Search Results for: LBP (Low Back Pain): Cosa dicono le linee guida del mal di schiena

Circulation, Volume 150, Issue Suppl_1, Page A4142952-A4142952, November 12, 2024. Background:The significance of left ventricular global longitudinal strain (LV-GLS) for risk stratification of sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM) without septal reduction therapy remains to be investigated.Aims:To evaluate the prognostic utility of LV-GLS in a long-term follow-up HCM cohort without septal reduction therapy.Methods:We retrospectively enrolled 871 consecutive patients with HCM (mean age 49±13 years, 71% men) who underwent cardiac MRI in our center between January 2010 and December 2013. All study participants never received alcohol septal ablation or surgical myectomy during follow-up. LV-GLS were derived from cine cardiac MRI by using feature tracking method. The primary endpoint was SCD or SCD-equivalent events. The association between LV-GLS and SCD-related endpoints was evaluated by using time-dependent receiver operating characteristic (ROC) analysis, Kaplan-Meier analysis, and multivariable competing risk regression analysis.Results:During median follow-up of 8.8 years, SCD-related endpoint occurred in 45 HCM patients (5.2%). Patients suffering from SCD had higher European Society of Cardiology (ESC) Risk-SCD score (2.2 ± 0.6 vs. 2.6 ± 0.6, P < .001) and absolute LV-GLS (11.4 ± 3.7% vs. 9.3 ± 3.4%, P < .001). According to time-dependent analysis, 9% is an optimal cut-off value for absolute LV-GLS in predicting the primary outcome after a 10-year follow-up. On competing risk regression analysis, absolute LV-GLS ≤ 9% was associated with a higher rate of primary endpoints (subhazard ratio: 2.66 [95% confidence interval: 1.96 to 3.36]) after adjustment for known risk factors. Finally, LV-GLS provided incremental prognostic value over 2020 American College of Cardiology (ACC)/American Heart Association (AHA) risk model (log-likelihood ratios, -262.2 vs -266.2; P = .003) and 2022 ESC risk model (log-likelihood ratios, -268.4 vs -264.9; P = .009), respectively. In the subgroup with Class 3 of recommendation for implantable cardioverter defibrillator, patients with absolute LV-GLS ≤ 9% showed significantly worse prognosis than those with absolute LV-GLS > 9% (p = .002 and .004 for 2020 AHA guideline and 2022 ESC guideline, respectively).Conclusion:Feature tracking LV-GLS derived by cardiac MRI may enable further risk stratification for the subgroup of HCM patients who never accept septal reduction therapy in their lifetime, especially for those recognized as low-risk for SCD based on current guidelines.

Circulation, Volume 150, Issue Suppl_1, Page A4145465-A4145465, November 12, 2024. Background:Myocardial bridging (MB) is a common congenital anomaly wherein a coronary artery segment takes an intramyocardial course. While often benign, MB may be associated with myocardial ischemia/stunning (MS), acute coronary syndromes (ACS), or even sudden cardiac death during periods of increased cardiac demand.Case presentation:A 47-year-old male with a history of type 1 diabetes mellitus was admitted to the Intensive Care Unit for diabetic ketoacidosis (DKA). He complained of epigastric pain with an electrocardiogram showing transient ST-elevation in the anterior and inferior leads. Cardiac troponin showed an upward trend with a peak of 0.202 ug/L and an elevated NT-proBNP of 5,014 pg/mL. A transthoracic echocardiogram (TTE) revealed left ventricular systolic dysfunction (LVEF 40%) with akinesis of the mid to apical anterior and septal walls, consistent with the left anterior descending (LAD) artery territory. Emergent left heart catheterization (LHC) revealed patent coronary arteries with severe mid-LAD MB with TIMI 3 flow. He was managed conservatively with guideline-directed medical therapy for heart failure, and subsequent TTE nine months later showed normalization of LV wall motion (LVEF 65%). Five months later, the patient was readmitted for DKA with elevated troponin. A repeat TTE demonstrated LV systolic dysfunction (LVEF 35%) with wall motion abnormalities (WMA) mirroring the initial presentation.Discussion:Our patient presented with recurrent episodes of ACS/MS complicated by LV systolic dysfunction along the LAD territory during periods of DKA, a known stressor for myocardial ischemia. The absence of obstructive coronary atherosclerosis on LHC, coupled with severe mid-LAD MB, suggests that the MB was the likely culprit for recurrent ACS/MS. Although stress cardiomyopathy was considered a differential diagnosis, this was less likely given the uncharacteristic pattern of WMA sparing the apical lateral and inferior walls as opposed to apical ballooning and the presence of an alternative diagnosis.Conclusion:This unique case underscores the importance of recognizing MB as a rare but potential cause of ACS/MS and LV dysfunction in patients with precipitating stressors such as DKA.

Circulation, Volume 150, Issue Suppl_1, Page A4141635-A4141635, November 12, 2024. Background:Pulse wave analysis (PWA) of aortic pressure waveforms carries valuable information about cardiovascular health. However, due to the invasiveness of direct measurement, peripheral pressure waveforms are commonly used as surrogates. Recent findings revealed that while algorithmic methods can preserve pressure dynamics in non-invasive measurements, significant waveform morphology changes disrupt the association between peripheral and central parameters(PMID: 38591330, 2024). There is a need for non-invasive methods to faithfully reconstruct the central pressure waveform.Aim:Evaluate the fidelity of reconstructed aortic waveforms using a machine learning method applied to non-invasive brachial measurements.Methods:This study analyzed concurrent aortic catheterization and brachial cuff waveform measurements in suprasystolic mode in subjects referred for non-emergent left heart catheterization (N=115; mean age 66, 63% male). Our machine learning method uses a non-linear mode mapping in the frequency domain between non-invasive calibrated brachial pressure waveforms and invasive aortic ones. PWA features captured waveform magnitude and shape: systolic blood pressure (SBP), diastolic blood pressure (DBP), systolic pressure-time integral (SPTI), diastolic pressure time integral (DPTI), peak timing (Tpeak), systole duration (Tsys), maximum pressure derivative ((+)dP/dt), and form factor (FF). Percentage error ((true–predicted)/true) was used to assess parameter correspondence in the testing population (N=35; cardiac cycles=994).Results:The non-linear mapping technique successfully reconstructed central pressure waveforms with good agreement between measured and estimated (MEAN=0.5 mmHg; SD=7.3 mmHg) as shown in Fig. 1A. PWA features showed low mean percentage errors for pressure (SBP=-0.7 ±5.9%; DBP=-2.9±9.4%), area (SPTI=0.2±8.7%; DPTI=-2.8±9.3%), timing (Tpeak=1.0±12.3%; Tsys=1.2±7.1%), and shape parameters ((+)dP/dt=11.5±24.3%; FF=1.4±4.7%) shown in Fig. 1B.Conclusion:Our results demonstrate that the machine learning method applied on brachial cuff measurements captures waveform morphological changes along the arterial system allowing for a faithful representation of the central pressure waveform.

Circulation, Volume 150, Issue Suppl_1, Page A4146419-A4146419, November 12, 2024. Introduction/Background:Gestational diabetes mellitus (GDM) is one of the most common pregnancy complications and a major risk factor for endothelial dysfunction and cardiovascular diseases in later life. The underlying pathophysiology is not well-understood. An important mediator of endothelial dysfunction and atherosclerosis is the lectin-like receptor for oxidized low-density lipoprotein, LOX-1.Research Question/Hypothesis:We hypothesize that maternal GDM leads to impaired fetal vascular function and increased endothelial LOX-1 expression.Goals/Aim:Our aim is a better understanding of the impact of maternal GDM on fetal vascular function and LOX-1 as potential mediator of endothelial dysfunction.Methods/Approach:We obtained maternal and fetal vessels of mature human placentas from normoglycemic mothers (n=32) and patients with insulin-treated GDM (iGDM) (n=8) or diet-treated GDM (dGDM) (n=8). Groups were defined by oral glucose tolerance test and clinical data of mothers and newborns. Vascular function of fetal vessels from mothers with iGDM, dGDM, or normoglycemic controls was analyzed by Mulvany Myograph. Gene expression was quantified by real-time PCR in RNA from fetal vessels of cotyledone base and maternal spiral arteries of patients.Results/Data:Birth weight to placenta weight-ratio showed a significantly reduced placenta efficiency in the iGDM group (P

Circulation, Volume 150, Issue Suppl_1, Page A4139236-A4139236, November 12, 2024. Background:New-onset atrial fibrillation (AF) is common among kidney transplant (KTx) recipients and is associated with reduced patient survival. Predictors of AF after KTx are not well understood, although AF can be associated with traditional and non-traditional risk factors. While artificial intelligence-enabled electrocardiography (AI-ECG) has shown promise in predicting incident AF, its predictive and prognostic implications in the KTx population have not yet been evaluated.Hypothesis:AI-ECG can predict new-onset AF and carries prognostic implications in patients undergoing KTx.Aims:To evaluate the clinical implications of applying AI-ECG to the preoperative ECGs of recipients of a KTx.Methods:Patients without a history of AF who underwent KTx at three referral centers between 2011 and 2021, with at least one preoperative ECG, were included in this retrospective study. Preoperative ECGs were analyzed using a previously developed AI-ECG algorithm to estimate the probabilities of new-onset AF. Based on these probabilities, patients were categorized into two groups: high and low probability of incident AF. The optimal cut-off value for the AI-ECG tool was determined using ROC analysis. The incidence of new-onset AF and mortality at 5 years post KTx were compared between these two groups using univariate and multivariate Cox regression analyses.Results:In total, 6246 patients were included (mean age 52.9 ±14.3 years, 58.7% males). A pre-transplant AI-ECG probability of AF >10% was identified as the most accurate cutoff point to distinguish between patients at low risk and high risk of incident AF (ROC = 0.72). The study found that a preoperative AI-ECG high risk of AF demonstrated not only a strong association with new-onset AF (HR 2.54, 95%CI 2.02-3.19, p

Circulation, Volume 150, Issue Suppl_1, Page A4143615-A4143615, November 12, 2024. Background:A coronary artery calcium score of zero (CAC=0) is generally accepted as a marker of a very low 5y risk for coronary events. However, whether the prognostic value of CAC=0 varies by sex is unclear. For example, non-atherosclerotic causes of coronary ischemia present more often in women, including spontaneous coronary artery dissection and microvascular angina, which may be undetected by CAC. Further, CAC is performed at a later age in women. Whether these factors impact the utility of CAC=0 in women vs men is uncertain.Methods:We tested whether the prognostic value of CAC=0 differs by sex. We searched the Intermountain Health electronic medical record (eMR) database for patients (pts) at primary coronary risk who underwent positron emission tomography/computed tomography (PET/CT) stress testing and had a zero CAC score. We assessed coronary prognosis (i.e., coronary death [CD] or non-fatal myocardial infarction [MI]) during follow-up. Primary events were adjudicated by chart review. We compared outcomes in women vs. men. Given the small number of events, chi-square rather than time-to-event analyses were performed. We also compared all-cause death or MI rates in those with CAC=0 vs. CAC >0 by sex.Results:The eMR search identified19,495 women and 20,523 men undergoing PET/CT who were at primary coronary risk. Of these, 7967 (19.9%) had CAC=0 on CT. Of CAC=0 patients, 5400 (67.8%) were women and 2567 (32.2%) were men. Overall age averaged 60.5y (SD 12.0) in women and 53.8y (SD 12.6) in men. In total, 13 events occurred (MI=12, CD=1) over a follow-up of 2.1y (SD 1.6). By sex, 7 events (0.13%) occurred in CAC=0 women and 6 (0.24%) in men (p=0.28). Rates of all-cause death or non-fatal MI comparing CAC=0 to CAC >0 were 3.3% vs 9.5% in women and 3.3% vs 10.2% in men (both p

Circulation, Volume 150, Issue Suppl_1, Page A4147562-A4147562, November 12, 2024. Background:Up to 20% of patients presenting with an acute coronary heart disease (CHD) event do not report any traditional modifiable cardiovascular risk factors (CVRFs) on admission. However, major predictors of CHD events in the absence of CVRFs are still unknown.Aims:To establish whether increased concentrations of emerging circulating biomarkers at baseline (hsCRP, cystatin C, fibrinogen, NT-proBNP and troponin I), might be associated with future CHD events in subjects from the general population, who demonstrated no traditional CVRFs (hypertension, diabetes mellitus, dyslipidemia, smoking) at time of enrollment.Methods:Overall 213,310 subjects (median age 50.6 yrs.; 57.0% males) from 21 European prospective population-based cohorts were included. All participants were free of CHD at baseline and were followed-up prospectively for incident CHD events. Subjects were characterized in accordance to CVRF burden into2not present” or having 1 or ≥2 CVRFs at baseline. Fine and Gray competing risk-adjusted models were performed for the association between biomarkers and future CHD events in an interaction with the CVRF groups.Results:Overall, 18.6% of subjects revealed no traditional CVRF at baseline (n=39,722). During a median follow-up of 13.95 years, 17,544 subjects developed an incident CHD event (event rate 20.0%). Of those, 532 events were among subjects, who were free of four traditional CVRFs at baseline (event rate 6.7%). Among all studied biomarkers, only fibrinogen was not associated with incident CHD among those without CVRFs, whereas the association between all remaining biomarkers and future events was found to be even more prominent in subjects without than in those with CVRFs. The corresponding sub-distribution Hazard Ratios (sHRs) with 95% CI were for hsCRP (

Circulation, Volume 150, Issue Suppl_1, Page A4125691-A4125691, November 12, 2024. Introduction:Physical activity (PA) is an important modifiable factor for cardiovascular disease (CVD). Sexual and gender minority (SGM; e.g., lesbian/gay, bisexual, transgender) adults face higher risks of inadequate PA and CVD due to increased exposure to minority stressors, such as experienced and anticipated discrimination, which may influence SGM adults’ willingness to engage in PA. To our knowledge, researchers have not investigated the impact of minority stressors on objectively-measured PA among SGM adults.Goal:Using k-means clustering, we sought to identify whether clusters characterized by greater exposure to minority stressors were associated with lower moderate and vigorous PA (MVPA) and higher sedentary behavior among SGM adults.Methods:This daily diary study included an online sample of SGM adults living in the United States. Participants completed daily surveys about personally experienced discrimination and anticipated discrimination (i.e., expectation of experiencing discrimination) and wore wrist accelerometers for 28 days to objectively measure PA. We used k-means clustering to identify clusters based on reports of experienced and anticipated discrimination. We first determined the optimal number of clusters using established partition criteria. Next, we ran linear regression models (adjusted for demographic factors) to examine the associations of minority stress clusters with MVPA and sedentary time per week.Results:Among 42 SGM adults (mean age 27.0±7.7 years) with 1133 person-days of accelerometry data (~3% missing data), we identified four minority stress clusters: low anticipated/low experienced (LALE; reference group); low anticipated/high experienced (LAHE); high anticipated/low experienced (HALE); and high anticipated/high experienced discrimination (HAHE). Participants in the HALE cluster (n=12) engaged in 202 fewer minutes of MVPA than those in the LALE cluster (n=7). Participants in the LAHE cluster (n=10) had 123 fewer minutes of vigorous PA than those in the LALE cluster. No differences were identified for sedentary time.Conclusions:This is the first study to examine the association of minority stressors with objective PA among SGM adults. Participants in the HALE and LAHE clusters engaged in significantly lower PA than those with low levels of both experienced and anticipated discrimination. Findings underscore the importance of assessing minority stressors and the need for interventions to improve PA among SGM adults.

Circulation, Volume 150, Issue Suppl_1, Page A4139955-A4139955, November 12, 2024. Background:Myocardial infarction (MI) is a leading cause of mortality worldwide, and adverse outcomes among hospitalized patients are notable, particularly among older patients who experience frailty. Frailty is characterized by poor physiologic reserve and often results in poor response to medical insults. This study aims to assess the utility of a health record-based Electronic Frailty Index (eFI) in predicting clinical outcomes among these patients.Methods:This study is a single-center, retrospective cohort study of 390 patients aged 65 and older admitted with MI from October 2017 to January 2021. Data was collected using the ACC Chest Pain-MI registry and the electronic health record. Patients were divided into two cohorts: Fit (eFI

Circulation, Volume 150, Issue Suppl_1, Page A4142856-A4142856, November 12, 2024. Background:Atherosclerosis (AS) progression involves complex interactions and phenotypic plasticity among vascular and immune cell lineages. Single-cell RNA-seq (scRNA-seq) studies have highlighted lineage-specific transcriptomic signatures, but human cell phenotypes and crucial pathogenic cell subsets remain controversial.Methods:We performed an integrated meta-analysis of single-cell sequencing data from our center along with four other scRNA-seq libraries (GSE247238, GSE235436, GSE155512, GSE159677) to generate a comprehensive map of human atherosclerotic plaques, including both coronary arteries with no discernible atherosclerotic lesions and diseased carotid plaques. To validate our conclusions, three independent datasets were used, including two bulk transcriptomics datasets and one proteomics dataset (GSE28829, GSE16315 and PXD031052). Besides, the Biobank of Karolinska Endarterectomy (BiKE) dataset was used for Kaplan–Meier (KM) analysis. Comparative analyses were performed between the groups, including cellular compositional analysis, cell type–resolved transcriptomic changes, and functional analysis.Results:The final integrated single-cell dataset, comprising 134,710 cells, consisted of 8 major cell types. The annotated cell subpopulations were generally present across the various studies, but their proportions varied between different studies. Pathway analysis identified that the most significantly impacted pathways were those associated with immune cell functions and cellular metabolism. Notably, SPP1 is highly expressed in macrophages. Survival analysis showed significantly lower ischemic event-free survival in the high SPP1 expression group compared to the low expression group. Besides, compared to atherosclerotic plaques with early stage (EA), non-intraplaque hemorrhage (IPH), and non-calcified conditions, SPP1 expression was highly up-regulated in all stages of plaque progression, including advanced plaques (AA), hemorrhagic plaques, and calcified plaques. Meanwhile, the differences in cellular composition and transcriptomic profiles between the lesion and non-lesion groups further highlighted the significance of lipid metabolism-related SPP1hifoamy macrophages.Conclusions:We created a unified atlas of human atherosclerosis informing cell state-specific mechanistic and translational studies of cardiovascular diseases. SPP1hifoamy macrophages contributed importantly to AS progression.

Circulation, Volume 150, Issue Suppl_1, Page A4136394-A4136394, November 12, 2024. Background:Arrhythmogenic cardiomyopathy (ACM) is a genetic heart disease characterized by fibrofatty replacement of ventricular myocardium. Arrhythmogenic left ventricular (LV) cardiomyopathy (ALVC) is a phenotypic variant of ACM predominantly involving the LV. Mutations in genes encoding for desmosome proteins and filamin C have been implicated in ALVC, especially in the setting of a ring-like late gadolinium enhancement (LGE) imaging pattern.Objective:To identify the underlying genetic substrate responsible for genetically elusive ring-like ALVC in a patient with seemingly sporadic/recessive disease.Methods:A 38-year-old male was referred for genetic investigation to determine the underlying genetic substrate responsible for his ALVC phenotype. The patient fulfilled both electrocardiographic (low voltage in the limb leads and anterolateral T-wave inversions) and imaging ( >1 segment of subepicardial LGE) criteria for ALVC. Additionally, the patient experienced unexplained episodes of tachycardia, shakiness, sweating, and nausea prompting concern for an underlying neuromuscular disease. Genome sequencing (GS) was performed on DNA isolated from the affected patient and both of his unaffected parents. Variants were filtered assuming either a sporadic de novo occurrence or an autosomal recessive inheritance pattern.Results:GS identified compound heterozygous GNPTAB variants in the affected patient. A previously reported maternally derived p.Leu257Leu (c.771G >A) variant involving the last nucleotide of exon 7 of theGNPTABgene and a novel paternally inherited Lys834fs*5 frame-shift variant were identified. The p.Leu257Leu variant has been reported to cause aberrant splicing and exon skipping of the GNPTAB mRNA transcript. Pathogenic variants in theGNPTABencoded N-acetylglucosamine-1 (GlcNAc)-phosphotransferase subunits alpha/beta cause mucolipidosis type III, a rare recessive lysosomal storage disease characterized by coarse facial features, developmental delay, short stature, skeletal deformities, and cardiac involvement including valvular thickening and cardiomyopathy.Conclusions:Here, using a genome sequencing trio analysis we identified a compound heterozygous GNPTAB pathogenic variants as the underlying genetic substrate in a patient with ring-like ALVC and concomitant neuromuscular disease manifestation. Genome sequencing may identify the genetic etiology responsible for an otherwise undifferentiated diagnosis of cardiomyopathy.

Circulation, Volume 150, Issue Suppl_1, Page A4116093-A4116093, November 12, 2024. Background:High intensity statin therapy is currently recommended for primary prevention of ASCVD in patients with severe hyperlipidemia (HLD), defined as low-density lipoprotein cholesterol (LDL-C) of ≥190 mg/dL. We examined statin use for patients with severe HLD and associated ASCVD outcomes in a large contemporary healthcare network.Methods:Using EMR data, patients between the ages of 20 and 79 with a lipid bloodwork result between 2013 and 2017 without ASCVD byICD9andICD10codes were identified. Patients with LDL-C ≥ 190 mg/dL were identified. Statin use was stratified by no statin, guideline directed statin intensity (GDSI), and less than guideline directed statin intensity (

Circulation, Volume 150, Issue Suppl_1, Page A4142989-A4142989, November 12, 2024. Background:Cardiovascular magnetic resonance (CMR) has an emerging role in graft surveillance for pediatric heart transplant recipients (PHTR). Transplanted grafts are susceptible to cardiac allograft vasculopathy, manifested as macrovascular narrowing on angiography, as well as micro-vessel disease. By CMR, myocardial perfusion abnormalities can be evaluated semi-quantitatively, by calculation of a myocardial perfusion reserve index (MPRI). However, normal MPRI values have not been well established in PHTR and prior investigation of associations between MPRI and graft pathology remain limited.Research Aims:The goals of this study were to describe the MPRI findings in a large cohort of PHTR and to evaluate clinical associations with low MPRI.Methods:We performed a retrospective chart review of consecutive, stress CMR studies at a single center from 2015-2024. Follow-up studies were excluded. Biventricular volume and function analyses were performed. A total dose of 0.15mg/kg gadobutrol was administered for rest and stress imaging. Regadenoson was the pharmacologic stressor at dose of 6-10mcg/kg, up to max 400mcg. Time signal intensity curves were obtained from perfusion datasets at stress and rest at the base, mid-ventricle, and apex. Segmental MPRI was calculated as a ratio of the maximal upslopes of the curves at stress versus rest. Global MPRI was computed as a mean of all segments.Results:128 PHTR were included. Mean age was 12.5±5.3y, with 5.9±3.8y since transplant. A clinical concern prompted CMR in 18% of studies; in 82% the indication was routine surveillance. History of CAV was present in 6% and moderate or severe rejection in 22%. In 11 studies, images were inadequate for MPRI analysis. In the 117 studies included for analysis, global MPRI was normally distributed with mean 1.38±5.3. Mean MPRI observed at the mid-ventricle (1.49±0.46) was higher than at the base (1.32±0.32) and apex (1.33±0.39), (p

Circulation, Volume 150, Issue Suppl_1, Page A4135791-A4135791, November 12, 2024. Background:While non-vitamin K antagonist oral anticoagulants (NOACs) are more effective than single antiplatelets (mostly low-dose aspirin) at reducing stroke risk in patients with atrial fibrillation (AF), differences in bleeding risk between NOACs and single-dose antiplatelets across various populations remain unclear.Aim:We performed a systematic review and meta-analysis of randomized controlled trials (RCTs) comparing bleeding outcomes of NOACs versus single antiplatelet therapy.Methods:We searched MEDLINE, EMBASE, and CENTRAL to June 2024 for RCTs that compared NOAC (therapeutic doses used for stroke prevention in AF patients) versus single antiplatelet therapy for a treatment duration of ≥3 months. For the meta-analyses, we used fixed-effects models and reported results as summary risk ratios (RRs). We used Risk of Bias 2 and GRADE to assess the quality and certainty of the evidence.Results:Eight RCTs with 26,194 participants were included. Mean follow-up time was 18 (±13) months. NOACs included in the studies were apixaban (4 studies), rivaroxaban (2 studies), and dabigatran (2 studies). All studies used low-dose aspirin as the comparator. When compared to aspirin, NOACs had a higher risk of major bleeding (326/13107 [2.5%] vs. 239/13087 [1.8%] events; RR 1.36 95% CI 1.15-1.60, I2=52%, 8 trials; high certainty) (Figure A), gastrointestinal bleeding (104/8803 [1.2%] vs. 74/8788 [0.8%] events; RR 1.39; 95%CI, 1.04-1.87; I2=0%; 5 trials; high certainty), and clinically relevant non-major bleeding (318/10397 [3.1%] vs. 230/10395 [2.2%] events; RR 1.38; 95%CI, 1.17-1.63; I2=16%; 5 trials; high certainty). There was no difference in the risk of intracranial hemorrhage (88/13107 [0.7%] vs. 84/13087 [0.6%] events; RR 1.04, 95%CI 0.78-1.41; I2=48%; 9 trials; high certainty) (Figure B) nor fatal bleeding (22/12412 [0.2%] vs. 28/12392 [0.2%] events; RR 0.78; 95%CI, 0.45-1.36; I2=8%; 6 trials; high certainty).Conclusion:When compared to aspirin, NOACs are associated with an increased risk of major bleeding and clinically relevant non-major bleeding, but not intracranial hemorrhage. These data are important to inform patients about the risks of antithrombotic treatment.

Circulation, Volume 150, Issue Suppl_1, Page A4145440-A4145440, November 12, 2024. Introduction:Post-infarction (post-MI) ventricular septal rupture (VSR) and papillary muscle rupture (PMR) are usually lethal complications of acute STEMI that have decreased in the fibrinolytic era and with rapid STEMI response teams. Delayed correction is preferred for recovery from MI and healing of the edges of the VSD but like emergent repair, delayed treatment is also associated with high mortality. We present a case of concomitant post-MI VSR and PMR successfully corrected by simultaneous percutaneous intervention.Case presentation:A 76-yo female with hypertension, obesity and asthma presented with progressively worsening dyspnea and mild substernal chest pain for 4 days. She appeared pale, diaphoretic, and hypoxic, with troponin of 22ng/mL and lactate of 9mmol/L. ECG showed Q waves with STE

Circulation, Volume 150, Issue Suppl_1, Page A4140060-A4140060, November 12, 2024. Introduction:Type 2 diabetes mellitus (T2DM) is a major risk factor for coronary artery disease (CAD). SGLT2 inhibitors (SGLT2i) are effective in reducing cardiovascular mortality in T2DM patients, but their benefits for those with both CAD and T2DM are uncertain.Objective:The primary outcome was to evaluate the efficacy of SGLT2i compared to other hypoglycemic agents or placebo in reducing the risk of all-cause mortality in patients with T2DM and CAD. Secondary outcomes included cardiovascular death, fatal or non-fatal stroke, and fatal or non-fatal myocardial infarction. We hypothesize that SGLT2i are more effective in mortality risk reduction in patients with T2DM and concomitant CAD.Methods:A systematic review following PRISMA-2020 guidelines was conducted across four databases to evaluate the efficacy of SGLT2i in reducing mortality risk in diabetic patients with CAD. Quantitative analysis using Stata v18 employed a random-effects model (Restricted Maximum Likelihood) with Hazard Ratios (HR) as the measure of association.Results:Out of 853 studies identified, 5 publications were included in the final quantitative analysis, which included 5225 patients. The Newcastle-Ottawa Quality Assessment Form showed all included cohort studies had a low risk of bias. Those patients taking SGLT2i had a significant reduction in 38% the risk of all-cause mortality (HR 0.62 [0.47, 0.80]), this same effect was observed when compared with each subgroup vs. other hypoglycemic agents, HR 0.52 [0.29, 0.93]; vs. placebo, HR 0.64 [0.46, 0.90]. Results show very low heterogeneity. In overall cardiovascular death analysis, a significantly greater reduction was observed with SGLT2i (HR 0.61 [0.46, 0.81]), as well as when compared with placebo (HR 0.64 [0.47, 0.86]). In contrast, when compared with other hypoglycemic agents, there was a reduction, but this was not significant (HR 0.45 [0.19, 1.03]). No statistically significant decrease in the risk of fatal or non-fatal stroke and myocardial infarction was found with SGLT2i.Conclusion:SGLT2i demonstrates a greater significant benefit in reducing all-cause and cardiovascular mortality in patients with T2DM and CAD.