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Objective: It has long been thought that anger is important in the development of essential hypertension. However, tests of this hypothesis have yielded conflicting findings. This study prospectively examined the relationship between anger expression style and incident hypertension in a population sample of middle-aged men.Methods: Participants were 537 initially normotensive men from eastern Finland, who completed a medical examination and series of psychological questionnaires at baseline and at 4-year follow-up. Anger expression was assessed by Spielberger's Anger-out and Anger-in scales.Results: At follow-up, 104 men (19.4%) were hypertensive (blood pressure > or = 165 mm Hg systolic and/or 95 mm Hg diastolic). Age-adjusted logistic regression analyses revealed that each 1-point increase in Anger-out was associated with a 12% increase in risk of hypertension after 4 years of follow-up (p < .002), which corresponded to a two-fold increased risk of hypertension among men with scores in the top tertile of the Anger-out scale, relative to those with scores in the bottom tertile (odds ratio = 2.00, 95% confidence interval 1.20-3.38). Each 1-point increase on the Anger-in scale also was related to a 12% increased risk of hypertension (p < .01). Adjustments for body mass index, smoking, alcohol consumption, physical activity, a positive parental history of hypertension, and baseline resting diastolic blood pressure had little impact on the findings.Conclusions: These data provide strong epidemiological evidence for a positive relationship between anger expression style and subsequent hypertension, independent of known risk factors. Findings support the hypothesis that extreme expression of anger in either direction has adverse cardiovascular consequences. [ABSTRACT FROM AUTHOR]

Most studies that examine the role of alcohol consumption in atherosclerosis and cardiovascular disease have overlooked the possible effect of drinking pattern. We investigated the association between the habit of heavy acute intake of beer and spirits (binging) and the 4-year progression of carotid atherosclerosis in a population-based sample of middle-aged Finnish men. Data from the Kuopio Ischemic Heart Disease Risk Factor Study (KIHD) were used to estimate changes in maximum and mean intima-media thickness (IMT) and the maximum plaque height in 764 KIHD participants who reported using beer and in 871 participants who used spirits. After adjustment for age, baseline carotid atherosclerosis, and average weekly alcohol consumption level, we observed the highest atherosclerosis progression in men who usually consumed a whole bottle of vodka or more in 1 session. For beer binging (>6 beers at a time), the magnitude of IMT progression was even higher, although this association was only marginally significant (P<0.1) because of smaller numbers. The associations were largely unaffected by adjustments for blood pressure, lipids, smoking, BMI, and medication. The magnitude of the difference was generally higher in a subgroup that was free of IHD at baseline. We conclude that the pattern of drinking associates with the progression of carotid atherosclerosis independently of the total level of alcohol consumption and risk factors.

Objective: The purpose of this study is to provide data on the prevalence of insomnia and hypersomnia among older persons, the stability of these sleep complaints over time, and factors associated with disturbed sleep, in particular age., Method: Data on symptoms of insomnia and hypersomnia were examined for the 1994 to 1995 cohort of the Alameda County Study. In addition to age, the effects of gender, education, marital status, chronic medical conditions, functional impairment, life events, financial strain, and mood disturbance were examined using multiple logistic analyses., Results: Prevalence in 1994 was 23.4% for insomnia and 6.8% for hypersomnia. There was moderate concordance between sleep complaints in 1994 and 1995 (kappa=.43). There was a tendency for insomnia and hypersomnia to increase with age in 1995, but not in 1994. Only gender, mood disturbance, and chronic health problems predicted insomnia. Life events, mood disturbance, and chronic conditions predicted hypersomnia. Age, net of the effects of other factors, was not associated with risk of either insomnia or hypersomnia., Conclusions: The results contribute to the expanding body of evidence concerning the important roles of psychological and somatic dysfunction in sleep disturbance. Age in and of itself is not a risk factor for insomnia or hypersomnia. That is, after adjustment for an array of putative risk factors for sleep problems, it seems the association between sleep difficulties and age is primarily due to depressed mood and physical health problems.

Background: Exaggerated cardiovascular reactivity to mental stress is hypothesized to increase atherosclerotic risk. We examined this hypothesis using cross-sectional data from the Kuopio Ischemic Heart Disease study, a population-based epidemiological sample., Methods and Results: 901 Eastern Finnish men from four age cohorts (age, 42 to 60 years) were administered a standardized testing battery to assess cardiovascular reactivity to mental stress. Ultrasound measures of intima-medial thickness (IMT) and plaque height from the common carotid arteries were used as noninvasive markers of atherosclerosis. Diastolic blood pressure (DBP) responses to mental stress were significantly associated with mean IMT (b=.021, P=.006), maximum IMT (b=.026, P=.013), and mean plaque height (b=.017, P=.041). Significant associations were also shown between stress-related systolic blood pressure (SBP) reactivity and mean IMT (b=.0151, P=.042). When examined separately by age, associations with IMT were significant only in the youngest half of the sample (age, 46 and 52 years, n=433; for mean IMT, DBP b=.033, P=.0002, SBP b=.0266, P=.003; for maximum IMT, DBP b=.039, P=.002, SBP b=.032, P=.011). Results remained significant in the younger subjects after adjustment for smoking, lipid profiles, fasting glucose, and resting blood pressure (b=.024, P=.011); results also remained significant in a subgroup of unmedicated younger subjects without symptomatic cardiovascular disease (n=135; for SBP reactivity, b=.031, P=.036; for DBP, b=.037, P=.007)., Conclusions: The tendency to show exaggerated pressor responses to mental stress is a significant independent correlate of atherosclerosis in this population sample of Finnish men. The effect does not appear to be accounted for by the confounding influence of other risk factors or preexisting clinical disease.

The importance of hope has long been recognized, whereas a lack of hope, or "giving up," is generally believed to have a negative impact on psychological well-being and physical health. Recently, hopelessness has been identified as a strong, independent predictor of cardiovascular disease morbidity and mortality in both American and Finnish populations. In this study we examined the association between high levels of hopelessness and progression of carotid atherosclerosis in participants (n = 942) in the Kuopio Ischemic Heart Disease Study, a population-based study of middle-aged men from eastern Finland who underwent carotid ultrasonography at baseline and 4 years later. Men reporting high levels of hopelessness at baseline had faster progression of carotid atherosclerosis, assessed by four measures of intima-media thickening (IMT), than men reporting low to moderate levels of hopelessness. Further analyses revealed significant interactions between hopelessness and initial level of atherosclerosis, such that the effects of high hopelessness on progression were greatest among men who had baseline mean IMT values at or above the median. Moreover, progression was greatest among men reporting high levels of hopelessness at both baseline and follow-up. Traditional coronary risk factors and use of cholesterol-lowering and antihypertensive medications did not account for much variance in the observed relationships. These findings indicate that hopelessness contributes to accelerated progression of carotid atherosclerosis, particularly among men with early evidence of atherosclerosis, and that chronically high levels of hopelessness may be especially detrimental. Additional research is needed to identify the contributory pathways and/or mechanisms underlying these relationships.

Background: Characteristics of the work environment have been associated with cardiovascular morbidity and mortality, but it is unclear whether these factors are associated with preclinical manifestations of disease., Methods and Results: We investigated the association between job demands, economic reward, and the 4-year progression of carotid atherosclerosis in a population-based sample of 940 Finnish men. Data from the Kuopio Ischemic Heart Disease Risk Factor Study were used to estimate changes in plaque height, maximum and mean intima-media thicknesses across combinations of job demands, and income. Associations were examined in relation to atherosclerotic risk factors and were stratified by baseline levels of atherosclerosis and prevalent ischemic heart disease. Men who had jobs with high demands and low economic rewards had significantly greater 4-year progression of plaque height (0.33 mm, P = .008) and maximum intima-media thickness (0.32, P = .03) than men with low-demand, high-income jobs. The magnitude of these differences was not greatly attenuated by risk factor adjustment and did not differ when examined by the level of workplace resources, social support, or employment status. Larger differences were observed in a subsample of men who had more advanced atherosclerosis at baseline., Conclusions: These results show that men with demanding work that produces little economic reward have significantly greater progression of carotid atherosclerosis than more advantaged men. The relationship between job demands and health should be understood in a broad framework of interacting economic conditions, social circumstances, and behaviors that cascade over the life course and may ultimately contribute to socioeconomic inequalities in morbidity and mortality.

Socioeconomic status (SES) is importantly associated with cardiovascular morbidity and mortality, but no information exists on the relationship between SES and progression of atherosclerotic vascular disease. We investigated the association between education and income and the 4-year progression of carotid atherosclerosis in a population-based sample of Finnish men. Data from the Kuopio Ischemic Heart Disease Risk Factor Study were used to estimate changes in maximum and mean intima-media thickness (IMT) and maximum plaque height across levels of SES in 1022 men. Associations between SES and atherosclerotic progression were examined in relation to risk factors and stratified by baseline levels of atherosclerosis and prevalent ischemic heart disease (IHD). There were significant, inverse, graded relationships between levels of education and income for all three progression measures, which were largely unaffected by risk factor adjustment. For education, the age- and baseline IMT-adjusted maximum progression for those with primary schooling or less was 0.28 mm and for those who graduated from high school, 0.24 mm (P = .05). Compared with the lowest SES group, men with the highest SES had 14% to 29% less atherosclerotic progression, depending on the measure used. Associations of the same magnitude were evident in subgroups without advanced baseline IMT and in men who were free of IHD. These results show that men with poor education and low income have significantly greater progression of carotid atherosclerosis than men with more advantages. The findings strengthen the contention that SES plays a significant role early in the atherosclerotic disease process and that reducing the burden of atherosclerotic vascular disease associated with lower SES will require approaches that focus on all stages of the life course.

Background: There is a consistent body of evidence that socioeconomic status (SES) is importantly associated with cardiovascular morbidity and mortality. However, little information currently exists on the relationship between SES and early manifestations of atherosclerotic vascular disease., Methods and Results: We investigated the association between education, income, and occupation and intima-media thickness (IMT) in a population-based sample of eastern Finnish men. Data from the Kuopio Ischemic Heart Disease Risk Factor Study were used to estimate mean IMT across levels of SES in 1140 men. The association between SES and IMT was examined in relation to atherosclerotic risk factors and was also stratified by degree of atherosclerotic progression and was also stratified by degree of atherosclerotic progression and prevalent cardiovascular disease. There were significant, inverse, graded differences between levels of SES and IMT. For education, the age-adjusted mean IMTs for those with primary schooling or less, some high school, and completed high school or more were 0.96, 0.94, and 0.82 mm, respectively. The difference in mean IMT between the most extreme categories of education corresponds to a 15.4% increase in the risk of myocardial infarction. Similar patterns were found for each measure of SES, although the differences between the highest and lowest levels of SES were attenuated by adjustment for risk factors. In men who had no carotid stenosis or nonstenotic plaque and in men who had no indication of prevalent cardiovascular disease, a graded, inverse association between SES and IMT persisted, even after risk factor adjustment., Conclusions: These findings demonstrate a strong association between SES and atherosclerosis in an unselected population. The results show that this association was mediated by known atherosclerotic risk factors, was evident in the early stages of atherosclerosis, and was apparent in a healthy subgroup. Our findings suggest that the impact of SES is evident early in the natural history of atherosclerotic vascular disease.

We studied the associations between 11 scales of social functioning and risk of death over an average follow-up time of 71 months in 42- to 60-year-old men in the Kuopio Ischemic Heart Disease Risk Factor Study. In age-adjusted analyses, men were at increased risk of death if they reported few persons to whom they gave or received social support, nonparticipation in organizations, low quality of social relationships, a small number of friends, or not currently being married. Frequency of interaction, shyness, and use of emotional support when troubled were not associated with risk of death; the use of instrumental support when troubled was associated with increased risk. There was little evidence of confounding of these associations by the presence of 31 chronic or acute conditions, perceived health status, or six risk factors. Consistent associations were found in a healthy subgroup. These data add to the growing body of literature linking mortality risk with social functioning, especially in relation to organizational participation and quality of relationships.

Despite recent declines in mortality, cardiovascular diseases are the leading cause of death in the United States today. It appears that many of the major risk factors for coronary disease have been identified. Researchers are still learning about different modifiable factors that may influence cardiovascular diseases. Socioeconomic status may provide a new focus. The principal measures of SES have been education, occupation, and income or combinations of these. Education has been the most frequent measure because it does not usually change (as occupation or income might) after young adulthood, information about education can be obtained easily, and it is unlikely that poor health in adulthood influences level of education. However, other measures of SES have merit, and the most informative strategy would incorporate multiple indicators of SES. A variety of psychosocial measures--for example, certain aspects of occupational status--may be important mediators of SES and disease. The hypothesis that high job strain may adversely affect health status has a rational basis and is supported by evidence from a limited number of studies. There is a considerable body of evidence for a relation between socioeconomic factors and all-cause mortality. These findings have been replicated repeatedly for 80 years across measures of socioeconomic level and in geographically diverse populations. During 40 years of study there has been a consistent inverse relation between cardiovascular disease, primarily coronary heart disease, and many of the indicators of SES. Evidence for this relation has been derived from prevalence, prospective, and retrospective cohort studies. Of particular importance to the hypothesis that SES is a risk factor for cardiovascular disease was the finding by several investigators that the patterns of association of SES with coronary disease had changed in men during the past 30 to 40 years and that SES has been associated with the decline of coronary mortality since the mid-1960s. However, the declines in coronary mortality of the last few decades have not affected all segments of society equally. There is some evidence that areas with the poorest socioenvironmental conditions experience later onset in the decline in cardiovascular mortality. A number of studies suggest that poor living conditions in childhood and adolescence contribute to increased risk of arteriosclerosis. Some of these studies have been criticized because of their nature, and others for inadequate control of confounding factors.(ABSTRACT TRUNCATED AT 400 WORDS)