Medical, Socialogical and environmental issues in cardiovascular disease epidemiology, prevention and rehabilitation.
Sheenu Jhawar
Apex Hospitals Pvt Ltd., Malviya Nagar, Jaipur302016 India
The global burden of coronary heart disease (CHD) is rapidly increasing to the effect that it is likely to be the most common cause of disability-adjusted life years (DALY) loss in year 2020 as compared to fifth position in 1990 (1). There have been two major changes in the epidemiology of CHD over recent years: (i) a changing social class distribution of the disease (2) and (ii) a rise and fall in CHD in different countries (3). In many European countries and in US as CHD became a mass disease it increased first in higher socio-economic groups and subsequently in lower classes. The social distribution changed to the now familiar pattern of inverse social gradient- higher rates as the social hierarchy is descended. More recently, the decline in CHD mortality both in the United Kingdom and the USA is being enjoyed to a greater extent by higher socio-economic groups leading to a widening of the social gap (4).
A study carried out by Professor Davey-Smith of the Northern and Yorkshire Research and Development Directorate (UK) investigated the same concept. The study was based on the premise that people in lower social classes have higher rates of morbidity and mortality from cardiovascular disease than those in higher classes. At the same time the following was also realised that there is debate about the extent to which this is related to early life experience or to a higher prevalence of risk factors. The prospective study showed that deprivation corresponding with socio-economic status in early life is strongly related to stroke risk, while coronary heart disease risk appears to be influenced by socially patterned exposures acting across the life course.
This debate about the origin of cardiovascular disease (CVD) in early life has important implications for health promotion and prevention of the disease. If the risk of disease in adulthood is substantially influenced by either biological programming in utero (5,6) or circumstances in early life (7,8,9) then, a serious thought is required to evaluate the importance of current attempts underway, which only target areas like encouraging healthy lifestyles in adults. It is imperative that policies for the control of the disease are revised in light of the recent and upcoming scientifically based evidence. Various disease prevention strategies, are usually focussed for the urban dwellers. The spotlight is on physical fitness programmes, change in diet programmes, and improvement in the sedentary lifestyles. Are we assuming that the urban rich are the only begetters of the disease?
Various studies done around the globe point out, that there is much more than meets the eye. The fact sheet by the World Health Organisation on cardiovascular disease states that in developed countries lower socio-economic groups have greater prevalence of risk factors, higher incidence of disease and higher mortality. In developing countries as the CVD epidemic matures the burden will shift to the lower socio-economic groups. The fact sheet points that newly emerging CVD risk factors like low birth weight, folate deficiency and infections are also more frequent among the poorest in low and middle income countries.
In India, the prevalence of CHD has been reported at 4% in the rural (10) and 11% (11) in the urban populations. However there may be many facets to these figures. One could be, given that, prevalence reflects the incidence times the duration of illness and with the apparent quality accessibility and availability of medical care distribution in the rural and urban areas, the mortality rates between the two may be quite different. As a result length of morbidity might confer greater magnitude to the disease profile in the urban population as opposed to rural population at any given point in time. While the determinants of health transition in the developing countries are similar to those that charted the course of the epidemics in the developed countries, their dynamics are different. The compressed time frame of transition in the developing countries imposes a large, double burden of communicable and non-communicable diseases. Unlike in the developed countries where urbanisation occurred in prospering economies, urbanisation in developing countries occurs in settings of high poverty levels and international debt, restricting resources for public health responses (12). There are several biological, behavioural, psychological and social risk factors that have been well recognised as risk factors for CHD. Sevaral aspects need to be recognised in this framework. Multiplicative risk arising from a combination of risk factors might help in explaining the recent emergence, and underlie the projected escalation, of the CVD epidemic in the developing countries (13).
Insight into south Asian coronary risk comes from study of the prevalence rates (mortality and morbidity data) amongst expatriate population which reveals that this group, as an ethnic entity, has increased prevalence and definite evidence of excess mortality from CHD as compared to other groups (14,15). This phenomenon was described initially for the colonial plantation workers in the Pacific Islands in the early 1950s (16). And was later confirmed by mortality and morbidity data from UK and USA (17,18) and subsequently from other parts of the world (19,20).
In developing countries low birth weight, thinness and short body length at birth are known to be associated with increased rates of cardiovascular disease and non-insulin dependent diabetes later in life (21,22). Recently low birth weight is reported to be associated with endothelial dysfunction in young adults; an effect most marked in individuals with lower risk factor profiles and may be relevant to the pathogenesis of atherosclerosis in later life (23). Data from India supports the high rates of CHD amongst those studied whose mothers had a low body weight during pregnancy. The highest prevalence of disease (20%) was in people who weighed 5.5 lb (2.5 kg) or less at birth and whose mothers weighed less than 100 lb (45 kg) in pregnancy (24).
Even though the current figures that in India, rural prevalence of the disease is a lesser than the urban areas, yet, in light of the evidenced based risk of CHD several many issues need to be borne in mind Firstly, when low birth weight is considered a risk factor for CHD, then it needs to be realised that since rural population has apparently a higher infant mortality rate (IMR), therefore many children of low birth weight (a phenomenon which is bound to occur more in the rural pop.) might succumb. On the other hand in urban areas, even children with low birth weight will survive due to better medical conditions. In later life this may contribute to a greater morbidity and mortality in urban population, because of the higher survival of such children. However in current years, due to increasing medical facilities, and with improving IMR, in rural areas , children with low birth weight might survive more in numbers as compared to previous times, leading to high CHD risk pool even in rural areas.
Childhood poverty followed by high standards of living is known to operate at least partly as a risk factor of coronary heart disease through conventional risk factors (25). Lower socioeconomic status (SES) in childhood is associated with higher levels of hostility, depression and hopelessness; greater tobacco consumption and alcohol abuse; less leisure time physical activity; obesity and a less nutritious diet in adulthood (26). Socioeconomic factors may be considered as important elements of the risk profile of this population in view of prevailing economic situation; there is potential to further explore this risk factor in the native South Asian setting. Several studies have confirmed a graded, inverse relation between SES and the risk of CHD, CVD and all-cause mortality (27-29), There is also an inverse relationship between SES and conventional risk factors (30) . Concurrence of risk factors; that can have a synergistic effect on the risk for CVD (31) has been shown to be higher in less educated groups.

In this context several studies in Norway have shown large differences in risk factors for arteriosclerotic heart disease among municipalities. Today it is difficult to show specific differences in the standard of living between the various municipalities to explain these findings. However, such differences have previously existed, and were expressed by, for example, the variations in infant mortality from one municipality to another. In this work a significant positive correlation is shown between the cholesterol values among men and women aged 35-49 years and the infant mortality rate previously present in the municipalities for the same cohort. The findings indicate that poverty in childhood and adolescence, followed by later prosperity, results in high cholesterol values. The findings are related to previous work where a significant positive correlation was shown between infant mortality rates and later mortality rates from arteriosclerotic heart disease. Besides childhood factors, it has been found that among a number of different diseases have been related to psychosocial conditions in the workplace, most notable is CHD.

Since then, a large number of prospective and cross-sectional studies on associations of stressful work as defined by high demand and low control (job strain) with cardiovascular risk and disease have been conducted (Karasek and Theorell 1990, Schnall and Landsbergis 1994, Kristensen 1995, Theorell and Karasek 1996, Hemingway and Marmot 1998). A number of these studies have focused on methodological considerations and have used new outcome measures, the majority of which have revealed positive findings.

The importance of work related psychosocial factors to the development of ill health and disease can be illustrated from the Whitehall studies of British civil servants.(32). In this, one hypothesis is that the lower the grade of employment in the civil service, the lower the level of control over the job, the lower the use of skills and the higher the level of monotony. These may be related to the higher rate of cardiovascular and other diseases in lower employment grades. The results of the study show that both men and women with low control, either self-reported or independently assessed, have a higher risk of newly reported CHD during a mean follow-up period of five years. The differing associations between aspects of the psychosocial work environment and CHD correspond to the review by Schnall and Landsbergis (1994), in which 17 out of 25 studies found significant associations between job control and cardiovascular outcome, whereas associations with job demands were significant in only eight out of 23 studies.
The soluble protein fibrinogen circulates in the blood and provides the material from which the insoluble fibrin clot is formed during blood coagulation. High plasma fibrinogen concentration predicts future CHD in men and women. High plasma fibrinogen concentration in adulthood is associated with elevated risk of CHD and stroke. Prospective studies in healthy men and women have shown that a single fibrinogen measurement predicts fatal and non-fatal cardiovascular events as much as 16 years later (33-36). The adult fibrinogen level appears to be determined by environmental factors operating throughout the life course, and levels are inversely related to socioeconomic status. The Whitehall II study shows that low control at work is associated with a high fibrinogen level, thus providing evidence that chronic psychosocial stress is indexed by plasma fibrinogen. An alternative view is that the prospective fibrinogen-cardiovascular disease association may be a consequence, rather than a cause, of the disease process, perhaps due to an inflammatory response to progressive endothelial damage. This view identifies fibrinogen as a marker of long-term pathophysiological changes. Both perspectives, which are certainly not mutually exclusive, support the use of fibrinogen as a cardiovascular risk factor in epidemiological studies (37).

About one half of the population variance of fibrinogen appears to be genetically determined. Weight at one year, but not birth weight, has been shown to be related to fibrinogen level: heavier infants have lower fibrinogen levels in adulthood. (38). Measures of childhood environment, adult height, father's social class, and level of education, are inversely associated with adult plasma fibrinogen level in both sexes (37).A pilot study (39) in male civil servants suggested that low control, monotony and under-utilisation of skills at work are related to raised fibrinogen levels. It may be that fibrinogen may account, in part, for the high rates of coronary disease experienced by people in unfavorable socioeconomic circumstances, which cannot be explained by the classical determinants of coronary risk (40). Fibrinogen may thus be a marker of the specific biological pathways which mediate the inverse socioeconomic gradient in coronary disease.

India is at a much earlier stage of the transition and only the urban areas are currently greatly affected by the disease profile. Nonetheless the burden of CHD is great and there is evidence based probability of a large, increase in all sectors of the society, particularly in the low socio-economic strata. The influence on mortality risk through CHD is an accumulative, acting throughout the individual's life. It starts from the previous generation, even before birth, as shown by the impact of mother's weight, and then antenatal characteristics, through the socioeconomic conditions, on any individual. It, therefore, requires a far reaching policy to address the growing disease burden. Bearing in mind the demographic diversity in India, the policies have to be customized, and targeted strategically for the prevention and control of the disease.
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