PURPOSE:We investigated the associations of depression and anxiety with the presence of coronary artery plaque amongst a diverse cohort of adults without clinical atherosclerotic cardiovascular disease. METHODS:This cross-sectional study analyzed data from the Miami Heart Study at baseline. Depression was ascertained by the 8-item Patient Health Questionnaire (PHQ-8) with a score ≥10 indicating depression. Anxiety was assessed by the Generalized Anxiety Disorder 7-item (GAD-7) questionnaire with a score ≥10 demonstrating anxiety. Multivariable logistic regression models were used to analyze the association of either depression or anxiety with the presence of any plaque on CCTA. Sensitivity analyses further examined the severity of depressive symptoms, severity of anxiety symptoms, individuals with either depression or anxiety, and individuals with both as predictors of coronary plaque. RESULTS:Of the 2356 individuals (mean age 53.4 ± 6.8 years), 50.4% were men and 47.1% were of Hispanic ethnicity. Depression and anxiety were identified in 143 (6.1%) and 224 (9.5%) of individuals, respectively. CCTA-identified plaque was present in 49.0% of participants with depression and 54.0% of those with anxiety, and the presence of any plaque did not significantly differ when compared to those without depression or without anxiety, respectively. There were no statistically significant associations between depression and plaque (adjusted odds ratio [aOR]: 1.03; 95%CI [0.70, 1.52]; p = 0.891) or between anxiety and plaque (aOR: 1.27; 95%CI [0.93, 1.73]; p = 0.138) in all regression models. CONCLUSIONS:Our study did not identify an association of depression, anxiety, their combination, or their severity with coronary plaque on CCTA among a large cohort of asymptomatic adults.

Purpose:To investigate the association of positive airway pressure (PAP) therapy and cardiometabolic factors in patients with sleep apnea (SA). Methods:Patients with cardiometabolic disease from a multicenter cardiometabolic registry from January 2019 to August 2023 were included. Baseline characteristics of patients with SA stratified by PAP use were compared. Logistic regression was used to assess the association of PAP use and cardiometabolic factors (Hemoglobin A1c [HbA1c], systolic and diastolic blood pressure [SBP and SDB], Triglycerides [TG] and body mass index [BMI]) in an unadjusted model (Model 1), after adjusting for age, sex, ethnicity, race, BMI (Model 2), and additionally for cardiac comorbidities, medications, and medication adherence (Model 3). Results:Of a total of 1575 patients (median age: 65 years [interquartile range 58.0-71.0], 683 (43.4 %) presented with SA, and of those, 447 (65.4 %) reported routine PAP use. Logistic regression analysis showed that PAP use was associated with lower HbA1c (-0.31 %, 95 % CI -0.59 to -0.04, p = 0.025) in Model 2, but not in Model 3 (-0.19 %, 95 % CI -0.46 to 0.08, p = 0.165). In addition, PAP use was associated with lower SBP (-3.99 mmHg, 95 % CI -7.18 to -0.8, p = 0.014) and lower DBP (-2.52 mmHg, 95 % CI -4.45 to -0.6, p = 0.010) in Model 3. Conclusions:In this multicenter registry of patients with cardiometabolic disease, PAP use was associated with improvement of cardiometabolic key risk factors. This effect was observed for SBP and DBP even after adjusting for medication adherence.

BackgroundThe relationship between atherogenic lipoproteins and subclinical coronary atherosclerosis has not been thoroughly evaluated in low-risk adults.ObjectivesThe purpose of this study was to assess the association of low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (HDL-C), and apolipoprotein B (apoB) with coronary atherosclerosis in adults without traditional risk factors.MethodsWe assessed atherosclerosis on coronary computed tomography angiography among asymptomatic adults in the Miami Heart Study not taking lipid-lowering therapy and without hypertension, diabetes, or active tobacco use. Prevalence of atherosclerosis was evaluated based on serum LDL-C, non-HDL-C, and apoB, and multivariable logistic regression with forward selection was used to assess variables associated with coronary plaque.ResultsAmong 1,033 adults 40 to 65 years of age, 55.0% were women and 86.3% had estimated 10-year atherosclerotic cardiovascular disease risk <5%. Coronary atherosclerosis prevalence was 35.9% (50.6% in men; 23.8% in women) and 3.4% had ≥1 high-risk plaque feature. Atherosclerosis prevalence increased with LDL-C, ranging from 13.2% in adults with LDL-C <70 mg/dL up to 48.2% with ≥160 mg/dL. Higher LDL-C (adjusted OR [aOR]: 1.13 [95% CI: 1.08-1.18] per 10 mg/dL), age (aOR: 1.43 [95% CI: 1.28-1.60] per 5 years), male sex (aOR: 3.81 [95% CI: 2.86-5.10]), and elevated lipoprotein(a) (aOR: 1.46 [95% CI: 1.01-2.09]) were associated with atherosclerosis. Higher serum non-HDL-C and apoB were similarly associated with atherosclerosis. In adults with optimal risk factors, 21.2% had atherosclerosis with greater prevalence at higher lipoprotein levels.ConclusionsAmong asymptomatic middle-aged adults without traditional risk factors, coronary atherosclerosis is common and increasingly prevalent at higher levels of atherogenic lipoproteins. These findings emphasize the importance of lipid-lowering strategies to prevent development and progression of atherosclerosis regardless of risk factors.

Background/Synopsis One in five individuals have elevated lipoprotein(a) [Lp(a)], an inherited risk factor for atherosclerotic cardiovascular disease (ASCVD). However, there is no clear consensus involving the appropriate testing criteria for Lp(a), specifically related to the role of a detailed family history of premature ASCVD for guidance. Objective/Purpose To assess the independent association between a detailed family history of premature ASCVD and Lp(a). Methods We studied 4,244 participants from the Multi-Ethnic Study of Atherosclerosis who had measures of Lp(a) (Visit 1) and completed detailed family history questionnaires (Visit 2). Family history of premature ASCVD (<55 years old in men, <65 years old in women) was defined as any myocardial infarction or stroke in a first-degree relative (mother, father, sibling). A combined family history of premature ASCVD score (0, 1, >2 first-degree relatives) was constructed. Modified Poisson regression modeling calculated prevalence ratios (PR) for Lp(a) >50 mg/dL according to family history of premature ASCVD after adjusting for age, sex, race/ethnicity, health insurance status, estimated glomerular filtration rate, and lipid-lowering medications. Results The mean age of participants was 61.7 years old, 52% were women, 28% were Black, and the median Lp(a) was 18 mg/dL (Q1: 8, Q3: 40). One in five individuals (21%) reported a family history of premature ASCVD, but the proportion of individuals who reported two or more first-degree relatives affected by premature ASCVD was two-fold higher among those with Lp(a) >50 versus <50 (4% versus 2%, p=0.003). There was a stepwise increment of Lp(a) and greater prevalence of Lp(a) >50 as the number of reported family members with premature ASCVD increased (Figure). In multivariable analyses considering individuals without a family history of premature ASCVD as reference, there was no significantly higher prevalence of Lp(a) >50 for individuals reporting one family member with premature ASCVD (PR=1.05, 95% CI: 0.90-1.22), though persons who had two or more family members affected by premature ASCVD had a 38% higher prevalence of Lp(a) >50 (PR=1.38, 95% CI: 1.03-1.84). Conclusions Consideration of an ordinal family history of premature ASCVD score may help to better identify those most likely to have elevated Lp(a) compared to current binary family history questionnaires. Detailed documentation involving family history of premature ASCVD may facilitate targeted use of Lp(a)-specific risk assessment in clinical practice.

BACKGROUND:Elevated levels of lipoprotein(a) (Lp(a)) are independently associated with an increased risk of atherosclerotic cardiovascular disease events. However, the mechanisms driving this association are poorly understood. We aimed to evaluate the association between Lp(a) and coronary plaque characteristics in a contemporary US cohort without clinical atherosclerotic cardiovascular disease, undergoing coronary computed tomography angiography, the noninvasive gold standard for the assessment of coronary atherosclerosis. METHODS:We used baseline data from the Miami Heart Study-a community-based, prospective cohort study-which included asymptomatic adults aged 40 to 65 years evaluated using coronary computed tomography angiography. Those taking any lipid-lowering therapies were excluded. Elevated Lp(a) was defined as >= 125 nmol/L. Outcomes included any plaque, coronary artery calcium score >0, maximal stenosis >= 50%, presence of any high-risk plaque feature (positive remodeling, spotty calcification, low-attenuation plaque, napkin ring), and the presence of >= 2 high-risk plaque features. RESULTS:Among 1795 participants (median age, 52 years; 54.3% women; 49.6% Hispanic), 291 (16.2%) had Lp(a) >= 125 nmol/L. In unadjusted analyses, individuals with Lp(a) >= 125 nmol/L had a higher prevalence of all outcomes compared with Lp(a) <125 nmol/L, although differences were only statistically significant for the presence of any coronary plaque and >= 2 high-risk features. In multivariable models, elevated Lp(a) was independently associated with the presence of any coronary plaque (odds ratio, 1.40, [95% CI, 1.05-1.86]) and with >= 2 high-risk features (odds ratio, 3.94, [95% CI, 1.82-8.52]), although only 35 participants had this finding. Among participants with a coronary artery calcium score of 0 (n=1200), those with Lp(a) >= 125 nmol/L had a significantly higher percentage of any plaque compared with those with Lp(a) <125 nmol/L (24.2% versus 14.2%; P<0.001). CONCLUSIONS:In this contemporary analysis, elevated Lp(a) was independently associated with the presence of coronary plaque. Larger studies are needed to confirm the strong association observed with the presence of multiple high-risk coronary plaque features.

There are limited data depicting the association between high risk of obstructive sleep apnea (OSA) and the levels of inflammatory markers in a population-based sample free from cardiovascular disease (CVD). In a large US cohort enriched with a Hispanic population and free of CVD, we aimed to assess the association between high risk of OSA and inflammatory markers. We analyzed data for 2,359 clinical CVD-free participants from the Miami Heart Study, aged 40–65 years (May 2015–September 2018). High risk of OSA included those with a high risk using the Berlin Questionnaire. Poisson regression analyses were used to examine the associations between high risk of OSA (reference: low risk of OSA) and high-sensitivity C-reactive protein (hs-CRP), interleukin 6, and tumor necrosis factor alpha levels (continuous) in univariate and multivariate models (adjusting for age, sex, race/ethnicity, and body mass index, diabetes, hypertension, high cholesterol, and smoking). A total of 552 (28

Background Increases in low-density lipoprotein cholesterol (LDL-C) can occur on carbohydrate restricted ketogenic diets. Lean metabolically healthy individuals with a low triglyceride-to-high-density lipoprotein cholesterol ratio appear particularly susceptible, giving rise to the novel “lean mass hyper-responder” (LMHR) phenotype. Objectives The purpose of the study was to assess coronary plaque burden in LMHR and near-LMHR individuals with LDL-C ≥190 mg/dL (ketogenic diet [KETO]) compared to matched controls with lower LDL-C from the Miami Heart (MiHeart) cohort. Methods There were 80 KETO individuals with carbohydrate restriction-induced LDL-C ≥190 mg/dL, high-density lipoprotein cholesterol ≥60 mg/dL, and triglyceride levels ≤80 mg/dL, without familial hypercholesterolemia, matched 1:1 with MiHeart subjects for age, gender, race, hyperlipidemia, hypertension, and smoking status. Coronary artery calcium and coronary computed tomography angiography (CCTA) were used to compare coronary plaque between groups and correlate LDL-C to plaque levels. Results The matched mean age was 55.5 years, with a mean LDL-C of 272 (maximum LDL-C of 591) mg/dl and a mean 4.7-year duration on a KETO. There was no significant difference in coronary plaque burden in the KETO group as compared to MiHeart controls (mean LDL 123 mg/dL): coronary artery calcium score (median 0 [IQR: 0-56]) vs (1 [IQR: 0-49]) (P = 0.520) CCTA total plaque score (0 [IQR: 0-2] vs [IQR: 0-4]) (P = 0.357). There was also no correlation between LDL-C level and CCTA coronary plaque. Conclusions Coronary plaque in metabolically healthy individuals with carbohydrate restriction-induced LDL-C ≥190 mg/dL on KETO for a mean of 4.7 years is not greater than a matched cohort with 149 mg/dL lower average LDL-C. There is no association between LDL-C and plaque burden in either cohort. (Diet-induced Elevations in LDL-C and Progression of Atherosclerosis [Keto-CTA]; NCT057333255)

This cross-sectional study included 18,797 participants from 6 longitudinal cohorts (CARDIA, FHS Gen III, HCHS/SOL, MESA, MiHeart, and REGARDS), and 5,806 of them had high-sensitivity C-reactive protein (hs-CRP) measurements. We found that exclusive electronic cigarette (EC) use was associated with significantly lower hs-CRP levels compared to exclusive combustible cigarette use, suggesting a potentially lower inflammatory burden. hs-CRP levels in dual users and former smokers currently using EC were comparable to those observed in exclusive cigarette smokers. Exclusive EC users showed no significant difference in hs-CRP levels compared to never cigarette smokers. These findings have important implications for tobacco regulation, public health, and clinical practice, highlighting the need for continued monitoring of potential EC-related health impacts.

This cross-sectional study included 18,797 participants from six longitudinal cohorts (CARDIA, FHS Gen III, HCHS/SOL, MESA, MiHeart, and REGARDS). 5,806 of them were with high-sensitivity C-reactive protein (hs-CRP) measurements. We found that among exclusive electronic cigarette (EC) use was associated with significantly lower high-sensitivity C-reactive protein (hs-CRP) levels compared to exclusive combustible cigarette use, suggesting a potentially lower inflammatory burden. hs-CRP levels in dual users and former smokers currently using EC were comparable to those observed in exclusive cigarette smokers. In contrast, individuals who exclusively used ECs showed no significant difference in hs-CRP levels compared to never smokers. These findings have important implications for tobacco regulation, public health, and clinical practice, highlighting the need for continued monitoring of EC-related health impacts.

BACKGROUND AND AIMS:We aimed to investigate the interplay between low-density lipoprotein-cholesterol (LDL-C) and coronary plaque in asymptomatic cohorts undergoing coronary tomography angiography (CCTA) assessment in the United States. METHODS:A cross-sectional analysis of baseline data from 1808 statin-naïve participants in the Miami Heart Study was conducted. We assessed CCTA-detected atherosclerosis (any plaque, noncalcified plaque, maximal stenosis ≥50%, high-risk plaque) across LDL-C levels, coronary artery calcium (CAC) scores (0, 1-99, ≥100), and 10-year cardiovascular risk categories. RESULTS:Atherosclerosis presence varied across LDL-C levels: 40% of those with LDL-C ≥190 mg/dL had no coronary plaque, while 33% with LDL-C <70 mg/dL had plaque (22.4% with noncalcified plaque). Among those with CAC 0, plaque prevalence ranged from 13.2% (LDL-C <70 mg/dL) to 28.2% (LDL-C ≥190 mg/dL), noncalcified plaque from 13.2% to 25.6%, stenosis ≥50% from 0 to 2.6%, and high-risk plaque from 0 to 5.1%. Conversely, with CAC ≥100, all had coronary plaque, with noncalcified plaque prevalence ranging from 25.0% (LDL-C <70 mg/dL) to 83.3% (LDL-C ≥190 mg/dL), stenosis ≥50% from 25.0% to 50.0%, and high-risk plaque from 0 to 66.7%. Among low-risk participants, 76.7% had CAC 0, yet 31.5% had any plaque and 18.3% had noncalcified plaque. Positive trends between LDL-C and any plaque (17.9%-45.2%) or noncalcified plaque (12.8%-23.8%) were observed in the low-risk group, but no clear trends were seen in higher-risk groups. CONCLUSIONS:Heterogeneity exists in subclinical atherosclerosis across LDL-C, CAC, and estimated cardiovascular risk levels. The value of CCTA in risk-stratifying asymptomatic adults should be further explored.

Background: Coronary computed tomography angiography -derived plaque burden is associated with the risk of cardiovascular events and is expected to be utilized in clinical practice. Understanding of CT quantitative plaque volume compares to normative values in the general population is clinically important for determining management. This study aimed to investigate the distribution of coronary artery plaque volume in general population and to develop nomographic quantitative plaque volume using the Miami Heart Study, a large community-based cohort study. Methods: A total of 2,301 asymptomatic subjects without coronary artery disease (CAD) enrolled in the Miami Heart Study were included. Quantitative assessments of atherosclerotic plaque volume (total, calcified, and non-calcified plaque) were performed using artificial intelligence-guided quantitative coronary computed tomography angiography analysis (AI-QCT). The percentiles of the plaque distribution by gender and age were estimated with nonparametric techniques. Results: The mean age was 53.5 years and 50.4% were male. The majority of study participants were Hispanic/Latino (47.2%) and White (85.5%). In terms of traditional risk factors, approximately one-third of the cohort were current or former smokers, 4.3% had diabetes, 24.9% had hypertension, and 34.9% had high cholesterol or lipid abnormalities. Overall, 93.1% of men and 84.6% of women had any plaque using AI-QCT. The median total plaque volume was 54 mm 3 (IQR 16-126 mm 3 ) and increased with age. Male subjects had more median total plaque volume, calcified plaque volume, and noncalcified plaque volume than female subjects (80 mm 3 vs 34mm 3 , 4 mm 3 vs 2 mm 3 , and 66 mm 3 vs 27 mm 3 , respectively). Younger individuals tend to have a higher percentage of noncalcified plaque. Conclusions: In this asymptomatic population without known CAD, 93.1% of men and 84.6% of women had CAD detected using AI-QCT. Additionally, we developed age- and sex-specific nomograms for atherosclerotic plaque volume. Our data enhance the understanding of plaque volume distribution in general population and should be an important indicator in clinical practice.

Introduction: A higher coronary artery calcium score (CACS) is an established indicator of short- to long-term adverse cardiovascular events. In general, CACS is considered to reflect only the ‘calcified’ plaque component of coronary atherosclerotic plaque burden, whereas its relationship with a non-calcified plaque burden is unknown. In this study, we aim to leverage recent developments in AI-based coronary plaque composition and quantification across the spectrum of CACS in a large asymptomatic U.S.

Introduction: The prevalence of psychological disorders have been increasing, especially since the COVID-19 pandemic. Multiple mechanisms such as medication nonadherence, negative coping behaviors, and systemic inflammation may mediate the potential effects of depression and anxiety on atherosclerosis. Question: Is there an association of depression or anxiety with the presence of plaque assessed by coronary computed tomography angiography (CCTA) among adults free of clinical coronary artery disease (CAD)? Aim: We aim to examine the association of psychological factors with CCTA-based plaque, as they may be key targets for prevention and CCTA could be considered for enhanced risk characterization. Methods: This cross-sectional study analyzed baseline data from the community-based Miami Heart Study (MiHeart). Depression was assessed by the Patient Health Questionnaire 8-item scale with a score ≥10 indicating binary depression. Anxiety was assessed by the Generalized Anxiety Disorder 7-item questionnaire with a score ≥10 demonstrating binary anxiety. The outcome was the binary presence of any plaque on CCTA. Multivariable logistic regression models were adjusted for potential confounders and clinically relevant risk factors. Sensitivity analyses further examined the severity of depressive symptoms, severity of anxiety symptoms, individuals with either depression or anxiety, and individuals with both depression and anxiety as predictors of coronary plaque. Results: Of the 2,356 individuals (mean age 53.4±6.8 years), 50.4% were men and 47.1% were of Hispanic ethnicity. Depression and anxiety were reported in 143 (6.1%) and 224 (9.5%) of individuals, respectively. CCTA-identified plaque was present in 49.0% of participants with depression and 54.0% of those with anxiety, and plaque presence did not significantly differ when compared to those without depression or without anxiety, respectively. There were no significant associations between depression and plaque (adjusted odds ratio [aOR]: 1.03; 95%CI [0.70, 1.52]; p=0.891) or between anxiety and plaque (aOR: 1.27; 95%CI [0.93, 1.73]; p=0.138) in all regression models. On sensitivity analysis, there were also no statistically significant associations found. Conclusion: Our study found no association of depression, anxiety, their combination, or their severity with coronary plaque on CCTA in asymptomatic adults. To our knowledge, this is the first large study on this topic utilizing CCTA data in a U.S. population.

Background: The Cardiometabolic Center Alliance (CMCA) has demonstrated that its comprehensive, coordinated care model achieved statistically significant increases in the use of guideline-directed medical therapies (GDMT) as well as reductions in cardiovascular risk factors. The durability and scalability of this approach and potential impact on care disparities have not yet been assessed. Methods: Using CMCA multicenter registry data (CMCA sites with ≥ 30 participants, each with ≥ 2 visits) we evaluated changes in GDMT utilization across cardiometabolic disease categories, and in the management of key cardiovascular risk factors. Results: In all, 1528 individuals across 6 sites with T2D and CVD and/or CKD were evaluated (median age 66 years, 43.7 % women, 14.1 % black, 63.4 % noncommercially insured, 6-month median follow-up). Sustained improvements in GDMT, reductions in weight, HbA1c, total/LDL cholesterol, triglycerides, and decreases in insulin requirements were observed (p< 0.001 for all); furthermore, the performance on key quality metrics was consistent across racial subgroups. (Figures A and B). Conclusion: The CMCA led implementation of a coordinated, team-based approach, produces durable improvements in GDMT and overall quality of care in patients with cardiometabolic disease and across racial subgroups. Disclosure M.N. Kosiborod: Research Support; AstraZeneca. Consultant; AstraZeneca. Other Relationship; AstraZeneca. Research Support; Boehringer-Ingelheim. Consultant; Boehringer-Ingelheim. Research Support; Pfizer Inc. Consultant; Pfizer Inc., 35Pharma, Alnylam, Amgen Inc., Applied Therapeutics, Arrowhead Pharmaceuticals, Inc., Bayer Inc., Cytokinetics Inc., Dexcom, Inc., Eli Lilly and Company, ESPERION Therapeutics, Inc., Imbria Pharmaceuticals, Janssen Pharmaceuticals, Inc., Lexicon Pharmaceuticals, Inc., Merck & Co., Inc., Novo Nordisk, Pharmacosmos A/S, Regeneron Pharmaceuticals Inc., Sanofi, scPharmaceuticals, Structure Therapeutics, Inc., Vifor Pharma. Other Relationship; Vifor Pharma. Consultant; Youngene Therapeutics. Stock/Shareholder; Artera Health, Saghmos Therapeuticals. M.L. Magwire: Consultant; Novo Nordisk, Boehringer-Ingelheim, Merck & Co., Inc. D.S. Aistrope: None. E. Andaya: None. A. Bashall: Stock/Shareholder; Lilly Diabetes, Lexicon Pharmaceuticals, Inc., Novo Nordisk. J. Butler: Consultant; Abbott, American Regent, Amgen, Applied Therapeutic. Other Relationship; AstraZeneca. Consultant; Bayer. Other Relationship; Boehringer Ingelheim. Consultant; Bristol Myers Squibb, Cardiac Dimension, Cardior, CVRx, Cytokinetics, Janssen, Daxor Edwards, Element Science. Other Relationship; Eli Lilly. Consultant; Innolife. Other Relationship; Impulse Dynamics. Consultant; Imbria, Inventiva, Lexicon, LivaNova, Medscape, Medtronics, Merck, Occlutech. Other Relationship; Novartis. Consultant; Novo Nordisk, Pfizer, Pharmacosmos, Pharmain, Roche, Secretome, Sequana, SQ Innovation, Tenex, Tricoq. Other Relationship; Vifor. K. Cummings: None. L. Davis: Speaker's Bureau; Amgen Inc. R.H. Eckel: Other Relationship; Amgen Inc. Consultant; Novo Nordisk. Advisory Panel; Ionis Pharmaceuticals, Arrowhead Pharmaceuticals, Inc. Other Relationship; Regeneron Pharmaceuticals Inc. J.A. Fialkow: Speaker's Bureau; Amarin Corporation, Amgen Inc. Advisory Panel; Novo Nordisk. Speaker's Bureau; ESPERION Therapeutics, Inc. L. Harness: None. K.A. Miller: Speaker's Bureau; Boehringer-Ingelheim. I. Neeland: Speaker's Bureau; Boehringer-Ingelheim. Consultant; Eli Lilly and Company. Advisory Panel; Novo Nordisk A/S. Speaker's Bureau; Bayer Inc. Consultant; Nestlé Health Science. J. Plutzky: Other Relationship; Novo Nordisk. Research Support; Boehringer-Ingelheim. Consultant; Boehringer-Ingelheim, Amgen Inc., Novartis Pharmaceuticals Corporation, Altimmune Inc., Merck & Co., Inc. R.K. Saalfeld: None. A. Stafos: None. S. Rajagopalan: Consultant; Novo Nordisk, Bayer Inc. Funding Funding/Sponsors: AstraZeneca, Boehringer Ingelheim, Amgen, Novo Nordisk

Background: Despite high risk, minority of individuals with Type 2 diabetes (T2D) and cardiovascular or chronic kidney disease (CVD/CKD) receives optimal guideline directed medical therapy (GDMT). Professional societies advocate for collaborative, team-based models to improve care in this group but successful multicenter implementation efforts are lacking. Methods: CMCA is a non for profit organization that seeks to transform care and outcomes in individuals with cardiometabolic disease. CMCA assists members in implementing team-based, coordinated care models (Cardiometabolic Centers) and GDMT driven pathways. Quality of care and outcomes are monitored via multicenter registry. Since launch in 2020, 14 US organizations joined CMCA. This initial report includes sites with data reported for ≥30 participants (each with ≥ 2 visits). Results: In total 606 individuals with T2D and CVD/CKD from 6 sites were evaluated (age 64 years, 44% women, 78% white, median follow up 6 months). After initiation of care at CMCA sites, large improvements in GDMT and reductions in weight, HbA1c, blood pressure, total/LDL cholesterol, triglycerides, and insulin requirements were observed (Figure panels 1 and 2; p< 0.001 for all). Conclusion: CMCA directed implementation of coordinated team-based care produced rapid and large improvements in GDMT and quality of care across multiple sites. Disclosure M.N.Kosiborod: Consultant; Alnylam Pharmaceuticals, Inc., Amgen Inc., Applied Therapeutics Inc., AstraZeneca, Bayer Inc., Boehringer Ingelheim Inc., Cytokinetics Inc., Dexcom, Inc., Eli Lilly and Company, ESPERION Therapeutics, Inc., Janssen Pharmaceuticals, Inc., Lexicon Pharmaceuticals, Inc., Merck & Co., Inc., Novo Nordisk, Pharmacosmos A/S, Pfizer Inc., Sanofi, Vifor Pharma Management Ltd., Youngene Therapeutics, Other Relationship; AstraZeneca, Research Support; AstraZeneca, Boehringer Ingelheim Inc. E.Fryoux: None. L.Harness: None. R.Heath: None. K.A.Miller: None. I.Neeland: Consultant; Nestlé Health Science, Speaker's Bureau; Boehringer Ingelheim and Eli Lilly Alliance, Bayer Inc. S.Patel: None. J.Plutzky: Advisory Panel; ESPERION Therapeutics, Inc., Consultant; Amgen Inc., Merck & Co., Inc., Novo Nordisk, Research Support; Boehringer Ingelheim Inc. R.K.Saalfeld: None. A.Stafos: None. S.Rajagopalan: Advisory Panel; Novartis, Novo Nordisk, Speaker's Bureau; Novo Nordisk. M.L.Magwire: Consultant; AstraZeneca, Novo Nordisk. D.S.Aistrope: None. E.Andaya: None. J.Butler: Consultant; Abbott,, Amgen, Applied Therapeutics, Array, Astra Zeneca, Bayer,, Boehringer Ingelheim, Bristol Myers Squibb, CVRx, G3 Pharma,, Impulse Dynamics, Innolife, Janssen, LivaNova, Luitpold, Medtronic, Merck, Novartis, NovoNordisk, Relypsa, Roche, Sequana Medical, Vifor, Speaker's Bureau; Novartis, Boehringer Ingelheim-Lilly, Astra Zeneca, Janssen. K.Cummings: None. L.Davis: Speaker's Bureau; Amgen Inc. R.H.Eckel: Advisory Panel; Amarin Corporation, 89bio, Inc., Novo Nordisk, Weight Watchers International, Board Member; Lexicon Pharmaceuticals, Inc., Consultant; Amgen Inc., Better Therapeutics, Inc, The Healthy Aging Company, Other Relationship; Arrowhead Pharmaceuticals, Inc. J.A.Fialkow: Speaker's Bureau; Amgen Inc., ESPERION Therapeutics, Inc., Amarin Corporation. Funding AstraZeneca; Boehringer Ingelheim; Novo Nordisk, Amgen Inc.; Eli Lilly and Company; Novartis