The worldwide epidemic of childhood obesity is progressing at an alarming rate. Risk factors for coronary heart disease (CHD) are already identifiable in overweight children. The severity of the long-term effects of excess childhood weight on CHD, however, remains unknown.
We investigated the association between body-mass index (BMI) in childhood (7 through 13 years of age) and CHD in adulthood (25 years of age or older), with and without adjustment for birth weight. The subjects were a cohort of 276,835 Danish schoolchildren for whom measurements of height and weight were available. CHD events were ascertained by linkage to national registers. Cox regression analyses were performed.
In 5,063,622 person-years of follow-up, 10,235 men and 4318 women for whom childhood BMI data were available received a diagnosis of CHD or died of CHD as adults. The risk of any CHD event, a nonfatal event, and a fatal event among adults was positively associated with BMI at 7 to 13 years of age for boys and 10 to 13 years of age for girls. The associations were linear for each age, and the risk increased across the entire BMI distribution. Furthermore, the risk increased as the age of the child increased. Adjustment for birth weight strengthened the results.
Higher BMI during childhood is associated with an increased risk of CHD in adulthood. The associations are stronger in boys than in girls and increase with the age of the child in both sexes. Our findings suggest that as children are becoming heavier worldwide, greater numbers of them are at risk of having CHD in adulthood.
STUDY OBJECTIVE: To analyse the association between self rated health and the incidence of fatal and non-fatal coronary heart disease (CHD) in a Danish cohort followed up over 16 years. DESIGN: This was a prospective epidemiological follow up study. SETTING: A cohort from the County of Copenhagen, Denmark. PARTICIPANTS: The study included 1052 men and women born in 1936. During the 16 years' follow up 50 cases of CHD were registered in either the Danish register of deaths or the register of hospital admissions. MAIN RESULTS: Univariate analysis showed the following relative risks of CHD in the four self rated health groups: 'extremely good': 1.0, 'good': 4.0, 'poor': 5.8, 'miserable': 12.1 (p = 0.02). After control for the conventional CHD risk factors and a substantial number of other potential confounders the relative risks were: 1.0, 4.2, 6.5, and 18.6 (p = 0.02) respectively. CONCLUSIONS: Self rated health was an independent predictor of CHD in the present cohort. If confirmed, the association between self rated health and CHD may lead to new insight into psychosocial processes leading to this disease.
Low birth weight and high childhood body mass index (BMI) is each associated with an increased risk of coronary heart disease (CHD) in adult life. We studied individual and combined associations of birth weight and childhood BMI with the risk of CHD in adulthood.
Birth weight and BMI at age seven years were available in 216,771 Danish and Finnish individuals born 1924–1976. Linkage to national registers for hospitalization and causes of death identified 8,805 CHD events during up to 33 years of follow-up (median = 24 years) after age 25 years. Analyses were conducted with Cox regression based on restricted cubic splines. Using median birth weight of 3.4 kg as reference, a non-linear relation between birth weight and CHD was found. It was not significantly different between cohorts, or between men and women, nor was the association altered by childhood BMI. For birth weights below 3.4 kg, the risk of CHD increased linearly and reached 1.28 (95% confidence limits: 1.13 to 1.44) at 2 kg. Above 3.4 kg the association weakened, and from about 4 kg there was virtually no association. BMI at age seven years was strongly positively associated with the risk of CHD and the relation was not altered by birth weight. The excess risk in individuals with a birth weight of 2.5 kg and a BMI of 17.7 kg/m2 at age seven years was 44% (95% CI: 30% to 59%) compared with individuals with median values of birth weight (3.4 kg) and BMI (15.3 kg/m2).
Birth weight and BMI at age seven years appeared independently associated with the risk of CHD in adulthood. From a public health perspective we suggest that particular attention should be paid to children with a birth weight below the average in combination with excess relative weight in childhood.
Objective: To assess the associations between components of adult height and coronary heart disease (CHD) in postmenopausal women.
Methods: Cross sectional analysis of 4286 women randomly selected from 23 British towns. The association of components of adult height with prevalent CHD (n = 694) were assessed.
Results: Shorter stature, shorter leg length, and trunk length were all associated with CHD in age adjusted analyses. The association between trunk length and CHD was attenuated to the null with adjustment for smoking. The leg length–CHD association was independent of smoking, socioeconomic position in childhood and adulthood, birth weight, and other potential confounders. Insulin resistance did not appear to be an important mediating factor in the association between leg length and CHD. After full adjustment for all potential confounding factors the odds ratio (95% confidence interval) of CHD for a 1 SD (4.3 cm) increase in leg length was 0.84 (0.77 to 0.93) and the odds ratio for a 1 SD (0.05) increase in the leg to trunk ratio was 0.85 (0.79 to 0.95).
Conclusions: The specific association between leg length and CHD suggests that early life environmental exposures that influence skeletal growth also influence CHD risk in later life.
anthropometry; coronary heart disease; leg length; life course epidemiology; stature
Short stature is associated with increased risk of coronary heart disease (CHD); although the mechanisms for this relationship are unknown, shared genetic factors have been proposed. Subclinical atherosclerosis, measured by coronary artery calcification (CAC), is associated with CHD events and represents part of the biological continuum to overt CHD. Many molecular mechanisms of CAC development are shared with bone growth. Thus, we examined whether there was evidence of shared genes (pleiotropy) between adult stature and CAC.
877 asymptomatic white adults (46% men) from 625 families in a community-based sample had computed tomography measures of CAC. Pleiotropy between height and CAC was determined using maximum-likelihood estimation implemented in SOLAR.
Adult height was significantly and inversely associated with CAC score (P=0.01). After adjusting for age, sex, and CHD risk factors, the estimated genetic correlation between height and CAC score was -0.37 and was significantly different than 0 (P=0.001) and -1 (P<0.001). The environmental correlation between height and CAC score was 0.60 and was significantly different than 0 (P=0.024).
Further studies of shared genetic factors between height and CAC may provide important insight into the complex genetic architecture of CHD, in part through increased understanding of the molecular pathways underlying the process of both normal growth and disease development. Bivariate genetic linkage analysis may provide a powerful mechanism for identifying specific genomic regions associated with both height and CAC.
Genetics; Atherosclerosis; Calcium; Imaging; Stature
Background and Purpose
Ultrasound measurements of arterial stiffness are associated with atherosclerosis risk factors, but limited data exist on their association with incident cardiovascular events. We evaluated the association of carotid ultrasound derived arterial stiffness measures with incident coronary heart disease (CHD) and ischemic stroke in the ARIC study.
Carotid arterial strain (CAS) and compliance (AC), distensibility (AD) and stiffness indices (SI), pressure-strain (Ep) and Young’s elastic moduli (YEM) were measured in 10,407 individuals using ultrasound. Hazard ratios for incident CHD (myocardial infarction [MI], fatal CHD, coronary revascularization) and stroke in minimally adjusted (age, sex, center, race) and fully adjusted models (minimally adjusted model + diabetes, height, weight, total cholesterol, high-density lipoprotein cholesterol, tobacco use, systolic blood pressure, antihypertensive medication use, and carotid intima-media thickness (CIMT) were calculated.
The mean age was 55.3 years. Over a mean follow up of 13.8 years, 1,267 incident CHD and 383 ischemic stroke events occurred. After full adjustment for risk factors and CIMT, all arterial stiffness parameters [CAS HR (95% confidence interval [CI]) =1.14 (1.02, 1.28); AD HR=1.19 (1.02, 1.39); SI HR=1.14 (1.04, 1.25); Ep HR=1.17 (1.06, 1.28); YEM HR=1.13 (1.03, 1.24)], except arterial compliance HR=1.02 (0.90, 1.16), were significantly associated with incident stroke but not with CHD.
After adjusting for cardiovascular risk factors, ultrasound measures of carotid arterial stiffness are associated with incident ischemic stroke but not incident CHD events, despite that the 2 outcomes sharing similar risk factors.
arterial stiffness; carotid ultrasound; coronary heart disease; stroke; ARIC
Background Adult height is known to be inversely related to coronary heart disease (CHD) risk. We sought to investigate transgenerational influence of parental height on offspring’s CHD risk.
Methods Parents took part in a cardiorespiratory disease survey in two Scottish towns during the 1970s, in which their physical stature was measured. In 1996, their offspring were invited to participate in a similar survey, which included an electrocardiogram recording and risk factor assessment.
Results A total of 2306 natural offspring aged 30–59 years from 1456 couples were subsequently flagged for notification of mortality and followed for CHD-related hospitalizations. Taller paternal and/or maternal height was associated with socio-economic advantage, heavier birthweight and increased high-density lipoprotein cholesterol in offspring. Increased height in fathers, but more strongly in mothers (risk ratio for 1 SD change in maternal height = 0.85; 95% confidence interval: 0.76 to 0.95), was associated with a lower risk of offspring CHD, adjusting for age, sex, other parental height and CHD risk factors.
Conclusion There is evidence of an association between taller parental, particularly maternal, height and lower offspring CHD risk. This may reflect an influence of early maternal growth on the intrauterine environment provided for her offspring.
Coronary heart disease; mortality; intergenerational; height
While several plausible biological mechanisms have been advanced for the association between greater physical stature and lower coronary heart disease (CHD) risk in prospective cohort studies, the importance of one of the principal artifactua explanations – reverse causality due to shrinkage – remains unresolved. To explore this issue, studies with repeat measurements of height are required, however, to date, such data have been lacking.
We analysed data from the Whitehall II prospective cohort study of 3802 men and 1615 women who participated in a physical examination in 1985/88, had their height re-measured in 1997/99, and were then followed for fatal and non-fatal CHD.
A mean follow-up of 7.4 years after the second height measurement gave rise to 69 CHD events in men (18 in women). After adjustment for baseline CHD risk factors, greater loss of physical stature between survey and resurvey was associated with an increased risk of CHD in men (hazard ratio; 95% CI for a one SD increase: 1.24; 1.00, 1.53) but not women (0.93; 0.58, 1.50).
It is possible that reverse causality due to shrinkage may contribute to the inverse association between a single measurement of height and later CHD in other studies.
Background: Taller people and those with better lung function are at reduced risk of coronary heart disease (CHD). Biological mechanisms for these associations are not well understood, but both measures may be markers for early life exposures. Some studies have shown that leg length, an indicator of pre-pubertal nutritional status, is the component of height most strongly associated with CHD risk. Other studies show that height-CHD associations are greatly attenuated when lung function is controlled for. This study examines (1) the association of height and the components of height (leg length and trunk length) with CHD risk factors and (2) the relative strength of the association of height and forced expiratory volume in one second (FEV1) with risk factors for CHD.
Subjects and methods: Cross sectional analysis of data collected at detailed cardiovascular screening examinations of 1040 men and 1298 women aged 30–59 whose parents were screened in 1972–76. Subjects come from 1477 families and are members of the Midspan Family Study.
Setting: The towns of Renfrew and Paisley in the West of Scotland.
Results: Taller subjects and those with better lung function had more favourable cardiovascular risk factor profiles, associations were strongest in relation to FEV1. Higher FEV1 was associated with lower blood pressure, cholesterol, glucose, fibrinogen, white blood cell count, and body mass index. Similar, but generally weaker, associations were seen with height. These associations were not attenuated in models controlling for parental height. Longer leg length, but not trunk length, was associated with lower systolic and diastolic blood pressure. Longer leg length was also associated with more favourable levels of cholesterol and body mass index than trunk length.
Conclusions: These findings provide indirect evidence that measures of lung development and pre-pubertal growth act as biomarkers for childhood exposures that may modify an individual's risk of developing CHD. Genetic influences do not seem to underlie height-CHD associations.
Peripheral arterial disease (PAD), defined by a low ankle-brachial index (ABI), is associated with an increased risk of cardiovascular events, but the risk of coronary heart disease (CHD) over the range of the ABI is not well characterized, nor described for African Americans.
The ABI was measured in 12186 white and African American men and women in the Atherosclerosis Risk in Communities Study in 1987–89. Fatal and non-fatal CHD events were ascertained through annual telephone contacts, surveys of hospital discharge lists and death certificate data, and clinical examinations, including electrocardiograms, every 3 years. Participants were followed for a median of 13.1 years. Age- and field-center-adjusted hazard ratios (HRs) were estimated using Cox regression models.
Over a median 13.1 years follow-up, 964 fatal or non-fatal CHD events accrued. In whites, the age- and field-center-adjusted CHD hazard ratio (HR, 95% CI) for PAD (ABI<0.90) was 2.81 (1.77–4.45) for men and 2.05 (1.20–3.53) for women. In African Americans, the HR for men was 4.86 (2.76–8.47) and for women was 2.34 (1.26–4.35). The CHD risk increased exponentially with decreasing ABI as a continuous function, and continued to decline at ABI values > 1.0, in all race-gender subgroups. The association between the ABI and CHD relative risk was similar for men and women in both race groups. A 0.10 lower ABI increased the CHD hazard by 25% (95% CI 17–34%) in white men, by 20% (8–33%) in white women, by 34% (19–50%) in African American men, and by 32% (17–50%) in African American women.
African American members of the ARIC cohort had higher prevalences of PAD and greater risk of CHD associated with ABI-defined PAD than did white participants. Unlike in other cohorts, in ARIC the CHD risk failed to increase at high (>1.3) ABI values. We conclude that at this time high ABI values should not be routinely considered a marker for increased CVD risk in the general population. Further research is needed on the value of the ABI at specific cutpoints for risk stratification in the context of traditional risk factors.
Multiple studies have identified single-nucleotide polymorphisms (SNPs) that are associated with coronary heart disease (CHD). We examined whether SNPs selected based on predefined criteria will improve CHD risk prediction when added to traditional risk factors (TRFs).
SNPs were selected from the literature based on association with CHD, lack of association with a known CHD risk factor, and successful replication. A genetic risk score (GRS) was constructed based on these SNPs. Cox proportional hazards model was used to calculate CHD risk based on the Atherosclerosis Risk in Communities (ARIC) and Framingham CHD risk scores with and without the GRS.
The GRS was associated with risk for CHD (hazard ratio [HR] = 1.10; 95% confidence interval [CI]: 1.07–1.13). Addition of the GRS to the ARIC risk score significantly improved discrimination, reclassification, and calibration beyond that afforded by TRFs alone in non-Hispanic whites in the ARIC study. The area under the receiver operating characteristic curve (AUC) increased from 0.742 to 0.749 (Δ= 0.007; 95% CI, 0.004–0.013), and the net reclassification index (NRI) was 6.3%. Although the risk estimates for CHD in the Framingham Offspring (HR = 1.12; 95% CI: 1.10–1.14) and Rotterdam (HR = 1.08; 95% CI: 1.02–1.14) Studies were significantly improved by adding the GRS to TRFs, improvements in AUC and NRI were modest.
Addition of a GRS based on direct associations with CHD to TRFs significantly improved discrimination and reclassification in white participants of the ARIC Study, with no significant improvement in the Rotterdam and Framingham Offspring Studies.
Genetics; Risk factors; Coronary disease
Lipoprotein-associated phospholipase A2 (Lp-PLA2) levels predict incident coronary heart disease (CHD) in adults without known CHD, independent of heart disease risk factors. We examined whether the independent association was apparent in older adults.
Serum levels of Lp-PLA2, an enzyme that hydrolyzes oxidized phospholipids to yield potentially proatherogenic particles, have been associated with CHD and may help predict cardiovascular risk.
Participants were 1,077 community-dwelling men and women, median age 72 years, who had no known CHD at baseline (1984 to 1987) when blood samples and risk factor data were collected. Participants were followed for CHD events for a mean of 16 years, through 2002. Cox proportional hazards regression models were used to examine the association of serum Lp-PLA2 with incident CHD (myocardial infarction, angina, or coronary revascularization).
The Lp-PLA2 levels positively correlated with age (r = 0.09), body mass index (r = 0.11), low-density lipoprotein (r = 0.37), triglycerides (r = 0.25), and C-reactive protein (r = 0.10), and negatively correlated with high-density lipoprotein (r = −0.27) (all p < 0.05). During follow-up, 228 participants had incident CHD events. Lipoprotein-associated phospholipase A2 levels in the second, third, and fourth quartiles predicted an increased risk of CHD compared with the lowest quartile (hazard ratios 1.66, 1.80, and 1.89, respectively; p < 0.05 for each). This association persisted after adjusting for C-reactive protein and other CHD risk factors.
Elevated Lp-PLA2 levels predict CHD events in apparently healthy older adults, independent of CHD risk factors.
China will experience an overall growth and aging of its adult population in coming decades. We used a computer model to forecast the future impact of these demographic changes on coronary heart disease (CHD) in China.
The CHD Policy Model is a validated state-transition, computer simulation of CHD on a national scale. China-specific CHD risk factor, incidence, case-fatality, and prevalence data were incorporated, and a CHD prediction model was generated from a Chinese cohort study and calibrated to age-specific Chinese mortality rates. Disability-adjusted life years (DALYs) due to CHD were calculated using standard methods. The projected population of China aged 35–84 years was entered, and CHD events, deaths, and DALYs were simulated over 2000–2029. CHD risk factors other than age and case-fatality were held at year 2000 levels. Sensitivity analyses tested uncertainty regarding CHD mortality coding, the proportion of total deaths attributable to CHD, and case-fatality.
We predicted 7.8 million excess CHD events (a 69% increase) and 3.4 million excess CHD deaths (a 64% increase) in the decade 2020–2029 compared with 2000–2009. For 2030, we predicted 71% of almost one million annual CHD deaths will occur in persons ≥65 years old, while 67% of the growing annual burden of CHD death and disability will weigh on adults <65 years old. Substituting alternate CHD mortality assumptions led to 17–20% more predicted CHD deaths over 2000–2029, though the pattern of increases in CHD events and deaths over time remained.
We forecast that absolute numbers of CHD events and deaths will increase dramatically in China over 2010–2029, due to a growing and aging population alone. Recent data suggest CHD risk factor levels are increasing, so our projections may underestimate the extent of the potential CHD epidemic in China.
To examine the association between overtime work and incident coronary heart disease (CHD) among middle-aged employees.
Methods and results
Six thousand and fourteen British civil servants (4262 men and 1752 women), aged 39–61 years who were free from CHD and worked full time at baseline (1991–1994), were followed until 2002–2004, an average of 11 years. The outcome measure was incident fatal CHD, clinically verified incident non-fatal myocardial infarction (MI), or definite angina (a total of 369 events). Cox proportional hazard models adjusted for sociodemographic characteristics showed that 3–4 h overtime work per day was associated with 1.60-fold (95% CI 1.15–2.23) increased risk of incident CHD compared with employees with no overtime work. Adjustment for all 21 cardiovascular risk factors measured made little difference to these estimates (HR 1.56, 95% CI 1.11–2.19). This association was replicated in multivariate analysis with only fatal cardiovascular disease and incident non-fatal MI as the outcome (HR 1.67, 95% CI 1.02–2.76).
Overtime work is related to increased risk of incident CHD independently of conventional risk factors. These findings suggest that overtime work adversely affects coronary health.
Working hours; Stress; CHD; Myocardial infarction; Angina; Middle-aged; Prospective
Several epidemiologic studies have suggested periodontitis as a risk factor for coronary heart disease (CHD), but results have been inconsistent.
Methods and Results:
We evaluated the association between clinical and radiographic measures of periodontitis, edentulism and incident CHD (angina, myocardial infarction or fatal CHD) among 1,203 men in the VA Normative Aging and Dental Longitudinal Studies who were followed with triennial comprehensive medical and dental exams up to 35 yrs (median: 24 yrs). Cox proportional hazards models with time-varying effects of exposure and potential confounders were fit. We found a significant, dose-dependent association between periodontitis and CHD incidence among men younger than 60 yrs of age (HR 2.12, 95% CI 1.26, 3.60 comparing highest vs. lowest category of radiographic bone loss, p for trend = 0.02), independent of age, BMI, smoking, alcohol intake, diabetes, fasting glucose, total cholesterol, HDL cholesterol, triglycerides, hypertension, systolic and diastolic blood pressure, education, marital status, income and occupation. No association was found among men older than 60 yrs. Similar results were found using the sum of probing pocket depths as a measure of periodontitis. Among men 60+ yrs, edentulous men tended to have higher risk of CHD compared to dentate men in the lowest bone loss (HR 1.61, 95% CI 0.95, 2.73) and lowest pocket depth categories (HR 1.72, 95% CI 1.03, 2.85), independent of confounders.
Chronic periodontitis is associated with incidence of CHD among younger men, independent of established cardiovascular risk factors.
coronary disease; epidemiology; infection; inflammation; risk factors
We examined whether a panel of SNPs, systematically selected from genome-wide association studies (GWAS), could improve risk prediction of coronary heart disease (CHD), over-and-above conventional risk factors. These SNPs have already demonstrated reproducible associations with CHD; here we examined their use in long-term risk prediction.
Study Design and Setting
SNPs identified from meta-analyses of GWAS of CHD were tested in 840 men and women aged 55–75 from the Edinburgh Artery Study, a prospective, population-based study with 15 years of follow-up. Cox proportional hazards models were used to evaluate the addition of SNPs to conventional risk factors in prediction of CHD risk. CHD was classified as myocardial infarction (MI), coronary intervention (angioplasty, or coronary artery bypass surgery), angina and/or unspecified ischaemic heart disease as a cause of death; additional analyses were limited to MI or coronary intervention. Model performance was assessed by changes in discrimination and net reclassification improvement (NRI).
There were significant improvements with addition of 27 SNPs to conventional risk factors for prediction of CHD (NRI of 54%, P<0.001; C-index 0.671 to 0.740, P = 0.001), as well as MI or coronary intervention, (NRI of 44%, P<0.001; C-index 0.717 to 0.750, P = 0.256). ROC curves showed that addition of SNPs better improved discrimination when the sensitivity of conventional risk factors was low for prediction of MI or coronary intervention.
There was significant improvement in risk prediction of CHD over 15 years when SNPs identified from GWAS were added to conventional risk factors. This effect may be particularly useful for identifying individuals with a low prognostic index who are in fact at increased risk of disease than indicated by conventional risk factors alone.
Recent studies show that retinal vascular signs such as quantitative retinal vascular caliber are associated with an increased risk of incident coronary heart disease (CHD), but whether these retinal vascular signs add to the prediction of CHD over and above traditional CHD risk factors has not been addressed. We investigated whether these signs add to the prediction of CHD over and above the Framingham risk score amongst people (n=9,155) without diabetes selected from the Atherosclerosis Risk in Communities (ARIC) study. Incident CHD was ascertained using standardized methods and retinal vascular caliber and other retinal signs were measured from retinal photographs. After a mean of 8.8 years of follow up, there were 700 incident CHD events. Women with wider retinal venular caliber (hazard ratio 1.27 per 1 standard deviation increase [95% confidence interval, 1.08, 1.50]) and narrower retinal arteriolar caliber (1.31 per 1 standard deviation decrease [1.10, 1.56]) had a higher risk of incident CHD after adjusting for the Framingham risk score variables. The area under the receiver operator characteristic curve increased from 0.695 to 0.706 (1.7% increase) with the addition of retinal vascular caliber to the Framingham risk model. The risk prediction models with and without the retinal vascular caliber both fitted the data and were well calibrated for women. In men, retinal vascular caliber was not associated with CHD risk after adjustment. Other retinal vascular signs were not associated with 10-year incident CHD in men or women. In conclusion, although retinal vascular caliber independently predicts CHD risk in women, the incremental predictive ability over that of the Framingham model is modest, and unlikely to translate meaningfully into clinical practice.
Coronary disease; retinal vascular disease; retinal imaging; risk prediction
To examine the sex-specific contributions of the metabolic syndrome and microalbuminuria to cardiovascular disease (CVD) and coronary heart disease (CHD) mortality in community-dwelling older adults, between 1992–1995, 869 women and 575 men aged 40–96 years (mean 71) completed questionnaires, physical examinations, and fasting laboratory tests. Participants were followed over an average of 8 years. CVD and CHD mortality were analyzed using Cox proportional hazards models. At baseline, 267 participants had the Adult Treatment Panel III metabolic syndrome, 151 had microalbuminuria, and 34 had both. During follow up, there were 180 CVD deaths, including 83 CHD deaths. In women, microalbuminuria was associated with a 2-fold increased risk of CVD and CHD mortality (p ≤ 0.01). Women with both microalbuminuria and the metabolic syndrome (n = 18) had a 3-fold increased risk of CVD mortality and a 5-fold increased risk of CHD mortality compared with women without either (n = 657). A significant interaction existed between microalbuminuria and the metabolic syndrome in the prediction of both CVD and CHD (p = 0.021). In men, neither the combination of the metabolic syndrome and microalbuminuria (n = 16), nor either alone, significantly increased the risk of CVD or CHD mortality. In conclusion, in this cohort, microalbuminuria and the metabolic syndrome together were a more powerful predictor of CVD mortality than either alone in women but not in men. Screening for microalbuminuria in older women may identify women at high risk for CVD mortality, beyond that conferred by risk factors included in the metabolic syndrome.
Cardiovascular disease; Elderly; Metabolic syndrome; Microalbuminuria
Negative psychological states such as stress and depression are associated with increased risk of coronary heart disease (CHD), but it is unclear whether some positive states are protective. We investigated satisfaction with specific life domains as predictors of incident CHD.
Methods and results
Coronary risk factors and satisfaction within seven life domains (e.g. job and family) were assessed in 7956 initially healthy members of the Whitehall II cohort. Incident CHD (angina, non-fatal myocardial infarction, or death from CHD) was ascertained from medical screening, hospital data, and registry linkage over five person-years of follow-up. Satisfaction averaged across domains was associated with reduced CHD risk (HR: 0.87; 95% CI: 0.78–0.98), controlling for demographic characteristics, health behaviours, blood pressure, and metabolic functioning. Associations with CHD risk were evident for satisfaction in four life domains—one's job, family, sex life, and self, but not one's love relationship, leisure activities, or standard of living. When examining CHD outcomes separately, average domain satisfaction was associated with angina but not myocardial infarction or coronary death.
Satisfaction in most life domains was associated with reduced CHD risk, with definite angina being mostly responsible for this association. These findings suggest that satisfaction with life may promote heart health. Further research should examine whether interventions to enhance life satisfaction in specific domains reduce CHD risk and whether life satisfaction is primarily associated with atherosclerosis rather than thrombotic factors associated with plaque rupture.
Coronary heart disease; Angina; Life satisfaction; Domain satisfaction; Well-being
To investigate whether the known diabetes mellitus (KDM) or newly diagnosed diabetes mellitus (NDM) could be regarded as a coronary heart disease (CHD) risk equivalent among a relatively young Middle East population with high prevalence of diabetes mellitus (DM).
A population based cohort study of 2267 men and 2931 women, aged ≥ 30 years. Prior CHD was defined as self-reported or ECG positive CHD at baseline, KDM as subjects using any kind of glucose-lowering medications and NDM according to fasting plasma glucose and 2-h postchallenge glycemia.
Participants were categorized to six groups according to the presence of known or newly diagnosed DM and CHD at baseline (DM-/CHD-, DM-/CHD+, NDM+/CHD-, NDM+/CHD+, KDM+/CHD-, KDM+/CHD+) and Cox regression analysis were used to estimate the hazard ratio (HR) of CHD events for these DM/CHD groups, given DM-/CHD-as the reference.
During 7.6-year follow up, 358 CHD events occurred. After controlling traditional risk factors, HRs of CHD events for DM-/CHD+ group were 2.1 (95% CI: 1.4-3.1) and 5.2 (3.2-8.3) in men and women respectively. Corresponding HRs for NDM+/CHD-were 1.7 (1.1-2.7) and 3.1 (1.8-5.6) and for KDM+/CHD-were 1.7 (0.9-3.3) and 6.2 (3.6-10.6) in men and women respectively. The HRs for NDM+/CHD+ and KDM+/CHD+ groups (i.e. participants with history of both diabetes and CHD) were 6.4 (3.2-12.9) and 8.0 (4.3-14.8) in women and 3.2 (1.9-5.6) and 4.2 (2.2-7.8) in men, respectively.
The hazard of CHD events did not differ between KDM+/CHD-and DM-/CHD+ in both genders using paired homogeneity test, however the HR for NDM+/CHD-was marginally lower than the HR for DM-/CHD+ in women (p = 0.085).
KDM patients in both genders and NDM especially in men exhibited a CHD risk comparable to nondiabetics with a prior CHD, furthermore diabetic subjects with prior CHD had the worst prognosis, by far more harmful in women than men; reinforcing the urgent need for intensive care and prophylactic treatment for cardiovascular diseases.
We evaluated whether carotid intima-media thickness (C-IMT) and the presence or absence of plaque improved coronary heart disease (CHD) risk prediction when added to traditional risk factors (TRF).
Traditional CHD risk prediction schemes need further improvement as the majority of the CHD events occur in the “low” and “intermediate” risk groups. C-IMT and presence of plaque on an ultrasound are associated with CHD and therefore could potentially help improve CHD risk prediction.
Risk prediction models (overall, in men and women) considered included TRF-only, TRF+C-IMT, TRF+plaque, and TRF+C-IMT+ plaque. Model predictivity was determined by calculating the area under the receiver operating characteristic curve (AUC) adjusted for optimism. Cox-proportional hazards models were used to estimate 10-year CHD risk for each model, and the number of individuals reclassified determined. Observed events were compared with expected events; and, the net reclassification index (NRI) was calculated.
Of 13,145 eligible individuals (5,682 men; 7,463 women), ~23% were reclassified by adding C-IMT+plaque information. Overall, the addition of C-IMT and plaque separately or together to the TRF model improved the AUC which increased from 0.742 to 0.750, 0.751 and 0.755 for the TRF-only, TRF+C-IMT, TRF+plaque and TRF+C-IMT+plaque model respectively. The C-IMT+TRF+plaque model had a NRI of 9.9% when compared to TRF-only in the overall population. However, comparison of TRF+C-IMT+plaque with TRF+C-IMT or TRF+plaque only resulted in non-significant or modestly significant changes of the various statistical tests. Sex-specific analyses are presented in the manuscript.
Adding plaque and C-IMT to TRF improves CHD risk prediction in the ARIC study.
C-IMT; plaque; risk prediction
Background The relationship between depression and cerebrovascular disease (CBVD) continues to be debated although little research has compared the predictive power of depression for coronary heart disease (CHD) with that for CBVD within the same population. This study aimed to compare the importance of depression for CHD and CBVD within the same population of adults free of apparent cardiovascular disease.
Methods A random sample of 23 282 adults (9507 men, 13 775 women) aged 20–54 years were followed up for 7 years. Fatal and first non-fatal CHD and CBVD events were documented by linkage to the National-hospital-discharge and mortality registers.
Results Sex–age–education-adjusted hazard ratio (HR) for CHD was 1.66 [95% confidence interval (CI) 1.24–2.24] for participants with mild to severe depressive symptoms, i.e. those scoring ≥10 on the 21-item Beck Depression Inventory, and 2.04 (1.27–3.27) for those who filled antidepressant prescriptions compared with those without depression markers in 1998, i.e. at study baseline. For CBVD, the corresponding HRs were 1.01 (0.67–1.53) and 1.77 (0.95–3.29). After adjustment for behavioural and biological risk factors these associations were reduced but remained evident for CHD, the adjusted HRs being 1.47 (1.08–1.99) and 1.72 (1.06–2.77). For CBVD, the corresponding multivariable adjusted HRs were 0.87 (0.57–1.32) and 1.52 (0.81–2.84).
Conclusions Self-reported depression using a standardized questionnaire and clinical markers of mild to severe depression were associated with an increased risk for CHD. There was no clear evidence that depression is a risk factor for CBVD, but this needs further confirmation.
Depression; coronary heart disease; cerebrovascular disease
The relationship between depression and cerebrovascular disease (CBVD) continues to be debated although little research has compared the predictive power of depression for coronary heart disease (CHD) to that for CBVD within the same population. This study aimed to compare the importance of depression for CHD and CBVD within the same population of adults free of apparent cardiovascular disease.
A random sample of 23282 adults (9507 men, 13775 women) aged 20–54 years were followed-up for 7 years. Fatal and first non-fatal CHD and CBVD events were documented by linkage to the National-hospital-discharge and mortality registers.
Sex-age-education-adjusted Hazard Ratio (HR) for CHD was 1.66 (95% confidence interval (CI) 1.24–2.24) for participants with mild to severe depressive symptoms, i.e. those scoring 10 or more on the 21-item Beck-Depression-Inventory, and 2.04 (1.27–3.27) for those who filled antidepressant prescriptions compared to those without depression markers in 1998, i.e., at study baseline. For CBVD, the corresponding HRs were 1.01 (0.67–1.53) and 1.77 (0.95–3.29). After adjustment for behavioural and biological risk factors these associations were reduced but remained evident for CHD, the adjusted HRs being 1.47 (1.08–1.99) and 1.72 (1.06–2.77). For CBVD, the corresponding multivariable adjusted HRs were 0.87 (0.57–1.32) and 1.52 (0.81–2.84).
Self-reported depression using a standardized questionnaire and clinical markers of mild to severe depression were associated with an increased risk for CHD. There was no clear evidence that depression is a risk factor for CBVD, but this needs further confirmation.
Adult; Coronary Disease; epidemiology; psychology; Depression; complications; Female; Finland; epidemiology; Humans; Incidence; Male; Middle Aged; Proportional Hazards Models; Prospective Studies; Risk Factors; Stroke; epidemiology; psychology; Young Adult; depression; coronary heart disease; cerebrovascular disease
To examine the relations between obesity or overweight and coronary heart disease (CHD) mortality in men with and without prevalent CHD in a prospective cohort study.
In the Whitehall study of London‐based male government employees, 18 403 middle age men were followed up for a maximum of 35 years having participated in a medical examination in the late 1960s in which weight, height, CHD status, and a range of other social, physiological, and behavioural characteristics were measured.
In age‐adjusted analyses of men with baseline CHD there was a modest raised risk in the overweight relative to normal weight groups for all cause mortality (hazard ratio 1.10, 95% confidence interval (CI) 1.00 to 1.20) and CHD mortality (1.28, 95% CI 1.11 to 1.47) but not for stroke mortality (1.01, 95% CI 0.73 to 1.40). Mortality was similarly raised in the obese group. While these slopes were much steeper in men who were apparently CHD‐free at study induction, the difference in the gradients according to baseline CHD status did not attain significance at conventional levels (p value for interaction ⩾ 0.24). The weight–mortality relations were somewhat attenuated when potential mediating and confounding factors were added to the multivariable models in both men with and men without a history of CHD.
Avoidance of obesity and overweight in adult life in men with and without CHD may reduce their later risk of total and CHD mortality.
obesity; overweight; coronary heart disease; mortality; cohort study
Background:Evidence on socioeconomic inequalities in coronary heart disease (CHD) and their pathways in the elderly is limited. Little is also known about the contributions that novel coronary risk factors (particularly inflammatory/hemostatic markers) make to socioeconomic inequalities in CHD. Objectives:To examine the extent of socioeconomic inequalities in CHD in older age, and the contributions (relative and absolute) of established and novel coronary risk factors. Methods:A population-based cohort of 3761 British men aged 60–79 years was followed up for 6.5 years for CHD mortality and incidence (fatal and non-fatal). Social class was based on longest-held occupation recorded at 40–59 years. Results:There was a graded relationship between social class and CHD incidence. The hazard ratio for CHD incidence comparing social class V (unskilled workers) with social class I (professionals) was 2.70 [95% confidence interval (CI) 1.37–5.35; P-value for trend = 0.008]. This was reduced to 2.14 (95% CI 1.06–4.33; P-value for trend = 0.11) after adjustment for behavioral factors (cigarette smoking, physical activity, body mass index, and alcohol consumption), which explained 38% of the relative risk gradient (41% of absolute risk). Additional adjustment for inflammatory markers (C-reactive protein, interleukin-6, and von Willebrand factor) explained 55% of the relative risk gradient (59% of absolute risk). Blood pressure and lipids made little difference to these estimates; results were similar for CHD mortality. Conclusions:Socioeconomic inequalities in CHD persist in the elderly and are at least partly explained by behavioral risk factors; novel (inflammatory) coronary risk markers made some further contribution. Reducing inequalities in behavioral factors (especially cigarette smoking) could reduce these social inequalities by at least one-third.
coronary heart disease; coronary risk factors; older age; social inequalities