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here are a series of well-established risk factors of coronary heart disease (CHD): hypertension, high total cholesterol, smoking, diabetes, older age and male sex. Some studies have paid attention to interactions between them, but have mainly looked at multiplicative interactions with age and/or sex. For example, relative risks associated with many risk factors are larger at younger compared to older ages. The dominant approach to quantifying the association of risk factors with disease is the use of multiplicative models, such as Cox regression. They allow estimation of the association between risk factor and disease as a ratio in hazard between exposed and unexposed groups as well as estimation of the multiplicative interactions between risk factors. An alternative approach is to fit additive hazards model that provides the excess risk due to the presence of risk factor and opportunity to quantify interactions on additive scale. The examination of interactions on the additive scale is rarely done, despite calls for the wider use of absolute measures in epidemiology and public health practice

here are a series of well-established risk factors of coronary heart disease (CHD): hypertension, high total cholesterol, smoking, diabetes, older age and male sex. Some studies have paid attention to interactions between them, but have mainly looked at multiplicative interactions with age and/or sex. For example, relative risks associated with many risk factors are larger at younger compared to older ages. The dominant approach to quantifying the association of risk factors with disease is the use of multiplicative models, such as Cox regression. They allow estimation of the association between risk factor and disease as a ratio in hazard between exposed and unexposed groups as well as estimation of the multiplicative interactions between risk factors. An alternative approach is to fit additive hazards model that provides the excess risk due to the presence of risk factor and opportunity to quantify interactions on additive scale. The examination of interactions on the additive scale is rarely done, despite calls for the wider use of absolute measures in epidemiology and public health practice

BACKGROUND: Patients with atherosclerotic vascular disease remain at high risk for cardiovascular events despite effective statin-based treatment of low-density lipoprotein (LDL) cholesterol levels. The inhibition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipoprotein (HDL) cholesterol levels. However, trials of other CETP inhibitors have shown neutral or adverse effects on cardiovascular outcomes.METHODS: We conducted a randomized, double-blind, placebo-controlled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving intensive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol per liter). The patients were assigned to receive either 100 mg of anacetrapib once daily (15,225 patients) or matching placebo (15,224 patients). The primary outcome was the first major coronary event, a composite of coronary death, myocardial infarction, or coronary revascularization.RESULTS: During the median follow-up period of 4.1 years, the primary outcome occurred in significantly fewer patients in the anacetrapib group than in the placebo group (1640 of 15,225 patients [10.8%] vs. 1803 of 15,224 patients [11.8%]; rate ratio, 0.91; 95% confidence interval, 0.85 to 0.97; P=0.004). The relative difference in risk was similar across multiple prespecified subgroups. At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the placebo group (a relative difference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%. There were no significant between-group differences in the risk of death, cancer, o

OBJECTIVE: The construct of vital exhaustion has been identified as a potential independent psychological risk factor for incident and recurrent coronary heart disease (CHD). Despite several decades of research, no systematic review or meta-analysis has previously attempted to collate the empirical evidence in this field. The purpose of this study was to review and quantify the impact of vital exhaustion on the development and progression of CHD.METHODS: Prospective and case-control studies reporting vital exhaustion at baseline and CHD outcomes at follow-up were derived from PubMed, PsycINFO (1980 to July 2015; articles in English and published articles only), and bibliographies. Information on aim, study design, sample size, inclusion and exclusion criteria, assessment methods of psychological risk factors, and results of crude and adjusted regression analyses were abstracted independently by two authors.RESULTS: Thirteen prospective (n = 52,636) and three case-control (cases, n = 244; controls, n = 457) studies assessed vital exhaustion and could be summarized in meta-analyses. The pooled adjusted risk of CHD in healthy populations was 1.50 (95% confidence interval [CI] = 1.22-1.85) for prospective studies, and 2.61 (95% CI = 1.66-4.10) for case-control studies using hospital controls. Risk of recurrent events in patients with CHD was 2.03 (95% CI = 1.54-2.68). The pooled adjusted risk of chronic heart failure in healthy populations was 1.37 (95% CI = 1.21-1.56), but this was based on results from only two studies.CONCLUSIONS: Vital exhaustion is associated with increased risk of incident and recurrent CHD.

Type III hyperlipoproteinemia (HLP) is mainly found in homozygous carriers of apolipoprotein E2 (apoE2, Arg158-->Cys). Only a small percentage (< 5%) of these apoE2 homozygotes develops hyperlipidemia, indicating that additional environmental and genetic factors contribute to the expression of type III HLP. In the present study, first, the prevalence of type III HLP among apoE2 homozygotes was estimated in a Dutch population sample of 8888 participants. Second, 68 normocholesterolemic and 162 hypercholesterolemic apoE2 homozygotes (type III HLP patients) were collected to investigate additional factors influencing type III HLP expression. In the Dutch population sample, apoE2 homozygosity occurred with a frequency of 0.6% (57 of 8888 individuals). Among the 57 E2/2 subjects, 10 type III HLP patients were identified (prevalence 18%). Comparison of normocholesterolemic E2/2 subjects and type III HLP patients showed that the latter had a significantly increased body mass index (25.6 +/- 4.0 versus 26.9 +/- 3.8 kg/m(2), respectively; P=0.03) and prevalence of hyperinsulinemia (26% versus 63%, respectively; P<0.001). Multiple linear regression analysis d