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CHD Risk (chd + risk)
Terms modified by CHD Risk Selected AbstractsImpact of substance use on the physical health of patients with bipolar disorderACTA PSYCHIATRICA SCANDINAVICA, Issue 6 2010M. P. Garcia-Portilla Garcia-Portilla MP, Saiz PA, Benabarre A, Florez G, Bascaran MT, Díaz EM, Bousoño M, Bobes J. Impact of substance use on the physical health of patients with bipolar disorder. Objective:, To describe the impact of tobacco, alcohol and cannabis on metabolic profile and cardiovascular risk in bipolar patients. Method:, Naturalistic, cross-sectional, multicenter Spanish study. Current use of tobacco, alcohol and cannabis was determined based on patient self-reports. Metabolic syndrome was defined using the National Health and Nutrition Examination Survey 1999,2000 and the American Heart Association/National Heart, Lung and Blood Institute criteria, and cardiovascular risk using the Framingham and the Systematic Coronary Risk Evaluation functions. Results:, Mean age was 46.6 years, 49% were male. Substance use: 51% tobacco, 13% alcohol and 12.5% cannabis. Patients who reported consuming any substance were significantly younger and a higher proportion was male. After controlling for confounding factors, tobacco was a risk factor for coronary heart disease (CHD) (unstandardized linear regression coefficient 3.47, 95% confidence interval 1.85,5.10). Conclusion:, Substance use, mainly tobacco, was common in bipolar patients. Tobacco use negatively impacted CHD risk. [source] Predicting CHD risk in patients with diabetes mellitusDIABETIC MEDICINE, Issue 5 2001W. W. Yeo First page of article [source] One-year changes in glucose and heart disease risk factors among participants in the WISEWOMAN programmeEUROPEAN DIABETES NURSING, Issue 2 2007JC Will PhD Abstract Background: WISEWOMAN provides chronic disease risk factor screening, referrals and lifestyle interventions to low-income, uninsured women, to reduce their heart disease and stroke risk. Participants learn behaviour-changing skills tailored to low-income populations, such as collaborative goal setting, the need to take small steps and other empowerment techniques. Aim: To quantify the baseline prevalence of pre-diabetes (fasting blood glucose 5.5,6.9 mmol/l) and diabetes among WISEWOMAN participants and assess one-year changes in glucose levels and other diabetes risk factors. Methods: We used 1998,2005 baseline and one-year follow-up data from WISEWOMAN participants. Using a multilevel regression model, we assessed one-year changes in glucose, blood pressure (BP), total cholesterol and 10-year risk of coronary heart disease (CHD) among participants with baseline pre-diabetes (n=688) or diabetes (n=338). Results: At baseline, 15% of participants had pre-diabetes and 10% had diabetes. Of those with diabetes, 26% were unaware of their condition before baseline screening. During the one-year follow-up period, participants with pre-diabetes experienced statistically significant improvements in glucose (2.9%) and cholesterol (2.1%) levels and 10-year CHD risk (4.3%). Participants with newly diagnosed diabetes experienced statistically significant improvements in glucose (11.5%), BP (3.1%,3.5%) and cholesterol (6.4%) levels. Participants with previously diagnosed diabetes experienced significant improvements in BP (1.9%,3.4%), cholesterol level (3.8%), and 10-year CHD risk (8.5%). Conclusions: Implementing patient-centered, comprehensive and multilevel interventions and demonstrating their effectiveness will likely lead to the adoption of this approach on a much broader scale. [source] Individuals at increased coronary heart disease risk are characterized by an impaired microvascular function in skinEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2003R. G. IJzerman Abstract Background To investigate whether microvascular function in skin is a valid model to study the relationships between cardiovascular risk factors and microvascular function, we investigated skin microvascular function in individuals with increased coronary heart disease (CHD) risk. Materials and methods Forty-six healthy White individuals aged 30,70 years were studied. Coronary heart disease risk was assessed with the use of the CHD risk score according to the Framingham Heart Study, which is based on the risk factors age, blood pressure, cigarette smoking, total cholesterol, HDL cholesterol and diabetes. Endothelium-dependent and -independent vasodilation in skin were evaluated with laser Doppler after iontophoresis of acetylcholine and sodium nitroprusside. Videomicroscopy was used to measure recruitment of skin capillaries after arterial occlusion. Results Coronary heart disease risk score (i.e. the 10-year probability of CHD) varied from 1,37%. Microvascular function decreased with increasing quartiles of CHD risk (for acetylcholine-mediated vasodilation: 687, 585, 420 and 326%, P = 0·002; for nitroprusside-mediated vasodilation: 776, 582, 513 and 366%, P = 0·02; for capillary recruitment: 49·9, 44·6, 27·2 and 26·7%, P = 0·001). These trends were similar in men and women (P for interaction > 0·2) and independent of body mass index. Conclusions Increased CHD risk is associated with an impaired endothelium-dependent vasodilatation and capillary recruitment in skin, suggesting that microvascular function in skin is a valid model to study the relationships between cardiovascular risk factors and microvascular function. [source] Paraoxonase activity in two healthy populations with differing rates of coronary heart diseaseEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2000Mackness Background The rate of coronary heart disease is over three-fold greater in Belfast than in Toulouse and the excess risk cannot be totally explained by ,classical' risk factors such as total cholesterol, LDL-cholesterol, smoking, etc. Design The effect of the human serum paraoxonase (PON1) 192-genetic polymorphism on plasma lipid and lipoprotein concentrations and on PON1 activity and concentration was investigated in 186 randomly selected healthy subjects from Toulouse and 165 from Belfast. Results The frequency of the R allele of PON1, which has been related to the risk of coronary heart disease, was significantly higher in Belfast (0.33) than in Toulouse (0.24; ,2 = 7.229, P = 0.0072). Subjects from Belfast also had significantly higher serum cholesterol, triglycerides, LDL-cholesterol, and apolipoprotein B, and significantly lower HDL-cholesterol and apolipoprotein A1, but these lipoprotein parameters were independent of the PON1 192-polymorphisms. PON1 activity towards paraoxon was significantly higher in the Belfast population than in Toulouse (median values: 179.7 vs. 129.4 nmol min,1 mL,1 serum, respectively; P < 0.05), which is consistent with our finding of a greater prevalence of the R allele. The median serum concentration of PON1 was 56.3 ,g mL,1 in Belfast, which was significantly lower (P < 0.005) than the level of 71 ,g mL,1 in Toulouse. Conclusions Our results thus provide further support for the hypothesis that populations at increased CHD risk have diminished serum PON1 concentration and an increased prevalence of the R allele of PON1. They are also consistent with reports that the ability of PON1 to hydrolyse paraoxon is inversely related to its capacity to hydrolyse lipid-peroxides, and thus to its antiatherogenic action. [source] Plasma antioxidative activity during atorvastatin and fluvastatin therapy used in coronary heart disease primary preventionFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 1 2004Jan Kowalski Abstract We estimated the effect of atorvastatin and fluvastatin on plasma antioxidative activity used in coronary heart disease (CHD) primary prevention. Anti-oxidative activity of blood plasma was determined by Bartosz et al. method [Curr. Top. Biophys. (1998)22:11,13], based on reduction of preformed cation radical of 2,2,azinobis(3-ethylbenzothiazoline-6-sulphonic acid) by blood plasma. The study comprised 35 patients with CHD risk who were randomly divided into two groups. The atorvastatin group comprised 17 patients who were administered the drug orally in a daily dose of 10 mg and the fluvastatin group consisted of 18 patients on an oral dose of 40 mg once daily. The control group comprised 12 healthy subjects with no drug administration. Blood samples were collected from cubital vein before and after 6-week therapy. Significantly (P < 0.05) increased , in comparison with the initial values , antioxidative activity of blood plasma was found in atorvastatin and fluvastatin groups after 6-week therapy. Moreover, the increase in antioxidative plasma activity in atorvastatin group was significantly higher in comparison with the fluvastatin group. The results of our study have demonstrated that atorvastatin and fluvastatin have an additional mechanism independent of the effect on cholesterol concentration. Thus, we presume that administration of these statins in CHD risk patients may have a beneficial effect. [source] Prevalence of risk factors for cardiovascular disease in HIV-infected patients over time: the Swiss HIV Cohort StudyHIV MEDICINE, Issue 6 2006TR Glass Objective Metabolic changes caused by antiretroviral therapy (ART) may increase the risk of coronary heart disease (CHD). We evaluated changes in the prevalence of cardiovascular risk factors (CVRFs) and 10-year risk of CHD in a large cohort of HIV-infected individuals. Methods All individuals from the Swiss HIV Cohort Study (SHCS) who completed at least one CVRF questionnaire and for whom laboratory data were available for the period February 2000 to February 2006 were included in the analysis. The presence of a risk factor was determined using cut-offs based on the guidelines of the National Cholesterol Education Program (NCEP ATP III), the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7), the American Diabetes Association, and the Swiss Society for Cardiology. Results Overall, 8033 individuals completed at least one CVRF questionnaire. The most common CVRFs in the first completed questionnaire were smoking (57.0%), low high-density lipoprotein (HDL) cholesterol (37.2%), high triglycerides (35.7%), and high blood pressure (26.1%). In total, 2.7 and 13.8% of patients were categorized as being at high (>20%) and moderate (10,20%) 10-year risk for CHD, respectively. Over 6 years the percentage of smokers decreased from 61.4 to 47.6% and the percentage of individuals with total cholesterol >6.2 mmol/L decreased from 21.1 to 12.3%. The prevalence of CVRFs and CHD risk was higher in patients currently on ART than in either pretreated or ART-naive patients. Conclusion During the 6-year observation period, the prevalence of CVRFs remains high in the SHCS. Time trends indicate a decrease in the percentage of smokers and individuals with high cholesterol. [source] Cardiovascular risk evaluation and antiretroviral therapy effects in an HIV cohort: implications for clinical management: the CREATE 1 studyINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2010M. Aboud Summary Aims:, The aim of this study is to determine the cardiovascular disease (CVD) risk profile of a large UK HIV cohort and how highly active antiretroviral therapy (HAART) affects this. Methods:, It is a cross-sectional study within a large inner city hospital and neighbouring district hospital. A total of 1021 HIV positive outpatients representative of the complete cohort and 990 who had no previous CVD were included in CVD risk analysis. We recorded demographics, HAART history and CVD risk factors. CVD and coronary heart disease (CHD) risks were calculated using the Framingham (1991) algorithm adjusted for family history. Results:, The non-CVD cohort (n = 990) was 74% men, 51% Caucasian and 73.1% were on HAART. Mean age was 41 ± 9 years, systolic blood pressure 120 ± 14 mmHg, total cholesterol 4.70 ± 1.05mmol/l, high-density lipoprotein-C 1.32 ± 0.48 mmol/l and 37% smoked. Median CVD risk was 4 (0,56) % in men and 1.4 (0,37) % in women; CHD risks were 3.5 (0,36) % and 0.6 (0,16) %. CVD risk was > 20% in 6% of men and 1% of women and > 10% in 12% of men and 4% of women. CVD risk was higher in Caucasians than other ethnicities; the risk factor contributing most was raised cholesterol. For patients on their first HAART, increased CHD risk (26.2% vs. 6.5%; odds ratio 4.03, p < 0.001) was strongly related to the duration of therapy. Conclusions:, Modifiable risk factors, especially cholesterol, and also duration of HAART, were key determinants of CVD risk. Discussion:, Regular CHD and/or CVD risk assessment should be performed on patients with HIV, especially during HAART therapy. The effect of different HAART regimens on CHD risk should be considered when selecting therapy. [source] Prospective Association Between Low and High Total and Low-Density Lipoprotein Cholesterol and Coronary Heart Disease in Elderly MenJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 12 2004J. David Curb MD Objectives: To examine the relationship between total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) and the incidence of coronary heart disease (CHD) in elderly men. Design: Prospective. Setting: Population based. Participants: A sample of 2,424, Japanese-American men aged 71 to 93 was used. Measurements: Six years of data on incident fatal plus nonfatal CHD were examined. Results: Analysis revealed a significant U-shaped relationship between age-adjusted CHD rates and both TC and LDL-C. The ranges of TC and LDL-C with the lowest risk of CHD were 200 to 219 mg/dL and 120 to 139 mg/dL, respectively. As cholesterol concentrations declined and increased beyond these ranges, the risk of CHD increased. These U-shaped relationships remained significant after adjusting for age and other risk factors. Conclusion: The U-shaped associations between TC and LDL-C and CHD imply a complex relationship between lipids and CHD in late life. The results indicate that elevated lipid levels should continue to be treated in healthy elderly individuals, as they are in those who are younger, although pharmacologically lowering lipids to excessively low levels in the elderly may warrant further study, as does the contribution of subclinical frailty to the relationship of lipids to CHD risk. [source] Risk factors for coronary heart disease in 55- and 35-year-old men and women in Sweden and EstoniaJOURNAL OF INTERNAL MEDICINE, Issue 6 2002J. Johansson Abstract., Johansson J, Viigimaa M, Jensen-Urstad M, Krakau I I, Hansson L-O (Karolinska Hospital, Stockholm, Sweden, Tartu University Hospital, Tartu, Estonia). Risk factors for coronary heart disease in 55- and 35-year-old men and women in Sweden and Estonia. J Intern Med 2002; 252:551,560. Objective., To illustrate the geographical West-to-East division of coronary heart disease (CHD) by comparing a population from Sweden, that represents a Western country to a population from Estonia, that represents an Eastern country. Estonia has an approximately 2,4-fold higher CHD prevalence for 55-year-old women and men, respectively, than Sweden. Design., Randomized screening of 35- and 55-year-old men and women in Sollentuna county, Sweden and Tartu county, Estonia. Eight hundred subjects, 100 from each cohort, were invited to participate in the study, 272 Swedes and 277 Estonians participated. Setting., Preventive cardiology, administered by a primary health care centre at the Karolinska Hospital, Sweden and a cardiology centre at Tartu University Hospital, Estonia. Main outcome measures., The CHD risk factors (smoking, blood pressure, concentrations of lipoproteins, fibrinogen, and glucose) and certain environmental factors and attitudes related to CHD risk by questionnaires (fat-type and alcohol ingestion, self-assessed rating of CHD susceptibility). Results., Of the 55-year-old men, 57% smoked in Estonia and 20% smoked in Sweden. Similar, although less pronounced differences showing higher smoking prevalence, were seen for 35-year-old Estonian men and women, whilst for 55-year-old women, less than 20% smoked in either country. Estonian 55-year-old women had lower HDL cholesterol and higher LDL cholesterol serum concentrations than Swedish 55-year-old women. Estonians reportedly ate food containing more saturated fats than Swedes, as indicated by the scale-score questionnaire. Estonians, relative to Swedes, rated their chance of developing CHD higher, and paradoxically, Estonians did to a much lesser degree believe that life style influences the risk of developing CHD. Conclusions., Elevated smoking prevalence is a striking difference between the Estonian and Swedish populations likely to explain the much higher CHD prevalence in Estonian men. The lower HDL cholesterol and higher LDL cholesterol in Estonian 55-year-old women may explain the higher CHD prevalence in Estonian women. Furthermore, the SWESTONIA CHD study (i.e. comparison between Sweden and Estonia) shows several environmental differences between the countries populations related to fat content in food, alcohol drinking patterns, and views on CHD risk and the importance of lifestyle intervention, that could contribute to the higher CHD prevalence in Estonia. [source] Low-fat diets, triglycerides and coronary heart disease riskNUTRITION BULLETIN, Issue 1 2000Helen M. Roche Summary Nutritionists are currently debating whether low-fat high-carbohydrate diets protect against coronary heart disease (CHD). Traditionally, low-fat diets were prescribed because they reduce plasma and low density lipoprotein (LDL) cholesterol concentrations. However, there is considerable concern because low-fat diets also increase plasma triglyceride (TG) and reduce high density lipoprotein (HDL) cholesterol concentrations. Recent prospective epidemiological studies have shown that these are independent risk factors for future CHD risk. It has been proposed that the adverse effects of low-fat, high-carbohydrate diets on TG and HDL may counteract or negate the beneficial effect of reducing LDL cholesterol concentrations. Although there is also strong epidemiological evidence that reduced total fat intake is not protective against CHD, high-fat diets predispose to obesity and insulin resistance, both of which adversely affect TG metabolism. This review presents the evidence in relation to the importance of TG as a risk factor for CHD, and explains the pathophysiology that may underlie the aetiological role of TG metabolism in the pathogenesis and progression of CHD. It also addresses the physiological consequences of advocating low-fat high-carbohydrate diets, with particular reference to the effects on lipoprotein metabolism and CHD risk. [source] Plasma Concentrations of Plant Sterols: Physiology and Relationship with Coronary Heart DiseaseNUTRITION REVIEWS, Issue 9 2006Yen-Ming Chan MSc Recently, it has been questioned whether elevated levels of circulating plant sterols increase the risk of coronary heart disease (CHD). To date, no definitive conclusions regarding such a relationship have been reached, nor have there been any studies summarizing the factors that contribute to the observed elevations in plant sterol concentrations in plasma. Thus, the purpose of this review is to systematically compare the plant sterol levels of subjects from the general population and to describe factors that contribute to the variations observed. The question of whether elevated plasma concentrations of plant sterols are associated with an increased risk of CHD was also assessed. Results indicate that the key factors accounting for variations in circulating plant sterol concentrations include: apolipoprotein E phenotypes, ATP-binding cassette transporter polymorphisms, use of statin drugs, presence of metabolic syndrome, dietary intake of plant sterols, gender, and analytical techniques used in the measurement of plant sterols in the plasma. An analysis of the studies examining the relationship between circulating levels of plant sterols and CHD risk in non-sitosterolemic populations revealed no clear associations. Furthermore, it was shown that the above-mentioned factors play an important role in determining the levels of plant sterols in plasma. Since these factors may act as potential confounders, they must be controlled for before more solid conclusions can be reached. [source] The association between effort,reward imbalance and coronary atherosclerosis in a Chinese sampleAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 7 2010Weixian Xu MD Abstract Background Previous studies of job strain and coronary heart disease (CHD) have produced mixed findings. We aimed to examine the association between job stress evaluated by the effort,reward imbalance (ERI) model and coronary atherosclerosis assessed by coronary angiography in a Chinese sample. Methods Three-hundred twenty participants accepting coronary angiography for the first time were enrolled in series. Job stressors were evaluated by the ERI model. The presence and severity of CHD were assessed by measuring the coronary artery stenosis (the presence of >50% luminal stenosis in one or more major coronary arteries). The association between job stressors and CHD was examined by multivariate analysis. Results Compared with the low-level group, high-level effort, overcommitment, and ERI increased CHD risk with odds ratio (OR) 2.5 (95% confidence interval (CI): 1.2,5.0), 2.5 (95% CI: 1.2,5.0), 2.4 (95% CI: 1.2,4.9), respectively, after adjustment for confounders. They were also significantly positively correlated with the complexity of coronary artery lesions, respectively. Dose,response relationships were observed. Conclusions ERI was associated with coronary artery lesions in a sample of Chinese workers. Longitudinal research and interventional designs are needed to confirm the mechanism and to provide evidence for the prevention of CHD. Am. J. Ind. Med. 53:655,661, 2010. © 2010 Wiley-Liss, Inc. [source] Is it effective to target treatment using just calculated CHD risk?PRESCRIBER, Issue 14 2010FRCPath, Tim Reynolds BSc Statin prescribing for the primary prevention of CHD is based on risk calculated from long-term population data. Here, the author discusses the issues with the current risk models and suggests that money could be better spent on improved targeting through the use of a diagnostic test. Copyright © 2010 Wiley Interface Ltd [source] Social stress, visceral obesity, and coronary artery atherosclerosis: product of a primate adaptationAMERICAN JOURNAL OF PRIMATOLOGY, Issue 9 2009Carol A. Shively Abstract Abdominal obesity is prevalent and often accompanied by an array of metabolic perturbations including elevated blood pressure, dyslipidemia, impaired glucose tolerance or insulin resistance, a prothrombotic state, and a proinflammatory state, together referred to as the metabolic syndrome. The metabolic syndrome greatly increases coronary heart disease (CHD) risk. Social stress also increases CHD although the mechanisms through which this occurs are not completely understood. Chronic stress may result in sustained glucocorticoid production, which is thought to promote visceral obesity. Thus, one hypothesis is that social stress may cause visceral fat deposition and the metabolic syndrome, which, in turn increases CHD. CHD is caused by coronary artery atherosclerosis (CAA) and its sequelae. Cynomolgus monkeys (Macaca fascicularis) are a well-established models of CAA. Social subordination may be stressful to cynomolgus monkeys and result in hypercortisolemia and exacerbated CAA in females. Herein is reviewed a body of literature which suggests that social stress increases visceral fat deposition in cynomolgus monkeys, that subordinate females are more likely than dominants to have visceral obesity, that females with visceral obesity have behavioral and physiological characteristics consistent with a stressed state, and that females with high ratios of visceral to subcutaneous abdominal fat develop more CAA. While these relationships have been most extensively studied in cynomolgus macaques, obesity-related metabolic disturbances are also observed in other primate species. Taken together, these observations support the view that the current obesity epidemic is the result of a primate adaptation involving the coevolution with encephalization of elaborate physiological systems to protect against starvation and defend stored body fat in order to feed a large and metabolically demanding brain. Social stress may be engaging these same physiological systems, increasing the visceral deposition of fat and its sequelae, which increase CHD risk. Am. J. Primatol. 71:742,751, 2009. © 2009 Wiley-Liss, Inc. [source] The A370T Variant (StuI Polymorphism) in the LDL Receptor Gene is not Associated with Plasma Lipid Levels or Cardiovascular Risk in UK MenANNALS OF HUMAN GENETICS, Issue 6 2006José Ricardo S. Vieira Summary Over 800 different missense mutations in the low density lipoprotein (LDL) receptor gene (LDLR) have been identified in patients with familial hypercholesterolaemia (FH). Only two of them, including the Alanine to Threonine change at position 370 (A370T), have been discovered in FH patients but do not cause FH. The frequency of the 370T allele has been reported worldwide to be between 0.022 and 0.070, with no clear association with high cholesterol levels or risk for coronary heart disease (CHD) and stroke. To explore this relationship in more detail we have determined this genotype in 2,659 healthy middle-aged (50,61 years) men participating in the prospective Second Northwick Park Heart Study, with 236 CHD and 67 stroke incident events. The genotype distribution was in Hardy-Weinberg equilibrium and in the no-event group the frequency of 370T was 0.046 (95% CI 0.040,0.052). Overall, there was no significant association of the 370T allele with any measured plasma lipid trait, and there was no difference in genotype distribution or allele frequency between the no-event and CHD (0.059; 95% CI 0.040,0.085) or stroke (0.037; 95% CI 0.012,0.085) groups ( p= 0.18 and 0.65, respectively). There was evidence for significant interaction ( p= 0.006) between body mass index (BMI) and genotype on CHD risk, with 370A homozygotes showing the expected higher CHD risk for those with higher BMI, whilst risk for 370T allele carriers was highest in men in the lowest tertile of BMI. The explanation for this association is unclear, and may simply be chance. Thus, these data confirm the absence of a significant impact of the A370T polymorphism on LDL receptor function, at least as measured by the effect on plasma lipid levels and CHD risk. [source] Interaction between smoking and the stromelysin-1 (MMP3) gene 5A/6A promoter polymorphism and risk of coronary heart disease in healthy menANNALS OF HUMAN GENETICS, Issue 5-6 2002S. E. HUMPHRIES Smoking is a major risk factor for coronary heart disease (CHD), but this risk may be modified by an individual's genotype. A common functional 5A/6A polymorphism in the promoter of the stromelysin-1 (matrix metalloproteinase 3, MMP3) gene has been identified. The 6A allele has been consistently associated with faster progression of angiographically determined CHD, while the 5A allele has recently been associated with risk of acute myocardial infarction (MI) in patients with unstable angina. To date there has been no prospective study of the relationship of this genotype to CHD risk in smokers and non-smokers. DNA was available from 2743 middle-aged men, free of CHD at baseline, recruited through nine general practices in the UK for prospective surveillance. To date there have been almost 24000 person-years of follow-up with 125 CHD events (fatal and non-fatal MI, sudden coronary death, need for coronary artery surgery or new major ECG Q-wave abnormality). Men with events were each matched for age, practice and cholesterol level with three healthy men. Smoking habit was determined by questionnaire. 5A/6A genotype was determined using a heteroduplex generator method. Associations between genotype and disease outcome, according to smoking status, were assessed using conditional logistic regression. Overall, current smoking was associated with a relative risk (RR) of 1.99 (95% CI 1.30,3.06) as compared with never-smokers and ex-smokers combined (p<0.002). In non-smoking men, and after adjustment for conventional risk factors, compared with the 5A5A group, the RR was 1.37 (0.64,2.94) in those with the genotype 5A6A and 3.02 (1.38,6.61) in those with the genotype 6A6A. Smoking increased risk 1.4 fold in the 5A6A group to 1.91 (1.84,4.36), by 1.3 fold in the 6A6A group to 4.01 (1.57,10.24), but by 3.81 fold (1.54,9.40) in the 5A5A group (smoking,genotype interaction p = 0.01). The data indicate a key role for stromelysin in the atherosclerotic process. Men with the stromelysin genotype 5A5A represent 29% of the general population, and their high risk, if smokers, provides a further strong argument for smoking avoidance. [source] EFFECT OF A SOYBEAN PRODUCT ON SERUM LIPID LEVELS IN FEMALE UNIVERSITY STUDENTSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2004Kyoko Takahashi SUMMARY 1.,A dietary intervention study targeting female students by using cake containing soybean protein and isoflavone was conducted. Female students (n = 120) were divided into three Groups (A, 6.26 g of soybean protein and isoflavone at 50 mg/day; B, 1.36 g soybean protein and isoflavone 50 mg; and C, a wheat puff as placebo). Intervention period was 4 weeks. The ratio of hypercholesterol in each group indicated a high value; A: 25%, B: 17.9% and C: 24.4%. 2.,Total cholesterol as well as the rate of hypercholesterolemia decreased in Group A. The average total cholesterol significantly reduced (P < 0.001) from 242 ± 17 to 220 ± 25 mg/dL in Group A. 3.,Dietary intake of soy protein for 4 weeks could be effective in reducing CHD risk among Japanese female students with a high plasma cholesterol level. [source] Epidemiology and burden of cardiovascular diseaseCLINICAL CARDIOLOGY, Issue S3 2004Laurence O. Watkins M.D., M.P.H. Coronary heart disease (CHD) is the leading cause of death in the United States. The rate of CHD and CHD death varies across racial groups, with higher rates among black men and women than among white men and women. The development of CHD is promoted by major CHD risk factors,dyslipidemia, hypertension, and smoking. These risk factors are independently associated with CHD risk and are common among adults in the United States. Diabetes mellitus is also a significant contributor to CHD risk and is associated with risk of a CHD event equivalent to that conferred by the presence of prior CHD. Metabolic syndrome, a related condition, also confers a high risk for CHD as well as for the development of type 2 diabetes. Diabetes and metabolic syndrome are characterized by the presence of central obesity and insulin resistance, which result in dyslipidemia, hypertension, and cardiovascular derangements that promote CHD. Diabetes and metabolic syndrome illustrate the significance of risk factor clustering, which contributes to CHD risk through the additive effect of each risk factor. Diabetes, metabolic syndrome, and risk factor clustering in general are becoming more prevalent, which illustrates the need for better CHD prevention strategies aimed at risk factor control. The pathologic process associated with risk factor clustering also contributes to the higher CHD burden among black men and women, who have a higher prevalence of risk factor clustering and type 2 diabetes. Furthermore, despite having a higher CHD risk, black men and women are less likely to receive adequate treatment or control of risk factors, including dyslipidemia or hypertension. Eliminating disparities among population groups will thus require aggressive efforts focused on risk assessment, guideline adherence, and risk factor control in populations in need. [source] Assessing coronary heart disease risk with traditional and novel risk factorsCLINICAL CARDIOLOGY, Issue S3 2004Peter W. F. Wilson M.D. Cardiovascular disease is the leading cause of death in the industrialized world, and a number of well-characterized factors, including advanced age, hypertension, dyslipidemia, diabetes, and smoking, contribute to cardiovascular risk. Integration of these factors using the Framingham calculation estimates the absolute 10-year risk for coronary heart disease (CHD), which can be used to guide therapy. Recent studies have demonstrated that additional markers, including elevated lipoprotein(a), homocysteine, sitosterol, and particularly C-reactive protein (CRP), are also associated with increased risk for CHD. In particular, high-sensitivity CRP has been shown to identify patients with high CHD risk who may not have elevated low-density lipoprotein cholesterol (LDL-C) and may add to the predictive value of the Framing-ham functions for CHD risk assessment. Assessment of global risk is particularly important in lipid management, as the LDL-C target goals are determined by risk category. [source] Cardiovascular risk evaluation and antiretroviral therapy effects in an HIV cohort: implications for clinical management: the CREATE 1 studyINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2010M. Aboud Summary Aims:, The aim of this study is to determine the cardiovascular disease (CVD) risk profile of a large UK HIV cohort and how highly active antiretroviral therapy (HAART) affects this. Methods:, It is a cross-sectional study within a large inner city hospital and neighbouring district hospital. A total of 1021 HIV positive outpatients representative of the complete cohort and 990 who had no previous CVD were included in CVD risk analysis. We recorded demographics, HAART history and CVD risk factors. CVD and coronary heart disease (CHD) risks were calculated using the Framingham (1991) algorithm adjusted for family history. Results:, The non-CVD cohort (n = 990) was 74% men, 51% Caucasian and 73.1% were on HAART. Mean age was 41 ± 9 years, systolic blood pressure 120 ± 14 mmHg, total cholesterol 4.70 ± 1.05mmol/l, high-density lipoprotein-C 1.32 ± 0.48 mmol/l and 37% smoked. Median CVD risk was 4 (0,56) % in men and 1.4 (0,37) % in women; CHD risks were 3.5 (0,36) % and 0.6 (0,16) %. CVD risk was > 20% in 6% of men and 1% of women and > 10% in 12% of men and 4% of women. CVD risk was higher in Caucasians than other ethnicities; the risk factor contributing most was raised cholesterol. For patients on their first HAART, increased CHD risk (26.2% vs. 6.5%; odds ratio 4.03, p < 0.001) was strongly related to the duration of therapy. Conclusions:, Modifiable risk factors, especially cholesterol, and also duration of HAART, were key determinants of CVD risk. Discussion:, Regular CHD and/or CVD risk assessment should be performed on patients with HIV, especially during HAART therapy. The effect of different HAART regimens on CHD risk should be considered when selecting therapy. [source] | ||||||||||||||||||||||||||||