Coronary Heart Disease Risk Reduction Research Articles

Markers of Endogenous Desaturase Activity and Risk of Coronary Heart Disease in the CAREMA Cohort Study

BackgroundIntakes of n-3 polyunsaturated fatty acids (PUFAs), especially EPA (C20∶5n-3) and DHA (C22∶6n-3), are known to prevent fatal coronary heart disease (CHD). The effects of n-6 PUFAs including arachidonic acid (C20∶4n-6), however, remain unclear. δ-5 and δ-6 desaturases are rate-limiting enzymes for synthesizing long-chain n-3 and n-6 PUFAs. C20∶4n-6 to C20∶3n-6 and C18∶3n-6 to C18∶2n-6 ratios are markers of endogenous δ-5 and δ-6 desaturase activities, but have never been studied in relation to incident CHD. Therefore, the aim of this study was to investigate the relation between these ratios as well as genotypes of FADS1 rs174547 and CHD incidence.MethodsWe applied a case-cohort design within the CAREMA cohort, a large prospective study among the general Dutch population followed up for a median of 12.1 years. Fatty acid profile in plasma cholesteryl esters and FADS1 genotype at baseline were measured in a random subcohort (n = 1323) and incident CHD cases (n = 537). Main outcome measures were hazard ratios (HRs) of incident CHD adjusted for major CHD risk factors.ResultsThe AA genotype of rs174547 was associated with increased plasma levels of C204n-6, C20∶5n-3 and C22∶6n-3 and increased δ-5 and δ-6 desaturase activities, but not with CHD risk. In multivariable adjusted models, high baseline δ-5 desaturase activity was associated with reduced CHD risk (P for trend = 0.02), especially among those carrying the high desaturase activity genotype (AA): HR (95% CI) = 0.35 (0.15–0.81) for comparing the extreme quintiles. High plasma DHA levels were also associated with reduced CHD risk.ConclusionIn this prospective cohort study, we observed a reduced CHD risk with an increased C20∶4n-6 to C20∶3n-6 ratio, suggesting that δ-5 desaturase activity plays a role in CHD etiology. This should be investigated further in other independent studies.

Coronary Heart Disease and Metabolic Risk Factors in Israel: Focus on Gender and Ethnicity

Israel is a small country with a highly diverse population in terms of ethnicity, religion, genetics and life- style, which all have an impact on coronary heart disease (CHD) and metabolic risk factors. This review focuses on gender and ethnic group differences in the risk factors associ- ated with CHD. Using the metabolic syndrome (MetSyn) as a guiding theoretical framework, 30 empirical studies from Israel published after the year 2000 were reviewed to elicit trends. Overall, the MetSyn framework appears to be less appropriate for women than for men in predicting CHD mor- bidity. In addition, ethnic minorities are more likely to have earlier and more severe risk factor profiles, and women are almost always disproportionately affected. Over a period of 5 to 15 years after arrival in Israel, immigrants from the former SovietUnionandEthiopiashowanincreaseinobesity.Recent intervention studies to reduce CHD risk have shown encour- aging results when the programs are culturally tailored.

Attainment of Normal Lipid Levels Among Patients on Lipid-Modifying Therapy in Hong Kong

Although low-density lipoprotein cholesterol (LDL-C) is the primary lipid target for coronary heart disease (CHD) risk reduction, high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) have also emerged as CHD risk factors. The objective of this study was to evaluate attainment of lipid goals and normal levels following lipid-modifying therapy (LMT) and its predictors in a representative sample of Chinese patients from Hong Kong. Using longitudinal data collected from patient medical records, the study identified 706 patients who initiated LMT from January 2004 to December 2006 and had full lipid panels 12 months before and after therapy. LDL-C goals and normal levels of HDL-C and TG were defined according to the National Cholesterol Education Program Adult Treatment Panel 3 guidelines. Patients with previous CHD, diabetes, and 10-year CHD risk > 20% were classified as high risk. Multiple logistic regressions evaluated predictors of normal lipid-level attainment. Among 706 patients (mean age 64.6 years, 58.6% male), 71.7% had elevated LDL-C, 32.4% had low HDL-C, and 24.9% had elevated TG before LMT. Despite therapy (91.2% statins only), 22.7% had elevated LDL-C, 31.9% had low HDL-C, 12.3% had elevated TG, and 13.9% had multiple abnormal lipid levels. The strongest predictors of attaining ≥ 2 normal lipid levels included male gender (odds ratio [OR]: 2.11 [1.12 to 4.01]), diabetes (OR: 0.43 [0.23 to 0.78]), obesity (OR: 0.91 [0.86 to 0.97]), and CHD risk > 20% (OR: 0.33 [0.15 to 0.71]). Current approaches to lipid management in Hong Kong, primarily using statins, considerably improve attainment of LDL-C goal. However, a large proportion of patients do not achieve normal HDL-C levels and control of multiple lipid parameters remains poor. Patients could benefit from a more comprehensive approach to lipid management that treats all three lipid risk factors, as suggested in clinical guidelines.

Gene panels to help identify subgroups at high and low risk of coronary heart disease among those randomized to antihypertensive treatment

To identify panels of genetic variants that predict treatment-related coronary heart disease (CHD) outcomes in hypertensive patients on one of four different classes of initial antihypertensive treatment. The goal was to identify subgroups of individuals on the basis of their genetic profile who benefit most from a particular treatment. Candidate genetic variants (n=78) were genotyped in 39 114 participants from Genetics of Hypertension Associated Treatment study, ancillary to Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial. Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial randomized hypertensive participants (≥55 years) to one of four treatments (amlodipine, chlorthalidone, doxazosin, lisinopril). The primary outcome was fatal CHD or nonfatal myocardial infarction (mean follow-up=4.9 years). A pharmacogenetic panel was derived within each of the four treatment groups. Receiver-operating characteristic (ROC) curves estimated the discrimination rate between those with and without a CHD event, on the basis of the addition of the genetic panel risk score. For each treatment group, we identified a panel of genetic variants that collectively improved the prediction of CHD to a small but statistically significant extent. Chlorthalidone (A): NOS3 rs3918226; SELE rs5361; ICAM1 rs1799969; AGT rs5051; GNAS rs7121; ROC comparison, P=0.004; Amlodipine (B): MMP1 rs1799750; Factor5 (F5) rs6025; NPPA rs5065; PDE4D rs6450512; MMP9 rs2274756; ROC comparison, P=0.006; Lisinopril (C): AGT rs5051; PON1 rs705379; MMP12 rs652438; F12 rs1801020; GP1BA rs6065; PDE4D rs27653; ROC comparison, P=0.01; Doxazosin (D): F2 rs1799963; PAI1 rs1799768; MMP7 rs11568818; AGT rs5051; ACE rs4343; MMP2 rs243865; ROC comparison, P=0.007. Each panel was tested for a pharmacogenetic effect; panels A, B, and D showed such evidence (P=0.009, 0.006, and 0.001, respectively) and panel C did not (P=0.09). Because each panel was associated with CHD in a specific treatment group but not the others, this research provides evidence that it may be possible to use gene panel scores as a tool to better assess antihypertensive treatment choices to reduce CHD risk in hypertensive individuals.

Treatment options for the management of hypertriglyceridemia: Strategies based on the best-available evidence

A severe elevation in triglycerides (TG; ≥500 mg/dL) increases the risk for pancreatitis. TG levels ≥200 mg/dL are associated with a greater risk of atherosclerotic coronary heart disease (CHD). However, no outcomes trials exist to assess the efficacy of TG lowering for preventing pancreatitis in patients with severe hypertriglyceridemia. Similarly, no completed prospective outcomes trial exists to support or refute a reduction in CHD risk resulting from lipid-altering therapy in patients specifically selected for the presence of hypertriglyceridemia. This review examines the available evidence for the use of statins, omega-3 fatty acids, fibrates, and niacin in the management of hypertriglyceridemic patients. Results from CHD outcomes trials support statins as the first-line lipid-altering drug therapy to reduce CHD in hypercholesterolemic patients, and subgroup analyses suggest statins are efficacious in hypertriglyceridemic patients with fasting TG levels <500 mg/dL. Omega-3 fatty acids and fibrates are reasonable first drug options for patients with TG ≥500 mg/dL and often are used to lower TG levels with the objective of reducing pancreatitis risk, although a statin or niacin may also be reasonable options. Combination lipid drug therapy may be needed to achieve both low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol treatment goals for CHD prevention in patients with elevated TG levels, particularly those with TG ≥500 mg/dL. Additional clinical outcomes data are needed to provide a more evidence-based rationale for clinical lipid management of hypertriglyceridemic patients.

Statin Therapy for Healthy Men Identified as “Increased Risk”

ATHEROSCLEROTIC CORONARY HEART DISEASE (CHD) is the most common cause of morbidity and mortality in the world. The “lipid hypothesis” of CHD is clearly established: (1) circulating cholesterol plays a central role in atherogenesis and is an integral component of the requisite lesion, the coronary plaque; (2) cholesterol levels beginning in childhood predict lifetime risk of atherosclerotic CHD events in a dose-response relationship; and (3) statins lower cholesterol levels and reduce CHD and cerebrovascular events directly proportional to the degree of low-density lipoprotein cholesterol (LDL-C) lowering. As a result, guidelines from around the world support a combined lifestyle and pharmacologic approach to cholesterol lowering directed at patients with elevated CHD risk. Assuming a high-density lipoprotein cholesterol (HDL-C) level of about 40 mg/dL, the patient in this common clinical scenario would have an “intermediate” 10-year risk for developing CHD (approximately 10%) based on the Framingham Risk Score (FRS). As always, lifestyle change is the first-line therapy. However, if this patient’s cholesterol level remains abnormal, despite sustained attempts at lifestyle optimization, statin therapy should be considered with the goal of reducing CHD risk. Current guidelines suggest an LDL-C goal of less than 130 mg/dL with an optional target of less than 100 mg/dL. In the shared decision-making process, the clinician should explicitly inform this patient that a statin is likely to reduce the chance of a first CHD event and reduce the chance of stroke and may offer a survival benefit that is likely to become more evident over a lifetime. Evidence Supporting Primary Prevention The WOSCOPS enrolled 6595 men aged 45 to 64 years with no previous history of myocardial infarction and a mean (SD) plasma cholesterol level of 272 (23) mg/dL. Treatment with pravastatin, 40 mg, resulted in a 31% reduction in myocardial infarction and CHD-related death (248 vs 174 events and 135 vs 106 deaths for placebo vs pravastatin, respectively). Similarly, the AFCAPS/TexCAPS randomized 6605 asymptomatic adults with a mean (SD) LDL-C level of 150 (17) mg/dL and low HDL-C (36 [5] mg/dL in men and 40 [5] mg/dL in women) to lovastatin, 20 to 40 mg, vs placebo. Treatment with lovastatin reduced the incidence of first major coronary events by 37% and myocardial infarction by 40% (183 vs 116 events and 95 vs 57 myocardial infarctions for placebo vs lovastatin, respectively). The JUPITER trial enrolled 17 802 healthy men and women with so-called normal LDL-C less than 130 mg/dL and elevated high-sensitivity C-reactive protein greater than 2.0 mg/L. Aggressive lowering of LDL-C in those randomized to receive rosuvastatin, 20 mg, reduced the risk of myocardial infarction, stroke, and revascularization by about 44% (251 vs 142 events for placebo vs rosuvastatin) and total mortality by 20% (247 vs 198 events, respectively). The effect of aggressive LDL-C lowering in JUPITER was substantial considering that the baseline median LDL-C was just 108 mg/dL. Subanalysis demonstrated the largest absolute reduction in patients with a FRS of 11% to 20% (145 vs 74 events for placebo vs rosuvastatin; hazard ratio [HR], 0.51; 95% CI, 0.39-0.68) followed by those with FRS of 5% to 10% (59 vs 32 events; HR, 0.55; 95% CI, 0.36-0.84).

Abstract MP025: Physical Activity and Risk of Coronary Heart Disease in Young Women

Background: The majority of studies on the association between physical activity and coronary heart disease (CHD) risk have been conducted in middle-aged and older populations. Although physical activity has been shown to lower risk of CHD in women by approximately 30%, evidence for the benefits of exercise for CHD in young women is very limited. Methods and Results: We conducted a prospective cohort study among 114 054 women, 25–42 years of age at baseline, enrolled in the Nurses’ Health Study II and followed from 1989 to 2009. Leisure-time physical activity was assessed at baseline and during follow-up through a series of questions on the specific type of activity and the average time per week spent on the activity over the previous year. Additionally, at baseline, women were asked the number of months per year they participated in strenuous exercise or sports during high school and ages 18–22. During 20 years of follow-up, we documented 518 new cases of non-fatal MI and fatal CHD. After adjusting for age and other cardiovascular risk factors, the rate ratios (RR) (95% confidence intervals [CI]) corresponding to 0, 0.1 – 3.5, 3.6 – 8.8, 8.9 – 21.0, and &gt; 21 MET-hours/week of physical activity were 1.0, 0.93 (0.71, 1.21), 0.73 (0.56, 0.95), 0.67 (0.52, 0.88), and 0.63 (0.49, 0.83) (p for trend = 0.001). There was no evidence of effect modification by age or body mass index. Specifically in women less than 50 years of age, the corresponding RR were 1.0, 0.97 (0.70, 1.35), 0.75 (0.53, 1.04), 0.69 (0.50, 0.96), and 0.63 (0.45, 0.88) (p for trend = 0.008). Brisk walking alone was also associated with significant reductions in CHD risk. In contrast to physical activity during adulthood, frequency of participation in strenuous activity in high school or during ages 18–22 was not associated with risk of CHD when adjusted for current physical activity. Conclusions: These prospective data suggest that physical activity is associated with substantial risk reductions in the incidence of coronary heart disease in young women.

An Evidence-Based Review of Exercise and Metabolic Syndrome

An Evidence-Based Review of Exercise and Metabolic Syndrome

Occupational physical activity and risk of coronary heart disease among active and non-active working-women of North Dakota: A Go Red North Dakota study

Currently less than half of the US adults meet physical activity (PA) recommendations, yet many more are sedentary in their occupations. Sedentary workers may therefore be at elevated risk for coronary heart disease (CHD). Therefore, the objective of the study is to examine the relationship of CHD risk with occupational PA (OCPA) and leisure time PA (LTPA) among working-women. The 10-year CHD risk and relative risk scores were calculated for 642 working-women. Self-report questionnaire determined levels of OCPA and LTPA. Biometric data were directly collected on all women. No direct relationship for OCPA and 'high risk' of CHD was determined. Insufficient LTPA was significantly associated with greater prevalence of 'high risk' of CHD. No dose response relationship was determined with PA and CHD risk. The odds of being 'high risk' were significantly greater for sedentary workers with insufficient LTPA compared to sufficient LTPA. The odds for being 'high risk' were similar among moderately active or heavy working women completing insufficient LTPA compared to women doing sufficient LTPA. For women with sedentary occupations, a sufficient amount of LTPA is essential to reduce CHD risk. Women in moderate to heavy working occupations may be acquiring adequate amounts of PA to minimize CHD risk.

Gut Microbiota, Diet, and Heart Disease

Modulation of the gut microbiota is an area of growing interest, particularly for its link to improving and maintaining the systemic health of the host. It has been suggested to have potential to reduce risk factors associated with chronic diseases, such as elevated cholesterol levels in coronary heart disease (CHD). Diets of our evolutionary ancestors were largely based on plant foods, high in dietary fiber and fermentable substrate, and our gut microbiota has evolved against a background of such diets. Therapeutic diets that mimic plant-based diets from the early phases of human evolution may result in drug-like cholesterol reductions. In contrast, typical Western diets low in dietary fiber and fermentable substrate, and high in saturated and trans fatty acids, are likely contributors to the increased need for pharmacological agents for cholesterol reduction. The gut microbiota of those consuming a Western diet are likely underutilized and depleted of metabolic fuels, resulting in a less than optimal gut microbial profile. As a result, this diet is mismatched to our archaic gut microbiota and, therefore, to our genome, which has changed relatively little since humans first appeared. While the exact mechanism by which the gut microbiota may modulate cholesterol levels still remains uncertain, end products of bacterial fermentation, particularly the short chain fatty acids (i.e., propionate), have been suggested as potential candidates. While more research is required to clarify the potential link between gut microbiota and CHD risk reduction, consuming a therapeutic diet rich in plant foods, dietary fiber, and fermentable substrate would be a useful strategy for improving systemic health, possibly by altering the gut microbiota.

Plant sterols and stanols as dietary factors reducing hypercholesterolemia by inhibiting intestinal cholesterol absorption

The review is focussed on the mechanisms of action, lipid-lowering activity, structural characteristics, and safety of plant sterins and stanols. Phytosterins and phytostanols inhibit intestinal cholesterol (CH) absorption, therefore decreasing plasma CH levels. The emphasis is put on prospective epidemiological studies of representative samples, which demonstrated that plasma concentrations of phytosterins and phytostanols in patients with coronary heart disease (CHD) are substantially lower than in CHD-free participants. A two-fold increase in serum sytosterin concentration was associated with a reduction in relative risk of CHD by 22 %. Plant sterin and sterol esters could be regarded as effective and safe dietary ingredients decreasing blood levels of CH — one of the major cardiovascular disease risk factors.

KIF6, LPA, TAS2R50, and VAMP8 genetic variation, low density lipoprotein cholesterol lowering response to pravastatin, and heart disease risk reduction in the elderly

Single nucleotide polymorphisms (SNPs) at the KIF6 (kinesin like protein 6, rs20455 or 719Arg), LPA (lipoprotein(a), rs3798220), TAS2R50 (taste receptor type 2, member 50, rs1376251) and VAMP8 (vesicle-associated membrane protein 8, rs1010) have previously been associated with low density lipoprotein cholesterol (LDL-C) lowering response to statins, coronary heart disease (CHD) at baseline, or CHD events on trial. We examined SNPs at the KIF6 (rs20455 or 719Arg), LPA (rs3798220), TAS2R50 (rs1376251) and VAMP8 (rs1010) in 5,411 participants in PROSPER (PROspective Study of Pravastatin in the Elderly at Risk) (mean age 75.3 years), who had been randomized to pravastatin 40 mg/day or placebo and were followed for a mean of 3.2 years. No SNP was related to vascular disease at baseline. Only the KIF6 SNP was related to LDL-C lowering with homozygous Arg 719 subjects being significantly less responsive than other groups ( p = 0.025, −34.2 vs. −36.1%). With regard to the primary CHD endpoint on trial (fatal or non-fatal myocardial infarction or stroke), we observed a significant relationship for KIF6 719Arg homozygotes ( p = 0.03, hazards ratio 0.47, 12.8% of the population) in women on pravastatin only, and for TAS2R50 for the AA genotype ( p = 0.03, hazards ratio 1.76, 8.9% of the population), also only in women on pravastatin. Our data indicate that the assessment of KIF6 rs20455 and TAS2R50 rs1376251 genotypes are not useful for predicting statin induced cardiovascular risk reduction in men, but do predict CHD risk reduction in women in this elderly population. However, these differences are no longer significant after correction for multiple comparisons, and we do not recommend the assessment of any of these SNPs in clinical practice.

Abstract 8968: Reduction of Non-hdl-cholesterol by More Than 5% with NCEP Diet Reduces CHD Risk

Background and aims: Dietary management is considered to be very important to lower plasma lipids. Non-HDL-cholesterol may be a better indicator of coronary heart disease (CHD) than traditional lipid risk markers (LDL-cholesterol, HDL-cholesterol), which was confirmed in previous studies. However the extent to which non-HDL-cholesterol must be lowered to decrease CHD risk with diet remains to be clarified. To answer this question, we conducted a post-hoc analysis of the dietary treatment group in a large-scale randomized primary prevention trial in Japanese. Materials and methods 7832 patients with mild hypercholesterolemia were randomly allocated to either diet alone (n=3966) or diet+pravastatin (n=3866) and followed for an average of 5 years. The patients were instructed to follow the National Cholesterol Education Program (NCEP) guideline step 1 diet, which is low in cholesterol and saturated fats, with the addition of fish, like in the usual Japanese diet. Incidence rates of CHD, CHD+cerebral infarction (CI), and all cardiovascular events were calculated by the Cox proportional hazard model according to the reduction rates of non-HDL-cholesterol. Results Baseline non-HDL-cholesterol level in the diet group was 184.4±18.6 mg/dL. CHD incidence was significantly reduced by 42% (p=0.02) and by 50% (p=0.007) in relation to a 3% and 5% lowering of non-HDL-cholesterol respectively. The total cardiovascular event rate was significantly reduced by 34% (p=0.02) with a 5% lowering of non-HDL-cholesterol. Neither stroke nor all-cause mortality was affected significantly. On treatment non-HDL-cholesterol levels were less than 174 mg/dL, indicating the reduction of CHD and cardiovascular events. Conclusion A reduction of 5% or more of non-HDL-cholesterol with the modified NCEP step 1 diet was associated with a significant reduction in CHD and cardiovascular events.

Translating HDL Science to Clinical Practice

It is an often-repeated axiom that high-density lipoprotein (HDL) cholesterol is protective, whereas low-density lipoprotein (LDL) cholesterol is causative, of the pathologic consequences of excess serum cholesterol, resulting in development of atherosclerotic plaques and coronary heart disease (CHD). Measurement of circulating LDL cholesterol has been well studied and correlated with CHD risk. HDL cholesterol levels, however, although correlated epidemiologically with reduction of CHD risk, have remained less-well defined as a biomarker. This Journal of Clinical Lipidology open-source eCME activity (accessed at http://multimedia.lipidjournal.com/2011/ HDL) presentation details a simple laboratory measure of the degree of risk-reduction that a given patient’s HDL cholesterol should provide, defined as the ‘‘cholesterol efflux’’ parameter. What it is, how it is calculated, and validation of its accuracy are discussed in this

HDL Functionality: How Do We Measure It and Is It Relevant for Everyday Clinical Practice?

It is an often-repeated axiom that high-density lipoprotein (HDL) cholesterol is protective, whereas low-density lipoprotein (LDL) cholesterol is causative, of the pathologic consequences of excess serum cholesterol, resulting in development of atherosclerotic plaques and coronary heart disease (CHD). Measurement of circulating LDL cholesterol has been well studied and correlated with CHD risk. HDL cholesterol levels, however, although correlated epidemiologically with reduction of CHD risk, have remained less-well defined as a biomarker. This Journal of Clinical Lipidology open-source eCME activity (accessed at http://multimedia.lipidjournal.com/2011/HDL) presentation details a simple laboratory measure of the degree of risk-reduction that a given patient’s HDL cholesterol should provide, defined as the “cholesterol efflux” parameter. What it is, how it is calculated, and validation of its accuracy are discussed in this presentation. Radar DJ. J Clin Lipidol. 2011; 5(6). Accessible at http://lipidjournal.com.

Hepatic lipase gene -514C&gt;T variant is associated with exercise training-induced changes in VLDL and HDL by lipoprotein lipase

Our objective was to test the hypothesis that a common polymorphism in the hepatic lipase (HL) gene (LIPC -514C>T, rs1800588) influences aerobic exercise training-induced changes in TG, very-low-density lipoprotein (VLDL), and high-density lipoprotein (HDL) through genotype-specific increases in lipoprotein lipase (LPL) activity and that sex may affect these responses. Seventy-six sedentary overweight to obese men and women aged 50-75 yr at risk for coronary heart disease (CHD) underwent a 24-wk prospective study of the LIPC -514 genotype-specific effects of exercise training on lipoproteins measured enzymatically and by nuclear magnetic resonance, postheparin LPL and HL activities, body composition by dual energy x-ray absorptiometry and computer tomography scan, and aerobic capacity. CT genotype subjects had higher baseline total cholesterol, HDL-C, HDL(2)-C, large HDL, HDL particle size, and large LDL than CC homozygotes. Exercise training elicited genotype-specific decreases in VLDL-TG (-22 vs. +7%; P < 0.05; CC vs. CT, respectively), total VLDL and medium VLDL, and increases in HDL-C (7 vs. 4%; P < 0.03) and HDL(3)-C with significant genotype×sex interactions for the changes in HDL-C and HDL(3)-C (P values = 0.01-0.02). There were also genotype-specific changes in LPL (+23 vs. -6%; P < 0.05) and HL (+7 vs. -24%; P < 0.01) activities, with LPL increasing only in CC subjects (P < 0.006) and HL decreasing only in CT subjects (P < 0.007). Reductions in TG, VLDL-TG, large VLDL, and medium VLDL and increases in HDL(3)-C and small HDL particles correlated significantly with changes in LPL, but not HL, activity only in CC subjects. This suggests that the LIPC -514C>T variant significantly affects training-induced anti-atherogenic changes in VLDL-TG, VLDL particles, and HDL through an association with increased LPL activity in CC subjects, which could guide therapeutic strategies to reduce CHD risk.

Heart health when life is satisfying: evidence from the Whitehall II cohort study.

Negative psychological states such as stress and depression are associated with increased risk of coronary heart disease (CHD), but it is unclear whether some positive states are protective. We investigated satisfaction with specific life domains as predictors of incident CHD. Coronary risk factors and satisfaction within seven life domains (e.g. job and family) were assessed in 7956 initially healthy members of the Whitehall II cohort. Incident CHD (angina, non-fatal myocardial infarction, or death from CHD) was ascertained from medical screening, hospital data, and registry linkage over five person-years of follow-up. Satisfaction averaged across domains was associated with reduced CHD risk (HR: 0.87; 95% CI: 0.78-0.98), controlling for demographic characteristics, health behaviours, blood pressure, and metabolic functioning. Associations with CHD risk were evident for satisfaction in four life domains-one's job, family, sex life, and self, but not one's love relationship, leisure activities, or standard of living. When examining CHD outcomes separately, average domain satisfaction was associated with angina but not myocardial infarction or coronary death. Satisfaction in most life domains was associated with reduced CHD risk, with definite angina being mostly responsible for this association. These findings suggest that satisfaction with life may promote heart health. Further research should examine whether interventions to enhance life satisfaction in specific domains reduce CHD risk and whether life satisfaction is primarily associated with atherosclerosis rather than thrombotic factors associated with plaque rupture.

Women's Risk Factors and Screening for Coronary Heart Disease

Age, race, poverty, hypertension, diabetes mellitus, hyperlipidemia, obesity, smoking, and sedentary lifestyle are risk factors for coronary heart disease (CHD) in women. Menstrual cycle irregularity, preeclampsia, and decreasing levels of sex hormones in postmenopausal women are also implicated. The U.S. Preventive Services Task Force does not recommend routine CHD risk stratification using nontraditional markers (e.g., lipoprotein(a), Ankle-Brachial Index [ABI], and inflammatory markers). Nurses should counsel all women regarding lifestyle behaviors to reduce CHD risk.

A Pharmacist Care Program

To investigate the effect of a pharmacist care program on cardiovascular risks in type 2 diabetic patients. A 9-month, prospective, randomized, controlled study was conducted in a public hospital in Hong Kong. Patients in the intervention group had regular drug-counseling sessions with pharmacists in addition to routine medical care, whereas patients in the control group received only routine medical care. The primary outcome was the change in coronary heart disease (CHD) risk. A total of 105 patients completed the study. Patients in the intervention group had a statistically significant reduction in CHD risk compared to those in the control group (-1.64% ± 3.56%; n = 51 vs -0.01% ± 3.08%; n = 54, P = .013). For stroke, a reduction in risk was noted in the intervention group, while an increased risk was noted in the control group (-1.06% ± 1.82% vs 0.31% ± 2.51%, P = .002). In addition, hemoglobin A1c levels were significantly reduced in the intervention group compared with the control group (-1.57% ± 1.50% vs -0.40% ± 1.19%, P < .001); a similar profile was seen with low-density lipoprotein cholesterol (-0.36 ± 0.76 vs -0.03 ± 0.74, P = .026). Furthermore, there were nonsignificant improvements in high-density lipoprotein cholesterol, triglyceride, and blood pressure in the intervention group. The increased level of understanding regarding medications in the intervention group was statistically significant (P < .001), yielding a better enhancement in compliance compared with patients in the control group (22.5% ± 13.4% vs 2.0% ± 5.0%, P < .001). The pharmacist care program implemented in this study demonstrated a significant cardiovascular risk reduction in type 2 diabetic patients; therefore such a program would be a valuable addition to a multidisciplinary care of diabetic patients.

Fruit, vegetables, and olive oil and risk of coronary heart disease in Italian women: the EPICOR Study

Many observational studies support the recommendation to eat sufficient amounts of fruit and vegetables as part of a healthy diet. The present study aimed to investigate the association between consumption of fruit, vegetables, and olive oil and the incidence of coronary heart disease (CHD) in 29,689 women enrolled between 1993 and 1998 in 5 European Prospective Investigation into Cancer and Nutrition (EPIC) cohorts in northern (Turin and Varese), central (Florence), and southern (Naples and Ragusa) Italy. Baseline dietary, anthropometric, and lifestyle characteristics were collected. Major events of CHD (fatal and nonfatal myocardial infarction and coronary revascularization) were identified through a review of clinical records. Analyses were stratified by center and adjusted for hypertension, smoking, education, menopause, physical activity, anthropometric measures, nonalcohol energy, alcohol, total meat, vegetables in analyses for fruit, and fruit in analyses for vegetables. During a mean follow-up of 7.85 y, 144 major CHD events were identified. A strong reduction in CHD risk among women in the highest quartile of consumption of leafy vegetables (hazard ratio: 0.54; 95% CI: 0.33, 0.90; P for trend = 0.03) and olive oil (hazard ratio: 0.56; 95% CI: 0.31, 0.99; P for trend = 0.04) was found. In contrast, no association emerged between fruit consumption and CHD risk. An inverse association between increasing consumption of leafy vegetables and olive oil and CHD risk emerged in this large cohort of Italian women.