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| 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 might help in explaining the recent emergence, and underlie the
projected escalation, of the CVD epidemic in the developing countries (13). |
| |  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,
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). |
| | | ANTENATAL
FACTORS | | | | 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. | | |
| 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).
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. | | |
| 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.
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. | | | | REFERENCES |
| |
| 1. |
Murray CJL, Lopez AD (1996). Global Health Statistics. Global Burden of Disease
and Injury Series. Boston. Harvard School of Public Health |
| 2. | Marmot,
M.G. (1992). Coronary heart disease: rise and fall of a modern epidemic. In: Marmot,
M.G. and Elliott, P. (eds.) Coronary Heart Disease Epidemiology. Oxford. Oxford
University Press. 3-19 | | 3. |
Uemura, K. and Pisa, Z. (1988). Trends in cardiovascular disease mortality in
industrialised countries since 1950. World Health Stat Q. 41:155-178 |
| 4. |
Wing, S. Casper M, Riggan, W. (1992). Geographic and socioeconomic variation in
the onset of decline of coronary heart disease mortality in white woman. Am J
Public Health. 82:204-209 | | 5. |
Barker DJP (1992). Fetal and infant origins of adult disease. London. BMJ Publishing. |
| 6. |
Barker DJP, Martyn CN (1992). The maternal and fetal origins of cardiovascular
disease. J Epidemiol Community Health. 46:8-11 | | 7. |
Forsdahl A (1978). Living conditions in childhood and subsequent development of
risk factors for arteriosclerotic heart disease: the cardiovascular survey in
Finmark 1974-75. J Epidemiol Community Health. 32:34-37 |
| 8. | Wadsworth
MEJ, Cripps HA, Midwinter RA, Colley JRT (1985). Blood pressure at age 36 years
and social and familial factors. BMJ. 291:1534-1538. |
| 9. | Bartley
M, Power C, Blane D, Davey Smith G, Shipley M (1994). Birthweight and later socioeconomic
disadvantage: evidence from the 1958 British cohort study. BMJ. 309:1475-1478 |
| 10. |
Gupta R (2001). Coronary heart disease epidemiology in India: the past, present
and future. In: Rao GHR, Kakkar VV. Editors. Coronary artery disease in South
Asians.. New Delhi (India): Jaypee Brothers. pp. 6-28 |
| 11. | Mohan V,
Deepa R, Rani SS, Premlatha G (2001). Prevalence of coronary heart disease and
its relationship to lipids in a selected population in South India: The Chennai
Urban Population Study. J Am Coll Cardiol. 38:682-687 |
| 12. | Reddy KS
(1997). Cardiovascular diseases in the developing countries: dimensions, determinants,
dynamics and directions for public health action. Public Health Nutrition. 5(1A):
231-237 | | 13. |
Pearson TA, Jamison DT, Trejo-Gutierrez H (1993). In: Jamison DT. Ed. Disease
control priorities in developing countries. New York. Oxford University Press.
577-599 | | 14. |
Enas EA, Mehta J (1995). Malignant coronary artery disease in young Asian Indians:
thoughts on pathogenesis, prevention and therapy. Clin Cardiol. 18:131-135 |
| 15. |
McKeigue PM, Miller GJ, Marmot MG (1989). Coronary heart disease in South Asian
overseas. J Clin Epidemiol. 42:597-609 | | 16. |
Tinker H(1974). A new system of slavery: the export of Indian labor overseas 1830-1920.
Oxford. Oxford University Press. | | 17. |
McKeigue PM. Marmot MG (1988). Mortality from coronary heart disease in Asian
communities in London. BMJ. 297:903-904 | | 18. |
Klatsky AL, TekawaI, Armstrong MA, Sidney S (1994). The risk of hospitalization
for ischaemic heart disease among Asian Americans in northern California. Am J
Public Health. 84:1672-1675 | | 19. |
Steinberg WJH,Balfe DL,Kustner HG (1988). Decline in the ischaemic heart disease
mortality rates of South Africans: 1968-1985. S Afr Med J. 74:547-550 |
| 20. |
Lee J, Heng D, Chia KS, Chew SK, Tan BY, Hughes K (2001). Risk factors and incident
coronary heart disease in Chinese, Malay and Asian Indian males: the Singapore
cardiovascular cohort study. Int J Epidemiol. 30:983-988 |
| 21. | Barker
DJP (2000). In-utero programming of cardiovascular disease. Theriogenology. 53:555-574 |
| 22. |
Godfrey DM, Barker DJ (2000). Fetal nutrition and adult disease. Am J Clin Nutr.
71(suppl):1344S-1352S | | 23. |
Leeson CPM, Kattenhorn M, Morley R, Lucas A, Deanfield JE (2001). Impact of low
birth weight and cardiovascular risk factors on endothelial function in early
adult life. Circulation.103:1264-1268 | | 24. |
Stein CE,Fall CH, Kumaran K, Osmond C, Cox V, Barker DJ (1996). Fetal growth and
coronary heart disease in South India. Lancet. 348:1269-1273 |
| 25. | Arnesen
E, Forsdahl A (1985). The Tromso heart study: coronary risk factors and their
association with living conditions during childhood. J Epidemiol Comm Health.
39:210-214 | | 26. |
Lynch JW, Kaplan GA, Salonen JT (1997). Why do poor people behave poorly? Variations
in adult health behaviours and psychological characteristics by stages of socioeconomic
life course. Soc Sci Med. 44:809-819 | | 27. |
Rose G, Marmot MG (1981). Social Class and coronary heart disease. Br Heart J.
45:13-19 | | 28. |
Liu K, Cedres LB, Stamler J, Dyer A, Stamler R, Nanas S (1982). Relationship of
education to major risk factors and death from coronary heart disease, cardiovascular
diseases and all causes: Finding of three Chicago epidemiological studies. Circulation.
66:308-314 | | 29. |
Lynch J, Kaplan GA, Salonen R, Cohen RD, Salonen JT (1995). Socioeconomic status
and carotid atherosclerosis. Circulation. 92:786-1792 |
| 30. | Gold MR,
Franks P (1990). The social origin of cardiovascular risk: an investigation in
a rural community. Int J Health Sec. 20:405-416 | | 31. |
Hoeymans N, SmitHA, Verkleij H, Kromhout D (1996). Cardiovascular risk factors
in relation to educational level in 36,000 men and women in the Netherlands. Eur
Heart J. 17:518-525 | | 32. |
Marmot MG, Davey Smith G, Stansfeld SA, Patel C, North F, Head J, White I, Brunner
EJ, Freeney A (1991). Health inequalities among British Civil Servants: the Whitehall
II study . Lancet. 337:1387-1393 | | 33. |
Meade TW, Ruddock V, Stirling Y, Chakrabarti R, Miller GJ (1993). Fibrinolytic
activity, clotting factors, and long-term incidence of ischaemic heart disease
in the Northwick Park Heart Study. Lancet. 342:1076-1079 |
| 34. | Wilhelmsen
L, Svardsudd K, Korsan-Bengsten K, et al (1984). Fibrinogen as a risk factor for
stroke and myocardial infarction. N Engl J Med. 311:501-505 |
| 35. | Kannel
WB, Wolf PA, Castelli WP, D'Agostino RB (1987). Fibrinogen and risk of cardiovascular
disease. JAMA. 258:1183-1186 | | 36. |
Yarnell JWG, Baker IA, Sweetnam PM, Bainton D, O'Brien JR, Whitehead PJ, Elwood
PC. Fibrinogen, viscosity and white blood cell count are major risk factors for
ischemic heart disease | | 37. |
Brunner EJ, Davey Smith G, Marmot M, Canner R, Beksinska M, O'Brien J (1996).
Childhood social circumstances and psychosocial and behavioural factors as determinants
of plasma fibrinogen. Lancet. 347:1008-1013 | | 38. |
Barker DJP, Meade TW, Fall CHD, Lee A, Osmond C, Phipps K, Stirling Y (1992).
Relation of fetal and infant growth to plasma fibrinogen and factor V concentrations
in adult life. BMJ. 304:148-152 | | 39. |
Markowe HLJ, Marmot MG, Shipley MJ, Bulpitt CJ, Meade TW, Stirling Y, Vickers
MV, Semmence A (1985). Fibrinogen: a possible link between social class and coronary
heart disease. BMJ. 291:1312-1314 | | 40. |
Marmot MG, Rose G, Shipley M, Hamilton PJS (1978). Employment grade and coronary
heart disease in British civil servants. J Epidemiol Comm Health. 32: 244-249 | | | |
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