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BACKGROUND: Duchenne muscular dystrophy (DMD) is frequently complicated by development of a cardiomyopathy. Despite significant medical advances provided to DMD patients over the past 2 decades, there remains a group of DMD patients who die prematurely. The current study sought to identify a set of prognostic factors that portend a worse outcome among adult DMD patients. METHODS AND RESULTS: A retrospective cohort of 43 consecutive patients was followed in the adult UT Southwestern Neuromuscular Cardiomyopathy Clinic. Clinical data were abstracted from the electronic medical record to generate baseline characteristics. The population was stratified by survival to time of analysis and compared with characteristics associated with death. The DMD population was in the early 20s, with median follow-up times over 2 years. All the patients had developed a cardiomyopathy, with the majority of the patients on angiotensin-converting enzyme inhibitors (86%) and steroids (56%), but few other guideline-directed heart failure medications. Comparison between the nonsurviving and surviving cohorts found several poor prognostic factors, including lower body mass index (17.3 [14.8-19.3] versus 25.8 [20.8-29.1] kg/m2, P

Background The plasma concentration of B‐type natriuretic peptide (BNP) is a strong predictor of adverse cardiovascular events. The aim of this study was to determine whether the association between plasma BNP concentration and cardiovascular mortality is sustained or diminishes with increasing time after BNP is measured. Methods and Results Six thousand seven hundred forty patients with a history of myocardial infarction or unstable angina who participated in the LIPID (Long‐Term Intervention with Pravastatin in Ischemic Disease) trial had plasma BNP concentration measured at baseline and after 1 year. Associations with cardiovascular mortality were evaluated in landmark analyses 1 to 1 BNP measurement improves long‐term risk prediction.

Background Biomarkers of myocardial stress and fibrosis are elevated in people living with HIV and are associated with cardiac dysfunction. It is unknown whether sex influences these markers of heart failure risk in sub‐Saharan Africa, where HIV burden is high and where the vast majority of women with HIV live. Methods and Results Echocardiograms and 6 plasma biomarkers (suppression of tumorigenicity‐2, growth differentiation factor 15, galectin 3, soluble fms‐like tyrosine kinase‐1, NT‐proBNP [N‐terminal pro‐B‐type natriuretic peptide], and cystatin C) were obtained from 100 people living with HIV on antiretroviral therapy and 100 HIV‐negative controls in Uganda. All participants were ≥45 years old with ≥1 major cardiovascular risk factor. Multivariable linear and logistic regression models were used to assess associations between biomarkers, echocardiographic variables, HIV status, and sex, and to assess whether sex modified these associations. Overall, mean age was 56 years and 62% were women. Suppression of tumorigenicity‐2 was higher in men versus women (P

Background Exhaled carbon monoxide (eCO) is directly associated with traditional cardiovascular disease risk factors and incident cardiovascular disease. However, its relation with the cardiovascular health score and incidence of heart failure (HF) has not been investigated. Methods and Results We measured eCO in 3521 Framingham Heart Study Offspring participants attending examination cycle 6 (mean age 59 years, 53% women). We related the cardiovascular health score (composite of blood pressure, fasting plasma glucose, total cholesterol, body mass index, smoking, diet, and physical activity) to eCO adjusting for age, sex, and smoking. Higher cardiovascular health scores were associated with lower eCO (β=−0.02, P

Background The Kansas City Cardiomyopathy Questionnaire (KCCQ) is a measure of heart failure (HF) health status. Worse KCCQ scores are common in patients with chronic kidney disease (CKD), even without diagnosed heart failure (HF). Elevations in the cardiac biomarkers GDF‐15 (growth differentiation factor‐15), galectin‐3, sST2 (soluble suppression of tumorigenesis‐2), hsTnT (high‐sensitivity troponin T), and NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide) likely reflect subclinical HF in CKD. Whether cardiac biomarkers are associated with low KCCQ scores is not known. Methods and Results We studied participants with CKD without HF in the multicenter prospective CRIC (Chronic Renal Insufficiency Cohort) Study. Outcomes included (1) low KCCQ score

Emergence of various highly sensitive cardiac troponin assays into clinical practice provides a new tool for clinicians diagnosing acute coronary syndrome. These assays also create a challenge for laboratories and clinicians who have yet to familiarize themselves with sex‐specific cutoffs. Healthy men and women, studied across various age groups and geographic locations, have notable differences in baseline values of highly sensitive cardiac troponin I and T, leading to establishment of sex‐specific upper reference limits and cutoffs. Several differences in cardiac physiology, size, and structure may account for baseline differences in highly sensitive cardiac troponins and outcomes between the sexes. The clinical utility of implementing sex‐specific cutoffs for diagnosis and management of acute coronary syndrome remains unclear. Presently, the only prospective study failed to show improved outcomes for men or women with use of sex‐specific cutoffs; however, a major limitation is the frequent lack of diagnostic, therapeutic, and preventive interventions prescribed to women with low‐level troponin elevations. Based on the current literature, we posit that there may nonetheless be clinical value in the use of sex‐specific cutoffs for evaluating suspected acute coronary syndrome, especially in select patient populations such as younger women who tend to have lower baseline values of highly sensitive cardiac troponins. Future studies should prospectively evaluate differences in diagnostic, pharmacologic, and interventional management in men and women using myocardial infarctions classified with sex‐specific cutoffs of the highly sensitive cardiac troponin assays.

Background DNA methylation is implicated in many chronic diseases and may contribute to mortality. Therefore, we conducted an epigenome‐wide association study (EWAS) for all‐cause mortality with whole‐transcriptome data in a cardiovascular cohort (CATHGEN [Catheterization Genetics]). Methods and Results Cases were participants with mortality≥7 days postcatheterization whereas controls were alive with≥2 years of follow‐up. The Illumina Human Methylation 450K and EPIC arrays (Illumina, San Diego, CA) were used for the discovery and validation sets, respectively. A linear model approach with empirical Bayes estimators adjusted for confounders was used to assess difference in methylation (Δβ). In the discovery set (55 cases, 49 controls), 25 629 (6.5%) probes were differently methylated (P0.05); the SLC4A9 transcript did not pass quality control. The cg17944110 probe is located within a potential regulatory element; expression of predicted targets (using GeneHancer) of the regulatory element, UBIAD1 (P=0.01) and CLSTN1 (P=0.03), were lower in cases. Conclusions We identified 6 novel methylation sites associated with all‐cause mortality. Methylation in CASZ1 may serve as a regulatory element associated with mortality in cardiovascular patients. Larger studies are necessary to confirm these observations.

Background Cardiac biomarkers may signal mechanistic pathways involved in heart failure (HF), a leading complication in chronic kidney disease. We tested the associations of NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide), high‐sensitivity troponin T (hsTnT), galectin‐3, growth differentiation factor‐15 (GDF‐15), and soluble ST2 (sST2) with incident HF in chronic kidney disease. Methods and Results We examined adults with chronic kidney disease enrolled in a prospective, multicenter study. All biomarkers were measured at baseline. The primary outcome was incident HF. Secondary outcomes included HF with preserved ejection fraction (EF≥50%) and reduced ejection fraction (EF

Background Cardiac troponin T (cTnT) is seen in many other conditions besides myocardial infarction, and recent studies demonstrated distinct forms of cTnT. At present, the in vivo formation of these different cTnT forms is incompletely understood. We therefore performed a study on the composition of cTnT during the course of myocardial infarction, including coronary venous system sampling, close to its site of release. Methods and Results Baseline samples were obtained from multiple coronary venous system locations, and a peripheral artery and vein in 71 non–ST‐segment–elevation myocardial infarction patients. Additionally, peripheral blood was drawn at 6‐ and 12‐hours postcatheterization. cTnT concentrations were measured using the high‐sensitivity‐cTnT immunoassay. The cTnT composition was determined via gel filtration chromatography and Western blotting in an early and late presenting patient. High‐sensitivity ‐cTnT concentrations were 28% higher in the coronary venous system than peripherally (n=71, P

Background Serial imaging studies in the general population remain important to evaluate the usefulness of pathophysiologically relevant biomarkers in predicting progression of left ventricular (LV) remodeling and dysfunction. Here, we assessed in a general population whether these circulating biomarkers at baseline predict longitudinal changes in LV structure and function. Methods and Results In 592 participants (mean age, 50.8 years; 51.4% women; 40.5% hypertensive), we derived echocardiographic indexes reflecting LV structure and function at baseline and after 4.7 years. At baseline, we measured alkaline phosphatase, markers of collagen turnover (procollagen type I, C‐terminal telopeptide, matrix metalloproteinase‐1) and high‐sensitivity cardiac troponin T. We regressed longitudinal changes in LV indexes on baseline biomarker levels and reported standardized effect sizes as a fraction of the standard deviation of LV change. After full adjustment, a decline in LV longitudinal strain (−14.2%) and increase in E/e′ ratio over time (+18.9%; P≤0.019) was associated with higher alkaline phosphatase activity at baseline. Furthermore, longitudinal strain decreased with higher levels of collagen I production and degradation at baseline (procollagen type I, −14.2%; C‐terminal telopeptide, −16.4%; P≤0.029). An increase in E/e′ ratio over time was borderline associated with lower matrix metalloproteinase‐1 (+9.8%) and lower matrix metalloproteinase‐1/tissue inhibitor of metalloproteinase‐1 ratio (+11.9%; P≤0.041). Higher high‐sensitivity cardiac troponin T levels at baseline correlated significantly with an increase in relative wall thickness (+23.1%) and LV mass index (+18.3%) during follow‐up (P≤0.035). Conclusions We identified a set of biomarkers predicting adverse changes in LV structure and function over time. Circulating biomarkers reflecting LV stiffness, injury, and collagen composition might improve the identification of subjects at risk for subclinical cardiac maladaptation.

Background We examined associations of objectively measured physical activity (PA) and sedentary time with cardiovascular disease biomarkers at age 60 to 64 years. This included investigation of sex differences and the extent to which associations may be mediated by adiposity. Methods and Results Participants were 795 men and 827 women aged 60 to 64 years from the Medical Research Council National Survey of Health and Development. Combined heart rate and movement sensors worn for 5 consecutive days were used to derive overall PA energy expenditure, kJ/kg per day) and time spent sedentary (3 metabolic equivalent of tasks). Linear regression models were used to relate each PA parameter to inflammatory (C‐reactive protein, interleukin‐6), endothelial (tissue‐plasminogen activator, E‐selectin) and adipokine (leptin, adiponectin) markers extracted from fasting blood samples. Greater time in light PA and moderate‐to‐vigorous intensity PA and less sedentary time were associated with more favorable biomarker levels. For C‐reactive protein, interleukin‐6, and leptin, these differences were greater among women than men. For example, % differences (95% confidence intervals) in leptin for men and women per SD increases in sedentary time: 7.9 (2.7, 13.0) and 20.6 (15.3, 25.8); light intensity PA: −3.8 (−8.9, 12.7) and −17.7 (−23.1, −12.4), moderate‐to‐vigorous intensity PA: −12.9 (−17.9, −8.0) and −18.3 (−23.4, −13.1). Fat mass mediated a greater proportion of these associations in women than men. Conclusions Greater light PA and moderate‐to‐vigorous intensity PA and less sedentary time in early old age were associated with more favorable cardiovascular biomarker profiles. Fat mass partially mediated these associations but more strongly in women than men, which explained sex differences.

Background Current preoperative models use clinical risk factors alone in estimating risk of in‐hospital mortality following cardiac surgery. However, novel biomarkers now exist to potentially improve preoperative prediction models. An assessment of Galectin‐3, N‐terminal pro b‐type natriuretic peptide (NT‐ProBNP), and soluble ST2 to improve the predictive ability of an existing prediction model of in‐hospital mortality may improve our capacity to risk‐stratify patients before surgery. Methods and Results We measured preoperative biomarkers in the NNECDSG (Northern New England Cardiovascular Disease Study Group), a prospective cohort of 1554 patients undergoing coronary artery bypass graft surgery. Exposures of interest were preoperative levels of galectin‐3, NT‐ProBNP, and ST2. In‐hospital mortality and adverse events occurring after coronary artery bypass graft were the outcomes. After adjustment, NT‐ProBNP and ST2 showed a statistically significant association with both their median and third tercile categories with NT‐ProBNP odds ratios of 2.89 (95% confidence interval [CI]: 1.04–8.05) and 5.43 (95% CI: 1.21–24.44) and ST2 odds ratios of 3.96 (95% CI: 1.60–9.82) and 3.21 (95% CI: 1.17–8.80), respectively. The model receiver operating characteristic score of the base prediction model (0.80 [95% CI: 0.72–0.89]) varied significantly from the new multi‐marker model (0.85 [95% CI: 0.79–0.91]). Compared with the Northern New England (NNE) model alone, the full prediction model with biomarkers NT‐proBNP and ST2 shows significant improvement in model classification of in‐hospital mortality. Conclusions This study demonstrates a significant improvement of preoperative prediction of in‐hospital mortality in patients undergoing coronary artery bypass graft and suggests that biomarkers can be used to identify patients at higher risk.

BackgroundSubclinical myocardial injury, as measured by high‐sensitivity cardiac troponin T (hsTnT), and myocardial stress, as measured by N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP), are related to glycemic control in patients with type 2 diabetes mellitus, and are strong predictors of adverse cardiovascular outcomes. We sought to determine whether antihyperglycemic therapy improves measures of myocardial injury and myocardial stress in patients with type 2 diabetes mellitus. Methods and ResultsWe randomized, in a 2×2 factorial fashion, 438 patients with type 2 diabetes mellitus to insulin glargine, metformin, the combination, or placebo and measured changes in NT‐proBNP and hsTnT after 12 weeks of therapy. At baseline, the median (Q1–Q3) plasma concentration was 35.4 (15.7–86.3) ng/L for NT‐proBNP and 6.7 (4.6–10.1) ng/L for hsTnT. The adjusted (95% confidence interval) change in NT‐proBNP concentration was 20.7% (7.9–35.0) in the insulin arm compared with 0.13% (−10.8 to 12.5) in the no‐insulin arm (P=0.03 for comparison). These changes were not related to changes in fasting or postprandial glucose, glycated hemoglobin, weight, blood pressure, or inflammation. In the metformin arm, the adjusted change in NT‐proBNP was 7.8% (−3.7 to 20.7) compared with 13.0% (0.72–26.8) in the no‐metformin arm (P=0.58). No significant changes in hsTnT concentrations were observed for any of the treatment arms. ConclusionsInsulin glargine was associated with a significant 20.7% increase in NT‐proBNP, a marker of myocardial stress, after 12 weeks of therapy. No change in hsTnT, a marker of myocardial injury, was observed. The changes were independent of substantial improvements in glucose control. Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT00366301.

BackgroundCardiac biomarkers are independent risk markers in atrial fibrillation, and the novel biomarker–based ABC stroke score (age, biomarkers, and clinical history of prior stroke) was recently shown to improve the prediction of stroke risk in patients with atrial fibrillation. Our aim was to investigate the short‐term variability of the cardiac biomarkers and evaluate whether the ABC stroke risk score provides a stable short‐term risk estimate. Methods and ResultsAccording to the study protocol, samples were obtained at entry and also at 2 months in 4796 patients with atrial fibrillation followed for a median of 1.8 years in the ARISTOTLE (Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation) trial. Cardiac troponin I, cardiac troponin T, and N‐terminal pro‐B‐type natriuretic peptide were measured with high‐sensitivity immunoassays. Associations with outcomes were evaluated by Cox regression. C indices and calibration plots were used to evaluate the ABC stroke score at 2 months. The average changes in biomarker levels during 2 months were small (median change cardiac troponin T +2.8%, troponin I +2.0%, and N‐terminal pro‐B‐type natriuretic peptide +13.5%) and within‐subject correlation was high (all ≥0.82). Repeated measurement of cardiac biomarkers provided some incremental prognostic value for mortality but not for stroke when combined with clinical risk factors and baseline levels of the biomarkers. Based on 8702 person‐years of follow‐up and 96 stroke/systemic embolic events, the ABC stroke score at 2 months achieved a similar C index of 0.70 (95% CI, 0.65–0.76) as compared with 0.70 (95% CI, 0.65–0.75) at baseline. The ABC stroke score remained well calibrated using predefined risk classes. ConclusionsIn patients with stable atrial fibrillation, the variability of the cardiac biomarkers and the biomarker‐based ABC stroke score during 2 months are small. The prognostic information by the ABC stroke score remains consistent and well calibrated with similar good predictive performance if patients are retested after 2 months. Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT00412984.

BackgroundThymosin beta‐4 (TB4) is an X‐linked gene product with cardioprotective properties. Little is known about plasma concentration of TB4 in heart failure (HF), and its relationship with other cardiovascular biomarkers. We sought to evaluate circulating TB4 in HF patients with preserved (HFpEF) or reduced (HFrEF) ejection fraction compared to non‐HF controls. Methods and ResultsTB4 was measured using a liquid chromatography and mass spectrometry assay in age‐ and sex‐matched HFpEF (n=219), HFrEF (n=219) patients, and controls (n=219) from a prospective nationwide study. Additionally, a 92‐marker multiplex proximity extension assay was measured to identify biomarker covariates. Compared with controls, plasma TB4 was elevated in HFpEF (985 [421–1723] ng/mL versus 1401 [720–2379] ng/mL, P

BackgroundDuchenne muscular dystrophy (DMD) is frequently complicated by development of a cardiomyopathy. Despite significant medical advances provided to DMD patients over the past 2 decades, there remains a group of DMD patients who die prematurely. The current study sought to identify a set of prognostic factors that portend a worse outcome among adult DMD patients. Methods and ResultsA retrospective cohort of 43 consecutive patients was followed in the adult UT Southwestern Neuromuscular Cardiomyopathy Clinic. Clinical data were abstracted from the electronic medical record to generate baseline characteristics. The population was stratified by survival to time of analysis and compared with characteristics associated with death. The DMD population was in the early 20s, with median follow‐up times over 2 years. All the patients had developed a cardiomyopathy, with the majority of the patients on angiotensin‐converting enzyme inhibitors (86%) and steroids (56%), but few other guideline‐directed heart failure medications. Comparison between the nonsurviving and surviving cohorts found several poor prognostic factors, including lower body mass index (17.3 [14.8–19.3] versus 25.8 [20.8–29.1] kg/m2, P

BackgroundVarious combinations of creatine kinase‐MB, myoglobin, and cardiac troponin I or T (cTnI/cTnT) have been used to evaluate patients with suspected acute coronary syndromes. The current recommendation is to use the 99th percentile of cTnI/cTnT as the sole marker for diagnosis of acute myocardial infarction. Methods and ResultsWe retrospectively analyzed cardiac marker protocols collected from 824 US hospitals undergoing Chest Pain Center Accreditation through the Society of Cardiovascular Patient Care from 2009 to 2014. Data were obtained by a self‐reported survey that addressed cardiac marker(s), sampling time periods, and cut points used for evaluation of suspected acute myocardial infarction. The combination of cTnI or cTnT with creatine kinase‐MB was the most commonly used biomarker strategy. Use of cTnI or cTnT as the sole marker increased over time (14–37%; P

BackgroundOur aim was to determine whether patients with embolic strokes of undetermined source (ESUS) have higher rates of elevated troponin than patients with noncardioembolic strokes. Methods and ResultsCAESAR (The Cornell Acute Stroke Academic Registry) prospectively enrolled all adults with acute stroke from 2011 to 2014. Two neurologists used standard definitions to retrospectively ascertain the etiology of stroke, with a third resolving disagreements. In this analysis we included patients with ESUS and, as controls, patients with small‐ and large‐artery strokes; only patients with a troponin measured within 24 hours of stroke onset were included. A troponin elevation was defined as a value exceeding our laboratory's upper limit (0.04 ng/mL) without a clinically recognized acute ST‐segment elevation myocardial infarction. Multiple logistic regression was used to evaluate the association between troponin elevation and ESUS after adjustment for demographics, stroke severity, insular infarction, and vascular risk factors. In a sensitivity analysis we excluded patients diagnosed with atrial fibrillation after discharge. Among 512 patients, 243 (47.5%) had ESUS, and 269 (52.5%) had small‐ or large‐artery stroke. In multivariable analysis an elevated troponin was independently associated with ESUS (odds ratio 3.3; 95% confidence interval 1.2, 8.8). This result was unchanged after excluding patients diagnosed with atrial fibrillation after discharge (odds ratio 3.4; 95% confidence interval 1.3, 9.1), and the association remained significant when troponin was considered a continuous variable (odds ratio for log[troponin], 1.4; 95% confidence interval 1.1, 1.7). ConclusionsElevations in cardiac troponin are more common in patients with ESUS than in those with noncardioembolic strokes.

BackgroundTroponin‐T elevation is seen commonly in sepsis and septic shock patients admitted to the intensive care unit. We sought to evaluate the role of admission and serial troponin‐T testing in the prognostication of these patients. Methods and ResultsThis was a retrospective cohort study from 2007 to 2014 on patients admitted to the intensive care units at the Mayo Clinic with severe sepsis and septic shock. Elevated admission troponin‐T and significant delta troponin‐T were defined as ≥0.01 ng/mL and ≥0.03 ng/mL in 3 hours, respectively. The primary outcome was in‐hospital mortality. Secondary outcomes included 1‐year mortality and lengths of stay. During this 8‐year period, 944 patients met the inclusion criteria with 845 (90%) having an admission troponin‐T ≥0.01 ng/mL. Serial troponin‐T values were available in 732 (78%) patients. Elevated admission troponin‐T was associated with older age, higher baseline comorbidity, and severity of illness, whereas significant delta troponin‐T was associated with higher severity of illness. Admission log10 troponin‐T was associated with unadjusted in‐hospital (odds ratio 1.6; P=0.003) and 1‐year mortality (odds ratio 1.3; P=0.04), but did not correlate with length of stay. Elevated delta troponin‐T and log10 delta troponin‐T were not significantly associated with any of the primary or secondary outcomes. Admission log10 troponin‐T remained an independent predictor of in‐hospital mortality (odds ratio 1.4; P=0.04) and 1‐year survival (hazard ratio 1.3; P=0.008). ConclusionsIn patients with sepsis and septic shock, elevated admission troponin‐T was associated with higher short‐ and long‐term mortality. Routine serial troponin‐T testing did not add incremental prognostic value in these patients.

BackgroundCardiac troponin T and brain natriuretic peptide (BNP) are elevated in >50% of dialysis patients and are associated with poor outcomes. Few data investigated these associations in earlier chronic kidney disease (CKD). Methods and ResultsWe studied whether CKD modified associations of elevated BNP, N‐terminal‐pro‐BNP, high‐sensitivity cardiac troponin T, coronary artery calcification, and left ventricular hypertrophy with all‐cause death and cardiovascular death/events in 3218 multiethnic individuals followed for 12.5 years, and whether biomarkers added prognostic information to traditional cardiovascular risk factors in CKD. Of the cohort, 279 (9%) had CKD. There were 296 deaths and 218 cardiovascular deaths/events. Of non‐CKD individuals, 7% died and 6% had cardiovascular death/event versus 32% and 30% of CKD participants, P

BackgroundDrug‐eluting stents (DESs) and bare metal stents (BMSs) are both recommended to improve coronary revascularization and to treat coronary artery disease in patients with chronic kidney disease (CKD). However, the potential superiority of DESs over BMSs for reducing the incidence of long‐term major adverse cardiovascular events and mortality in CKD patients has not been established, and the results remain controversial. We aimed to systematically assess and quantify the total weight of evidence regarding the use of DESs versus BMSs in CKD patients. Methods and ResultsIn this systematic review and conventional meta‐analysis, electronic studies published in any language until May 20, 2016, were systematically searched through PubMed, Embase, Web of Science, and the Cochrane Central Register of Controlled Trials. We included randomized controlled trials and observational studies comparing outcomes in CKD patients with DESs versus BMSs and extracted data in a standard form. Pooled odd ratios and 95% CIs were calculated using random‐ and fixed‐effects models. Finally, 38 studies involving 123 396 patients were included. The use of DESs versus BMSs was associated with significant reductions in major adverse cardiovascular events (pooled odds ratio 0.75; 95% CI, 0.64–0.88; P

BackgroundPrior studies show an increased risk of ischemic stroke (IS) after myocardial infarction; however, there is limited evidence on long‐term risk and whether it is directly related to cardiac injury. We hypothesized that the risk of IS after acute coronary syndrome is significantly higher if there is evidence of cardiac injury, such as ST‐segment elevation myocardial infarction (STEMI) or non‐STEMI, than when there is no evidence of cardiac injury, such as in unstable angina. Methods and ResultsAdministrative claims data were obtained from all emergency department encounters and hospitalizations at California's nonfederal acute care hospitals between 2008 and 2011. Patients with STEMI, non‐STEMI, and unstable angina were identified using appropriate International Classification of Diseases, Ninth Revision, Clinical Modification codes. The primary outcome was IS during 2 years of follow‐up. Unadjusted and adjusted Cox proportional hazards models were used to determine the association between acute coronary syndrome subtype and IS risk. We identified 73 059 patients with a diagnosis of STEMI (n=26 427), non‐STEMI (n=39 833), or unstable angina (n=6819) during the study period. In the fully adjusted models that included potential confounders such as atrial fibrillation and congestive heart failure, the risk of IS was higher with STEMI (hazard ratio 4.17, 95% CI 3.00–5.83; P

BackgroundDespite evidence for higher risk of coronary artery disease among HIV+ individuals, the underlying mechanisms are not well understood. We investigated associations of inflammatory markers with subclinical coronary artery disease in 923 participants of the Multicenter AIDS Cohort Study (575 HIV+ and 348 HIV− men) who underwent noncontrast computed tomography scans for coronary artery calcification, the majority (n=692) also undergoing coronary computed tomography angiography. Methods and ResultsOutcomes included presence and extent of coronary artery calcification, plus computed tomography angiography analysis of presence, composition, and extent of coronary plaques and severity of coronary stenosis. HIV+ men had significantly higher levels of interleukin‐6 (IL‐6), intercellular adhesion molecule‐1, C‐reactive protein, and soluble‐tumor necrosis factor‐α receptor (sTNFαR) I and II (all P