Multiple Coronary Heart Disease Risk Research Articles

Nonalcoholic Fatty Liver Disease and Cardiovascular Disease.

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Modifiable Coronary Heart Disease Risk Factors Trends in Urban Black South African Females and the Implications for Health Promotion Interventions

BACKGROUND: Multiple risk factors can contribute to the development of coronary heart disease (CHD) in an individual, yet any change in the modifiable CHD risk status of Black South African females in recent times is unknown.AIM: The researcher aimed to establish the current CHD risk status of urban Black African females and to report on any trends over a 10-year period with the purpose to direct health promotion programs.METHODS: Data from 62 urban Black females (Mean age 32.4 ± 8.5 years) in 2006 was paired for age with that of 67 women (Mean age 32.0 ± 9.0 years) in 2016. The modifiable CHD risk factors assessed were cigarette smoking, sedentary lifestyle, obesity, hypertension, and hypercholesterolemia.RESULTS: Physical inactivity (72.6% of the sample in 2006 vs. 75.8% in 2016) and obesity (42% in 2006 vs. 38.8% in 2016) were the top-ranked risk factors for CHD with the pattern unchanged in 2016. Significantly fewer participants (4.5% vs. 16.6%; p < 0.05) were hypertensive and significantly more women had hypercholesterolemia (5.6% vs. 23.9%; p < 0.05) in 2016. The multiple CHD risk profile showed that 42.4% had at least one CHD risk factor (an increase of 25%) and significantly fewer (27.3% vs. 45.2%; p < 0.05) had two CHD risk factors in 2016.CONCLUSION: A sedentary lifestyle and obesity were the highest CHD risk factors. Also, the multiple CHD risk profile of Black African women changed over a period of 10 years from higher to lower and normal risk. Health promotion strategies must be directed towards weight reduction, increasing physical activity levels and be tailored for the population for which the health promotion programs have been designed.

Abstract MP064: Dietary Contributors to Glycemic load in the REasons for Geographic and Racial Differences in Stroke (REGARDS) Study

Glycemic load (GL) is a measure that incorporates both the quality (i.e., glycemic index) and quantity of dietary carbohydrate and is a measure of the overall glycemic impact of the diet. In observational studies, high-GL diets have been associated with a greater prevalence of multiple coronary heart disease risk factors, including type 2 diabetes, overweight/obesity, dyslipidemia, inflammation, and abnormal blood clotting. To begin to develop interventions to reduce dietary GL, it is necessary to identify the major contributors to GL at the population level. We studied contributors to GL in 21,636 participants in the REasons for Geographic And Racial Differences in Stroke (REGARDS) study (7074 white men, 2472 black men, 7287 white women, and 4803 black women) whose mean (SD) age was 64.9 (9.3) years at baseline (2003-2007). Mean daily GL, as well as individual carbohydrate food and food group contributors to GL, were determined for each participant using intake data from the Block 1998 semi-quantitative food frequency questionnaire administered at baseline. Mean (SD) daily GL was 107.1 (44.1), 115.0 (53.8), 89.9 (40.6), and 100.0 (49.6) g/d in white men, black men, white women, and black women, respectively. Sugar-sweetened beverages was the main carbohydrate food group contributing to GL in both black men and women and were important contributors to GL in white men and women (Figure). Regular soft drinks in particular were the leading individual carbohydrate contributor to GL in black men (4.0 median % of daily GL). The main carbohydrate food group contributing to GL in both white men and women was breads. Dark breads were the leading individual carbohydrate contributors to GL in white men, white women, and black women (2.7, 3.2, and 2.4 median % of daily GL, respectively). Sugar-sweetened beverages were a major contributor to dietary GL in this sample of US adults, especially in blacks. Decreasing the consumption of these beverages should be considered in future interventions to reduce dietary GL.

Hypothyroidism and Moderate Subclinical Hypothyroidism Are Associated with Increased All-Cause Mortality Independent of Coronary Heart Disease Risk Factors: A PreCIS Database Study

Thyroid hormones have profound effect on the heart and peripheral vasculature. Hypothyroidism is associated with an increase in a number of coronary heart disease (CHD) risk factors including dyslipidemia, hypertension, and elevated levels of homocysteine. Our objective was to assess the effects of hypothyroidism (thyroid-stimulating hormone [TSH]: >10 μ U/mL), moderate subclinical hypothyroidism (SCH; TSH: 6.1-10 μ U/mL), and mild SCH (TSH: 3.1-6.0 μ U/mL) on cardiovascular risk factors, CHD prevalence, and all-cause mortality in patients at high risk for CHD seen in a preventive cardiology clinic. All patients seen in the Cleveland Clinic Preventive Cardiology clinic have demographic and laboratory tests including TSH and multiple CHD risk factors obtained at the baseline visit. All data are entered into a database (called PreCIS). The social security death index is queried monthly to determine all-cause mortality. Several CHD risk factors including age, male gender, systolic blood pressure, triglycerides, and fibrinogen were more common in hypothyroid patients. Prevalence of CHD was more common in hypothyroid and moderate SCH patients. All-cause mortality was higher in hypothyroid and moderate SCH patients, but not in mild SCH patients. Higher mortality in these groups was observed in both genders, patients under 65 years of age, and patients not on thyroid replacement therapy, but was not observed in patients over 65 years of age. Hypothyroidism and moderate, but not mild, SCH are associated with increased CHD prevalence and all-cause mortality. These observations suggest patients with moderate, but not mild, SCH and patients at high risk for CHD should be treated with thyroid replacement therapy.

Insights Gained from 20 Years of Soy Research ,

Soyfoods have long been recognized for their high-protein and low-saturated fat content, but over the past 20 y an impressive amount of soy-related research has evaluated the role of these foods in reducing chronic disease risk. Much of this research has been undertaken because the soybean is essentially a unique dietary source of isoflavones, a group of chemicals classified as phytoestrogens. The estrogen-like properties of isoflavones have also raised concern, however, that soyfoods might exert adverse effects in some individuals. There is intriguing animal and epidemiologic evidence indicating that modest amounts of soy consumed during childhood and/or adolescence reduces breast cancer risk. Evidence also suggests that soy reduces prostate cancer risk and inhibits prostate tumor metastasis, but additional clinical support for the chemopreventive effects of soyfoods is needed. Soy protein is modestly hypocholesterolemic and there is suggestive epidemiologic evidence that soyfoods lower risk of coronary heart disease (CHD) independent of effects on cholesterol. In clinical studies, soy favorably affects multiple CHD risk factors; however, with the exception of improved endothelial function, the data are too limited and/or inconsistent to allow definitive conclusions to be made. In regard to bone health, although recent clinical data have not supported the skeletal benefits of isoflavones, 2 large prospective epidemiologic studies found soy intake is associated with marked reductions in fracture risk. Soybean isoflavones also modestly alleviate hot flashes in menopausal women. Finally, other than allergic reactions, there is almost no credible evidence to suggest traditional soyfoods exert clinically relevant adverse effects in healthy individuals when consumed in amounts consistent with Asian intake.

Quantitative effects on cardiovascular risk factors and coronary heart disease risk of replacing partially hydrogenated vegetable oils with other fats and oils

Reduced consumption of trans-fatty acids (TFA) is desirable to lower coronary heart disease (CHD) risk. In practice, partially hydrogenated vegetable oils (PHVO) that contain both TFAs and other fatty acids are the unit of replacement and could be replaced with diverse alternative fats and oils. We performed quantitative estimates of CHD effects if a person's PHVO consumption were to be replaced with alternative fats and oils based on (1) randomized dietary trials and (2) prospective observational studies. We performed meta-analyses of (1) the effects of TFAs on blood lipids and lipoproteins in controlled dietary trials and (2) associations of habitual TFA consumption with CHD outcomes in prospective cohort studies. On the basis of these results and corresponding findings for saturated fatty acids (SFA), cis-monounsaturated fatty acids (MUFA) and cis-polyunsaturated fatty acids (PUFA), we calculated the effects on CHD risk for replacing 7.5% of energy from three different PHVO formulations (containing 20, 35 or 45% TFAs) with butter, lard, palm or vegetable oils. In controlled trials, each 1% energy replacement of TFAs with SFAs, MUFAs or PUFAs, respectively, decreased the total cholesterol (TC)/high-density lipoprotein cholesterol (HDL-C) ratio by 0.31, 0.54 and 0.67; the apolipoprotein (Apo)-B/ApoAI ratio by 0.007, 0.010 and 0.011; and lipoprotein (Lp)(a) by 3.76, 1.39 and 1.11 mg/l (P<0.05 for each). We also included possible effects on C-reactive protein (CRP) of TFAs vs other fats from one trial. On the basis of these risk factor changes in controlled trials, CHD risk would be variably decreased by different fats and oils replacing 7.5% of energy from 20% TFA PHVO (CHD risk reduction: -2.7% (butter) to -9.9% (canola)); 35% TFA PHVO (-11.9% (butter) to -16.0% (canola)); or 45% TFA PHVO (-17.6% (butter) to -19.8% (canola)). In prospective cohort studies, each 2% energy replacement of TFAs with SFAs, MUFAs or PUFAs would lower CHD risk by 17% (95% confidence interval (CI)=7-25%), 21% (95% CI=12-30%) or 24% (95% CI=15-33%), respectively. On the basis of these associations in observational studies, CHD risk would be variably decreased by different fats and oils replacing 7.5% of energy from 20% TFA PHVO (CHD risk reduction: +0.5% (butter) to -21.8% (soybean)); 35% TFA PHVO (-14.4% (butter) to -33.4% (soybean)); or 45% TFA PHVO (-22.4% (butter) to -39.6% (soybean)). The demonstrated effects on TC/HDL-C, ApoB/ApoAI, Lp(a), and CRP in randomized feeding trials together accounted for approximately 65-80% and approximately 50% of the estimated risk reduction for replacing PHVO with animal fats and vegetable oils, respectively, that would be calculated from prospective cohort studies. Effects on CHD risk of removing PHVO from a person's diet vary depending on the TFA content of the PHVO and the fatty acid composition of the replacement fat or oil, with direct implications for reformulation of individual food products. Accounting for the summed effects of TFAs on multiple CHD risk factors provides more accurate estimates of potential risk reduction than considering each risk factor in isolation, and approaches the estimated risk reduction derived from prospective cohort studies.

Depressive behavior and coronary artery atherogenesis in adult female cynomolgus monkeys.

To examine depressive behavior and early coronary artery atherogenesis in 36 socially housed female cynomolgus monkeys, an established model of atherogenesis and depression. Coronary heart disease (CHD) is caused by coronary artery atherosclerosis (CAA) and its sequelae which develop over a period of decades. Thus, in prospective studies of depression and CHD, CAA was likely present at baseline in most subjects who experienced cardiac events. Little is known about the relationship between depression and CAA. The monkeys were free of atherosclerosis before being fed a diet containing moderate amounts of fat and cholesterol for 52 months. Depressed behavior and activity levels recorded in weekly 15-minute focal samples, telemetered 24-hour heart rate, plasma total (TPC) and high-density lipoprotein cholesterol (HDLC), luteal phase serum progesterone concentrations, basal cortisol, cortisol response to corticotrophin-releasing hormone (CRH), and CAA extent were assessed. Time spent in depressed behavior over 4 years was significantly associated with early CAA (r = .73, p < .001), as were activity level, 24-hour heart rate, TPC, HDLC, cortisol response to CRH, and mean peak progesterone (all p < or = 0.05). Depressed females had four times the CAA compared with nondepressed females. Depression in primates is associated with perturbations in multiple CHD risk factors and accelerated early atherogenesis. These data are consistent with the hypotheses that depression and CAA both stem from a common mechanism and that depression may cause CAA.

Reduced Incidence of Invasive Breast Cancer With Raloxifene Among Women at Increased Coronary Risk

In the Raloxifene Use for The Heart trial, 10 101 postmenopausal women with coronary heart disease (CHD) or multiple CHD risk factors were randomly assigned to 60 mg/d raloxifene or to placebo and followed for a median of 5.6 years. Raloxifene, a selective estrogen receptor modulator, was found to reduce the risk of invasive breast cancer and vertebral fractures but not the risk of cardiovascular events. Here, we provide further details about breast cancer incidence by tumor characteristics, duration of treatment, and subgroup. Reported breast cancer was adjudicated by an independent committee based on medical records and pathology reports. The primary analyses used Cox proportional hazards models with time to first breast cancer as the outcome. Subgroup effects were analyzed using similar models with terms for treatment by subgroup. All statistical tests were two-sided. As previously reported, raloxifene reduced the incidence of invasive breast cancer by 44% (hazard ratio [HR] = 0.56; 95% confidence interval [CI] = 0.38 to 0.83; absolute risk reduction = 1.2 invasive breast cancers per 1000 women treated for 1 year). The lower incidence of invasive breast cancer reflected a 55% lower incidence of invasive estrogen receptor (ER)-positive tumors (HR = 0.45; 95% CI = 0.28 to 0.72). However, raloxifene treatment did not reduce the incidence of noninvasive breast cancer or of invasive ER-negative breast cancer. The reduced incidence of invasive breast cancer was similar across subgroups, including those defined by age, body mass index, family history of breast cancer, prior use of postmenopausal hormones, and 5-year estimated risk of invasive breast cancer. Raloxifene reduces risk of invasive ER-positive breast cancer regardless of a woman's baseline breast cancer risk but does not reduce risk of noninvasive or ER-negative breast cancers. These results confirm those of the Multiple Outcomes of Raloxifene Evaluation, a previous randomized trial among women with osteoporosis.

Vitamin D Supplementation and Cardiovascular Disease Risk

Many studies,1,2 but not all, have shown that low bone density is associated with increased cardiovascular disease (CVD) risk. Vitamin D deficiency is common in the elderly and is associated with osteoporosis; however, the association of endogenous 25-OH vitamin D (25-OH D) levels with CVD events is controversial.3,4 CVD rates are higher during winter seasons and at increased geographic latitudes where average serum vitamin D levels are lowest.5 Low 25-OH D levels have been found in stroke6 and heart failure patients.7 Moreover, 25-OH D deficiency is associated with hypertension, obesity,8 glucose intolerance,8 and the metabolic syndrome,9 which may be responsible, at least in part, for its association with increased CVD risk. Article p 846 Although vitamin D supplementation improves bone strength, elevated serum vitamin D levels may be associated with lower levels of vascular calcification. In subjects at moderately high risk for coronary heart disease, endogenous serum vitamin D levels were inversely correlated with the extent of coronary artery calcification as determined by cardiac computed tomography.10 Vitamin D also has intriguing antiinflammatory properties11 that have potential therapeutic benefit in several autoimmune diseases and allograft rejection. In 2 small clinical trials,12,13 vitamin D supplementation lowered C-reactive protein levels. Additionally, 1,25(OH)2D induces relaxation of vascular smooth muscle cells …

Effect of lifestyle intervention on metabolic coronary heart disease risk factors in obese older adults

Coronary heart disease (CHD) risk factors increase with age and body mass index (BMI; in kg/m2). However, whether lifestyle intervention ameliorates metabolic CHD risk factors in obese older adults is unknown. The objective was to determine whether lifestyle intervention improves metabolic CHD risk factors in obese older adults. A 6-mo outpatient randomized controlled trial was conducted in obese (BMI >or= 30) older (>or=65 y) adults randomly assigned to diet and exercise therapy (treatment group; n = 17) or no therapy (control group; n = 10). The main outcomes were CHD risk factors. Body weight decreased by 8.4% (8.2 kg) in the treatment group; weight did not change significantly (0.7 kg) in the control group (P < 0.001 between groups). Changes between the control and treatment groups, respectively, in waist circumference (1 and -10 cm), plasma glucose (4 and -4 mg/dL), serum triacylglycerols (0 and -45 mg/dL), and systolic (-2 and -10 mm Hg) and diastolic (0 and -8 mm Hg) blood pressure were different (P < 0.05 for all). The number of subjects with the metabolic syndrome decreased by 59% in the treatment group but did not change significantly in the control group (P < 0.05). Serum free fatty acids increased by 10 micromol/L in the control group and decreased by 99 micromol/L in the treatment group (P < 0.05). Changes between the control and treatment groups, respectively, in C-reactive protein (0.8 and -2.5 mg/L) and interleukin 6 (1.6 and -2.4 pg/mL) were different (P < 0.05 for both). Lifestyle intervention decreases multiple metabolic CHD risk factors simultaneously in obese older adults.

Endothelial dysfunction in HIV infection

Highly active antiretroviral therapy (HAART) has significantly improved the prognosis of patients with HIV infection; however, the use of protease inhibitors has been associated with increased cardiovascular events and worsening of multiple coronary heart disease risk factors including dyslipidemia, insulin resistance, and endothelial dysfunction. Endothelial dysfunction may be caused by the infection itself, the immunologic responses due to the HIV virus, and also by the effects of HAART through their effects on both lipid and glucose metabolism. The study of endothelial function in HIV infection and its modifications by HAART is an exciting new field in clinical research, limited by multiple factors such as viral factors, immunologic conditions, and metabolic drug effects that could affect the interpretation of endothelial impairment. Further studies are still needed to understand the significance of endothelial dysfunction in the cardiovascular risk assessment of patients with HIV infection.

Effect of Short‐Term Pritikin Diet Therapy on the Metabolic Syndrome

The Pritikin Program (Aventura, FL) involves the use of a very-low-fat, low-sodium, high-fiber diet and exercise to decrease the risk of coronary heart disease (CHD). This study evaluated the effect of short-term Pritikin therapy on the metabolic risk factors for CHD in patients with the metabolic syndrome. Sixty-seven subjects who had the metabolic syndrome and attended the Pritikin Longevity Center & Spa for 12-15 days were studied. Short-term Pritikin therapy improved most CHD risk factors: body mass index decreased by 3% (P<.001); systolic and diastolic blood pressure, and serum glucose and low-density lipoprotein cholesterol concentrations decreased by 10%-15% (P<.001); serum triglyceride concentration decreased by 36% (P<.001); and 37% of subjects no longer met National Cholesterol Education Program criteria for the metabolic syndrome. Serum high-density lipoprotein cholesterol, however, decreased by 3% (P<.05). These data demonstrate that brief treatment with a very-low-fat, low-sodium, high-fiber diet and regular exercise simultaneously improves multiple CHD risk factors in patients with the metabolic syndrome.

Age and Time Need Not and Should Not Be Eliminated From the Coronary Risk Prediction Models

Risk assessment, risk communication, and risk management are 3 fundamental steps in the primary and secondary prevention of coronary heart disease (CHD). Consequently, national and international guidelines1–4 have been formulated to assist clinicians in providing standardized care for treating coronary risk factors. These guidelines are consistent with the best available scientific evidence on risks of developing CHD and potential strategies to reduce those risks via nonpharmacological and pharmacological interventions. One of the critical concepts on which contemporary guidelines are founded is the notion that the choice and intensity of an intervention strategy should in part be based on the underlying risk—ie, the absolute risk of experiencing a CHD event during a short-term period. This is typically estimated as the 10-year risk of CHD for a man or a woman of a specific age.1,3,4 In this issue of Circulation , Ridker and Cook5 present an argument to eliminate both the age and the time dependency of CHD risk prediction algorithms. On the basis of the objectives of current guidelines and risk prediction algorithms, we disagree with the suggestion made by Ridker and Cook. We submit that not only is removal of age and time from the risk prediction equations not necessary, but, to the contrary, such removal may be inappropriate. Furthermore, as we demonstrate below, the objectives desired by Ridker and Cook are already available with the existing prediction algorithms and often have been incorporated into the standard use of the current guidelines. See p 657 Before we proceed, it would be useful to summarize the observations made by Ridker and Cook. First, they point out the possibility that young individuals with multiple risk factors and very low short-term CHD risk but a much higher lifetime CHD risk (patient example 1 in their article) may not be targeted …

Target value of intraabdominal fat area for improving coronary heart disease risk factors.

The goal of this study was to determine an intraabdominal fat (IF) area target value for improving coronary heart disease (CHD) risk factors in response to weight reduction. Subjects were 279 obese Japanese women, 21 to 66 years old, who were divided into diet-alone and diet-plus-exercise groups and participated in a 14-week weight reduction program. The IF area was measured by computerized tomography scans. Systolic blood pressure > or = 140 mm Hg, diastolic blood pressure > or = 90 mm Hg, total cholesterol > or = 5.70 mM, triglycerides > or = 1.70 mM, and fasting plasma glucose > or = 6.99 mM were defined as CHD risk factors. The best trade-off between sensitivity (probability of correctly detecting true positive) and specificity (probability of correctly detecting true negative) was found at 100 cm2 pretreatment in combined data of the two groups. At posttreatment, although a slight difference was found in the target value between the treatment groups (60 cm2 for diet alone and 50 cm2 for diet plus exercise), the combined data showed that the best trade-off occurred at 60 cm2 (sensitivity and specificity were 0.55 and 0.63, respectively). The percentage of subjects having no CHD risk factors was significantly lower in the group that had large IF areas (> or = 60 cm2) (46%) compared with the group that had normal IF areas (<60 cm2) (65%). However, the percentage of subjects having multiple CHD risk factors was significantly greater in the group that had large IF areas (16%) compared with the group with normal IF areas (7%) at posttreatment. Our longitudinal data suggest that obese Japanese women should reduce their IF areas to < 60 cm2 through weight reduction to improve CHD risk factors independent of treatment.

Clinical aspects of endothelial dysfunction associated with human immunodeficiency virus infection and antiretroviral agents.

Endothelial dysfunction is a critical initial step of atherogenesis that subsequently contributes to the progression and clinical manifestations of atherosclerosis. The use of human immunodeficiency virus type 1 (HIV-1) protease inhibitor (PI) agents has been associated with increased cardiovascular events and worsening of multiple coronary heart disease risk factors including dys-lipidemia, insulin resistance, and endothelial dysfunction. Endothelial dysfunction may be caused by HIV infection itself as well as treatment-related effects of the antiretroviral agents used to treat HIV. The available evidence suggests that PIs may induce endothelial dysfunction via their effects on both lipid and glucose metabolism. Studies in healthy subjects confirm a role for reduced endothelial nitric oxide production in the endothelial dysfunction associated with the PI indinavir. Further work is needed to determine the relative tendencies of other antiretroviral agents to induce endothelial dysfunction, the physiologic mechanisms involved, and the contribution of the metabolic and body shape changes associated with HIV treatment-related lipodystrophy, and to establish effective interventions for endothelial dysfunction in HIV-infected patients.

Multiple lipoprotein abnormalities associated with insulin resistance in healthy volunteers are identified by the vertical auto profile-II methodology.

The lipoprotein abnormalities first associated with insulin resistance (IR) and compensatory hyperinsulinemia were high plasma triglyceride (TG) and low HDL-cholesterol (HDL-C) concentrations (1)(2). It is now known that the characteristic IR-associated dyslipidemia also includes a shift to smaller, denser LDL particles (pattern B), enhanced postprandial lipemia, and decreased concentration of the more buoyant HDL particle, HDL2 (3)(4)(5). Recently, the IR-associated lipoprotein abnormalities that increase risk of coronary heart disease (CHD) have continued to expand. In addition to high plasma TG and low HDL-C concentrations (6)(7), at least three classes of TG-rich lipoproteins are both atherogenic and associated with increased CHD risk, including intermediate density lipoprotein (IDL; a TG-rich remnant product derived from VLDL metabolism) (8)(9), VLDL3 (the dense VLDL subclass) (10)(11), and TG-rich chylomicron remnants (8)(12)(13). Despite awareness of the myriad IR-associated proatherogenic lipoprotein abnormalities (1)(2)(3)(4)(5)(14)(15)(16)(17), we are unaware of previous publications in which both IR and all relevant lipoproteins were quantified in the same cohort of individuals. This is likely partly attributable to the unavailability of analytical methods to measure multiple lipoprotein CHD risk factors in a clinically useful manner. However, the validated vertical auto profile-II (VAP-II) methodology (18) provides a means to comprehensively identify the IR-associated dyslipidemic profile, and we have used VAP-II to compare lipoprotein characteristics of nondiabetic individuals stratified into IR and insulin-sensitive (IS) groups. The Stanford University Human Subjects Committee approved this study, and healthy volunteers from the San Francisco Bay Area gave informed consent. Participants underwent medical interview, anthropometric measurements, and a physical examination. Exclusion criteria included fasting plasma glucose >7.0 mmol/L (126 mg/dL), total bilirubin >34 μmol/L (2.0 …

Baseline characteristics of participants in the Raloxifene Use for The Heart (RUTH) trial

The Raloxifene Use for The Heart (RUTH) trial is a randomized, placebo-controlled, double-blind trial designed to determine whether raloxifene 60 mg/day compared with placebo lowers the risk of coronary events (coronary death, nonfatal myocardial infarction [MI], or hospitalized acute coronary syndromes other than MI) and reduces the risk of invasive breast cancer in women at risk for a major coronary event. Raloxifene is a selective estrogen receptor modulator that improves cardiovascular risk factors, reduces the risk of vertebral fracture, and is associated with a reduced incidence of invasive breast cancer in postmenopausal women with osteoporosis. Between June 1998 and August 2000, 10,101 women were enrolled at 187 sites in 26 countries. Approximately half of the women had documented coronary heart disease (CHD) (n = 5,031); the remainder had multiple CHD risk factors that increased their risk for a CHD event (n = 5,070). The mean age of participants was 68 years (39% were >70 years old), and did not differ between those with documented CHD and those at increased CHD risk. Most women were Caucasian (84%); 60% had a body mass index ≥27 kg/m 2, 46% had diabetes mellitus, 78% had systemic hypertension, and 14% had low-density lipoprotein cholesterol >160 mg/dl. Compared with women at increased CHD risk, women with documented CHD had higher cardiovascular risk scores, a higher prevalence of abnormal electrocardiograms, greater use of cardiovascular medications, were more likely to have had cardiac rehabilitation, and were more likely to have previously used estrogen or oral contraceptives, but had a slightly lower prevalence of CHD risk factors such as smoking, obesity, diabetes mellitus, and systemic hypertension, and had lower serum levels of total and low-density lipoprotein cholesterol. The RUTH cohort is the largest group of postmenopausal women at increased risk of CHD events ever assembled in a clinical trial, and is the first trial designed to determine the effect of a selective estrogen receptor modulator on the risk of CHD events.

Multiple coronary risk factors in healthy older Kuwaiti males.

The objective was to examine the percentage and severity of obesity and some common biochemical coronary heart disease (CHD) risk factors in a sample of healthy Kuwaiti adult males > or =45 y of age. We also sought to determine the percentage of males at increased risk due to the presence of multiple CHD risk factors. The study was a cross-sectional study. The study was conducted in all men who underwent a mandatory job related physical examination or who sought to obtain retirement benefits. A total of 740 healthy Kuwaiti males between the ages of 45 to 80 y. In all, 37% of the men were obese, 26% had elevated glucose values and 52% had elevated or high cholesterol levels. Some had multiple risk factors for CHD, including age > or =45 y, obesity, male gender, hyperglycemia and hypercholesterolemia. Blood glucose values increased consistently from younger (45-54 y) to older age groups (55-64 and > or =65 y). Blood glucose values varied inversely with education level. In societies with relatively uniform income levels, educational level may be a better indicator of chronic disease risk than income per se. These results, showing a high percentage of men with several risk factors and high mean values, suggesting more severe risk, suggest that immediate action should be taken to develop a public health intervention strategy to educate Kuwaiti men to become aware of the causes and correlates of CHD and how to decrease their risk for CHD and heart attack, the leading cause of death in Kuwait.

Effect of a multimodality natural medicine program on carotid atherosclerosis in older subjects: a pilot trial of Maharishi Vedic Medicine

Although the onset and progression of coronary heart disease (CHD) involve multiple risk factors, few intervention studies have attempted to modify these factors simultaneously. This pilot study tested the effect of a multimodality intervention involving dietary, exercise, herbal food supplement, and stress reduction approaches from a traditional system of natural medicine, Maharishi Vedic Medicine (MVM). The primary outcome measure was carotid intima-media thickness (IMT), a noninvasive measure of peripheral atherosclerosis and surrogate measure of coronary atherosclerosis. Comparison groups included modern medicine (conventional dietary, exercise, and multivitamin approaches) and usual care (no added intervention). Of 57 healthy seniors (mean age 74 years) randomized to the 3 treatment groups, 46 completed IMT post-testing. Carotid IMT was determined by B-mode ultrasound before and after 1 year of treatment. IMT decreased in a larger fraction of MVM subjects (16 of 20) than in the modern (5 of 9) and usual care (7 of 14) groups combined (i.e., 12 of 23; odds ratio 3.7, p = 0.05). For subjects with multiple CHD risk factors (“high-risk” subjects, n = 15), IMT decreased more in the MVM (−0.32 ± 0.23 mm, mean ± SD) than in the usual care (+0.022 ± 0.085; p = 0.009) or modern (−0.082 ± 0.095, p = 0.10) groups. Within-group reductions in IMT were significant for all MVM subjects (−0.15 ± 0.21, n = 20, p = 0.004) and for high-risk MVM subjects (n = 6, p = 0.01). These results show that this multimodality traditional approach can attenuate atherosclerosis in older subjects, particularly those with marked CHD risk.

National cholesterol education program keeps a priority on lifestyle modification to decrease cardiovascular disease risk.

The National Cholesterol Education Program's updated third Adult Treatment Panel report on clinical guidelines for cholesterol testing and management adds to the base of knowledge provided by two previous Adult Treatment Panel reports. Similar to the other reports, it has distinctive features and goals that are in accord with the most currently available clinical trial evidence. The major new feature of the third report is a focus on primary prevention of coronary heart disease in persons with multiple coronary heart disease risk factors. The guidelines provide the rationale for intensive cholesterol-lowering therapy in clinical management, and they provide detailed information to help inform clinical judgment for implementation of both medical nutrition management (therapeutic lifestyle changes) and drug therapy for treatment of high blood cholesterol.