Introduction:While prior studies have documented suboptimal lipid management and low rates of low-density lipoprotein cholesterol (LDL-C) goal achievement in patients with atherosclerotic cardiovascular disease (ASCVD), the degree of variability in lipid-lowering therapy (LLT) practice patterns between clinicians is less well described. Methods:In this cohort study, we evaluated the use of LLTs and achievement of LDL-C <70 mg/dL among adults with ASCVD (coronary artery disease, peripheral arterial disease, or ischemic cerebrovascular disease) followed by a cardiology physician or advanced practice provider (APP) at a large academic medical center in north Texas from 01/01/22-06/30/24. LLT utilization and LDL-C goal achievement were modeled using mixed-effects logistic regression with clustering at the clinician level, adjusting for patient age, insurance, ASCVD type, and diabetes. We quantified clinician-level variability using the adjusted median odds ratios (aMORs) from these models. Results:Among 9098 patients with ASCVD (median age 71.0 years, 61.6% male, 70.5% White) seen across 77 cardiology clinicians (56 physicians, 21 APPs), 52.8% were on a high-intensity statin, 17.1% were on ezetimibe, 7.8% were on novel LLT (proprotein convertase subtilisin/kexin type 9 monoclonal antibody, inclisiran, or bempedoic acid). Of those with an available lipid panel in the past year (n = 7122), 48.5% achieved an LDL-C <70 mg/dL. Lipid management strategies varied substantially across clinicians. In mixed-effects models adjusting for patient-level factors, significant clinician-level variation was observed in the use of high-intensity statins (aMOR 1.44, 95% CI 1.34-1.59), ezetimibe (aMOR 1.68, 95% CI 1.52-1.91), and novel LLT (aMOR 2.21, 95% CI 1.90-2.68). Variation in achieving LDL-C <70 mg/dL was more modest (aMOR 1.31, 95% CI 1.23-1.42). Sequential adjustment for clinician prescribing patterns explained nearly half of the observed variability in LDL-C goal achievement, reducing the aMOR to 1.16 (95% CI 1.09-1.27). Conclusion:We found suboptimal rates of high-intensity statin and LDL-C control among patients with ASCVD. Even among cardiology clinicians at the same academic medical center, practice patterns varied widely in using LLT and achieving LDL-C goals for secondary prevention. Understanding the reasons for this variability and standardizing lipid management across the specialty may improve quality of care for patients with ASCVD.

Background The Agatston score quantifies coronary artery calcium (CAC) burden but does not account for its spatial distribution. The CAC diffusivity index (DI) may refine cardiovascular risk stratification in individuals with Agatston CAC>0. This study assessed whether CAC distribution improves cardiovascular event prediction beyond the Agatston score in a young cohort. Methods Among DHS2 (Dallas Heart Study 2) participants with CAC>0 and no prior cardiovascular disease (35% of the cohort), we studied 1013 participants with CAC DI. CAC DI was calculated as 1−(CAC in most affected vessel/total CAC) and categorized as concentrated (<25th percentile), standard (25th–75th percentile), and diffuse (>75th percentile). Cox proportional hazards models and C‐statistics assessed coronary heart disease (CHD), atherosclerotic cardiovascular disease, and mortality, adjusting for Agatston CAC, demographics, and traditional risk factors. Results Mean±SD age was 55±9.4 years (49% women, and 47% Black), with a median follow‐up of 9±2.5 years (57 CHD and 92 atherosclerotic cardiovascular disease events). Compared with a concentrated CAC pattern, standard and diffuse patterns were associated with incident CHD (hazard ratio, 5.97 [95% CI, 1.24–28.78] and 5.48 [95% CI, 1.04–29.04], respectively; P<0.05) but not atherosclerotic cardiovascular disease in fully adjusted models. Positive and negative changes in CAC DI were associated with increased CHD and atherosclerotic cardiovascular disease risk in models adjusted for pooled cohort equation variables, although effects were attenuated in fully adjusted models. Adding continuous CAC DI did not significantly improve model performance. Conclusions Higher CAC DI at baseline significantly contributes to adjusted models for incident CHD in a young population‐based cohort, but temporal changes provided little additional benefit.

OBJECTIVE:Traumatic brain injury (TBI) is recognized as a chronic health condition. The primary objective was to investigate the association between TBI and cardiovascular disease (CVD). SETTING:Ovid MEDLINE, Ovid MEDLINE Epub Ahead of Print and In-Process, In-Data-Review and Other Non-Indexed Citations, Ovid Embase, Ovid APA PsycInfo, and the Cochrane Library were systematically searched until June 5, 2025. DESIGN:Observational studies that compared diagnoses of CVD, including atherosclerosis, coronary artery disease (CAD), heart failure, cardiomyopathy, arrhythmias, myocardial infarction, hypertension, hyperlipidemia, and cardiac death, between adults with and without TBI were included. Studies that focused on preinjury CVD and conditions, case reports, case series, letters, editorials, conference abstracts, reviews, and interventional studies were excluded. Study quality was evaluated using the National Institutes of Health quality assessment tool. DerSimonian-Laird random-effects meta-analyses were performed. MAIN MEASURES:The outcomes of interest were presence of any CVD, including atherosclerosis, CAD, heart failure, cardiomyopathy, arrhythmias, myocardial infarction, hypertension, hyperlipidemia, and cardiac death. RESULTS:This systematic review included 21 studies, with 18 studies involving 3,954,962 participants included in the meta-analysis. Two studies were rated as poor quality, with the rest fair to good. Individuals with TBI had higher odds of any CVD (odds ratio [OR] 1.78, 95% confidence interval [CI] 1.39-2.29), CAD (OR 1.40, 95% CI 1.20-1.63), arrhythmia (OR 1.42, 95% CI 1.12-1.80), cardiac death (risk ratio [RR] 3.07, 95% CI 2.17-3.98), hypertension (OR 1.42, 95% CI 1.07-1.90), and hyperlipidemia (OR 1.86, 95% CI 1.25-2.77) in unadjusted analysis. No association was found with heart failure (OR 1.16, 95% CI 0.96-1.39). The adjusted analysis was consistent with unadjusted findings for CAD, cardiac death, hypertension, and heart failure. CONCLUSION:Individuals with TBI have higher odds of CVD, hypertension, hyperlipidemia, CAD, arrhythmia, and cardiovascular death than the general population, highlighting the need for clinical screening, prevention, and management strategies after TBI.

Background: Lipoprotein(a) [Lp(a)] is associated with atherosclerotic cardiovascular disease (ASCVD). An Lp(a) threshold of ≥125 nmol/L is commonly used to identify those at higher risk, but there is paucity of data on Hispanic/Latino individuals. Methods: We evaluated the association between Lp(a) and myocardial infarction (MI), ischemic stroke (IS), and all-cause mortality (ACM) among 16,117 self-identified Hispanic/Latino HCHS/SOL participants. Event rates were compared across Lp(a) quintiles and below/above median IQR. Multivariable Cox proportional hazard models assessed the relationship between events and Lp(a) (log-transformed, per quintiles and above/below 125 nmol/L). Kaplan-Meier curves showed outcome-free survival across quintiles. Sampling weights and survey methods were used to accommodate the stratified probability sampling of the cohort. Results: Among HCHS/SOL participants (median age 41.1 years, 52.4% female), the median Lp(a) was 19.7 nmol/L (IQR 7.3-60.6), 11.4% had an Lp(a) over 125 nmol/L, and the highest quintile of Lp(a) was >77 nmol/L. Over a median of 9.8 years, 883 events (135 MI, 99 stroke, 649 ACM) occurred. Incident MI and ACM, but not IS, occurred more often in those in the highest quintile of Lp(a) compared with other quintiles. In multivariable models, continuous log-transformed Lp(a) and categorial Lp(a) (fifth quintile) were independently associated with incident MI but not IS or ACM. Lp(a) ≥125 nmol/L was associated with a higher risk of both incident MI and ACM. Outcome-free survival was significantly lower for the highest Lp(a) quintiles, Figure 1. Conclusion: Hispanic/Latino individuals with elevated Lp(a) are at increased risk of MI and ACM. Although Lp(a) ≥125 nmol/L is a valid risk threshold, Hispanics/Latinos show an increased risk at a lower Lp(a) threshold.

Background Lipoprotein(a) [Lp(a)] is associated with atherosclerotic cardiovascular disease. An Lp(a) threshold of ≥125 nmol/L is commonly used to identify individuals at higher risk for events, but there is a paucity of data on individuals of Hispanic/Latino descent. Objectives The purpose of this study was to provide a comprehensive evaluation of Lp(a) and its association with 10-year cardiovascular disease risk and mortality among Hispanic/Latino adults in the United States. Methods We evaluated the association between Lp(a) and myocardial infarction (MI), ischemic stroke, and all-cause mortality among 16,117 Hispanic Community Health Study/Study of Latinos individuals. Event rates were compared across Lp(a) quintiles. Multivariable Cox proportional hazards models assessed the relationship between events and Lp(a) across increasing quintiles, log-transformed Lp(a), and ≥125 nmol/L vs <125 nmol/L. Sampling weights and survey methods were used to account for the stratified probability sampling of the cohort. Results Among the Hispanic Community Health Study/Study of Latinos target population (median age 41.1 years, 52.4% women), the median Lp(a) was 19.7 nmol/L (Q1-Q3: 7.3-60.6 nmol/L), with 11.4% having Lp(a) ≥125 nmol/L, and the highest Lp(a) quintile defined as >77 nmol/L. Over a median follow-up of 9.8 years, 883 events (135 MI, 99 stroke, 649 all-cause mortality) occurred. The age-adjusted incidence rate of the composite events (MI, stroke, and all-cause mortality) was 505.2 per 100,000 person-years. After multivariable adjustment, each 1-SD increase in log-transformed Lp(a) was associated with a higher risk of MI (HR: 1.47; 95% CI: 1.14-1.89). Compared with Lp(a) <125 nmol/L, elevated Lp(a) ≥125 nmol/L conferred an increased risk of MI (HR: 2.29; 95% CI: 1.45-3.63), all-cause mortality (HR: 1.43; 95% CI: 1.05-1.93), and composite events (HR: 1.56; 95% CI: 1.22-2.01), but not stroke. Findings were consistent when comparing the highest Lp(a) quintile to the lower 4 quintiles, but the elevated risk was observed only for MI and composite events. Conclusions Hispanic/Latino individuals with elevated Lp(a) are at an increased risk of MI and all-cause mortality. Although Lp(a) ≥125 nmol/L is a valid risk threshold, Hispanics/Latinos show a continuous relationship between increasing Lp(a) levels and MI risk.

Introduction: The recent AHA presidential advisory on Cardiovascular-Kidney-Metabolic Syndrome (CKM) proposed a novel staging scheme, but limited data exist regarding CKM stage prevalence in the community. Prior population-based studies have lacked subclinical imaging measures, and have not reported variability by age, gender, and race/ethnicity. Methods: We estimated the population prevalence of CKM stages in Dallas County, from among 2,817 participants in the population-sampled Dallas Heart Study who attended study Visit 1 (2000-2002). Participants underwent protocol measurement of body composition, lipids, fasting blood sugar, serum creatinine, NT-proBNP, hs-cTnT, urinary albumin and creatinine, coronary artery calcium by cardiac CT (CAC), and cardiac function and mass by cardiac MRI. These were used to operationalize the following CKM stages: 0 – no CKM risk factors; 1 – excess or dysfunctional adiposity (body mass index, waist circumference, and fasting blood glucose); 2 – metabolic risk factors (hypertriglyceridemia, hypertension, diabetes, metabolic syndrome) and chronic kidney disease; 3 – subclinical cardiovascular diseases (CAC, LV hypertrophy or dysfunction by cardiac MRI, elevated cardiac biomarkers (NT-proBNP or hs-cTnT), high AHA-PREVENT or KDIGO scores); 4 – prevalent cardiovascular diseases (coronary heart disease, heart failure, atrial fibrillation, stroke). We used sampling weights to estimate the prevalence of CKM stages in Dallas County in 2000-2002 overall and by age category (30-44, 45-59, 60-65 years), gender, and race/ethnicity. Results: Among the 2,817 participants with a mean age of 44±10 years, the sample weighted demographics were 50% women, 52% non-Hispanic White, 20% non-Hispanic Black, and 26% Hispanic race/ethnicity. Among Dallas County adults, only 10% were CKM Stage 0 (no risk factors). The weighted prevalence of CKM Stages 1 through 4 was 16%, 46%, 23%, and 5%, respectively ( Figure A) . CKM stage prevalence was similar between men and women, while CKM Stage 4 was more frequent among older individuals and among non-Hispanic Black compared with non-Hispanic White and Hispanic individuals ( Figure B ). Conclusion: The public health burden of CKM is substantial. Ninety percent of Dallas County residents in 2000-2002 had some form of CKM syndrome, nearly half demonstrated metabolic dysfunction (Stage 2), and nearly one-fourth had subclinical cardiovascular disease (Stage 3).

ImportanceApolipoprotein B (apoB) distribution and its implications as an atherosclerotic cardiovascular disease (ASCVD) risk-enhancing factor among individuals of diverse Hispanic or Latino backgrounds have not been described.ObjectiveTo describe the distribution of apoB in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) cohort and to characterize associations of baseline sociodemographic and clinical variables with apoB and self-identified Hispanic or Latino background.Design, Setting, and ParticipantsThe HCHS/SOL was a prospective, population-based cohort study of diverse Hispanic or Latino adults living in the US who were recruited and screened between March 2008 and June 2011. Sampling weights were used to generate a population-based sample of Hispanic or Latino participants aged 18 to 74 years who resided in 4 US metropolitan areas (Bronx, New York; Chicago, Illinois; Miami, Florida; and San Diego, California). ApoB concentration was measured in participants from the HCHS/SOL, and apoB tertiles were compared across demographic groups, including self-identified Hispanic or Latino background. Median percentage continental genetic ancestry (West African, Amerindian, and European) was compared across apoB tertiles.ExposureApoB measured in mg/dL from serum or plasma using an immunoturbidimetric assay.Main Outcomes and MeasuresApoB tertiles were determined, and traditional lipids were evaluated across apoB tertiles. ApoB and traditional lipid measurements were assessed across ASCVD risk categories. Additionally, scatterplots were created to observe correlations between apoB and low-density lipoprotein cholesterol or non–high-density lipoprotein cholesterol.ResultsOverall mean (SD) apoB concentration was 99.8 (0.4) mg/dL, with male participants displaying significantly higher mean levels than female participants (102.4 vs 97.4 mg/dL, respectively). Mean (SD) participant age was 41.1 (0.8) years, and 8376 participants (51.9%) were female. ApoB levels were higher among older age groups. There was significant heterogeneity in mean apoB concentrations across self-identified Hispanic or Latino background groups, ranging from 95.1 mg/dL in Dominican individuals to 104.8 mg/dL in Cuban individuals. The prevalence of elevated apoB (≥130 mg/dL) was greater across higher predicted ASCVD risk categories. Among participants with a 10-year predicted ASCVD risk of 7.5% or higher, 26.5% had an elevated apoB. Median West African ancestry was lower across higher tertiles of apoB.Conclusions and RelevanceIn this cohort study among participants from the HCHS/SOL, elevated apoB was present in one-quarter of a diverse cohort study of Hispanic or Latino individuals who were at intermediate or high predicted ASCVD risk. Differences in apoB distribution among Hispanic or Latino individuals may have important implications for apoB’s use in ASCVD risk assessment.

South Asians (SAs) represent an increasing proportion of North American populations and demonstrate excess cardiometabolic risk. Multiple factors likely contribute; however, much is not yet known about what leads to this excess risk. Diet composition, physical activity, and mental health are important lifestyle contributors. Specific adverse pregnancy outcomes are higher in SA women and represent an early opportunity for intervention. More broadly, comprehensive assessments of adiposity, diabetes, hypertension, dyslipidemia, coronary atherosclerosis via imaging, and genetic risk may improve detection and awareness among SAs and those treating SAs. At an individual level, culturally tailored preventive clinics may foster awareness and detection, leading to improved prevention and management of cardiometabolic risk. At a community and population level, assessments of the impact of social determinants, acculturation, and the environment may lead to broader initiatives to improve health in SAs. Lastly, supporting expanded investigation, policy, and other health and science measures at an institutional and societal level may lead to broad but impactful changes across the North American diaspora. In this clinical practice statement, we aim to provide a roadmap of the path forward in each of these domains for health care providers and health systems, community outreach groups, and stakeholders invested in investigation and policy to mitigate risk and empower SAs to lead healthy lives.

BACKGROUND:Lp(a) (lipoprotein[a]) is a risk factor for cardiovascular disease; however, its association with cerebrovascular disease is not as well established. METHODS:Data from a population-based cohort of Hispanics/Latinos included 16 333 individuals with baseline Lp(a) levels (nmol/L) and self-reported prevalent stroke or transient ischemic attack (TIA). A subset of 2642 individuals with brain magnetic resonance imaging was also included. Linear and multivariate logistic regression assessed the association of Lp(a) with (1) self-reported stroke or TIA, (2) cerebral injury defined as self-reported stroke or TIA or evidence of a stroke on brain magnetic resonance imaging, (3) white matter hyperintensity volume, and (4) silent brain infarcts. Sampling weights were utilized given the HCHS/SOL (Hispanic Community Health Study/Study of Latinos) complex sample design. RESULTS:Mean age±SE was 41.1±0.3 years, 52.0% women, and median interquartile range (Q1, Q3) Lp(a) level of 19.7 (7.3-60.6) nmol/L; brain magnetic resonance imaging subset mean age±SE was 49.9±0.4 years, 56.4% women, and median (interquartile range) Lp(a) level of 21.7 (8.1-62.9) nmol/L. Each unit increase in log-transformed Lp(a) was associated with higher odds of self-reported stroke or TIA (odds ratio, 1.13 [95% CI, 1.01-1.27]; P=0.03). Lp(a) levels in the highest quintile (>77 nmol/L) were significantly associated with higher odds of prevalent stroke or TIA compared with Lp(a) <6 nmol/L (first quintile: odds ratio, 1.74 [95% CI, 1.09-2.77]; P=0.02). The highest proportion of cerebral injury was noted in Q5, while the lowest proportion was noted in Q2. When comparing Lp(a) >77 nmol/L with Lp(a) of 6 to <13 nmol/L (second quintile), a significant association was found between Lp(a) and cerebral injury that persisted after fully adjusted models (odds ratio, 2.03 [95% CI, 1.05-3.93]; P=0.03). Each unit increase in log-Lp(a) was associated with a 0.10 increase in log-white matter hyperintensity (β, 0.10; P=0.005). No significant association was found between Lp(a) and silent brain infarcts. CONCLUSIONS:Lp(a) is independently and significantly associated with prevalent stroke/TIA, and white matter hyperintensity, in a large diverse population of Hispanics/Latinos.

BACKGROUND:Tools for mortality prediction in patients with the severe hypercholesterolemia phenotype (low-density lipoprotein cholesterol ≥190 mg/dL) are limited and restricted to specific racial and ethnic cohorts. We sought to evaluate the predictors of long-term mortality in a large racially and ethnically diverse US patient cohort with low-density lipoprotein cholesterol ≥190 mg/dL.METHODS:We conducted a retrospective analysis of all patients with a low-density lipoprotein cholesterol ≥190 mg/dL seeking care at Montefiore from 2010 through 2020. Patients <18 years of age or with previous malignancy were excluded. The primary end point was all-cause mortality. Analyses were stratified by age, sex, and race and ethnicity. Patients were stratified by primary and secondary prevention. Cox regression analyses were used to adjust for demographic, clinical, and treatment variables.RESULTS:A total of 18 740 patients were included (37% non-Hispanic Black, 30% Hispanic, 12% non-Hispanic White, and 2% non-Hispanic Asian patients). The mean age was 53.9 years, and median follow-up was 5.2 years. Both high-density lipoprotein cholesterol and body mass index extremes were associated with higher mortality in univariate analyses. In adjusted models, higher low-density lipoprotein cholesterol and triglyceride levels were associated with an increased 9-year mortality risk (adjusted hazard ratio [HR], 1.08 [95% CI, 1.05-1.11] and 1.04 [95% CI, 1.02-1.06] per 20-mg/dL increase, respectively). Clinical factors associated with higher mortality included male sex (adjusted HR, 1.31 [95% CI, 1.08-1.58]), older age (adjusted HR, 1.19 per 5-year increase [95% CI, 1.15-1.23]), hypertension (adjusted HR, 2.01 [95% CI, 1.57-2.57]), chronic kidney disease (adjusted HR, 1.68 [95% CI, 1.36-2.09]), diabetes (adjusted HR, 1.79 [95% CI, 1.50-2.15]), heart failure (adjusted HR, 1.51 [95% CI, 1.16-1.95]), myocardial infarction (adjusted HR, 1.41 [95% CI, 1.05-1.90]), and body mass index <20 kg/m2 (adjusted HR, 3.36 [95% CI, 2.29-4.93]). A significant survival benefit was conferred by lipid-lowering therapy (adjusted HR, 0.57 [95% CI, 0.42-0.77]). In the primary prevention group, high-density lipoprotein cholesterol <40 mg/dL was independently associated with higher mortality (adjusted HR, 1.49 [95% CI, 1.06-2.09]). Temporal trend analyses showed a reduction in statin use over time (P<0.001). In the most recent time period (2019-2020), 56% of patients on primary prevention and 85% of those on secondary prevention were on statin therapy.CONCLUSIONS:In a large, diverse cohort of US patients with the severe hypercholesterolemia phenotype, we identified several patient characteristics associated with increased 9-year all-cause mortality and observed a decrease in statin use over time, in particular for primary prevention. Our results support efforts geared toward early recognition and consistent treatment for patients with severe hypercholesterolemia.

BACKGROUND AND AIMS:Identifying the association of novel plasma biomarkers with coronary artery calcium (CAC) incidence or progression may provide insights into the pathophysiology of atherogenesis and plaque formation. METHODS:Participants of the Dallas Heart Study (DHS), a multi-ethnic cohort of ambulatory individuals at low-intermediate risk for future atherosclerotic cardiovascular disease (ASCVD), who had their blood tested for 31 biomarkers reflecting multiple pathophysiological pathways, underwent 2 serial non-contrast computed tomography assessments for CAC a median ∼7 years apart. The collected biomarkers were explored for association with CAC incidence or progression using univariate and multivariate analysis. RESULTS:A total of 1424 participants were included; mean age 43 years, 39 % male, and nearly half African-American. Over a 7-year interval between the two CAC measurements, 340 participants (23.9 %) had CAC incidence or progression, 105 (7.4 %) with incident CAC, and 309 (21.7 %) with CAC progression. Although several plasma biomarkers were associated with CAC incidence or progression in a univariate model, only soluble intercellular adhesion molecule-1 (sICAM-1), related to atherosclerosis by the inflammatory pathway, remained independently associated in a multivariate model adjusted for traditional risk factors. CONCLUSIONS:Further studies are needed to characterize the role of sICAM-1 in CAC evolvement to establish whether it has a pivotal mechanistic contribution or is rather an innocent bystander. Alternate measures of coronary atherosclerosis may be needed to elucidate contributors to atherosclerosis incidence or progression.

AbstractBackgroundExcess muscle fat is observed in obesity and associated with greater burden of cardiovascular risk factors and higher risk of mortality. Liraglutide reduces total body weight and visceral fat but its effect on muscle fat and adverse muscle composition is unknown.MethodsThis is a pre‐specified secondary analysis of a randomized, double‐blind, placebo‐controlled trial that examined the effects of liraglutide plus a lifestyle intervention on visceral adipose tissue and ectopic fat among adults without diabetes with body mass index ≥30 kg/m2 or ≥27 kg/m2 and metabolic syndrome. Participants were randomly assigned to a once‐daily subcutaneous injection of liraglutide (target dose 3.0 mg) or matching placebo for 40 weeks. Body fat distribution and muscle composition was assessed by magnetic resonance imaging at baseline and 40‐week follow‐up. Muscle composition was described by the combination of thigh muscle fat and muscle volume. Treatment difference (95% confidence intervals [CI]) was calculated by least‐square means adjusted for baseline thigh muscle fat. The association between changes in thigh muscle fat and changes in body weight were assessed using Spearman correlation coefficients. The effect of liraglutide versus placebo on adverse muscle composition, denoted by high thigh muscle fat and low thigh muscle volume, was explored.ResultsAmong the 128 participants with follow‐up imaging (92.2% women, 36.7% Black), median muscle fat at baseline was 7.8%. The mean percent change in thigh muscle fat over median follow‐up of 36 weeks was −2.87% among participants randomized to liraglutide (n = 73) and 0.05% in the placebo group (absolute change: −0.23% vs. 0.01%). The estimated treatment difference adjusted for baseline thigh muscle fat was −0.24% (95% CI, −0.41 to −0.06, P‐value 0.009). Longitudinal change in thigh muscle fat was significantly associated with change in body weight in the placebo group but not the liraglutide group. The proportion of participants with adverse muscle composition decreased from 11.0% to 8.2% over follow‐up with liraglutide, but there was no change with placebo.ConclusionsIn a cohort of predominantly women with overweight or obesity in the absence of diabetes, once‐daily subcutaneous liraglutide was associated with a reduction in thigh muscle fat and adverse muscle composition compared with placebo. The contribution of muscle fat improvement to the cardiometabolic benefits of liraglutide requires further study.

Background: Lipoprotein(a) [Lp(a)] is causally linked to ASCVD events and aortic stenosis. Some guidelines now recommend screening of Lp(a) at least once in an adult’s lifetime. Currently, there is inconsistency in measurement modality (mg/dL vs. nmol/L), but most guidelines recommending testing in nmol/L due to less variability and improved standardization. We sought to determine the Lp(a) measurement practices, including testing modality and downstream interventions, at a large academic medical institution. Methods: We evaluated all patient encounter data at UT Southwestern Medical Center (UTSW) between January 1, 2017 to December 31, 2021 for any Lp(a) measurement. High Lp(a) was defined as >50mg/dL or >125 nmol/L. Aggregate data were used to summarize patient demographics, relevant ASCVD co-morbidities, and lipid lowering prescriptions. Chart-review was conducted on patients with high Lp(a) to assess referrals to specialty clinics. Results: From 2017 to 2021, there were 1,065 Lp(a) measurements among 938 patients, representing fewer than 0.1% of all patients with labs at UTSW. Most were ordered by cardiologists (71%). Lp(a) tests ordered by cardiologists increased 69% annually but remained stagnant for other specialties (figure 1, lines). Median Lp(a) levels across all tests were 17mg/dL and 43nmol/L. Lp(a) was high in 30% of all initial tests. A higher proportion of tests ordered in 2021 by cardiologists (84%) were in nmol/L, the recommended standard, compared with other specialties (55%) (figure 1, bars). Patients with high Lp(a) found by a non-cardiologist were infrequently referred to cardiology (16%), and 53% of patients with high Lp(a) were prescribed lipid lowering therapy within 3 months. Conclusion: Lp(a) testing at a major academic medical center was rare and only marginally increased during the 5-year study period. Measurement frequency and assay varied widely between specialties, and there were potential opportunities for downstream interventions. In addition to improving awareness of Lp(a), there is an opportunity to standardize practice patterns regarding its measurement and implications.

Introduction: Lipoprotein(a) [Lp(a)] is a known risk factor for cardiovascular disease; however, its association with cerebrovascular disease is not as well established. Methods: Data from HCHS/SOL, a population-based cohort of Hispanics/Latinos, was utilized. We included 16,039 participants with measured Lp(a) levels (nmol/L) and self-reported history of prevalent stroke or transient-ischemic attack (TIA) from Visit 1. Data from SOL-INCA MRI (ancillary study conducted after Visit 2) was utilized to identify a subset of 2,668 HCHS/SOL participants with brain MRI. Linear and logistic regression was used to study the association of Lp(a) with 1. Self-reported stroke or TIA; 2. Cerebral injury defined as self-reported stroke or TIA or evidence of a stroke on brain MRI; and 3. White matter hyperintensity (WMH) volume modeled as log (WMH/total cranial volume). Lp(a) was modeled as a continuous variable and as quintiles. Sampling weights and surveys methods were used to account for the complex HCHS/SOL design. Results: HCHS/SOL mean age ± SE was 41.1 ± 0.3 years, 52.0% female, and median (IQR) Lp(a) level 19.7 (7.3-60.6) nmol/L. SOL-INCA MRI mean age ± SE was 49.9 ± 0.4 years, 56.4% female, and median (IQR) Lp(a) level 21.7 (8.1-62.9). A ten nmol/L unit increase in Lp(a) was significantly associated with a higher risk of self-reported prevalent stroke or TIA (OR 1.03, 95% CI: 1.02-1.05, p = 0.0002). Lp(a)>77 nmol/L (5 th quintile) was significantly associated with higher risk of self-reported prevalent stroke or TIA (OR 1.8, 95% CI: 1.2-2.8, p = 0.009) compared to Lp(a) <6 nmol/L (1 st quintile) as reference. A ten unit increase in Lp(a) was significantly associated with higher odds of cerebral injury (OR 1.03, 95% CI: 1.02-1.05, p<0.0001). Lp(a)>77 nmol/L was significantly associated with cerebral injury (OR 1.8, 95% CI 1.3- 2.6, p=0.002) as compared to Lp(a) <6 nmol/L. A ten unit increase in Lp(a) was also significantly associated with increasing WMH volume (β 0.02, p=0.0002). Conclusions: Lp(a) is significantly associated with self-reported prevalent stroke or TIA, brain MRI evidence of cerebral injury, and WMH, in a large diverse population of Hispanics/Latinos, suggesting that Lp(a) may be a modifiable risk factor for cerebrovascular disease.