Variation In Coronary Heart Disease Research Articles

The contribution of diet and lifestyle to socioeconomic inequalities in cardiovascular morbidity and mortality

BackgroundThe role of differences in diet on the relationship between socioeconomic factors and cardiovascular diseases remains unclear. We studied the contribution of diet and other lifestyle factors to the explanation of socioeconomic inequalities in cardiovascular diseases. MethodsWe prospectively examined the incidence of coronary heart disease (CHD) and stroke events amongst 33,106 adults of the EPIC-NL cohort. Education and employment status indicated socioeconomic status. We used Cox proportional models to estimate hazard ratios ((HR (95% confidence intervals)) for the association of socioeconomic factors with CHD and stroke and the contribution of diet and lifestyle. ResultsDuring 12years of follow-up, 1617 cases of CHD and 531 cases of stroke occurred. The risks of CHD and stroke were higher in lowest (HR=1.98 (1.67;2.35); HR=1.55 (1.15;2.10)) and lower (HR=1.50 (1.29;1.75); HR=1.42 (1.08;1.86)) educated groups than in the highest. Unemployed and retired subjects more often suffered from CHD (HR=1.37 (1.19;1.58); HR=1.20 (1.05;1.37), respectively), but not from stroke, than the employed. Diet and lifestyle, mainly smoking and alcohol, explained more than 70% of the educational differences in CHD and stroke and 65% of employment status variation in CHD. Diet explained more than other lifestyle factors of educational and employment status differences in CHD and stroke (36% to 67% vs. 9% to 27%). ConclusionThe socioeconomic distribution of diet, smoking and alcohol consumption largely explained the inequalities in CHD and stroke in the Netherlands. These findings need to be considered when developing policies to reduce socioeconomic inequalities in cardiovascular diseases.

Contribution of Climate and Air Pollution to Variation in Coronary Heart Disease Mortality Rates in England

There are substantial geographic variations in coronary heart disease (CHD) mortality rates in England that may in part be due to differences in climate and air pollution. An ecological cross-sectional multi-level analysis of male and female CHD mortality rates in all wards in England (1999–2004) was conducted to estimate the relative strength of the association between CHD mortality rates and three aspects of the physical environment - temperature, hours of sunshine and air quality. Models were adjusted for deprivation, an index measuring the healthiness of the lifestyle of populations, and urbanicity. In the fully adjusted model, air quality was not significantly associated with CHD mortality rates, but temperature and sunshine were both significantly negatively associated (p<0.05), suggesting that CHD mortality rates were higher in areas with lower average temperature and hours of sunshine. After adjustment for the unhealthy lifestyle of populations and deprivation, the climate variables explained at least 15% of large scale variation in CHD mortality rates. The results suggest that the climate has a small but significant independent association with CHD mortality rates in England.

Differences in coronary heart disease, stroke and cancer mortality rates between England, Wales, Scotland and Northern Ireland: the role of diet and nutrition

IntroductionIt is unclear how much of the geographical variation in coronary heart disease (CHD), stroke and cancer mortality rates within the UK is associated with diet. The aim of this...

Predicting Coronary Heart Disease after Kidney Transplantation: Patient Outcomes in Renal Transplantation (PORT) Study

Traditional risk factors do not adequately explain coronary heart disease (CHD) risk after kidney transplantation. We used a large, multicenter database to compare traditional and nontraditional CHD risk factors, and to develop risk-prediction equations for kidney transplant patients in standard clinical practice. We retrospectively assessed risk factors for CHD (acute myocardial infarction, coronary artery revascularization or sudden death) in 23,575 adult kidney transplant patients from 14 transplant centers worldwide. The CHD cumulative incidence was 3.1%, 5.2% and 7.6%, at 1, 3 and 5 years posttransplant, respectively. In separate Cox proportional hazards analyses of CHD in the first posttransplant year (predicted at time of transplant), and predicted within 3 years after a clinic visit occurring in posttransplant years 1-5, important risk factors included pretransplant diabetes, new onset posttransplant diabetes, prior pre- and posttransplant cardiovascular disease events, estimated glomerular filtration rate, delayed graft function, acute rejection, age, sex, race and duration of pretransplant end-stage kidney disease. The risk-prediction equations performed well, with the time-dependent c-statistic greater than 0.75. Traditional risk factors (e.g. hypertension, dyslipidemia and cigarette smoking) added little additional predictive value. Thus, transplant-related risk factors, particularly those linked to graft function, explain much of the variation in CHD after kidney transplantation.

Diagnostic Certainty as a Source of Medical Practice Variation in Coronary Heart Disease: Results from a Cross-National Experiment of Clinical Decision Making

The authors examined physician diagnostic certainty as one reason for cross-national medical practice variation. Data are from a factorial experiment conducted in the United States, the United Kingdom, and Germany, estimating 384 generalist physicians' diagnostic and treatment decisions for videotaped vignettes of actor patients depicting a presentation consistent with coronary heart disease (CHD). Despite identical vignette presentations, the authors observed significant differences across health care systems, with US physicians being the most certain and German physicians the least certain (P < 0.0001). Physicians were least certain of a CHD diagnoses when patients were younger and female (P < 0.0086), and there was additional variation by health care system (as represented by country) depending on patient age (P < 0.0100) and race (P < 0.0021). Certainty was positively correlated with several clinical actions, including test ordering, prescriptions, referrals to specialists, and time to follow-up.

Does surveillance impact on cardiovascular prevention?

Many epidemiological projects and clinical trials on determinants of atherosclerotic cardiovascular diseases (CVDs) have been conducted to identify risk factors and demonstrate the reversibility of risk through actions directed at their reduction, both in healthy subjects and in patients with established CVDs. At the international level, the Seven Countries Study identified risk factors common to different cultures, consistent for their importance, predictive power, and frequency among the general population.1 Smoking habit, and a rich diet with consequent high levels of total cholesterol and high blood pressure, were ascertained to be partly responsible for differences in the incidence of stroke and coronary heart disease (CHD) between countries.2,3 The WHO's European Collaborative Trial of the multifactorial prevention of CHD demonstrated the reversibility of risk among European populations, through healthier lifestyles and treatment of high risk subjects.4 To this extent the North Karelia Project represents the best example of community-based primary prevention.5 In all these studies, risk factors were carefully standardized and CVD incident events and deaths validated. The scenario may be different when evaluating whole countries. In fact in most industrialized countries CHD mortality has decreased since 1960, but in others it has increased. Time trends have been described for total cholesterol, smoking habit, blood pressure, and body mass index. However, the comparability of mortality and risk factors data was poor. The MONICA-WHO Project (Monitoring Trends and Determinants in Cardiovascular Disease) was the first multinational large-scale study specifically designed to understand the wide variations in CHD and stroke mortality among different countries, … *Corresponding author. Tel: +39 0432 554449, Fax: +39 0432 554448, Email: dichiara.antonio{at}aoud.sanita.fvg.it

Estimation of seasonal variations in risk factor profiles and mortality from coronary heart disease

Seasonal variations in coronary heart disease (CHD) and related risk factors have been reported previously. However, no studies to date quantify the contribution of seasonal variations in risk factors to actual mortality in both men and women using a single database of sufficient size and follow-up. We investigated the database from the Western Austrian Vorarlberg Health Monitoring and Promotion Programme (VHM&PP) including over 450,000 repeated measurements of 149,650 individuals between 1985 and 1999. Of a total of 1266 deaths from CHD (ICD-9 410-414), 353 deaths occurred between December and February (27.9%), in contrast to 275 (21.7%) between June and August. While the frequency of deaths through acute myocardial infarction (ICD-9 410) was similar over the seasons, chronic forms of CHD (ICD-9 414) occurred significantly (p < 0.001) more frequently in winter. Total cholesterol, blood pressure and body mass index showed pronounced seasonal variations with average levels significantly higher during the winter months in all age groups and both sexes, giving an estimated increase in score risk of 6.8% in men and 3.6% in women. However by contrast, use of single time point risk factor data tended to over-estimate subsequent 10 year mortality if measured in winter and the converse in summer. For the first time, this study quantifies the contribution of seasonal risk factor variation to CHD mortality. The consistent effect across demographic groups suggests that this is a real physiological phenomenon and not an artefact of living conditions. Interpretation of standard risk scores should take account of this seasonal fluctuation in subsequent investigation and follow-up.

The British Regional Heart Study 1975-2004.

During the early 1970s, mortality rates from coronary heart disease (CHD) were exceptionally high in the UK. A twofold regional variation existed with particularly high rates in South Wales, Northern England, Scotland, and Northern Ireland. There was considerable interest in the possibility that ‘soft’ drinking water was a risk factor for CHD and that variations in water hardness/softness across Britain might account for these geographical variations. Professor Gerry Shaper and colleagues submitted a 5-year proposal to the Medical Research Council: to examine the factors responsible for the considerable regional variation in coronary heart disease, hypertension, and stroke in Great Britain, and to determine the causes of these conditions in order to provide a rational basis for recommendations towards their prevention. This proposal embraced the water hardness hypothesis but extended the potential of the data collected to produce a more substantial and wider ranging enquiry into the causes of CHD both at the individual and the regional level: The British Regional Heart Study (BRHS).

Chronic Stress Accelerates Atherosclerosis in the Apolipoprotein E Deficient Mouse

Conventional cardiovascular risk factors such as cholesterol and blood pressure do not account fully for variation in coronary heart disease suggesting the involvement of additional mechanisms. We have examined the effects of a chronic psychological stress protocol on the development of atherosclerosis in the apolipoprotein E knockout mouse. We observed a 3-fold increase in staining for atheroma accompanied by a 10-fold increase in corticosterone concentrations in mice stressed for 12 weeks. These data suggest that chronic mild stress can induce or accelerate the development of atherosclerosis.

Effects of seasonal mood changes on seasonal variations in coronary heart disease: role of immune system, infection, and inflammation

Coronary heart disease shows a winter peak and summer trough in incidence and mortality. A substantial part of a general population experiences seasonal mood changes including winter depression. Many studies demonstrate that depression is associated with increased incidence, morbidity, and mortality of cardiovascular disease. Therefore, the author previously suggested that persons with high levels of seasonality may be at increased risk of developing or worsening of coronary heart disease in the winter. Some psychological factors promote the development of disorders of the cardiovascular system. The same psychological factors decrease immunity and promote infection. There is evidence that the infectious process is involved in the pathogenesis of coronary heart disease. Therefore, the author previously proposed that the development of infection and inflammation in the atherosclerotic plaque may be related to the psychological disorders that suppress the immune system. In this paper, the author suggests that winter depression-induced suppression of the immune system may contribute to the winter increase in incidence and mortality of cardiovascular disease.

Respiratory infection and coronary heart disease: progression of a paradigm.

We have developed a previously published paradigm concerning causation of coronary heart disease, based on the probability that the fundamental cause is a microbe, probably Chlamydia pneumoniae, and that the progress of the disease is influenced by number of accelerating and inhibiting factors. We propose that cigarette smoking acts via respiratory infection, this itself being influenced by immunocompetence resulting from sunlight exposure. We also propose an immuno-enhancing effect of oestrogen and an anti-inflammatory effect of statin therapy. In respect of the geographical variation of coronary heart disease, we emphasize that this must be viewed as part of the bigger picture of a high mortality from all causes in countries of North-west Europe that have a particularly low level of sunlight exposure. Finally, we draw attention to the Albanian, French, Italian, Northern Ireland and Scottish paradoxes which should lead to a major review of the conventional wisdom concerning the aetiogenesis of coronary heart disease.

Genotypng:Genetic variation in coronary heart disease and myocardial infarction: methodological overview and clinical evidence

The precise molecular mechanisrms that lead to coronary artery disease (CAD) and myocardial infarction (MI) are not understood, despite a wealth of knowledge on predisposing risk factors and pathomechanisms. CAD and MI are complex genetic diseases; neither the environment alone nor a single gene cause disease, but a mix of environmental and genetic factors lead to atherosclerosis of the coronary arteries and subsequent manifestation of clinical disease. The biological complexity of atherosclerotic disease results from unknown or unpredictable interactions of many genetic and environmental factors which, by themselves, have only been partially identified. According to current knowledge, genetic variations in causative or susceptihility genes form the basis of molecular mechanisms that, together with environmental impact, lead to CAD/MI and determine its clinical course. Linkage analysis, which follows 'disease' alleles in families, or genetic association in a population of unrelated individuals are tools used in the search for chromosomal loci and candidate genes that are involved in these complex diseases. Progress in sequencing and mapping of the human genorne and efforts to identify all of the expected one million single nucleotide polymorphisms (SNPs) expected to be present in mankind will allow new approaches such as genome-wide association studies. The contribution of the current state of knowledge on genetic variation in man towards the dissection of CAD/MI as complex traits is sobering. Raised expectations with regard to the power of molecular genetic studies as compared to the traditional pathophysiological experimental approaches, lack of precise clinical phenotyping, lack of functional characterisation of gene variants, and the vast number of yet undetected genes may provide some explanation. Except for certain polymorphisms in lipid genes (i.e., apolipoprotein E [apo E]) or rare genetic variations (i.e., LDL receptor), which have a causal effect on both the intermediate (LDL-cholesterol level in plasma) and the clinical phenotypes (CAD/MI), the role of most gene polymorphisms is controversial or unknown. Despite the enormous progress in sequencing the human genome and in molecular genetic and bioinformatic techniques during the past decade, the progress in mapping and identifying genes responsible for complex traits such as CAD/MI has been modest and presents a formidable challenge to medical research in the 21st century.

Seasonal variations in coronary heart disease.

Coronary heart disease exhibits a winter peak and summer trough in incidence and mortality, in countries both north and south of the equator. In England and Wales, the winter peak accounts for an additional 20,000 deaths per annum. It is likely that this reflects seasonal variations in risk factors. Seasonal variations have been demonstrated in a number of lifestyle risk factors such a physical activity and diet. However, a number of studies have also suggested a direct effect of environmental temperature on physiological and rheological factors. We review the available evidence on seasonal variations in coronary heart disease and possible explanations for them.

Racial Disparities in CHD Mortality from 1968–1992 in the State Economic Areas Surrounding the ARIC Study Communities

PURPOSE: This study examined racial variations in CHD (coronary heart disease) mortality rates (1968–1992) of residents aged 35–84 in the state economic areas (SEAs) surrounding the ARIC (Atherosclerosis Risk in Communities) study. The quarter century of CHD mortality rates are discussed in relation to racial and gender differences in baseline risk factors measured in the ARIC cohort and to the incidence of hospitalized myocardial infarction and case fatality rates obtained from the community surveillance component of the ARIC study between 1987 and 1994, inclusive. METHODS: Five-year average annual, gender- and age-specific CHD mortality rates were compared across race groups, based on National Vital Statistics data for state economic areas. RESULTS: Five-year average annual CHD mortality declined 2.6% for white men and women and 1.6% and 2.2% for black men and women, respectively. The black-white mortality rate ratio increased over time for men and women. The black-white mortality age crossover (higher black than white mortality in young men, lower black than white mortality at older ages) had disappeared by the end of the observation. CHD mortality was markedly greater in black than white women at all ages and time periods. The black disadvantage in CHD mortality was increasingly greater in the ARIC SEAs than in the United States as a whole. CONCLUSIONS: Persistent and increasing racial disparities in CHD mortality occurred in the ARIC SEAs concurrently with racial differences in risk factors, the incidence of myocardial infarction, and case fatality rates.

Socio-economic, migrant and geographic differentials in coronary heart disease occurrence in New South Wales

ObjectiveThis study examines the variation in coronary heart disease (CHD) mortality and acute myocardial infarction (AMI) by socio-economic status (SES), country of birth (COB) and geography (urban/rural) in the total population of New South Wales (Australia) in 1991-95. MethodCHD deaths and AMI are from complete enumerations of deaths and hospital admissions, respectively; and population denominators are from census information. Data are examined separately by sex, and comparisons of SES groups (based on municipalities), COB and region are analysed using Poisson regression, after adjustment for age. ResultsThe study identified higher risk for AMI admissions and CHD mortality in lower SES populations with significant linear trends, for both sexes, adjusted for age, region and COB. According to the population attributable fractions (PAF), 23-41 % of the risk of CHD occurrence is due to SES lower than the highest quartile. The higher age-adjusted risk for CHD occurrence in rural and remote populations for both sexes, compared with urban communities, was lessened by adjustment for COB, and all but abolished when also adjusted for SES. COB analysis indicated significantly lower age-adjusted AMI admissions and CHD mortality compared with the Australian-born. ConclusionsHigher risks for CHD in rural populations compared with the capital city (Sydney) are due, in part, to lower SES, lesser migrant composition. ImplicationsStrategies for reducing CHD differentials should consider demographic factors and the fundamental need to reduce socio-economic inequalities, as well as targeting appropriate prevention measures.

People, places and coronary heart disease risk factors: A multilevel analysis of the Scottish heart health study archive

The Scottish Heart Health Study (SHHS), which recruited 5123 men and 5236 women between 1984 and 1986, was set up in part to investigate geographical variation in coronary heart disease in Scotland. Multilevel models are particularly appropriate for such hierarchical data, in which the individuals in the study can be represented by the lower level and the districts in which they live by the higher level. Multilevel models are presented for four coronary heart disease risk factors—diastolic blood pressure, cholesterol, alcohol consumption (defined both as units of alcohol consumed per week and as being a non-drinker) and smoking, for men and women separately. Significant district level variance was found for three out of the four variables studied, after controlling for socioeconomic and other variables considered at the level of the individual. These were for diastolic blood pressure, cholesterol and alcohol. Although the large majority of the variance was present at the individual level, the existence of significant variance at the district level is evidence that places may have a role in the distribution of coronary heart disease risk. Health policy aimed at reducing coronary heart disease should therefore consider the characteristics of places as well as individuals.

Sunlight, cholesterol and coronary heart disease.

We investigated the relationship between geography and incidence of coronary heart disease, looking at deficiency of sunlight and thus of vitamin D as a factor that might influence susceptibility and thus disease incidence. Sunlight deficiency could increase blood cholesterol by allowing squalene metabolism to progress to cholesterol synthesis rather than to vitamin D synthesis as would occur with greater amounts of sunlight exposure, and the increased concentration of blood cholesterol during the winter months, confirmed in this study, may well be due to reduced sunlight exposure. We show evidence that outdoor activity (gardening) is associated with a lower concentration of blood cholesterol in the summer but not in the winter. We suggest that the geographical variation of coronary heart disease is not specific, but is seen in other diseases and sunlight influences susceptibility to a number of chronic diseases, of which coronary heart disease is one.

Seasonal variation in coronary heart disease in Scotland.

Seasonality of coronary heart disease (CHD) was examined to determine whether fatal and non-fatal disease have the same annual rhythm. Time series analysis was carried out on retrospective data over a 10 year period and analysed by age groups ( < 45 to > 75 years) and gender. Data by month were obtained for the years 1962-71. The Registrar General provided information on deaths and the Research and Intelligence Unit of the Scottish Home and Health Department on hospital admissions. In Scotland, between 1962 and 1971, 123 000 patients were admitted to hospital for CHD, of whom 29 000 died. There were a further 97 000 CHD deaths outside hospital. These two groups were also examined as one (coronary incidence) - that is, all coronary deaths and coronary admissions discharged alive. STATISTICAL ANALYSIS AND MAIN RESULTS: Where there was a single annual peak, the sine curve was analysed by cosinor analysis. When there were two peaks the analysis was by normal approximation to Poisson distribution. In younger men (under 45 years) admitted to hospital there was a dominant spring peak and an autumn trough. A bimodal pattern of spring and winter peaks was evident for hospital admissions in older male age groups: with increasing age the spring peak diminished and the winter peak increased. In contrast, female hospital admissions showed a dominant winter/summer pattern of seasonal variation. In male and female CHD deaths seasonal variation showed a dominant pattern of winter peaks and summer troughs, with the winter peak spreading into spring in the two youngest male age groups. CHD incidence in women showed a winter/summer rhythm, but in men the spring peak was dominant up to the age of 55. The male, age related spring peak in CHD hospital admissions suggests there is an androgenic risk factor for myocardial infarction operating through an unknown effector mechanism. As age advances and reproduction becomes less important, the well defined winter/summer pattern of seasonal variation of CHD is superimposed, and shows a close relationship with the environment, especially temperature, or the autumn and early winter fall in temperature.

An investigation of the relationship between antioxidant vitamin intake and coronary heart disease in men and women using discriminant analysis

Smoking, high blood pressure and elevated blood cholesterol are the well-established ‘ classical’ risk factors for coronary heart disease (CHD) in men and women. However, it is also well-known that there is a considerable degree of residual variation in CHD after these factors have been taken into account. Consideration of antioxidant vitamin status may help to reduce this unexplained variation. Here, discriminant analysis is applied to the baseline cross-sectional data from the Scottish Heart Health Study. The problem of possible behavioural changes after diagnosis for CHD is addressed by analysing diagnosed and undiagnosed CHD cases separately. Results show that the combined dietary intakes of the antioxidant vitamins C, E and carotene (assessed using a food frequency questionnaire) differentiate CHD prevalence as well as do the classical risk factors. For women, stepwise discriminant analysis shows that the effect of the antioxidant vitamins on CHD is removed by adjustment for the classical risk factors and age. For men, however, the antioxidant vitamins still contribute to the discriminant function. It is concluded that dietary antioxidant vitamins appear to have a significant effect on the prevalence of CHD, especially amongst men. The benefits and problems of using discriminant analysis in this practical context are discussed, including the assumptions that need to be tested.

An analysis of the seasonal variation of coronary heart disease and respiratory disease mortality in New Zealand.

The seasonal variation of coronary heart disease mortality rates in New Zealand is analysed by age, sex and race using monthly national mortality data for the period 1970-83. A 35% variation from the winter peak to summer low is found in the crude mortality rate, but the size of the seasonal variation is age-dependent, being more pronounced in the elderly, and more so in males than in females. The hypothesis that respiratory infections are linked to coronary heart disease, and that their seasonal occurrence explains the seasonal variation in coronary rates, is examined by an analysis of the association between coronary disease and respiratory disease mortality rates. By partial correlation analysis and by examining the residual correlation after filtering the seasonal variation from both series, it is suggested that the season acts as a confounding factor to cause an apparent association between the two rates. After controlling for season there is a tenuous relationship, but it is apparent only in the elderly.