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Background and aims Recently, a pro-inflammatory diet based on a dietary inflammatory index (DII) has been related to higher CVD risk in general population, but this has not been investigated among women. Methods We investigated the relationship between DII and risk of total CVD and CVD subgroups (myocardial infarction, ischemic heart disease, stroke and cerebrovascular disease) in a prospective cohort of 6972 Australian women aged 50–55 years at baseline in 2001. We used clinical and procedure information from inpatient hospital separation registries, information on use of health care services, and from the causes-of-death registry to ascertain CVD outcomes during 11-year follow up. The association between baseline DII score and cardiovascular endpoints was analysed through cox-regression, with correction for demographic and cardiovascular risk factors. Results We identified 335 incident cases of CVD and 191 cases of ischaemic heart disease (including 69 myocardial infarctions) and 59 cases of cerebrovascular disease (including 40 cases of stroke). A statistically significant higher risk of myocardial infarction was observed in analyses using DII scores as a continuous variable with a hazard ratio of 1.46 (95% confidence interval 1.12–1.89), but this was attenuated by further adjustment for other known cardiovascular risk factors. No association was found for total CVD, ischaemic heart diseases, or cerebrovascular disease. Conclusions There was no statistically significant association between the dietary inflammatory index and risk of total cardiovascular disease, ischemic heart disease, myocardial infarction, cerebrovascular disease or stroke in this population of mid-aged Australian women. Associations were not different for postmenopausal women. [ABSTRACT FROM AUTHOR]

Objectives Cardiovascular risk estimation is a key element of current primary prevention strategies, despite its limited accuracy. Several biomarkers are being tested to assess their capacity to improve coronary (CHD) and cardiovascular (CVD) prediction. One of these biomarkers is ankle brachial index (ABI). The aim of this study was to assess whether the inclusion of ABI improved the predictive capacity of the Framingham-REGICOR risk function in an area of low CVD incidence. Methods A total of 5248 individuals, aged 35–74 years, from a prospective population-based cohort study were followed up for a median 5.9 years. Baseline ABI was measured using a standardized method. All incident CHD (angina, myocardial infarction, coronary revascularization, CHD death) and CVD (also including fatal and non-fatal stroke) events were recorded. Improvements in discrimination (ΔC-statistics) and reclassification by net reclassification index (NRI) were assessed. Results During follow-up, 111 and 64 subjects presented with a coronary or cerebrovascular event. Pathological ABI (≤0.9) was associated with increased CHD and CVD risk (HR: 2.08 and HR: 2.24, respectively; p-value < 0.001). Including ABI in the Framingham-REGICOR function improved both its discrimination and its reclassification capacity for CVD events but not for CHD events; the ΔC-statistic for CVD events was 0.007 (95% Confidence Interval: 0.001; 0.017) and the NRI was 0.029 (95% CI: 0.014–0.045; p-value < 0.001). Conclusion Inclusion of the ABI improves the predictive capacity of the Framingham-REGICOR risk function. The study results indicate the potential value of including this simple test in cardiovascular risk stratification and support current guidelines recommendations. [ABSTRACT FROM AUTHOR]

Objective While recent genomic studies have focused attention on triglyceride (TG) rich lipoproteins in cardiovascular disease (CVD), little is known of very low-density lipoprotein cholesterol (VLDL-C) relationship with atherosclerosis and CVD. We examined, in a high-risk type-2 diabetic population, the association of plasma VLDL-C with coronary artery calcification (CAC). Methods The Penn Diabetes Heart Study (PDHS) is a cross-sectional study of CVD risk factors in type-2 diabetics ( n = 2118, mean age 59.1 years, 36.5% female, 34.1% Black). Plasma lipids including VLDL-C were calculated ( n = 1879) after ultracentrifugation. Results In Tobit regression, VLDL-C levels were positively associated with increasing CAC after adjusting for age, race, gender, Framingham risk score, body mass index, C-reactive protein, exercise, medication and alcohol use, hemoglobin A1c, and diabetes duration [Tobit ratio (TR) and 95% confidence interval (CI) 0.38 (0.12–0.65), P = 0.005] and even after inclusion of apolipoprotein B data [TR 0.31 (0.03–0.58), P = 0.030]. Approximately 3-fold stronger effect was observed in women [TR 0.75 (0.16–1.34), P = 0.013] than men [TR 0.20 (−0.10–0.50), P = 0.189; gender interaction P = 0.034]. Plasma VLDL-C was related more strongly to CAC scores than TG levels (e.g., Akaike information criteria of 7263.65 vs. 7263.94) and had stronger CAC association in individuals with TGs >150 mg/dl (TR 0.80, P = 0.010) vs. those with TGs <150 mg/dl (TR 0.27, P = 0.185). Conclusions In PDHS, VLDL-C is associated with CAC independent of established CVD risk factors, particularly in women, and may have value even beyond apolipoprotein B levels and in patients with elevated TGs. [ABSTRACT FROM AUTHOR]

Objective Non-alcoholic fatty liver disease (NAFLD) is an obesity-related condition associated with cardiovascular mortality. Yet, whether or not NAFLD is independently related to atherosclerosis is unclear. In a population-based cross-sectional sample of middle-aged adults free from liver or heart disease, we tested the hypothesis that NAFLD is associated with subclinical atherosclerosis (coronary artery (CAC) and abdominal aortic calcification (AAC)) independent of obesity. Methods Participants from the Coronary Artery Risk Development in Young Adults study with CT quantification of liver fat, CAC and AAC were included (n = 2424). NAFLD was defined as liver attenuation ≤40 Hounsfield Units after exclusion of other causes of liver fat. CAC and AAC presence was defined as Agatston score >0. Results Mean participant age was 50.1 ± 3.6 years, (42.7% men, 50.0% black) and BMI was 30.6 ± 7.2 kg/m². The prevalence of NAFLD, CAC, and AAC was 9.6%, 27.1%, and 51.4%. NAFLD participants had increased prevalence of CAC (37.9% vs. 26.0%, p < 0.001) and AAC (65.1% vs. 49.9%, p < 0.001). NAFLD remained associated with CAC (OR, 1.33; 95% CI, 1.001-1.82) and AAC (OR, 1.74; 95% CI, 1.29-2.35) after adjustment for demographics and health behaviors. However, these associations were attenuated after additional adjustment for visceral adipose tissue (CAC OR, 1.05; 95% CI, 0.74-1.48, AAC OR = 1.20; 95% CI, 0.86-1.67). There was no interaction by race or sex. Conclusion In contrast to prior research, these findings suggest that obesity attenuates the relationship between NAFLD and subclinical atherosclerosis. Further studies evaluating the role of NAFLD duration on atherosclerotic progression and cardiovascular events are needed. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Amongst middle-aged men, haplogroup I is associated with ≈50% higher risk of coronary artery disease than other paternal lineages of Y chromosome. We hypothesised that carriers of haplogroup I had higher levels of aggression and estrogens and/or lower levels of androgens early in life and thus might be more prone to cardiovascular disease than men with other lineages of Y chromosome. Methods: We reconstructed phylogenetic tree of the Y chromosome in >1000 young apparently healthy white men from the general population. Each Y chromosome was classified into one of 13 most common European lineages. Androgens (DHEA-S, androstenedione, total testosterone) and their metabolites (total estradiol, estrone) were measured by radioimmunoassays. Information on five dimensions of aggression (total, physical, verbal, anger and hostility) was collected using Buss and Perry questionnaire. Results: Approximately 17% men inherited haplogroup I from their fathers. Carriers of haplogroup I showed lower scores of verbal aggression than men with other haplogroups (β = −0.72, SE = 0.29, P = 0.012) and when further compared to carriers of most common R1a lineage and other haplogroups (β = −1.03, SE = 0.34, P = 0.003). However, these associations did not survive a correction for multiple testing. Sex steroids did not show even nominal level of association with haplogroup I. Conclusion: Our data show no overall association between haplogroup I and sex-related phenotypes in young white men. These results also suggest that the previously identified association between haplogroup I and coronary artery disease is not likely mediated by unfavourable profile of sex steroids or heightened aggression early in life. [Copyright &y& Elsevier]

Abstract: Objective: High-sensitivity C-reactive protein (hsCRP) and coronary artery plaque characteristics have been separately evaluated as prognosticators of adverse cardiovascular events; however, their relationship remains unclear. We therefore evaluated the prognostic value of hsCRP in relation to plaque subtypes in predicting adverse cardiovascular outcome in asymptomatic patients without known coronary artery disease. Methods: A total of 4690 asymptomatic patients who underwent coronary computed tomography angiography for screening purposes were included. HsCRP was categorized as <1 mg/L, 1–3 mg/L and >3 mg/L. Cardiovascular events were defined as cardiovascular death, acute coronary syndrome, and stroke. Results: During follow-up (median 49 months, interquartile range 34–59 months), adverse cardiovascular events were observed in 56 (1.2%) patients. Higher hsCRP was associated with poor outcome in overall patients (OR 2.716, 95% CI 1.512–4.880, p = 0.001 for hsCRP 1–3 mg/L, OR 2.705, 95% CI 1.239–5.908, p = 0.013 for hsCRP > 3 mg/L, hsCRP <1 mg/L as reference). When patients were evaluated according to plaque subtype, hsCRP > 3 mg/L was a significant predictor of poor outcome only in patients with noncalcified plaques (NCP; p = 0.038). After adjusting for Framingham risk and coronary artery calcium score, hsCRP > 3 mg/L was a significant predictor of adverse outcomes in the presence of NCP (p = 0.048) but not in the presence of CP or MCP (p = 0.742). Conclusion: Elevated hsCRP is a predictor of adverse cardiovascular events in asymptomatic patients with NCP. After adjusting for Framingham risk and coronary artery calcium scores, hsCRP > 3 mgL remained an independent predictor of risk in patients with NCP but not in patients with CP or MCP. [Copyright &y& Elsevier]

Abstract: Objective: Although diabetes has a great impact on coronary heart disease (CHD) in Western populations, there is limited evidence that diabetes influences CHD in the Japanese population. Methods: The Japan Public Health Center-based prospective (JPHC) study conducted a follow-up of 31,192 individuals aged 40–69 years with no history of cardiovascular disease or cancer. Subjects were classified at baseline as normal, borderline diabetic or diabetic based on fasting and non-fasting blood glucose levels and the use of medication to treat diabetes. A Cox proportional hazards model was used to determine the association between diabetes and the risk of fatal and non-fatal CHD events after adjustment for potential confounders. Results: During 12.9 years of follow-up (1990–2006), we identified 266 fatal and non-fatal coronary events using validated criteria. With normal individuals serving as a control, the hazard ratios for total incident CHD events after adjusting for sex, age, study community and fasting were 1.65 (95% CI, 1.19–2.29) and 3.05 (2.03–4.59) in the borderline and diabetic groups, respectively. These associations remained significant after adjustment for conventional risk factors. The population attributable fractions (PAF) of borderline diabetes and diabetes for CHD events were 6.9% and 6.3%, respectively. Furthermore, there was a trend for an association between an impaired fasting glucose (5.6–6.9mmol/l) and an increased risk of CHD events. Conclusions: This prospective study suggests that diabetes and elevated glucose levels are associated with incident CHD in the general Japanese population. The PAF of diabetes for fatal and non-fatal coronary events was estimated to be moderate. [Copyright &y& Elsevier]

Abstract: Coronary heart disease (CHD) is a leading cause of death worldwide. CHD is complex and despite increased knowledge within vascular biology, traditional risk factors appear not to contribute to risk in a proportion of the population. Within this review, we look at the concept of gene–environment interaction in relation to plasma markers of oxidative stress and cardiovascular disease (CVD) risk. Growing evidence suggests that increased oxidative burden plays an important role in CVD. Genetic variation in antioxidant genes may determine the homeostatic response in an environment (e.g. smoking) of increased oxidative burden. To date, the influence of genetic variation on such plasma markers has been limited due to the lack of a robust measurement in a large number of samples often required in gene-association studies. This also explains the inability to look at gene–environment interaction within the limited number of published studies. We examine in detail the association between plasma markers of oxidative stress and LDL-oxidation with variants from three specific candidate genes: apolipoprotein E (a plasma lipoprotein), mitochondrial uncoupling protein 2 (a mitochondrial antioxidant) and glutathione-S-transferase (a cellular antioxidant protein). [Copyright &y& Elsevier]