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Cardiovascular disease remains the biggest killer of south Asians in the UK ­ Dr Kiran Patel, Professor Raj Bhopal and Professor Jaspal Kooner explain how knowledge has grown

and what GPs can do

South Asians have the highest overall and premature CHD mortalities of any UK ethnic group. And as CHD rates have fallen in the general UK population, the disparity between south Asians and their white counterparts has become even more marked. For example CHD mortality is 46 per cent higher in south Asian males and 51 per cent higher in south Asian females, compared with the UK white European population.

And the young are most at risk with mortality rates double in the 30-40 age group and triple in the 20-30 age group1.

Speculation about the increased mortality from CHD in migrant south Asians began more than 50 years ago. Since then the higher CHD mortality in migrant south Asian populations compared with the indigent population has become a consistent finding. The causes, consequences, prevention and treatment of CHD must be confronted in these populations, which as the largest UK ethnic group comprise 4 per cent of the population.

Why are disease rates so high?

South Asians are a heterogeneous group that includes Bangladeshi, Gujarati, Punjabi, Pakistani and Sri Lankan, with a diversity of culture and religion. But they all have one thing in common ­ current CHD risk prediction models underestimate the levels of risk for all of them by at least 50 per cent.

Classical risk factors

Another big question is whether there is an increased prevalence of classical risk factors in south Asians. Conventional risk factors are undoubtedly important. Let us discuss these individually and highlight where there is potential for disparity with the general population.


·Male sex

·Family history Supporting this is evidence that a component of insulin resistance is inherited in south Asians.

·Socioeconomic deprivation South Asians are more likely to live in areas of socioeconomic deprivation.

·Smoking Paradoxically, despite Sikhs and Hindus having lower rates of smoking than the general population, CHD rates are higher, suggesting increased potency of/or additional risk factors.

·Blood pressure BP levels are actually lower in UK Bangladeshi and Pakistani populations compared with the general population.

·Lipids Low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol (HDL) levels are similar to the general

population. Rapid changes in levels per se may confer an increased risk but, for example, Punjabis in Southall have a mean cholesterol of 6.5mmol/L compared with 4.9mmol/L for their siblings in India.

·Diabetes and the metabolic syndrome Diabetes prevalence is 2-5 per cent in rural Indians, 5-10 per cent in urban Indians, almost 20 per cent in UK south Asians and 4 per cent in UK white Europeans. There is a striking five-fold increased CV mortality rate in the diabetic south Asian population4. UK south Asians also develop diabetes on average 10 years earlier than their white counterparts. Elevated fasting and post-prandial glucose concentrations are associated with increased CHD risk, even in non-diabetic subjects.

·Obesity Body fat distribution follows an adverse centripetal pattern with increased visceral adiposity (higher waist-hip ratio) compared with white Europeans, for the same level of BMI. Such fat and its distribution has different metabolic characteristics and is associated with the metabolic syndrome, diabetes, inflammation and CHD. The World Health Organisation has suggested lower BMI thresholds to define obesity and 'overweight' than those used conventionally for the general population.

·Physical inactivity Exceptionally low rates of physical activity are seen from childhood into adulthood. More physical activity would promote reduction in weight, serum insulin, hyperuricaemia and diastolic blood pressure, and increases HDL. It may also delay or prevent the onset of diabetes.

·An atherogenic diet Ghee and other cooking oils are often advocated to be a major determinant of CHD in south Asians but their contribution may be exaggerated. UK south Asians have higher intakes of polyunsaturated fat and carbohydrate, and lower saturated fat intakes, compared with white Europeans. Some have therefore described this diet as favourable. However, total dietary fat constitutes less than 15 per cent of energy in rural India, compared with more than 30 per cent in the UK, suggesting that what might initially be perceived as a favourable diet may, in these populations, still promote insulin resistance.

·Metabolic syndrome Interestingly, south Asians may be 12-40 per cent more insulin resistant than their white counterparts, ie they require larger amounts of insulin to maintain normoglycaemia. Insulin resistance increases levels of free fatty acids and promotes a pattern of dyslipidaemia which is associated with increased entry of cholesterol into, and reduced clearance from, the arterial wall. Insulin resistance and its related metabolic abnormalities (central obesity, glucose intolerance, increased triglycerides, raised plasminogen activator inhibitor, and reduced HDL) are more common among south Asians.

Non-classical risk factors

The prevalence of non-classical risk factors is high. Several factors have been postulated, but there is a paucity of data to confirm or refute their contribution.

·Increased lipoprotein(a) may influence cholesterol uptake, and combined with a Westernised lifestyle, it is plausible that such a genetic tendency is translated into increased clinical risk.

·Sub-clinical hypothyroidism

·Homocysteine levels are higher in south Asians.

·Infection and inflammation Inflammation is central to atherogenesis and destabilisation of the atherosclerotic plaque. C-reactive protein levels, a sensitive index of inflammation, are higher in healthy asymptomatic south Asians than in white Europeans.

·Quality of care Despite being more likely than white Europeans to seek medical advice for symptoms suggestive of angina, south Asians are less likely to be referred for exercise testing, have to wait longer to be seen by a cardiologist, face longer waits for angiography, and are less likely to receive thrombolysis for acute myocardial infarction.

·Endothelial dysfunction is impaired in healthy UK south Asians compared with white Europeans and may be the final common pathway in CHD pathogenesis.

·Migration and urbanisation The Indian subcontinent is beginning to show increased levels of CHD among city dwellers compared with their rural counterparts. However, migration per se is not the sole reason, since not all migrants suffer adversely from CHD, eg UK Afro-Caribbean and Chinese populations do not have an increased risk of CHD compared with the general population.

Causal factors

Is there is a potent interaction of known causal factors specific to south Asian groups?

The INTERHEART study5 indicated a common base of nine risk factors responsible for CHD worldwide. Variation in CHD rates therefore implies differential interaction of risk factors or the presence of additional risk factor(s) to account for increased risk in the south Asian population.

What needs to be done2

Lost time needs to be made up. Past attention focused on 'Asian specific problems', for example rickets, with little attention to the CHD epidemic which was accountable for up to 50 per cent of deaths. Only recently have we witnessed an increase in educational materials tailored for south Asians. Confronting the challenge of CHD in south Asians requires a co-ordinated public health strategy based on evidence and expected standards specified in guidelines such as the national service framework. This strategy must incorporate2:

·Valid ethnic coding of disease registers and practice lists. Ethnic monitoring is not mandatory within primary care, which partly explains the paucity of routine data.

·Research support. No large-scale prospective study has examined CHD and risk factors and mortality in south Asians.

·Clear guidelines. Intervention thresholds may be lower than in European origin populations and guidelines for primary prevention must reflect this, for example a 50 per cent increase in CHD rates in south Asians suggests that statin therapy should commence at a 10-year risk of 10 per cent in south Asian diabetics rather than 15 per cent as current NICE guidance recommends.

·Ensure south Asian patients and communities are well informed about CHD.

·Monitor and address inequity of care to achieve equity in service delivery, quality and outcome.

What GPs can do

GPs must focus on established risk factors, taking into account language and cultural needs, relative poverty and the heterogeneity of south Asians. Until conventional treatments for CHD are validated in south Asians one must assume that they are effective.

Treatments should target:

·Patients with proven CHD.

·First-degree relatives of patients with premature CHD.

·Asymptomatic high-risk individuals. Prevention requires identification and treatment of high-risk persons but essential risk assessment tools validated in south Asians are unfortunately lacking.

·Dyslipidaemia ­ 'normal' cholesterol levels, should be redefined. Levels have risen by almost 2mmol/L with migration to the UK. Lipid lowering should be considered in all high-risk south Asians, irrespective of baseline cholesterol level. Ideally, aim for lipid profiles of non-migrants; ie total cholesterol <4.5mmol ,="" ldl=""><2.5mmol ,="" triglycerides=""><1.5mmol ,="" and="" hdl="">1.0mmol/L.

·Blood pressure ­ should probably not exceed

the non-migrant blood pressure of


·Diabetes and the associated metabolic syndrome ­ screening and early intervention will inevitably reduce end organ damage, eg CHD.

·Smoking and chewing of tobacco ­ must be aggressively tackled. The British Heart Foundation 'Asian Quitline' must be commended here.

·Physical activity ­ it is important to address obesity and maintain increased physical activity, otherwise effects on insulin resistance and improved endothelial function are lost within four weeks.

·Diet ­ energy intake from fat is twice that of non-migrants and must be reduced.

Continued support from the Department of Health, British Heart Foundation and research funding bodies and increasing interest from the pharmaceutical industry is essential. The implementation of specific measures targeted at populations such as the south Asian community is now on the department's and pharmaceutical industry's agenda.

We must keep it there, implement strategies and not lose momentum.

Hypotheses relating to increased

CHD in south Asians2,3

·Are high CHD rates statistical artefact? Unlikely as data collection is fairly robust.

·Are south Asians less likely to die of other causes (eg cancer) and so have a relatively high rate of CHD? This competing causes hypothesis is unlikely given the higher rates in younger Asians.

·Is there an increased or varying genetic susceptibility? The south Asian CHD epidemic within one generation following migration may be a reaction to an adverse environment. No specific genetic or gene-environment interactions have been described although a genetic predisposition to diabetes and insulin resistance is likely to play a major role. The thrifty genotype hypothesis proposes that a genotype which was at one time protective when calories were sparse, becomes harmful in an environment where calories are plentiful.

·Are south Asians more susceptible for non-genetic reasons? This forms the basis of the metabolic adaptation-dysadaptation hypothesis suggesting increased risk for south Asian populations who make the transition from a relatively poor to affluent environment. The fetal origins hypothesis, that metabolism is programmed in early life, suggests adverse circumstances in the womb and early life increase CHD risk, among other health problems. A later mismatch between the metabolism a person is programmed for and the lifestyle adopted, precipitates disease.


1 Balarajan R. Ethnicity and variations in mortality from coronary heart disease. Health Trends 1996; 28:45-51

2 Bhopal R. Book Chapter in The Epidemic of Coronary Heart Disease in South Asian Populations: Causes and Consequences (Eds Patel K and Bhopal R). SAHF Publishers 2004

3 Kooner J and Chambers J. Book Chapter in The Epidemic of Coronary Heart Disease in South Asian Populations: Causes and Consequences (Eds Patel K and Bhopal R). SAHF Publishers 2004

4 O'Hare JP et al for the UKADS Study Group. Evaluation of delivery of enhanced diabetes care to patients of south Asian ethnicity: the UK Asian Diabetes Study (UKADS). Diabet Med. 2004 Dec;21(12):1357-65

5 Yusuf S et al for the INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (INTERHEART study): case-control study. Lancet. 2004 Sep 11;364 (9438):937-52

Kiran Patel

specialist registrar in cardiology, University Hospitals Birmingham, Edgbaston, Birmingham, and chair of trustees of the South Asian Health Foundation

Raj Bhopal

professor of public health, University of Edinburgh, and patron of the South Asian Health Foundation

Jaspal Kooner

professor of cardiology, National Heart and Lung Institute, Imperial College, London

The above article is based on extracts from the book

'The Epidemic ofCoronary HeartDisease in south Asian Populations: causes and consequences', edited by Dr Patel and Professor Bhopal, published by the SouthAsian Health Foundation ­ copiescan be ordered via

the sahf website

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