Etiology Of Coronary Heart Disease Research Articles

Fifty percent of patients with coronary artery disease do not have any of the conventional risk factors

Prinzmetal's variant angina, primarily a vasospastic disease, is a glaring example of the gaps in our knowledge regarding the etiology of coronary heart disease. Half of all patients with coronary heart disease do not have any of the established coronary risk factors. Prinzmetal's variant angina, syndrome X, coronary embolization, and congenital coronary anomalies, are a few examples of conditions that may not be associated with established risk factors. New risk factors that are emerging in an attempt to establish an etiology in this group of patients are homocysteine plasma fibrinogen, estrogen-deficiency lipoprotein (a), C-reactive protein, Chlamydia pneumoniae, factor VII endogenous tissue plasminogen, and endogenous plasminogen activator/inhibitor type I. The battle against cardiovascular disease continues!

Effects of milk and fermented dairy products on the blood cholesterol content and profile of mammals in relation to coronary heart disease

Abstract In the recent past, dairy products have received adverse publicity in terms of their effect on the blood cholesterol content of consumers. They have been perceived to increase blood cholesterol content, which is a risk factor in the aetiology of coronary heart disease. The relationship between diet and blood cholesterol content is by no means clear and this applies certainly to the role of dietary dairy products. The effects of milk and of fermented dairy products have been reviewed in this paper and, although there are conflicting data in the scientific literature, the consensus view indicates that the dairy products discussed do not increase the plasma cholesterol concentration and, in many studies, hypocholesterolaemic effects have been reported.

Coronary heart disease: a review of the role of psychosocial stress and social support.

The role of psychosocial factors in the aetiology of coronary heart disease continues to be debated. Despite public perception of a major role for their effect, scientific opinion on their relevance remains divided. This paper reviews the literature on the influence of social support and life stress on coronary heart disease incidence and mortality. Observational studies published in English, based on over 100 human subjects from the general population, investigating life stress or social support were considered. Fourteen studies derived from MEDLINE searches on MeSH headings: coronary disease; stress, psychological; social support; social isolation; life change events. An equivalent search of BIDS and studies referenced by papers identified using these sources was carried out. The review concludes that both life stress and social support were found to have an influence on coronary heart disease, social support more so than stress. Both have a stronger influence on coronary heart disease mortality than on initial incidence of clinical disease. Measures of the quality of support, in particular emotion support, show the largest effects. The review highlights problems in drawing conclusions from the available literature; in particular, the inconsistency in measures used to define the psychosocial factors. Further studies are needed to investigate interrelationships between stress and social support, and a recommendation is made to adopt pragmatic measures in future studies, which if proven to have an effect, may be open to modification.

Preliminary report The effect of low-glycemic carbohydrate on insulin and glucose response in vivo and in vitro in patients with coronary heart disease

The insulin resistance syndrome has recently been implicated in the etiology of coronary heart disease, with a possible metabolic defect at the level of the adipocyte. We report the effects of a low— versus high—glycemic-index (LGI and HGI, respectively) diet on insulin and glucose response as assessed by oral glucose tolerance test (OGTT) and insulin-stimulated glucose uptake in isolated adipocytes in a group of 32 patients with advanced coronary heart disease. The area under the insulin curve following OGTT was significantly reduced after 4 weeks in the LGI group ( P < .03), but not in the HGI group. Insulin-stimulated glucose uptake in isolated adipocytes harvested from a presternal fat biopsy was significantly greater following the LGI diet ( P < .05). This study demonstrates that simple short-term dietary measures can improve insulin sensitivity in patients with coronary heart disease.

Plasminogen Activator Inhibitor 1 (PAI-1) in Plasma: Its Role in Thrombotic Disease

Impaired fibrinolytic function, mainly due to an elevation of the plasma PAI-1 concentration, is a common finding in patients with thrombotic disease. Unfortunately, regarding patients with idiopathic deep vein thrombosis (DVT), no reliable prospective or genetic studies have been published. Concerning postoperative DVT, preoperatively increased PAI-1 level seems to predict a postoperative DVT in patients subjected to hip surgery. Several longitudinal cohort studies of patients with manifest coronary heart disease (CHD) have linked elevated plasma PAI-1 or tPA antigen concentrations to future cardiovascular events, particularly myocardial infarction. Before PAI-1 can be regarded as a risk factor in the conventional epidemiological sense, its relationship to myocardial infarction must be demonstrated in prospective studies of healthy populations. Regulation of the plasma concentration of PAI-1 is complex and at present not well understood. Multiple interactions with disturbances of both carbohydrate and lipoprotein metabolism are evident. Many studies have been carried out in cultured cells, but data can hardly be transformed into human pathophysiology. It seems that both environmental and genetic factors are of importance for the plasma PAI-1 concentration. Recently, knowledge of the importance of genetic factors involved in the regulation of plasma PAI-1 concentration has become available. Interestingly, preliminary data suggest that the 4G/5G polymorphism located within the PAI-1 promoter is connected to CHD. More data on larger patient groups are needed and will certainly shed new light on the importance of impaired fibrinolytic function in the etiology of CHD in the near future.

Short note: Iron, infection and acute myocardial infarction

Recent studies have noted an association between both increased serum ferritin and dietary iron intake and acute myocardial infarction (AMI). The possible role of increased serum ferritin and dietary iron intake in the promotion of infection, and in the etiology of AMI, is discussed. In addition, the possible role of infection in the etiology of coronary heart disease and AMI is also discussed.

Association of early-onset coronary heart disease in South Asian men with glucose intolerance and hyperinsulinemia.

Rates of coronary heart disease are higher in South Asians (Indians, Pakistanis, and Bangladeshis) settled overseas than in other ethnic groups. We tested the hypothesis that this excess risk results from metabolic disturbances associated with insulin resistance. There were 1,421 South Asian men and 1,515 European men aged 40-69 years in London examined in the Southall Study. Prevalence of ischemic ECG abnormalities was higher in South Asians than in Europeans (17% versus 12%, p < 0.001), with an excess of major Q waves (Minnesota codes 1-1 or 1-2) in younger South Asian men (p = 0.01 for the age-ethnicity interaction). Major Q waves were strongly associated with glucose intolerance and hyperinsulinemia in younger South Asians; these factors accounted statistically for 73% of major Q waves in those aged 40-54 years. Age-standardized prevalence of a positive history of coronary heart disease was similar in South Asians and Europeans (8.5% versus 8.2%, NS), and positive history without Q waves was not associated with glucose intolerance or hyperinsulinemia in South Asians. Smoking rates and average plasma cholesterol were lower in South Asians than in Europeans; in a logistic model controlling for smoking and cholesterol, the odds ratio for major Q waves in South Asians compared with Europeans was 2.4 (95% CI, 1.5-3.8). Adjusting for glucose intolerance and hyperinsulinemia reduced this ratio to 1.5 (95% CI, 0.9-2.5). These results are consistent with the hypothesis that insulin resistance underlies the high coronary risk in South Asian people and strengthen the evidence for a fundamental role of this metabolic pattern in the etiology of coronary heart disease.

The role of insulin resistance and hyperinsulinemia in coronary heart disease

Patients with impaired glucose tolerance (IGT) and non-insulin-dependent diabetes mellitus (NIDDM) are more resistant to insulin-stimulated glucose uptake than are individuals with normal glucose tolerance. Evidence has also been published showing that first-degree relatives of patients with NIDDM are insulin resistant when compared with a matched group of relatives of subjects with normal glucose tolerance. In addition, the ability of insulin to stimulate glucose uptake varies approximately fourfold in individuals with normal glucose tolerance, and insulin resistance of a degree comparable to that seen in patients with IGT or with Type II diabetes is present in a significant portion of the normal population. Given a defect in insulin-stimulated glucose uptake, glucose tolerance can only be maintained if insulin-resistant individuals continue to secrete greater than normal amounts of insulin. As a corollary, glucose homeostasis will decompensate when the insulin secretory response begins to decrease, and the greater the decline in insulin secretion, the larger the increase in plasma glucose concentration. Resistance to insulin-stimulated glucose uptake and compensatory hyperinsulinemia seems to represent the basic defect in patients with NIDDM, with failure of β-cell function and subsequent development of fasting hyperglycemia only occurring later. This general formulation has received considerable support from longitudinal studies of the natural history of NIDDM. The fact that an increase in ambient insulin concentration can prevent gross decompensation of glucose tolerance in an insulin-resistant individual does not mean that this compensatory response is benign. It now appears that resistance to insulin-stimulated glucose uptake and compensatory hyperinsulinemia are associated not only with states of IGT, but are also seen in individuals with high blood pressure, hypertriglyceridemia, and low plasma concentrations of high-density lipoprotein (HDL) cholesterol. All of these events have been identified as increasing the risk of coronary heart disease (CHD), and there is increasing evidence that they tend to cluster in the same individual. As a consequence, it has been suggested that this constellation of abnormalities constitutes a syndrome (X) that plays an important role in the etiology of CHD. Indeed, in some populations it can be argued that Syndrome X is involved in the etiology of CHD to a greater degree than is an increase in plasma low-density lipoprotein (LDL) cholesterol concentration. In summary, resistance to insulin-stimulated glucose uptake seems to be a relatively common phenomenon, and is present in the majority of patients with IGT or NIDDM. The normal physiologic response to this defect in insulin action is to secrete more insulin in an effort to minimize the degree of IGT. If this compensatory response fails, glucose tolerance decompensates. Unfortunately, even if the hyperinsulinemia can be maintained, such individuals appear to be at increased risk of CHD, either directly as a result of the hyperinsulinemia, or secondary to the increase in blood pressure and the dyslipidemia shown to be associated with resistance to insulin-stimulated glucose uptake and elevation of plasma insulin concentration. As a result of these considerations, it seems possible that insulin resistance plays a major role in several important human diseases.

The effects of demographic shift on coronary heart disease mortality in a large migrant population at high risk

Asian immigrants to the United Kingdom and elsewhere are at greater risk of mortality and morbidity from coronary heart disease (CHD) than UK whites. This predisposition has yet to be explained. More than 63,000 Asian people, a high proportion of whom are under 40, live in Leicester. Projections of the local Asian and non-Asian populations indicate that numbers of Asian people in higher-risk age groups will more than double between 1988 and 2008. In the absence of effective intervention, numbers of CHD deaths among Asian people, and the prevalence of other manifestations of CHD in this group, will rise by an equivalent amount. This predicted shift in the ethnic distribution of CHD has important implications for the planning of acute services in Leicester. Our predictions also demonstrate both a valuable opportunity and a pressing need for local research into the aetiology of CHD among Asian people, upon which preventative strategies may be based.

Use of graded exercise to evaluate physiological hyperreactivity to mental stress

Physiological hyperreactivity (i.e., response in excess of metabolic requirements) to mental stress has been implicated in the etiology of coronary heart disease. This study evaluated potential hyperreactivity of cardiovascular, pulmonary, and biochemical variables to mental stress. Thirty healthy males, 19-36 yr, performed a mental arithmetic task and cycle ergometry at three powerloads. Linear regressions were calculated for each of 17 dependent variables during exercise, with oxygen uptake (VO2) serving as the independent variable. Ten variables were significantly correlated (P less than 0.003) with VO2 during exercise and, therefore, were predicted at the VO2 observed during the arithmetic task. The actual level of each variable observed during the arithmetic task was compared with the level predicted from the exercise by paired t-tests. Heart rate, systolic and diastolic blood pressure, rate-pressure product, minute ventilation, respiratory frequency, and respiratory exchange ratio were significantly greater (7-32%, P less than 0.005) during the arithmetic task than predicted from the exercise at an equivalent VO2. Plasma cortisol and serum lipid variables were not useful for evaluating hyperreactivity. Results demonstrated that graded aerobic exercise can serve as a reference for evaluating physiological hyperreactivity to mental stress for a group of ten variables which were significantly correlated with VO2 during graded exercise.

Cigarette Smoking As a Cause of Lung Cancer and Coronary Heart Disease. A Study of Smoking-Discordant Twin Pairs

Despite increasing scientific evidence for a causal role of tobacco smoking in lung cancer and coronary heart disease, an alternative hypothesis was put forward several decades ago. The constitutional hypothesis has stated that there are genetic or other common factors, which predispose both to smoking and disease. A critical test of this hypothesis was considered the pattern of occurrence of disease in monozygotic (MZ) twin pairs in which one is a smoker and the other never has been a smoker. Initial twin studies found only small differences in the mortality of smoking and nonsmoking twins of discordant pairs. In the Finnish Twin Cohort, a population-based panel of adult like-sexed twin pairs, a questionnaire study carried out in 1975 permitted identification of 2488 twin pairs discordant for cigarette smoking. Analyses of total mortality and mortality due to coronary heart disease and lung cancer indicate that the smoking members of discordant MZ pairs are at higher risk than their nonsmoking cotwins; increased mortality of smoking cotwins was also found on 21-year follow-up of smoking-discordant pairs in Sweden. Incidence data and noninvasive studies of atherosclerosis in the Finnish sample provide confirmatory evidence for the causal role of smoking in the etiology of coronary heart disease and lung cancer.

Reliability of the Jenkins Activity Survey in Assessing Type a Behavior Pattern in Middle-Aged Nigerians

Contemporary psychosomatic research has implicated Type A behaviour pattern in the etiology of coronary heart disease (3). This pattern is characterized by extremes of competitive-achievement striving, time urgency, impatience, easily aroused anger and aggression (1). Persons showing relative absence of these characteristics are designated Type B. The Jenkins Activity Survey has been used extensively as a reasonably valid and reliable selfreport test for assessing these behaviour tendencies (2). It has not been established, however, whether the Jenkins survey could be reliably applied to measure the Type A behaviour pattern in adult Nigerians. This hypothesis was tested for 285 male university administrators and lecturers who were ages 29 to 45 yr. (M = 34.7 yr.). Subjects responded to the scale (3) at three-week intervals. Their scale scores were calculated from items with high factor loadings (1): Type A (M = 3.87, SD = 1.21), Hard Driving (M = 3.57, SD = 0.79), Job Involvement (M=4.31, SD= 1.63)) Speed-impatience (M =2.46, SD= 1.12); Type B (M = 1.79, SD = 0.64), Hard Driving (M = 2.01, SD = 1.02), Job Involvement (M = 1.32, SD = 0.97), Speed-impatience (M = 1.82, SD = 0.79). Analysis indicated that the survey was internally consistent (Cronbach cw: Hard Driving, .86; Job Involvement, .82; Speed-impatience, .77) and yielded significant, positive and moderate test-retest correlations (Hard Driving, .71; Job Involvement, .66; Speed-impatience, 38; Pearson r, p<.01). As these scores and coefficients are comparable to values obtained from other research, these data suggest the Jenkins Activity Survey could reliably assess coronary-prone behavior pattern in employed middle-aged Nigerians. Confirmation of coronary heart disease in this group was not possible, but such data are needed.

The multifactorial aetiology of coronary heart disease: a dangerous delusion.

THE MULTIFACTORIAL AETIOLOGY OF CORONARY HEART DISEASE: A DANGEROUS DELUSION JAMES McCORMICK* Introduction The term multifactorial when applied to aetiology is a tautology that has led to unreal expectations and delusion. AU diseases are multifactorial in origin. Infectious disease does not inevitably follow exposure to pathogenic organisms; many other conditions need to be satisfied before disease ensues. Road accidents depend on the conjunction of many factors , factors as various as blood alcohol, temper and temperament, eyesight and weather. Nobody refers to road accidents as having a multifactorial aetiology, the phrase being reserved for diseases whose aetiology is unknown, most commonly coronary heart disease and sometimes cancers . The phrase is a synonym for "unknown" and thus a euphemism for ignorance. Risk Factors Are Risk Markers Since the end of the Second World War the new epidemiology has been largely concerned with the identification of risk factors. A risk factor strictly defined is a factor which is associated with an altered probability of disease occurrence. Unfortunately, not everyone makes a clear distinction between associations and causal relationships, and it is common to find doctors and others talking about risk factors as if causal relationships had been established. Such an assumption leads almost inevitably to the belief that modification of risk factors will lead to a reduction of disease incidence. It is this faulty logic which is responsible for the dangerous delusion. It would be better if the term risk factor were dropped and replaced by risk marker. *Department of Community Health, University of Dublin, 196 Pearse Street, Dublin 2, Ireland.© 1988 by The University of Chicago. AU rights reserved. 0031-5982/89/3201-0613$01 .00 Perspectives in Biology and Medicine, 32, 1 ¦ Autumn 1988 | 103 The initial identification of risk markers usually derives from casecontrol studies, but associations have also been described in prospective studies. Case-control studies are a quick, dirty, and relatively cheap way of generating aetiological hypotheses, and their use has been extremely fruitful. Nonetheless, they are prone to bias and never of themselves prove causal relationships [I]. The results of such studies are usually expressed in terms of odds ratio or relative risk, nowadays happily accompanied with confidence limits. As a rule the relative risks which emerge from most of these studies are small, usually less than two. Quite inappropriately, such relative risks once published are often taken up by the popular press and some enthusiasts and translated into advice about life-style or the avoidance of this pill or that article ofdiet. Because ofthe flaws in the method and the possibility of error, small relative risks so derived should never serve as a basis for action other than further, preferably prospective or experimental, studies. Good prospective studies provide more secure evidence of the strength ofassociations, but only experiment can prove causality. The list of risk "factors" for coronary heart disease grows daily. It now includes, and this is by no means an exhaustive list, cigarette smoking, serum cholesterol, hypertension, obesity, diabetes mellitus, low levels of high-density lipoproteins, high levels of low-density lipoproteins and triglycerides, selenium, thiazide diuretics, not drinking, not exercising, not having siestas, not eating fish, especially mackerel, living in Scotland, having a high level of phobic anxiety, being scrupulous about keeping appointments, not taking cod-liver oil, and snoring. The important associations include age, being male, a family history, a high level of fibrinogen , and—perhaps most important of all—being poor in the rich world. Multifactorial Aetiology On the basis of such associations it is stated that diseases such as ischaemic heart disease have a multifactorial aetiology. That is, unlike infectious disease and accidents, they do not have a single necessary cause but are the result of some combination or amalgam of risk markers , none of which is by itself necessary. The concept of cause is difficult. Even simple examples, such as being hit on the head by a falling hammer, can be made complex. The immediate cause, that is, the falling hammer, is both sufficient and necessary , but the antecedent causes involve being under the scaffolding at the right time and can be pursued backward in time to the accident of birth without which the possibility ofbeing rendered unconscious in...

Relationship between pseudocholinesterase and lipids in hyperlipoproteinaemia

The biological r d e of serum pseudocholinesterase (PChE) is enigmatic: the protein is normally detected and defined in terms of its catalytic hydrolysis of choline esters but no necessity for such enzymic activity in serum has ever been demonstrated. However, the now well-established association between obesity and PChE in genetic and dietary animal models (Kutty et a[., 1981, 1983), and also in clinical situations (Cucuianu et al., 1968; Chu et al., 1978), suggests that PChE may play a significant part in the aetiology of coronary heart disease (CHD), a common end-stage consequence of obesity and hyperlipoproteinaemia. Serum was collected after an overnight fast from 66 patients with confirmed C H D (80% males; age 35-60 years) and 83 matched controls. Sixteen of the C H D patients were re-investigated after treatment for 2-3 months with diet, or medication, or both, to reduce serum lipids. Cholesterol and triglycerides were measured by standard methods. Lowdensity lipoprotein (LDL) was measured by a turbidimetric method (Walton & Scott, 1964) that included both LDL and very-low-density lipoprotein (VLDL). PChE was measured with butyrylthiocholine iodide substrate (Dietz et al., 1973). Serum PChE activities in the control (mean = 3.15 pmol of thiocholine/min per ml of serum; S.D. = 0.40) did not differ significantly with age or sex in adult subjects. However, 34 C H D patients (50%) had PChE activities exceeding the control 95th percentile, and all C H D patients’ PChE activities exceeded the control mean (Fig. 1). As expected, 50% of the patients were hypercholesterolaemic and 80% were hypertriglyceridaemic by accepted clinical criteria. Correlation analysis of the combined observations from patients and controls demonstrated that PChE is positively correlated with LDL (r = 0.51) and its associated lipids, cholesterol ( r = 0.48) and triglycerides (r = 0.52). Of even greater potential significance is that 18% of the C H D patients with significantly elevated PChE had normal lipid levels. During treatment, the patients’ PChE activities dropped from 4.7 f 0.34 to 3.9 k 0.26pmol of thiocholinelmin per ml ( I = 10.1) in concert with declines in cholesterol, triglyceride and total LDL levels. Animal models (Kutty et al., 1981, 1983) suggest that excess dietary intake is a major determinant of the PChE levels. Genetically obese (oblob), diabetic (dbldb) and normal mice with gold thioglucose-induced obesity exhibit a marked increase (50-150%) in liver and serum PChE activity when diet is unrestricted. Levels of PChE are almost normal when these hyperphagic animals are maintained on restricted diets. The parallel between these experimental models and hypertrophic obesity in humans is clear. However, the problem remains of non-obese, normolipidaemic C H D patients with significantly elevated serum PChE: what is the aetiology of hyperpseudocholinesterasaemia in these individuals and is non-dietary elevated serum PChE an independent risk factor in susceptibility to atheroscleortic heart disease? How could elevated PChE levels be implicated in atherosclerosis? It is possible that the true function of PChE

Relative value of plasma copper, zinc, lipids and lipoproteins as markers for coronary artery disease

Studies in experimental animals have suggested an association between dietary copper deficiency, alone or with an attendant elevated intake of zinc, and an increase in serum total cholesterol. These findings led some to theorize that a dietary imbalance of zinc and copper may be a factor in the etiology of coronary heart disease. Plasma zinc and copper levels were measured in 60 adult male patients with confirmed coronary artery disease and compared with serum levels of lipids and lipoproteins in the same patients. The results were compared to the accepted values in normal adult males. In subjects with significant coronary artery atherosclerosis (≧ 50% luminal occlusion) there was no correlation between plasma zinc or copper with serum lipids or lipoproteins. However, total cholesterol was significantly correlated with low density lipoprotein (LDL) cholesterol, triglycerides, and inversely correlated with HDL-C : T-Chol ratio. Although dietary zinc and/or copper may influence the plasma levels of these trace metals, our studies show that there was no association between plasma zinc or copper and the serum levels of lipids or lipoproteins; we believe that this indicates that these trace metals are of doubtful value as markers for coronary atherosclerosis.

The importance of obesity in the development of coronary risk factors and disease: the epidemiologic evidence.

Coronary heart disease (CHD) is caused by a complex interaction of genetic and life-style factors that begin to exert their effects many years prior to diagnosis of the disease. Numerous epidemiologic studies in middle-aged populations have shown the importance of attributes such as elevated blood pressure and blood lipids in the etiology of CHD; as a result, intervention in high-risk individuals has been focused on reduction of risk factors with pharmacologic treatment and a modified-fat diet. While such approaches to risk reduction are important and can decrease mortality, it is also clear that optimal preventive strategies will require modification of early markers for the development of CHD, hyperten­ sion, and hyperlipidemia. The accumulated evidence strongly suggests that overweight or obesity is such a precursor to disease development and that prevention of CHD can be greatly promoted by the control of this attribute in overfed and sedentary populations such as those in North America.

The influence of exercise training on plasma lipids and lipoproteins in health and disease.

There is a very high probability that lipoprotein metabolism plays a central role in the etiology of coronary heart disease. In sedentary persons one way to favorably alter lipoprotein metabolism and possibly delay the progression of coronary atherosclerosis is by an increase in their habitual physical activity. More physically active persons tend to have lower plasma triglycerides and very low density lipoprotein concentrations, and a greater high-density lipoprotein mass due to higher concentrations of the subfraction HDL2 and apoprotein A-I. Plasma low-density lipoprotein concentrations usually are not significantly reduced by exercise unless accompanied by weight loss, but there may be important changes in the distribution among the low-density subfractions. These exercise effects are most likely mediated by alterations in the activity of enzymes involved in the synthesis, transport and catabolism of the various lipoproteins including lipoprotein lipase, hepatic lipase and lecithin: cholesterol acyltransferase. In healthy persons as well as in patients with ischemic heart disease, diabetes and renal failure, an increase in moderate-intensity, endurance-type activity requiring an expenditure of approximately 4 MJ (1,000 kcal) per week usually produce favorable lipoprotein changes. Above this level a dose-response relationship exists, with greater changes occurring up to energy expenditures of 19 MJ (4,500 kcal) per week.

Fibrinogen: a possible link between social class and coronary heart disease.

Mortality from coronary heart disease in civil servants in the lowest grade of employment has been found to be about three times that of men in the highest grade of employment. As part of an investigation of this finding several haemostatic variables were measured in a sample of 29 men in lower grades of employment and 45 men in higher grades. There was a significant difference in plasma fibrinogen concentrations between men in lower grades of employment and those in higher grades (mean 3.39 g/l v 2.95 g/l, respectively; p less than 0.01) but not in other haemostatic variables. Multiple regression analyses showed significant independent associations of fibrinogen concentration with smoking (p less than 0.05) and grade of employment (p less than 0.05). The size of the observed difference between the grades of employment was similar to that between those dying of coronary heart disease or surviving during longitudinal study; it may therefore be an important part of the mechanism underlying social class differences in coronary heart disease. The statistical relation between fibrinogen concentrations and other characteristics that may be concerned in the aetiology of coronary heart disease was examined. A summary measure of job stress was significantly related to fibrinogen concentration (p less than 0.01) and made a substantial contribution to explaining the differences between grades of employment. Behaviour type and a score of physical activity were not significantly related to fibrinogen concentration.

Atherosclerosis precursors in Finnish children and adolescents. XI. Psychological aspects.

The role of psychic risk factors in the early history of atherosclerosis was studied in 3,596 Finnish children and adolescents, aged 3, 6, 9, 12, 15, and 18 years. The family atmosphere, behavioural pattern and self-esteem were tested. The results showed that the abuse of alcohol by the parents and daily smoking by the child were the factors most clearly indicating the existence of psychic problems. The results showed that boys manifested in every age group behaviour most disposed to coronary heart disease (CHD). Furthermore, low serum HDL-cholesterol, high serum triglycerides, thick triceps skinfold and self-esteem problems coexisted and they can be supposed to independently contribute to the aetiology of CHD.

Social and psychologic factors in the etiology of coronary heart disease in black populations: An exploration of research needs

A number of findings that have broad relevance for the planning of future studies of psychosocial risk factors for coronary heart disease (CHD) in blacks were examined. These included data on marital status, social networks, health practices, well-being, distress, mental health, the residential environment, components of high blood pressure control, and health attitudes among youth. It is concluded that the specific research literature on psychosocial risk factors for CHD is almost entirely based on the study of white populations and does not constitute a compelling basis for recommending research programs on blacks. Instead, it is suggested that the starting point be a comprehensive examination of the psychosocial aspects of the black experience and of its etiologic linkages to a variety of health outcomes.