CORONARY HEART DISEASE RISK FACTORS : NEW PRIORITIES FOR THE DEVELOPING WORLD

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

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. in rural areas . rural prevalence of the disease is a lesser than the urban areas.might help in explaining the recent emergence. therefore many children of low birth weight (a phenomenon which is bound to occur more in the rural pop. Since then. leading to high CHD risk pool even in rural areas. Several studies have confirmed a graded. the variations in infant mortality from one municipality to another. greater tobacco consumption and alcohol abuse. Recently low birth weight is reported to be associated with endothelial dysfunction in young adults. The findings indicate that poverty in childhood and adolescence. yet. as an ethnic entity. Today it is difficult to show specific differences in the standard of living between the various municipalities to explain these findings. GENETIC FACTORS 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. of the CVD epidemic in the developing countries (13). 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. has increased prevalence and definite evidence of excess mortality from CHD as compared to other groups (14. However in current years.18) and subsequently from other parts of the world (19. This phenomenon was described initially for the colonial plantation workers in the Pacific Islands in the early 1950s (16). ANTENATAL FACTORS In developing countries low birth weight. CVD and all-cause mortality (27-29). one hypothesis is that the lower the grade of employment in . the majority of which have revealed positive findings. Data from India supports the high rates of CHD amongst those studied whose mothers had a low body weight during pregnancy. inverse relation between SES and the risk of CHD. there is potential to further explore this risk factor in the native South Asian setting. In this context several studies in Norway have shown large differences in risk factors for arteriosclerotic heart disease among municipalities. depression and hopelessness. Besides childhood factors. followed by later prosperity. Kristensen 1995. There is also an inverse relationship between SES and conventional risk factors (30) . less leisure time physical activity. Socioeconomic factors may be considered as important elements of the risk profile of this population in view of prevailing economic situation. Schnall and Landsbergis 1994. results in high cholesterol values. Hemingway and Marmot 1998). A number of these studies have focused on methodological considerations and have used new outcome measures. and were expressed by. And was later confirmed by mortality and morbidity data from UK and USA (17. such differences have previously existed. Lower socioeconomic status (SES) in childhood is associated with higher levels of hostility. In later life this may contribute to a greater morbidity and mortality in urban population. and with improving IMR. it has been found that among a number of different diseases have been related to psychosocial conditions in the workplace. due to increasing medical facilities.5 lb (2. most notable is CHD. that can have a synergistic effect on the risk for CVD (31) has been shown to be higher in less educated groups.) might succumb.15).22). 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. for example.20).(32). In this. and underlie the projected escalation. because of the higher survival of such children. Even though the current figures that in India. SOCIOECONOMIC FACTORS 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). an effect most marked in individuals with lower risk factor profiles and may be relevant to the pathogenesis of atherosclerosis in later life (23). children with low birth weight might survive more in numbers as compared to previous times. even children with low birth weight will survive due to better medical conditions. in light of the evidenced based risk of CHD several many issues need to be borne in mind Firstly. On the other hand in urban areas. However. The highest prevalence of disease (20%) was in people who weighed 5. 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. 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. Concurrence of risk factors. obesity and a less nutritious diet in adulthood (26). then it needs to be realised that since rural population has apparently a higher infant mortality rate (IMR). Theorell and Karasek 1996. when low birth weight is considered a risk factor for CHD.5 kg) or less at birth and whose mothers weighed less than 100 lb (45 kg) in pregnancy (24).

father's social class. An alternative view is that the prospective fibrinogen-cardiovascular disease association may be a consequence. High plasma fibrinogen concentration predicts future CHD in men and women. About one half of the population variance of fibrinogen appears to be genetically determined. and Pisa. Martyn CN (1992). 7. The results of the study show that both men and women with low control. either self-reported or independently assessed. and targeted strategically for the prevention and control of the disease. as shown by the impact of mother's weight. High plasma fibrinogen concentration in adulthood is associated with elevated risk of CHD and stroke. and level of education. through the socioeconomic conditions. Fetal and infant origins of adult disease. (1988). J Epidemiol Community Health. The influence on mortality risk through CHD is an accumulative. has been shown to be related to fibrinogen level: heavier infants have lower fibrinogen levels in adulthood. Am J Public Health. have a higher risk of newly reported CHD during a mean follow-up period of five years.G. for the high rates of coronary disease experienced by people in unfavorable socioeconomic circumstances. These may be related to the higher rate of cardiovascular and other diseases in lower employment grades. 3-19 Uemura.A pilot study (39) in male civil servants suggested that low control. the lower the use of skills and the higher the level of monotony. 82:204-209 Barker DJP (1992). (1992). Measures of childhood environment. Riggan. Weight at one year. It starts from the previous generation. London. (eds. in which 17 out of 25 studies found significant associations between job control and cardiovascular outcome. Oxford University Press.) Coronary Heart Disease Epidemiology. which are certainly not mutually exclusive. Oxford. in part. W. M. S. which cannot be explained by the classical determinants of coronary risk (40). therefore. the lower the level of control over the job. but not birth weight. Global Burden of Disease and Injury Series. Z. 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. Geographic and socioeconomic variation in the onset of decline of coronary heart disease mortality in white woman. Nonetheless the burden of CHD is great and there is evidence based probability of a large. 6. Murray CJL. 41:155-178 Wing. monotony and under-utilisation of skills at work are related to raised fibrinogen levels. adult height. Both perspectives. of the disease process. support the use of fibrinogen as a cardiovascular risk factor in epidemiological studies (37). on any individual. M.the civil service. Trends in cardiovascular disease mortality in industrialised countries since 1950. BMJ Publishing. are inversely associated with adult plasma fibrinogen level in both sexes (37). rather than a cause. Casper M. thus providing evidence that chronic psychosocial stress is indexed by plasma fibrinogen. The adult fibrinogen level appears to be determined by environmental factors operating throughout the life course. Harvard School of Public Health Marmot. Lopez AD (1996). particularly in the low socio-economic strata. Boston. Global Health Statistics. This view identifies fibrinogen as a marker of long-term pathophysiological changes. The differing associations between aspects of the psychosocial work environment and CHD correspond to the review by Schnall and Landsbergis (1994). even before birth. whereas associations with job demands were significant in only eight out of 23 studies. REFERENCES 1. Barker DJP. Fibrinogen may thus be a marker of the specific biological pathways which mediate the inverse socioeconomic gradient in coronary disease. requires a far reaching policy to address the growing disease burden. (38). K. It may be that fibrinogen may account. perhaps due to an inflammatory response to progressive endothelial damage. 3. 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). World Health Stat Q. 4. Bearing in mind the demographic diversity in India. In: Marmot. (1992). and then antenatal characteristics. P. Coronary heart disease: rise and fall of a modern epidemic. and Elliott. India is at a much earlier stage of the transition and only the urban areas are currently greatly affected by the disease profile. 5.G. 46:8-11 Forsdahl A (1978). It. acting throughout the individual's life. increase in all sectors of the society. FIBRINOGEN AS MARKER OF SOCIOECONOMIC STATUS The soluble protein fibrinogen circulates in the blood and provides the material from which the insoluble fibrin clot is formed during blood coagulation. J Epidemiol Community . 2. The maternal and fetal origins of cardiovascular disease. the policies have to be customized. Living conditions in childhood and subsequent development of risk factors for arteriosclerotic heart disease: the cardiovascular survey in Finmark 1974-75.

Armstrong MA. Kakkar VV. Trejo-Gutierrez H (1993). Cohen RD. J Clin Epidemiol. Wadsworth MEJ. Why do poor people behave poorly? Variations in adult health behaviours and psychological characteristics by stages of socioeconomic life course. Kattenhorn M. 9. J Am Coll Cardiol. Coronary heart disease in South Asian overseas. Dyer A. Malignant coronary artery disease in young Asian Indians: thoughts on pathogenesis.. Cripps HA. Lancet. Oxford University Press. 18:131-135 15. Barker DJP (2000). 53:555-574 22. Salonen R. Mohan V. Relationship of education to major risk factors and death from coronary heart disease. Deanfield JE (2001). Ed. Colley JRT (1985). pp. 32:34-37 8. Socioeconomic status and carotid atherosclerosis. Miller GJ. Impact of low birth weight and cardiovascular risk factors on endothelial function in early adult life. prevention and therapy. Chew SK. BMJ. Rose G. Coronary heart disease epidemiology in India: the past.Health. 39:210-214 26. 17. J Epidemiol Comm Health. The Tromso heart study: coronary risk factors and their association with living conditions during childhood. Klatsky AL. Oxford University Press.Kustner HG (1988). 6-28 11. Soc Sci Med. Theriogenology.103:1264-1268 24. Prevalence of coronary heart disease and its relationship to lipids in a selected population in South India: The Chennai Urban Population Study. Salonen JT (1995). 30:983-988 21. Gupta R (2001).Balfe DL. Arnesen E. The risk of hospitalization for ischaemic heart disease among Asian Americans in northern California. Blane D. Fetal growth and coronary heart disease in South India. Mehta J (1995). 84:1672-1675 19. 297:903-904 18. Marmot MG (1989). Fetal nutrition and adult disease. 291:1534-1538. BMJ. Tan BY. McKeigue PM. Tinker H(1974). 5(1A): 231-237 13. Salonen JT (1997). dynamics and directions for public health action. 309:1475-1478 10. Circulation. Stamler R. BMJ. determinants. 577-599 14. A new system of slavery: the export of Indian labor overseas 1830-1920. Br Heart J. Davey Smith G. Reddy KS (1997). Stamler J. Osmond C. 42:597-609 16. Birthweight and later socioeconomic disadvantage: evidence from the 1958 British cohort study. Bartley M. Kumaran K. Cox V. Heng D. Barker DJ (1996). Risk factors and incident coronary heart disease in Chinese. Marmot MG (1981). Coronary artery disease in South Asians. Editors. Premlatha G (2001). Circulation. Nanas S (1982). McKeigue PM. In-utero programming of cardiovascular disease. present and future. 92:786-1792 . 71(suppl):1344S1352S 23. 74:547-550 20. In: Rao GHR. Sidney S (1994). Decline in the ischaemic heart disease mortality rates of South Africans: 1968-1985. Chia KS. 66:308-314 29. Disease control priorities in developing countries. Am J Public Health. Liu K. Circulation. Kaplan GA. Oxford. New York. New Delhi (India): Jaypee Brothers. Godfrey DM. Kaplan GA. Midwinter RA. 44:809-819 27. Social Class and coronary heart disease. Lynch JW. Blood pressure at age 36 years and social and familial factors. Barker DJ (2000). 348:1269-1273 25. Shipley M (1994). Steinberg WJH. Deepa R. Malay and Asian Indian males: the Singapore cardiovascular cohort study. Stein CE. Lynch J. Morley R. Jamison DT. Forsdahl A (1985). Marmot MG (1988). cardiovascular diseases and all causes: Finding of three Chicago epidemiological studies. S Afr Med J. Cardiovascular diseases in the developing countries: dimensions. Public Health Nutrition. Pearson TA. Hughes K (2001).Fall CH. Int J Epidemiol. Cedres LB. Am J Clin Nutr. Leeson CPM. Rani SS. TekawaI. Clin Cardiol. Enas EA. Mortality from coronary heart disease in Asian communities in London. Power C. In: Jamison DT. Lee J. 45:13-19 28. Lucas A. 38:682-687 12.

Freeney A (1991). 311:501-505 35. Head J. Relation of fetal and infant growth to plasma fibrinogen and factor V concentrations in adult life. Meade TW. Meade TW. Verkleij H. BMJ. Lancet. Bainton D. North F. Baker IA. Stirling Y (1992). and long-term incidence of ischaemic heart disease in the Northwick Park Heart Study. Barker DJP. Int J Health Sec. Fall CHD. D'Agostino RB (1987). Elwood PC. JAMA. Semmence A (1985). J Epidemiol Comm Health. 20:405-416 31. Kromhout D (1996). Bulpitt CJ. Brunner EJ. Hamilton PJS (1978). Stirling Y. BMJ. 291:13121314 40. Stirling Y. Canner R. Marmot MG. White I. Shipley MJ. Franks P (1990). Childhood social circumstances and psychosocial and behavioural factors as determinants of plasma fibrinogen. 258:1183-1186 36. et al (1984). viscosity and white blood cell count are major risk factors for ischemic heart disease 37. Meade TW. Beksinska M. Fibrinogen as a risk factor for stroke and myocardial infarction. O'Brien JR. Gold MR. Korsan-Bengsten K. Davey Smith G. Svardsudd K. 337:1387-1393 33. Miller GJ (1993). Fibrinogen and risk of cardiovascular disease. Fibrinolytic activity. Castelli WP. Whitehead PJ. clotting factors. Employment grade and coronary heart disease in British civil servants. Eur Heart J. 342:1076-1079 34. 304:148-152 39. Wolf PA. Fibrinogen: a possible link between social class and coronary heart disease. Davey Smith G. SmitHA. Hoeymans N. Rose G. Markowe HLJ. Wilhelmsen L. Marmot MG. 347:1008-1013 38. Health inequalities among British Civil Servants: the Whitehall II study . N Engl J Med. Stansfeld SA. Marmot M. Lancet. Yarnell JWG. Marmot MG. Lancet.000 men and women in the Netherlands. Phipps K. Vickers MV. 17:518-525 32. Brunner EJ. Fibrinogen. Ruddock V. Patel C. Lee A. Chakrabarti R. Sweetnam PM. O'Brien J (1996). Cardiovascular risk factors in relation to educational level in 36. 32: 244-249 .30. The social origin of cardiovascular risk: an investigation in a rural community. Shipley M. Kannel WB. Osmond C.

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