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Inflammatory bowel disease (IBD) is associated with higher incidence of atherosclerotic cardiovascular disease (ASCVD). Data investigating the role of coronary artery calcium (CAC) scoring in identifying subclinical atherosclerotic disease in IBD patients is scarce. Using data obtained from the CLARIFY registry, a prospective study of no-charge coronary artery calcium (CAC) testing at University Hospitals, we reviewed patients with ulcerative colitis (UC) or Crohn's disease (CD) who underwent CAC scoring from 2014 to 2020. We investigated the concordance between CAC risk and 10-year estimated ASCVD risk by AHA/ACC pooled cohort equation using pre-established thresholds for statin prescription (CAC≥100, 10-year ASCVD risk ≥7.5%). We additionally investigated the association between CAC, preventive therapy initiation and Major Adverse Cardiovascular Events (MACE). A total of 369 patients with IBD were included (174 UC, 195 CD), with median age of 60 years. The median CAC score was 14.9 with no significant difference between UC and CD (P =.76). Overall, 151 (41%) had CAC of 0, 108 (29%) had CAC 1-99, 61 (17%) had CAC 100 to 399, and 49 (13%) had CAC ≥400 with no difference in CAC distribution between CD and UC (P =.17). There was no difference in median CAC between IBD or age/sex-matched controls (P =.34). Approximately half of the patients (52%) with IBD had 10-year estimated ASCVD risk of 7.5% or higher. Among patients with ASCVD risk <7.5% (n = 163), 29 (18%) had CAC≥100 and among patients with ASCVD risk ≥7.5% (n = 178), 102 (57%) had CAC <100. There was no difference between CAC<100 vs CAC≥100 with respect to CRP, use of immunosuppressive or amino-salicylate therapy, IBD severity or complications. CAC score (AUROC 0.67 [0.56-0.78]), but not PCE ASCVD risk (AUROC 0.60 [0.48-0.73]), was predictive of MACE. The best cut-off for CAC score was 76 (sensitivity = 60%, specificity = 69%), and was associated with 4-fold increase in MACE (Hazard Ratio 4.0 [2.0-8.1], P <.001). Subclinical atherosclerosis, as evaluated by CAC scoring, is prevalent in patients with IBD, and is associated with cardiovascular events. Further studies are needed to understand underlying biological processes of increased atherosclerotic disease risk among adults with IBD. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) risk amongst those with type 2 diabetes (T2D) is heterogenous. The role of imaging-based cardiometabolic biomarkers (e.g., coronary artery calcium [CAC] score, and hepatic triglyceride content [HTC]) in CVD risk stratification in T2D is unclear. To better understand this, we sought to evaluate the individual and joint associations between CAC and hepatic steatosis (HS) with clinical atherosclerotic CVD (ASCVD) in Dallas Heart Study (DHS) participants with and without T2D. We examined participants in the DHS, a multi-ethnic cohort study, without self-reported ASCVD. CAC scoring was performed via computed tomography with the mean of two consecutive scores used. HTC was measured using magnetic resonance spectroscopy, and HS was defined as HTC >5.5% The primary outcome was incident ASCVD, defined as coronary heart disease (CHD; myocardial infarction, percutaneous coronary intervention, or coronary artery bypass graft surgery), ischemic stroke, transient ischemic attack, or CVD death. Cox regression analyses, and interaction testing was performed to evaluate the individual and joint associations between CAC and HS with ASCVD. The association between HS and coronary heart disease was validated in the UK Biobank (UKB). A total of 1252 DHS participants were included with mean age 44.8 ± 9.3 years, mean body mass index 28.7 ± 5.9 kg/m2, 55% female, and 59% black with an overall prevalence of T2D of 9.7%. CAC scores were significantly higher (p < 0.01) and HS was significantly more prevalent in those with T2D (p < 0.01). Over a median of 12.3 years, 8.3% of participants experienced ASCVD events. The ASCVD event rate was significantly higher in participants with T2D (20.5% vs 7.0%, p < 0.01). Continuous CAC was associated with ASCVD events in the overall cohort regardless of T2D status with a significant interaction present between CAC and T2D status on ASCVD, P interaction = 0.02. HTC was not associated with ASCVD risk in participants without T2D but was inversely associated with risk in participants with T2D (HR 0.91, 95% CI 0.83–0.99 per 1% increase in HTC, p = 0.02), P interaction = 0.02. Amongst 37,266 UKB participants, 4.5% had T2D. CHD events occurred in 2.2% of participants, with 10.2% of events occurring amongst those with T2D. An inverse relationship between HTC and CHD was also found amongst those with T2D in UKB with a significant interaction between T2D status and HTC on CHD (HR per 1% increase in HTC 0.95, 95% CI 0.91–0.99, p = 0.01, P interaction = 0.02). In the DHS, we found that CAC was associated with ASCVD risk independent of T2D status. We did not observe an association between HTC and ASCVD in participants without T2D, but there was an inverse association between HTC and ASCVD in those with T2D that was replicated in the UKB cohort. Further investigation is warranted to understand the possible protective association of HS in participants with T2D. [ABSTRACT FROM AUTHOR]

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Background: Low cardiorespiratory fitness (CRF), high body mass index, and excess visceral adiposity are each associated with impairment in left ventricular (LV) peak circumferential strain (Ecc), an intermediate phenotype that precedes the development of clinical heart failure (HF). However, the association of regional fat distribution and CRF with Ecc independent of each other and other potential confounders is not known. Methods: Participants from the Dallas Heart Study Phase 2 who underwent dual energy X-ray absorptiometry assessment of regional fat distribution, CRF assessment by submaximal treadmill test, and Ecc quantification by tissue-tagged cardiovascular magnetic resonance were included in the analysis. The cross-sectional associations of measures of regional adiposity, namely visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and lower-body fat (LBF) with Ecc after adjustment for CRF and other potential confounders (independent variables) were assessed using multivariable linear regression analysis. Results: The study included 1089 participants (55% female, 39% black). In the unadjusted analysis, higher VAT was associated with greater impairment in Ecc. After adjustment for baseline risk factors, CRF, parameters of LV structure and function, and other fat depots such as SAT and LBF, higher VAT remained associated with greater impairment in Ecc (β: 0.19, P = 0.002). SAT and LBF were not significantly associated with Ecc, however, CRF remained associated with Ecc in the fully adjusted model including all fat depots (β: - 0.15, P < 0.001). Conclusions: VAT and CRF are each independently associated with impairment in Ecc, suggesting that higher VAT burden and low CRF mediate pathological cardiac remodeling through distinct mechanisms. [ABSTRACT FROM AUTHOR]

Although obesity is typically defined by body mass index criteria, this does not differentiate true body fatness, as this includes both body fat and muscle. Therefore, other fat depots may better define cardiometabolic and cardiovascular disease (CVD) risk imposed by obesity. Data from translational, epidemiological, and clinical studies over the past 3 decades have clearly demonstrated that accumulation of adiposity in the abdominal viscera and within tissue depots lacking physiological adipose tissue storage capacity (termed "ectopic fat") is strongly associated with the development of a clinical syndrome characterized by atherogenic dyslipidemia, hyperinsulinemia/glucose intolerance/type 2 diabetes mellitus, hypertension, atherosclerosis, and abnormal cardiac remodeling and heart failure. This state-of-the-art paper discusses the impact of various body fat depots on cardiometabolic parameters and CVD risk. Specifically, it reviews novel and emerging imaging techniques to evaluate adiposity and the risk of cardiometabolic diseases and CVD. • Anthropometric and laboratory markers of obesity have limited utility for personalized treatment. Direct imaging measures of obesity may improve diagnosis, guide decision-making for appropriate interventions, and monitor responses to treatment. • Multimodality imaging is used to assess visceral and ectopic fat depots (such as within the heart, liver, skeletal muscle, pancreas, and kidney) to improve evaluation of metabolic disease and CVD risk. • Future studies will combine body fat assessment with physical activity/cardiorespiratory fitness to further improve efforts to prevent and treat obesity and its progression to CVD. [ABSTRACT FROM AUTHOR]

Natriuretic peptides (NPs, B-type natriuretic peptide /BNP and NT-proBNP) are universally used biomarkers with established cut-points to aid in the diagnosis of heart failure (HF). It has been demonstrated that an inverse relationship exists between obesity, defined by the body mass index (BMI), and NPs, such that the application of NPs to diagnostic algorithms in HF remains challenging in overweight and obese patients. Some have advocated that lowering the cut-offs for NPs or using a correction for high BMI may improve the diagnostic accuracy in obese individuals. The inverse relationship of NPs with high BMI is present in both HF with reduced (HFrEF) and with preserved (HFpEF) ejection fraction, although levels tend to be higher in HFrEF. Nevertheless, data from several studies have shown that the prognostic value of NPs is preserved across BMI classes, and that increasing circulating levels of NPs correlate with adverse outcomes including all-cause mortality and HF hospitalizations. While NPs can still be used in diagnosis of HF in obese individuals, lower thresholds and the clinical context should be utilized in decision making. Additionally, given the validated prognostic value even in obesity, NPs can be employed in risk-stratification of individuals with obesity and HF, although there remains limited evidence about use in those with severe obesity (BMI >40 kg/m2). [ABSTRACT FROM AUTHOR]

Background: Cardiovascular disease is a leading economic and medical burden in the United States (US). As an important risk factor for cardiovascular disease, hypertension represents a critical point of intervention. Less is known about longitudinal effects of neighborhood deprivation on blood pressure outcomes, especially in light of new hypertension guidelines.Methods: Longitudinal data from the Dallas Heart Study facilitated multilevel regression analysis of the relationship between neighborhood deprivation, blood pressure change, and incident hypertension over a 9-year period. Factor analysis explored neighborhood perception, which was controlled for in all analyses. Neighborhood deprivation was derived from US Census data and divided into tertiles for analysis. Hypertension status was compared using pre-2017 and 2017 hypertension guidelines.Results: After adjusting for covariates, including moving status and residential self-selection, we observed significant associations between residing in the more deprived neighborhoods and 1) increasing blood pressure over time and 2) incident hypertension. In the fully adjusted model of continuous blood pressure change, significant relationships were seen for both medium (SBP: β = 4.81, SE = 1.39, P = .0005; DBP: β = 2.61, SE = 0.71, P = .0003) and high deprivation (SBP: β = 7.64, SE = 1.55, P < .0001; DBP: β = 4.64, SE = 0.78, P < .0001). In the fully adjusted model of incident hypertension, participants in areas of high deprivation had 1.69 higher odds of developing HTN (OR 1.69; 95% CI 1.02, 2.82), as defined by 2017 hypertension guidelines. Results varied based on definition of hypertension used (pre-2017 vs. 2017 guidelines).Conclusion: These findings highlight the potential impact of adverse neighborhood conditions on cardiometabolic outcomes, such as hypertension. [ABSTRACT FROM AUTHOR]

Background Development and change of coronary artery calcium (CAC) are associated with coronary heart disease. Interpretation of serial CAC measurements will require better understanding of changes in CAC beyond the variability in the test itself. Methods Dallas Heart Study participants (2888) with duplicate CAC scans obtained minutes apart were analyzed to determine interscan concordance and 95% confidence bounds (ie: repeatability limits) for each discrete CAC value. These data derived cutoffs were then used to define change above measurement variation and determine the frequency of CAC development and change among 1779 subjects with follow up CAC scans performed 6.9 years later. Results Binary concordance (0 vs. >0) was 91%. The value of CAC denoting true development of CAC by exceeding the 95% confidence bounds for a single score of 0 was 2.7 Agatston units (AU). Among those with scores >0, the 95% confidence bounds for CAC change were determined by the following formulas: for CAC≤100AU: 5.6√CAC + 0.3*CAC – 3.1; for CAC>100AU: 12.4√CAC – 67.7. Using these parameters, CAC development occurred in 15.0% and CAC change occurred in 48.9%. Although 225 individuals (24.9%) had a decrease in CAC over follow up, only 1 (0.1%) crossed the lower confidence bound. Compared with prior reported definition of CAC development (ie: >0), the novel threshold of 2.7AU resulted in better measures of model performance. In contrast, for CAC change, no consistent differences in performance metrics were observed compared with previously reported definitions. Conclusion There is significant interscan variability in CAC measurement, including around scores of 0. Incorporating repeatability estimates may help discern true differences from those due to measurement variability, an approach that may enhance determination of CAC development and change. [ABSTRACT FROM AUTHOR]

Objective To determine the feasibility of using oral 13 C labeled glycerol to assess effects of visceral adiposity on gluconeogenic pathways in obese humans. Research Design and Methods Obese (BMI ≥ 30 kg/m 2 ) participants without type 2 diabetes underwent visceral adipose tissue (VAT) assessment and stratification by median VAT into high VAT-fasting (n = 3), low VAT-fasting (n = 4), and high VAT-refed (n = 2) groups. Participants ingested [U- 13 C 3 ] glycerol and blood samples were subsequently analyzed at multiple time points over 3 h by NMR spectroscopy. The fractions of plasma glucose (enrichment) derived from [U- 13 C 3 ] glycerol via hepatic gluconeogenesis, pentose phosphate pathway (PPP), and tricarboxylic acid (TCA) cycle were assessed using 13 C NMR analysis of glucose. Mixed linear models were used to compare 13 C enrichment in glucose between groups. Results Mean age, BMI, and baseline glucose were 49 years, 40.1 kg/m 2 , and 98 mg/dl, respectively. Up to 20% of glycerol was metabolized in the TCA cycle prior to gluconeogenesis and PPP activity was minor (< 1% of total glucose) in all participants. There was a 21% decrease in 13 C enrichment in plasma glucose in the high VAT-fasting compared with low VAT-fasting group ( p = 0.03), suggesting dilution by endogenous glycerol. High VAT-refed participants had 37% less 13 C enrichment in glucose compared with high VAT-fasting ( p = 0.02). There was a trend toward lower [1,2- 13 C 2 ] (via PPP) and [5,6- 13 C 2 ]/[4,5,6- 13 C 3 ] (via TCA cycle) glucose in high VAT versus low VAT groups. Conclusions We applied a simple method to detect gluconeogenesis from glycerol in obese humans. Our findings provide preliminary evidence that excess visceral fat disrupts multiple pathways in hepatic gluconeogenesis from glycerol. [ABSTRACT FROM AUTHOR]

Therapies targeting high-density lipoprotein cholesterol content (HDL-C) have not improved coronary heart disease (CHD) outcomes. High-density lipoprotein particle concentration (HDL-P) may better predict CHD. However, the impact of race/ethnicity on the relations between HDL-P and subclinical atherosclerosis and incident CHD events has not been described. Participants from the Dallas Heart Study (DHS), a multiethnic, probabilitybased, population cohort of Dallas County adults, underwent the following baseline measurements: HDL-C, HDL-P by nuclear magnetic resonance imaging, and coronary artery calcium by electron-beam computed tomography. Participants were followed for a median of 9.3 years for incident CHD events (composite of first myocardial infarction, stroke, coronary revascularization, or cardiovascular death). The study comprised 1,977 participants free of CHD (51% women, 46% black). In adjusted models, HDL-C was not associated with prevalent coronary artery calcium (p = 0.13) or incident CHD overall (hazard ratio [HR] per 1 SD 0.89, 95% confidence interval [CI] 0.76 to 1.05). However, HDL-C was inversely associated with incident CHD among nonblack (adjusted HR per 1 SD 0.67, 95% CI 0.46 to 0.97) but not black participants (HR 0.94,95% CI 0.78 to 1.13, Pinteraction = 0.05). Conversely, HDL-P, adjusted for risk factors and HDL-C, was inversely associated with prevalent coronary artery calcium (p = 0.009) and with incident CHD overall (adjusted HR per 1 SD 0.73, 95% CI 0.62 to 0.86), with no interaction by black race/ethnicity (Pinteraction = 0.57). In conclusion, in contrast to HDL-C, the inverse relation between HDL-P and incident CHD events is consistent across ethnicities. These findings suggest that HDL-P is superior to HDL-C in predicting prevalent atherosclerosis as well as incident CHD events across a diverse population and should be considered as a therapeutic target. [ABSTRACT FROM AUTHOR]

Background Obesity has been linked to the development of hypertension, but whether total adiposity or site-specific fat accumulation underpins this relationship is unclear. Objectives This study sought to determine the relationship between adipose tissue distribution and incident hypertension. Methods Normotensive participants enrolled in the Dallas Heart Study were followed for a median of 7 years for the development of hypertension (systolic blood pressure [SBP] ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of blood pressure medications). Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) was quantified by magnetic resonance imaging and proton-spectroscopic imaging, and lower body fat (LBF) was imaged by dual-energy x-ray absorptiometry. Multivariable relative risk regression was performed to test the association between individual fat depots and incident hypertension, adjusting for age, sex, race/ethnicity, diabetes, smoking, SBP, and body mass index (BMI). Results Among 903 participants (median age, 40 years; 57% women; 60% nonwhite; median BMI 27.5 kg/m 2 ), 230 (25%) developed incident hypertension. In multivariable analyses, higher BMI was significantly associated with incident hypertension (relative risk: 1.24; 95% confidence interval: 1.12 to 1.36, per 1-SD increase). However, when VAT, SAT, and LBF were added to the model, only VAT remained independently associated with incident hypertension (relative risk: 1.22; 95% confidence interval: 1.06 to 1.39, per 1-SD increase). Conclusions Increased visceral adiposity, but not total or subcutaneous adiposity, was robustly associated with incident hypertension. Additional studies will be needed to elucidate the mechanisms behind this association. [ABSTRACT FROM AUTHOR]

Objectives This study aimed to investigate the independent and joint associations between family history of myocardial infarction (FH) and coronary artery calcification (CAC) with incident coronary heart disease (CHD). Background FH and CAC are associated with each other and with incident CHD. It is not known whether FH retains its predictive value after CAC results are accounted for. Methods Among 2,390 participants without cardiovascular disease enrolled in the Dallas Heart Study, we assessed FH (myocardial infarction in a first-degree relative) and prevalent CAC by electron-beam computed tomography. The primary outcome, a composite of CHD-related death, myocardial infarction, and percutaneous or surgical coronary revascularization, was assessed over a mean follow-up of 8.0 ± 1.2 years. The individual and joint associations with the CHD composite outcome were determined for FH and CAC. Results The mean age of the population was 44 ± 9 years; 32% had FH and 47% had a CAC score of 0. In multivariate models adjusted for traditional risk factors, FH was independently associated with CHD (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). Further adjustment for prevalent CAC did not diminish this association (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). FH and CAC were additive: CHD event rates in those with both FH and CAC were 8.8% vs. 3.3% in those with prevalent CAC alone (p < 0.001). CHD rates were 1.9% in those with FH alone compared with 0.4% in those with neither FH nor CAC (p < 0.017). Among subjects without CAC, FH characterized a group with a more unfavorable cardiometabolic profile. Conclusions FH provided prognostic information that was independent of and additive to CAC. Among those with CAC, FH identified subjects at particularly high short-term risk, and, among those without it, selected a group with an adverse risk-factor profile. [ABSTRACT FROM AUTHOR]

Background: Previous studies that reported an association of dietary Na+ intake with metabolic syndrome were limited by the use of imprecise measures of obesity, Na+ intake, or exclusion of multiethnic populations. The effect of dietary K+ intake on obesity is less well described. Objective: We hypothesized that high dietary Na+ and low K+, based on the ratio of urinary Na+ to K+ (U[Na+]/[K+]) in a first-void morning urinary sample, is independently associated with total body fat. Design: In a prospective population-based cohort, 2782 participants in the community-dwelling, probability-sampled, multiethnic Dallas Heart Study were analyzed. The primary outcome established a priori was total-body percentage fat (TBPF) measured by dual-energy X-ray absorptiometry. The main predictor was U[Na+]/[K+]. Robust linear regression was used to explore an independent association between U[Na+]/[K+] and TBPF. The analyses were stratified by sex and race after their effect modifications were analyzed. Results: Of the cohort, 55.4% were female, 49.8% African American, 30.8% white, 17.2% Hispanic, and 2.2% other races. The mean (6SD) age was 44 6 10 y, BMI (in kg/m2) was 30 6 7, TBPF was 32 6 10%, and U[Na+]/[K+] was 4.2 6 2.6; 12% had diabetes. In the unadjusted and adjusted models, TBPF increased by 0.75 (95% CI: 0.25, 1.25) and 0.43 (0.15, 0.72), respectively (P = 0.003 for both), for every 3-unit increase in U[Na+]/[K+]. A statistically significant interaction was found between race and U[Na+] /[K+], so that the non-African American races had a higher TBPF than did the African Americans per unit increase in U[Na+]/[K+] (P-interaction, 0.0001 for both). No interaction was found between sex and U[Na+]/[K+]. Conclusions: The ratio of dietary Na+ to K+ intake may be independently associated with TBPF, and this association may be more pronounced in non-African Americans. Future studies should explore whether easily measured spot U[Na+]/[K+] can be used to monitor dietary patterns and guide strategies for obesity management. [ABSTRACT FROM AUTHOR]

Objectives: The goal of this study was to investigate the association between natriuretic peptides and body fat distribution in a multiethnic cohort. Background: Natriuretic peptides stimulate lipolysis, reduce weight gain, and promote adipocyte browning in animal models, but data are lacking in humans. Methods: A total of 2,619 participants without heart failure in the Dallas Heart Study underwent measurements of 1) B-type natriuretic peptide (BNP) and N-terminal pro–B-type natriuretic peptide (NT-proBNP); and 2) body fat distribution by dual energy x-ray absorptiometry and magnetic resonance imaging. Cross-sectional associations of natriuretic peptides with adiposity phenotypes were examined after adjustment for age, sex, race, comorbidities, and body mass index. Results: Median BNP and NT-proBNP levels in the study cohort (mean age 44 years; 56% women, 48% African Americans, 32% obese) were 3.0 and 28.1 pg/ml, respectively. Natriuretic peptide levels above the median were associated with a more favorable body fat profile and less insulin resistance, including lower visceral fat, liver fat, and homeostasis model assessment of insulin resistance index, and increased lower body fat and higher adiponectin (p < 0.05 for each). In multivariable analyses, NT-proBNP remained inversely associated with visceral fat (beta coefficient = −0.08; p < 0.0001) and liver fat (beta coefficient = −0.14; p < 0.0001) and positively associated with lower body fat (beta coefficient = 0.07; p < 0.0001) independent of age, sex, race, and obesity status; findings were similar with BNP. Adjustment for body composition, homeostasis model assessment of insulin resistance index, circulating androgens, and adipocytokines did not attenuate the associations. Conclusions: Higher natriuretic peptide levels were independently associated with a favorable adiposity profile, characterized by decreased visceral and liver fat and increased lower body fat, suggesting a link between the heart and adipose tissue distribution mediated through natriuretic peptides. [Copyright &y& Elsevier]

Objectives: The goal of this study was to determine if biomarkers of subclinical myocardial injury and hemodynamic stress identify asymptomatic individuals with left ventricular hypertrophy (LVH) at higher risk for heart failure (HF) and death. Background: The interaction between LVH, low but detectable cardiac troponin T (cTnT), and elevated N-terminal pro–B-type natriuretic peptide (NT-proBNP) on cardiovascular (CV) outcomes in the general population is unknown. Methods: Participants in the Dallas Heart Study without clinical HF, LV dysfunction, or chronic kidney disease underwent measurement of LV mass by magnetic resonance imaging (MRI), cTnT by highly sensitive assay, and NT-proBNP analysis (n = 2,413). Subjects were stratified according to LVH and by detectable cTnT (≥3 pg/ml) and increased NT-proBNP (>75th age- and sex-specific percentile) levels. For each analysis, participants were categorized into groups based on the presence (+) or absence (–) of LVH and biomarker levels above (+) or below (–) the predefined threshold. Results: Nine percent of participants were LVH+, 25% cTnT+, and 24% NT-proBNP+. Those LVH+ and cTnT+ and/or NT-proBNP+ (n = 144) were older and more likely to be male, with a greater risk factor burden and more severe LVH compared with those who were LVH+ biomarker– (p < 0.01 for each). The cumulative incidence of HF or CV death over 8 years among LVH+ cTnT+ was 21% versus 1% (LVH– cTnT–), 4% (LVH– cTnT+), and 6% (LVH+ cTnT–) (p < 0.0001). The interactions between LVH and cTnT (pinteraction = 0.0005) and LVH and NT-proBNP (pinteraction = 0.014) were highly significant. Individuals who were LVH+ and either cTnT+ or NT-proBNP+ remained at >4-fold higher risk for HF or CV death after multivariable adjustment for CV risk factors, renal function, and LV mass compared with those who were LVH– biomarker–. Conclusions: Minimal elevations in biomarkers of subclinical cardiac injury and hemodynamic stress modify the association of LVH with adverse outcomes, identifying a malignant subphenotype of LVH with high risk for progression to HF and CV death. [Copyright &y& Elsevier]

Patients with a suspected acute coronary syndrome and left bundle branch block (LBBB) present a unique diagnostic and therapeutic challenge to the clinician. Although current guidelines recommend that patients with new or presumed new LBBB undergo early reperfusion therapy, data suggest that only a minority of patients with LBBB are ultimately diagnosed with acute myocardial infarction, regardless of LBBB chronicity, and that a significant proportion of patients will not have an occluded culprit artery at cardiac catheterization. The current treatment approach exposes a significant proportion of patients to the risks of fibrinolytic therapy without the likelihood of significant benefit and leads to increased rates of false-positive cardiac catheterization laboratory activation, unnecessary risks, and costs. Therefore, alternative strategies to those for patients with ST-segment elevation myocardial infarction are needed to guide selection of appropriate patients with a suspected acute coronary syndrome and LBBB for urgent reperfusion therapy. In this article, we describe the evolving epidemiology of LBBB in acute coronary syndromes and discuss controversies related to current clinical practice. We propose a more judicious diagnostic approach among clinically stable patients with LBBB who do not have electrocardiographic findings highly specific for ST-segment elevation myocardial infarction. [ABSTRACT FROM AUTHOR]

Abstract: Background: The electrocardiographic (ECG) pattern of ST-segment deviation in myocardial infarction is integral to the proper assessment of the location, extent, and functional significance of the infarct but may be modified by the underlying coronary artery anatomy. Methods: We describe the ECG findings in 2 cases of proximal left anterior descending (LAD) artery occlusion in ST-elevation myocardial infarction (STEMI) associated with 3-vessel coronary artery disease. Results: Both patients had atypical ECG patterns of ST-segment elevation in leads V2, I, and aVL and ST-segment depression with positive T waves suggestive of extensive subendocardial ischemia in leads II, III, aVF, and V3 through V6; acute proximal LAD occlusion and concomitant 3-vessel coronary artery disease were observed angiographically. Conclusion: Electrocardiographic changes in proximal LAD STEMI may be modified by the presence of significant atherosclerotic disease elsewhere in the coronary vasculature. Recognition of this ECG pattern may aid the clinician in the rapid identification of high-risk STEMI. [Copyright &y& Elsevier]

Background & Aims We performed a systematic review and network meta-analysis to evaluate the overall and comparative effects of weight-loss medications approved by the Food and Drug Administration for long-term use on cardiometabolic risk profiles of obese adults. Methods We performed a systematic literature review through February 28, 2017 to identify randomized clinical trials of the effects of Food and Drug Administration−approved weight-loss medications (ie, orlistat, lorcaserin, naltrexone-bupropion, phentermine-topiramate, and liraglutide) administered to obese adults for 1 year or more, compared with placebo or another active agent. Outcomes of interest included changes in blood glucose (fasting blood glucose [FBG] and hemoglobin A1c), cholesterol profile (low-density lipoprotein and high-density lipoproteins), blood pressure (BP; systolic/diastolic), and waist circumference (WC). We performed pair-wise and network meta-analyses with outcomes reported as weighted and standardized mean differences. Quality of evidence was rated using GRADE (Grading of Recommendations Assessment, Development and Evaluation). Results In a meta-analysis of 28 randomized controlled trials (29,018 participants; median body mass index, 36.1 kg/m 2 ), we associated weight-loss medications with a modest decrease in FBG (weighted mean difference, 4.0 mg/dL; 95% confidence interval, –4.4 to –3.6 mg/dL) and WC (weighted mean difference, reduction of 3.3 cm; 95% confidence interval, –3.5 to –3.1 cm), without clinically meaningful changes in systolic/diastolic BP or cholesterol profile vs placebo (standardized mean difference <0.2); effects varied among drugs. Phentermine-topiramate use was associated with a substantial decrease in WC and a modest decrease in FBG, hemoglobin A1c, and BP, and had minimal effect on cholesterol. Liraglutide use was associated with a substantial decrease in FBG, hemoglobin A1c, and WC, and a minimal effect on BP and cholesterol. Naltrexone-bupropion use was associated with moderate increase in high-density lipoprotein cholesterol, but had a minimal effect on FBG and WC. Orlistat use was associated with a decrease in low-density lipoprotein and high-density lipoprotein cholesterol. No drug improved all cardiometabolic risk factors. Conclusions In a systematic review and network meta-analysis, we found Food and Drug Administration−approved weight-loss medications to have only modest positive effects on cardiometabolic risk profile. Further research is needed to evaluate the long-term cardiometabolic benefits of these medications. PROSPERO: CRD42016039486. [ABSTRACT FROM AUTHOR]

Aims Metabolic syndrome (MetS) increases atherosclerotic cardiovascular disease (ASCVD) risk. Low HDL cholesterol (HDL-C) is a diagnostic criterion of MetS and a major ASCVD risk factor. HDL particle concentration (HDL-P) associates with incident ASCVD independent of HDL-C, but its association with incident MetS has not been studied. We hypothesized that HDL-P would be inversely associated with incident metabolic syndrome independent of HDL-C and markers of adiposity and insulin resistance. Materials and methods HDL-P was measured by NMR and visceral fat by MRI in participants of the Dallas Heart Study, a probability-based population sample of adults age 30–65. Participants with prevalent MetS, DM, CVD, and any systemic illlness were excluded. Incident MetS as defined by NCEP ATPIII criteria was determined in all participants after median follow-up period of 7.0 years. Results Among 1120 participants without DM or MetS at baseline (57% women, 45% Black, mean age 43), 22.8% had incident MetS at follow-up. HDL-P and HDL-C were modestly correlated (r = 0.54, p < 0.0001). In models adjusted for traditional risk factors and MetS risk factors including visceral fat, HS-CRP, triglyceride to HDL-C ratio, and HOMA-IR, the lowest quartile of HDL-P was associated with a 2-fold increased risk of incident MetS (OR 2.1, 95%CI 1.4–3.1; p = 0.0003). Conclusions Low HDL-P is independently associated with incident MetS after adjustment for traditional risk factors, lipid parameters, adiposity, inflammation, and markers of insulin resistance. Further studies are warranted to validate these findings and elucidate the mechanisms underpinning this association. [ABSTRACT FROM AUTHOR]

Deficiencies in the care of patients with diabetes are the norm rather than the exception. We propose a reframing of diabetes care quality, which encompasses four key principles ('the 4 BEs') that together can help address deficiencies in the care of the patient with Type 2 diabetes (T2D) and eliminate these missed opportunities. [ABSTRACT FROM AUTHOR]

Background: Multiple scoring systems have been devised to quantify angiographic coronary artery disease (CAD) burden, but it is unclear how these scores relate to each other and which scores are most accurate. The aim of this study was to compare coronary angiographic scoring systems (1) with each other and (2) with intravascular ultrasound (IVUS)–derived plaque burden in a population undergoing angiographic evaluation for CAD. Methods: Coronary angiographic data from 3600 patients were scored using 10 commonly used angiographic scoring systems and interscore correlations were calculated. In a subset of 50 patients, plaque burden and plaque area in the left anterior descending coronary artery were quantified using IVUS and correlated with angiographic scores. Results: All angiographic scores correlated with each other (range for Spearman coefficient [ρ] 0.79-0.98, P < .0001); the 2 most widely used scores, Gensini and CASS-70, had a ρ = 0.90 (P < .0001). All scores correlated significantly with average plaque burden and plaque area by IVUS (range ρ 0.56-0.78, P < .0001 and 0.43-0.62, P < .01, respectively). The CASS-50 score had the strongest correlation (ρ 0.78 and 0.62, P < .0001) and the Duke Jeopardy score the weakest correlation (ρ 0.56 and 0.43, P < .01) with plaque burden and area, respectively. Conclusions: Angiographic scoring systems are strongly correlated with each other and with atherosclerotic plaque burden. Scoring systems therefore appear to be a valid estimate of CAD plaque burden. [ABSTRACT FROM AUTHOR]

Background: Left ventricular hypertrophy (LVH) combined with elevations in cardiac biomarkers reflecting myocardial injury and neurohormonal stress (malignant LVH) is associated with a high risk for heart failure and death.Objectives: The aim of this study was to determine the impact of intensive systolic blood pressure (SBP) control on the prevention of malignant LVH and its consequences.Methods: A total of 8,820 participants in SPRINT (Systolic Blood Pressure Intervention Trial) were classified into groups based on the presence or absence of LVH assessed by 12-lead ECG, and elevations in biomarker levels (high-sensitivity cardiac troponin T ≥14 ng/L or N-terminal pro-B-type natriuretic peptide ≥125 pg/mL) at baseline. The effects of intensive vs standard SBP lowering on rates of acute decompensated heart failure (ADHF) events and death and on the incidence and regression of malignant LVH were determined.Results: Randomization to intensive SBP lowering led to similar relative reductions in ADHF events and death across the combined LVH/biomarker groups (P for interaction = 0.68). The absolute risk reduction over 4 years in ADHF events and death was 4.4% (95% CI: -5.2% to 13.9%) among participants with baseline malignant LVH (n = 449) and 1.2% (95% CI: 0.0%-2.5%) for those without LVH and nonelevated biomarkers (n = 4,361). Intensive SBP lowering also reduced the incidence of malignant LVH over 2 years (2.5% vs 1.1%; OR: 0.44; 95% CI: 0.30-0.63).Conclusions: Intensive SBP lowering prevented malignant LVH and may provide substantial absolute risk reduction in the composite of ADHF events and death among SPRINT participants with baseline malignant LVH. [ABSTRACT FROM AUTHOR]

The Cardiometabolic Think Tank was convened on June 20, 2014, in Washington, DC, as a “call to action” activity focused on defining new patient care models and approaches to address contemporary issues of cardiometabolic risk and disease. Individual experts representing >20 professional organizations participated in this roundtable discussion. The Think Tank consensus was that the metabolic syndrome (MetS) is a complex pathophysiological state comprised of a cluster of clinically measured and typically unmeasured risk factors, is progressive in its course, and is associated with serious and extensive comorbidity, but tends to be clinically under-recognized. The ideal patient care model for MetS must accurately identify those at risk before MetS develops and must recognize subtypes and stages of MetS to more effectively direct prevention and therapies. This new MetS care model introduces both affirmed and emerging concepts that will require consensus development, validation, and optimization in the future. [ABSTRACT FROM AUTHOR]

Obesity contributes to reduced life expectancy because of its link with type 2 diabetes and cardiovascular disease. Yet, targeting this poorly diagnosed, ill-defined, and underaddressed modifiable risk factor remains a challenge. In this review, we emphasize that the tendency among health care professionals to amalgam all forms of obesity altogether as a single entity may contribute to such difficulties and discrepancies. Obesity is a heterogeneous condition both in terms of causes and health consequences. Attention should be given to 2 prevalent subgroups of individuals: 1) patients who are overweight or moderately obese with excess visceral adipose tissue; and 2) patients with severe obesity, the latter group having distinct additional health issues related to their large body fat mass. The challenge of tackling high-cardiovascular-risk forms of obesity through a combination of personalized clinical approaches and population-based solutions is compounded by the current obesogenic environment and economy. [ABSTRACT FROM AUTHOR]

Aim: To investigate the reliability of multicompartmental volumetric mesenchymal segmentations on MRI and their correlations with anthropomorphic and clinical parameters.Materials and Methods: A consecutive series of middle-age (35-50 year old) female volunteers with variable body mass index (BMI) and MRI scans performed as a part of the Dallas Heart Study were included. A semi-automatic segmentation tool was used to partition different mesenchymal tissues- fat, muscle, and bone on MRI of pelvis. Total volumes of each compartment were calculated and compared between overweight/obese (BMI> = 25 kg/m2) and non-obese (BMI < 25 kg/m2) groups, and with physical performance measurements, i.e. mean activity counts per minute (MVPA) and cardiorespiratory fitness (CRF) estimated by submaximal treadmill test (TT). Kruskal Wallis, Mann-Whitney U test, intraclass correlation coefficient (ICC) and Spearman correlations were used. P value <0.05 was considered statistically significant.Results: There were statistically significant positive correlations between fat volume and BMI (p < 0.0001), muscle volume and height (p = 0.03), and bone volume and height (p < 0.0001). Significant inverse correlations were found between bone volume and BMI (p = 0.002). Fair to good interobserver reliability was seen with muscle and fat volumes (ICC = 0.43-0.64) and excellent reliability was seen with bone volumes (ICC = 0.78-0.79). Statistically significant inverse correlations were found between MVPA and age (p = 0.01), and TT with BMI and weight (p = 0.01, 0.03).Conclusion: Multi-compartment mesenchymal tissue volume quantification on pelvic MRI is reliable in females. Inverse correlation of bone volume with BMI has potential implications for future risk of fracture. [ABSTRACT FROM AUTHOR]

The few available population-based longitudinal studies examining the link between change in neighborhood condition and weight change to date have only examined neighborhood changes generated by residential mobility. Applying a difference-in-difference analytic framework to data from the Dallas Heart Study (DHS), a multi-ethnic, population-based cohort in Dallas County, TX, we evaluated the relationship between changes in neighborhood condition and weight change for both movers and non-movers over an approximate seven-year follow-up period. We employed a novel measure of neighborhood condition based on property appraisal data to capture temporally consistent measures of change in neighborhood condition regardless of residential mobility. We observed an inverse relationship between weight change and change in neighborhood condition which was more pronounced for non-movers (1.9 fewer kilograms gained per 1-standard deviation improvement in neighborhood condition) than for movers (1.5 fewer kilograms gained per 1-standard deviation improvement in neighborhood condition). [ABSTRACT FROM AUTHOR]

Introduction: Coronary artery calcium (CAC) scoring is not routinely performed in patients with diabetes based on an existing class I indication for statin therapy in these patients. However, CAC scoring may improve risk classification and prediction of atherosclerotic cardiovascular disease (ASCVD) events beyond risk scores in asymptomatic individuals with prediabetes and diabetes, warranting CAC assessment in this population. The routine availability through provision of no-charge CAC as an alternative to routine probabilistic risk scores may improve utilization of preventive therapies especially in traditionally underserved populations.Methods: Prospective observational study in a large health system offering no-charge CAC scoring for primary prevention risk prediction with available glycosylated hemoglobin (HbA1c) measurements between June 2015 and March 2019 were divided according to no diabetes (HbA1c <5.7 %), prediabetes (HbA1c 5.7 %-6.4 %), or diabetes (HbA1c ≥ 6.5 % or charted history) and followed for major adverse cardiovascular events [myocardial infarction, stroke, death (MACE) or coronary revascularization]. Patient characteristics, health history, laboratory data, and statin prescription rates were measured at baseline and at one year after CAC scoring.Results: A total of 12,194 subjects with available HbA1c underwent CAC scoring during the study period (6462 diabetes, 2062 prediabetes, and 3670 without diabetes). At a median follow-up of 1.2 years, there were 458 MACE events (71 patients without diabetes, 66 patients with prediabetes, and 321 patients with diabetes). Among patients with diabetes or prediabetes, increased CAC was associated with MACE (HR 1.38 [1.26-1.51], p < 0.001) and MACE or revascularization (HR 1.70 [1.57-1.85], p < 0.001). In patients with diabetes, CAC category was associated with greater statin initiation (89.6 % for CAC≥400 vs 60.1 % for CAC = 0, p < 0.001) and high intensity statin initiation (42.2 % for CAC≥400 vs 16.8 % for CAC = 0, p < 0.001) at one year post CAC scoring. Patients with diabetes had greater reductions in systolic blood pressure, LDL-C, total cholesterol, and triglycerides from baseline with a CAC ≥400 compared to a lower CAC category (p = 0.007).Conclusions: CAC burden is associated with ASCVD risk in patients with diabetes. CAC scoring increases statin prescriptions and reduces ASCVD risk in patients with diabetes, potentially warranting routine CAC assessment in this population. [ABSTRACT FROM AUTHOR]