularly in the context of acute coronary syndrome.Case Presentation:A 49-year-old male with a medical history of dextrocardia, hypothyroidism, dyslipidemia and hypertension was referred to a cardiologist by his primary physician due to a 3-week history of unstable angina. His vital signs were normal, and the physical examination was unremarkable. Electrocardiogram (ECG) showed a prominent S wave in the left-sided leads and a prominent R wave in the right-sided chest leads, suggesting dextrocardia. Although he had a normal echocardiogram and stress test a year ago at a different hospital, due to his symptoms and intermediate-high risk probability of coronary artery disease (CAD), the decision was made to proceed with a cardiac catheterization using a trans-radial approach with a horizontal sweep technique. During the procedure, a 6-French tiger catheter (TIG) was guided into the left coronary sinus and advanced into the left ventricle under fluoroscopic guidance.The left main coronary artery was widely patent bifurcating into the left anterior descending and left circumflex. The left circumflex had 80% proximal stenosis with minimal luminal irregularities in the mid to distal portion. After guidewire crossing, balloon angioplasty was performed, and a drug-eluting stent was deployed. An intravascular ultrasound was also performed, which was negative for vessel dissection. There were no post-procedure complications, and the patient was discharged on beta blockers and dual antiplatelet agents.Conclusion:Performing cardiac catheterization in patients with dextrocardia presents unique technical challenges due to the mirror-image anatomy. This case report highlights the modifications in standard techniques, emphasizing the need for specialized skills and strategies to achieve successful outcomes in such cases.

Circulation, Volume 150, Issue Suppl_1, Page A4140616-A4140616, November 12, 2024. Introduction:Cardiovascular events occur in patients without obstructive coronary artery disease (oCAD), indicating a need for better risk stratification tools. CT angiography (CTA)-based high-risk plaque (HRP) characteristics predict such events effectively but are not widely available. We performed comprehensive proteomics profiling in the PROMISE trial to identify biomarkers associated with HRP, oCAD, and major adverse cardiovascular events (MACE).Methods:The PROMISE trial randomized patients with stable chest pain to CTA vs. stress testing. Proteomic profiling (Olink, 524 proteins) was performed on 1724 participants with CTA and biospecimens. A high-risk composite phenotype (HRCP) was defined as presence of oCAD (≥50% stenosis in any major vessel), Leaman score >5, coronary artery calcium score ≥400, or HRP features on CTA. Individual proteins were tested for association with HRCP (false discovery rate-adjusted p-value [q]