Skip to main content

The current status of primary prevention in coronary heart disease


During the second part of the twentieth century, research advances caused a substantial decline in the rate of coronary heart disease. The decline lasted from the mid-1960s until the early 1990s and occurred primarily in Western countries. However, an unfavourable trend in coronary heart disease related mortality has gradually developed during the 1990s, with cardiovascular diseases anticipated to remain the main cause of overall mortality for the foreseeable future. The present paper aims at analyzing the current status of the main determinants of population-wide coronary heart disease prevention.


Research has resulted in major improvements in health-care in the past 50 years. Advances in the field of genomics/genetics are anticipated to lead to further acceleration in the progress of research development, with the promise of a new era for diagnosis, treatment and prevention of disease. But despite spectacular progress in medicine and general improvement of health across the world, cardiovascular diseases remain a global problem, and coronary heart disease (CHD) in particular is anticipated to be a problem over the next 30 years, both for the developed and developing world.

Retrospective analysis of health and social problems illustrates limited success in identifying and dealing with potentially preventable health problems. Recent conclusions from the European Action on Secondary Prevention through Intervention to Reduce Events (EUROASPIRE) II [1] drawn by Wood, who coordinated the study, are relevant here. Among the many disappointing results was the fact that 81% of the individuals surveyed in 1999/2000 were overweight, with a third of them obese. The proportion of obese people increased sharply from 25% in 1995/96, while the number of smokers was unchanged, despite anti-smoking campaigns. Further, 61% of those surveyed had hypertension and 59% had abnormally high cholesterol, despite increased use of antihypertensive and cholesterol lowering drug treatment. Wood argued that the findings revealed "inadequate standard of care" and "a collective failure of the medical practice." He claimed that cardiologists are too focused on acute management and are paying insufficient attention to prevention and long-term treatment.

The multifaceted clinical complexity of CHD, with a bias towards acute treatment, neglect of preventive care, and inappropriate long-term treatment of patients after acute coronary events, requires fundamental reform to improve patients' outcomes and quality of life, as well as the cost-effectiveness of treatment. Future preventive measures need to focus on establishing risk factor profiles in individual patients, accurately identifying those at risk, and actively intervening to maximize the ability to change that risk. Moreover, prevention strategies need to begin in childhood.

Public health impact of CHD

Despite declining mortality rates from cardiovascular disease during the past three decades, cardiovascular disorders still account for the highest mortality rates both in developed and in developing countries. Coronary heart diseases are in turn the most prevalent of the cardiovascular disorders, accounting for 6.3 million deaths in 1990, at a time when a steady decline in heart disease mortality was stated to be ongoing [2].

CHD remains a massive public health problem in the developed world, both for survival and for work capacity. In the USA alone, more than 10 million individuals have symptomatic CHD, resulting each year in approximately 1.5 million myocardial infarctions, almost 1 million deaths, and an economic burden of $12 billion. "CHD is the single largest killer of American males and females" [3].

In European countries, cardiovascular mortality represents around 40% of all mortality before the age of 74. Despite decreasing age-specific cardiovascular disease mortality rates in Western European countries, there has been no decrease in the absolute number of people who die from cardiovascular diseases. The number of chronically ill cardiovascular patients may even be increasing in these countries due to the ageing of the population. Because of a fall in early mortality, currently available treatments for diseases such as acute myocardial infarction may lead to an increase in the number of patients who reinfarct and the number with congestive heart failure. For this reason, and because of the increasing trend in cardiovascular mortality in Central and Eastern European countries, the burden of cardiovascular diseases in European societies will not decrease and may even increase in the forthcoming decades [4].

Despite national and international guidance, evidence of clinical effectiveness, and widespread agreement on management of risk factors, primary prevention of CHD is inadequate and remains underdeveloped and under-funded [5,6].

The joint European Task Force set up in 1998 has emphasized the need for national guidelines to establish a "model for care" for preventive cardiology and for promotion of greater collaboration between hospitals and primary care. Representatives from the European Society of Cardiology, European Atherosclerosis Society, International Society of Behavioral Medicine, European Society of General Practice/Family Medicine, and from the European Heart Network underlined the concern that Europe is not capitalizing upon the extensive life-saving potential of preventive cardiology [7]. The task force proposals are focusing upon the need that each country should draw up its own model of care with the aim of implementing routine screening for cardiovascular disease, medical record keeping, systematic follow-up of patients, and coronary risk management.

This paper will attempt to draw attention to different factors encountered in daily practice that may potentially have a negative impact on the provision of long-term care to patients with CHD and, particularly, on the primary prevention of CHD in the general population.

The author proposes a paradigm shift in the approach to primary and secondary prevention of CHD, with their integration into a common management strategy for the different stages of the same pathological entity: the coronary heart disease.

Barriers in the implementation of preventive strategies

Surveys of CHD prevention-related services such as smoking cessations advice, measurement and treatment of lipid disorders, and physical activity assessment and counseling are disappointing [8,9,10,11,12]. Significant variation exists among the risk control therapies of patients with cardiovascular diseases. Major drugs in the cardiovascular therapy arsenal such as beta-blockers, angiotensin-converting enzyme inhibitors, aspirin, and lipid lowering drugs are currently underused [13,14,15]. A variety of factors at the levels of the patient, physician, health care setting and community/society, as well as the lack of a third party payment, may interfere with the provision of these services (see Table 1 [14]).

Table 1 Barriers to Implementation of Preventive Services

Low physician adherence

In spite of international consensus guidelines and tremendous amounts of health information surrounding CHD prevention, it seems that substantial confusion perpetuates among both physicians and their patients [16]. Unfortunately, conflicting messages in different guidelines [17,18,19] and inaccuracy in identifying high-risk patients are often contributing factors [20].

It is generally assumed that physicians are aware of the relative importance of the various risk factors for CHD. However, the busy schedules of both primary care and specialist clinicians, combined with defective training in the field of disease prevention, and the lack of financial incentives for prevention measures have combined to produce very poor systematic prevention of CHD in clinical practice [21,22].

Poor patient compliance

Nowadays we witness a rising interest in health, healthy living, and healthy environment. Successful campaigns in the field of 'prevention and health promotion' focusing on hot topics such as smoking, alcohol consumption, and high cholesterol have undoubtedly raised the level of awareness of health issues in the general population. However, closer scrutiny uncovers a poor compliance of the general, still healthy population, with the need for lifestyle changes and risk factor modification strategies. This may simply be explained by the fact that people are generally attracted by the prospect of a benefit which is visible early, and which they can definitely gain from. Health benefits rarely meet these criteria; they may be real, but they are likely to be delayed and to come to only a few of those who seek them. This phenomenon has been called "prevention paradox" [23], meaning that preventive measures that bring large benefits to the community offer little to individual participants.

Lastly, there is a lack of structured and systematic information on different treatments and decisions, which physicians are supposed to give to their patients to help them come to informed decisions about their healthcare. Failure to provide patients with basic information such as the potential risks and benefits of a certain therapy, the inconvenience, the side effects, and the cost may result in the rejection of a proposed therapy, instead of long-term adherence to it. It should also be noted that individual patients expect quite a lot, but carry too little responsibility for their own actions or participation in decisions. Most probably, the rights of individuals will increase in the next decades, but so will the responsibility of individuals and the acceptance of risk associated with medical decisions agreed between physician and patient [24].

Lack of third party payment

Medical thinking has been largely concerned with responding to the need of the sick individual. This has shaped its ethics (responsibility for the sick), its research (why do individuals become sick?), and the planning of medical services. A disease-oriented model of healthcare has emerged, with highest priority given to the prevention of death and acute illness. This reflects the particular outlook common to both doctors and healthcare policy makers of viewing ill health through a dichotomous paradigm of yes/no decisions, such as to investigate or not to investigate, to admit or to send home, to treat or not to treat, with the ultimate aim of reducing the number of people requiring medical care in order to cut cost.

This type of reasoning struggles to achieve the defined purpose-triad of medicine: to prevent occurrence of disease, to prolong life, and to improve quality of life by minimizing unwanted symptoms.

In an era of cost consciousness, there are increasingly demands that health promotion and disease prevention programs be proven economically worthwhile by means of cost-effectiveness analysis. People generally agree that it is worth investing in health promotion activities; however, it is difficult to prove that the value of benefits obtained outweigh the cost of those investments or that they, at least, equal the clear benefits obtained from managing medical emergencies and waiting lists, both being focused by policy makers [25,26]. The continuous increase of the percentage of aging population demands allocation of greater amount of resources.

Demographic changes

The progressive ageing of the population in the twentieth century, caused by unprecedented gains in life expectancy, offers not only great opportunities but also formidable challenges for all societies. The global population of people over the age of 65 is increasing by 750,000 a month. Increases in the older population of up to 300% are expected in many developing countries within the next 30 years [27].

Another demographic feature that makes the process of ageing much more complicated is the fact that, in the next 25 years, while the population aged 65 years and above is likely to grow by 88%, the working-age population will increase by only 45%. The direct consequence of this fact is that a steadily declining number of people of productive age will have to provide for an expanding number of dependants, in the form of direct support to older relatives and through escalating taxation to cover the provision of health and social services [28,29,30].

Population ageing is beginning to transform health care and social systems, with new public policies in health and social care being widely adopted throughout the world [31]. Public interest and discussion of healthcare issues is at an all-time high. Because of the cost of healthcare, which is continually escalating both in developed and developing countries, there is a widespread trend toward structural reform of healthcare systems [32].

Nowadays, there is a growing discrepancy between what is possible in modern healthcare provision and what is affordable within limited budgets. Perverse incentives, which are inherent to all healthcare systems, result in ineffective and inefficient delivery of care. A competitive healthcare market with the separation of purchasers and providers has been introduced in several Western countries as a means of increasing the efficiency of healthcare provision. A common feature is that health authorities, hospital administrators, and providers are looking for additional means of financing through raised patient copayments and private insurance.

The impact of IT on healthcare

It is apparent that the development and diffusion of effective medical technology must not be limited, and that a well-organized assessment capability in close collaboration between physicians and health care insurers should be developed, if we want to maintain delivery and access to high quality care in the future [33].

This concrete strategy for change calls for joint investment by government and industry into healthcare infrastructure, applications for healthcare information systems, and the development of the pre-requisite technology for these applications.

New practice paradigms and administrative functions should be targeted for strategic investment in order to enhance the development of new medical practice paradigms that incorporate a trend towards patient-centered healthcare, including a focus on wellness, prevention programs, and evidence-based healthcare.

Implementing community-wide networks for healthcare information will lead to the development of information systems that allow clinical and administrative data to be readily accessed, regardless of location, with appropriate safeguards for protecting patient confidentiality, and in a manner convenient for practitioners and patients.

Integrated vision of primary and secondary prevention of CHD

Increasingly sensitive technologies that can identify pathophysiologic states, early lesions, or silent disease in persons who have never been symptomatic have permitted an expanded definition of health that extends far beyond 'absence of disease' and emphasizes the need for prevention of disease occurrence. Despite the large overlap of the primary and secondary prevention of CHD, the first can be defined as the prevention of the athero-sclerotic process itself, with the latter being the treatment of the atherosclerotic disease process [35].

Since the risk factors concept was introduced in 1948 by the Framingham Study investigators, tens of risk factors have been suggested as determinants of CHD. Several modifiable, or behavioral, risk factors (cigarette smoking, poor diet, hypercholesterolemia, excessive alcohol intake, lack of exercise) have been shown to be causally related to CHD [36,37,38], and these may be approached either on a population-wide or an individual basis. Nonmodifiable factors, such as age, sex, race and family history of CHD, may be used to identify high-risk groups of individuals who would benefit from specific programs. Additional factors termed physiological, such as hypertension, diabetes, obesity and different types of dyslipidemias, interact with the nonmodifiable and behavioural risk factors, leading to the clinical manifestations of atheroclerosis: coronary heart disease, hypertensive heart disease, thrombotic or hemorrhagic stroke and peripheral vascular disease (Fig. 1) [39].

Figure 1
figure 1

Relationship between cardiovascular risk factors and cardiovascular diseases. HDL, high-density lipoprotein; LDL, low-density lipoprotein.

During the past 5 decades, and in particular during the past 10 years, we not only accumulated knowledge on risk factors and CHD pathophysiology, we also witnessed a continual metamorphosis of recommendations and guidelines for prevention and treatment of coronary heart disease. Nevertheless, during the first years of the last decade, individual risk factors such as raised blood pressure and high cholesterol were focused on by separate guidelines, which recommended treatment on the basis of specified cut-off points. Not only that, but professional societies both in the US and in Europe had separate guidelines on coronary prevention [40], hyperlipidemia [41,42], hypertension [43], and diabetes [44]. However, there is nowadays a universal consensus as to similar management of the modifiable risk factors in the context of both primary and secondary prevention of CHD (Table 2).

Table 2 Evidence base for benefit of risk factor modification

In 1989 Rose described two approaches for the practical management of risk factors [22]: the 'population approach' and the 'high risk approach'. The recommendation of combining both approaches in clinical practice is based on reasoning from epidemiological explanations of the risk factor distribution in populations.

The bell-shaped distribution of values (Fig. 2) of a particular risk factor, (eg cholesterol) suggests that most people are found in its middle part and have cholesterol levels around the average. However, one tail of the distribution contains individuals with higher values. A more concrete example is reflected by Fig. 3, which has been assembled from Multiple Risk Factor Intervention Trial (MRFIT) data [89]. The bar diagram presents the distribution of serum cholesterol levels, with the commonest values being around 5-5.5 mmol/l. The broken curve shows that the incidence of fatal heart attacks rises steeply with increasing levels of cholesterol. At the highest level (8 mmol/l) 20 deaths per 1000 individuals are registered, although the prevalence of such exposure is only 2%.

Figure 2
figure 2

Cholesterol distribution and its shift (dashed line) with application of population approach. Data from Carleton et al [95].

Figure 3
figure 3

Prevalence distribution (bars) of serum cholesterol concentration related to age-adjusted mortality from coronary heart disease (CHD) (broken curve) in men aged 40-59 years. The number above each bar is the percentage of death "attributable" to the cholesterol effect and arising at that level. Data from Martin et al [96].

Persons with risk levels in the tail of a distribution are a deviant high-risk minority. They qualify for special attention and are the target of high-risk preventive strategy, which normally takes place when the physician is treating a patient for ailments such as hypertension or high cholesterol. With this approach, the remaining individuals in the population are classified as normal and can be left in peace. However, while the rate of cardiovascular disease is higher in the high-risk individuals, they only account for a small percentage of those who suffer from the disease. Most cases of CHD occur among those falling in the average risk group, classified as normal. The 'population approach' is concerned with this latter group and the reduction of the population burden of CHD that may result from shifting the entire population level of risk factors (the dashed bell-shaped curve, Fig. 2).

The population and high-risk approaches are not mutually exclusive. They should be used in combination and constitute one of the main pillars of any health policy. However, the two approaches are somewhat different, primarily from a logistic and organizational point of view.

The population approach proceeds from the basic axiom that CHDs are epiphenomenona in populations that adopt a Western lifestyle, characterized by high-fat and high-cholesterol diet, tobacco use, and lack of physical activity. It is therefore a matter of application of essential public services such as surveillance, education, organizational partnerships, assurance of personal health services, and legislation/policy [90] in a variety of community settings including work sites, healthcare facilities, religious organizations, schools, and whole communities [91], with the main goal of achieving reduced impact of risk factors and risk behaviors on the health of the general population. Epidemiological evidence and results from clinical trials have demonstrated that such goals are achievable in practice [92].

Fig. 4 illustrates the specific means applicable in specific community settings, with the aim of controlling risk factors and risk behaviors on a population basis.

Figure 4
figure 4

A conceptual framework for public health practice in cardiovascular disease prevention.

Individual risk assessment

Gradually, previous guidelines based on relative risk have been replaced by joint American and European recommendations and guidelines based on absolute measures of risk [65]. The absolute risk of cardiovascular disease is strongly influenced by the combination of risk factors present, particularly a history of cardiovascular disease, age, gender, diabetes, smoking, blood pressure, and blood lipid concentrations [66]. The assessment of these factors through careful history taking, physical examination, and selected laboratory testing is absolutely necessary for quantification of global risk score. Specific target levels for particular risk factors are used to prioritize goals for behavioral and pharmacological intervention (Table 3) [93]. The new clinical guidelines recommend that priority for treatment should be given to patients at high absolute risk of coronary heart disease, defined as probability of developing coronary heart disease over a specified period, rather than emphasis being placed on an individual risk factor [67].

Table 3 Guide to primary prevention of cardiovascular disease

Fig. 5 attempts to present CHD in its whole spectrum, as a continuum in which the dichotomy of having or not having an acute coronary event is only one level of the same disease, which actually starts many years before the occurrence of that acute event.

Figure 5
figure 5

Preventive strategies in CHD. A holistic approach to quantitative assessment.

The Primary Prevention section in Fig. 5 summarizes the distribution of high absolute risk (>20% probability of developing CHD in the next 10 years) in the high risk (H) group and part of the medium risk (M) group individuals. The high absolute risk individuals may sustain acute coronary events in their late thirties or early forties, depending upon a multitude of factors that are difficult to predict. Individuals with relative risk corresponding to the low-risk group and part of the medium risk group individuals in the general population, run the risk of coronary events at a later age, usually in their sixties or even later.

The risk of a coronary heart disease event (death, non-fatal myocardial infarction, and angina) in 10 years has been adopted as the standard measure in both Europe and the United States [68] and proposed as the common instrument to guide treatment for raised blood pressure as well as treatment with aspirin and statins [69,70].

The Framingham equations computed on the basis of pre-specified categorical variables have been the mathematical background for calculation of absolute risk in the most popular charts, tables and computer programs so far [71,72]. However, it has been emphasized that the Fram-ingham equations based on North American high-risk population may have limited applicability to other high-risk groups, such as South Asians, Polynesians, African Ameri-cans and South Europeans [73]. Evidence indicates that risk prediction is quite reliable in central and western populations [74,75], but is overestimated for southern populations [76,77].

Several methods are available at present for the assessment of a patient's risk of developing CHD. All of these methods are based on estimates from the Framingham study and they only take into account the standard risk factors - gender, smoking, blood pressure, ratio of total cholesterol to high-density lipoprotein cholesterol (HDL), and presence of diabetes. Other factors such as family history of premature CHD, ethnicity, obesity, and lifestyle may need to be considered in clinical interpretation and decision making in individual patients. The most commonly used tools are the New Zealand Guidelines [78], the Sheffield Table [79], and the Joint British Societies coronary prediction chart [80].

The Sheffield table has been used to identify those patients where measurements of total cholesterol and HDL cholesterol are indicated. The modified Sheffield table requires only yes/no categorization of the patient as hypertensive, rather than a systolic blood pressure measurement [79]. The Joint British Societies chart requires more information and is not intended for use in treated hypertensive patients. In these patients, the use of current blood pressure measurements gives an underestimate of risk. None of the charts are used in patients who already have a diagnosis of CHD.

The Joint European societies have used the multiple-risk approach to develop figures that allow the visual calculation of previous absolute risk of developing CHD over the next 10 years, based on age, sex, smoking, systolic blood pressure, and total cholesterol level [81] (Figs 6 and 7).

Figure 6
figure 6

Coronary risk chart for primary CHD prevention in men. Published with permission from [97].

Figure 7
figure 7

Coronary risk chart for primary CHD prevention in women. Published with permission from [97].

Cardiovascular risk is defined as the CHD risk plus the risk of stroke, vascular disease and heart failure. Cardiovascular risk can be estimated from the CHD risk since the two are correlated; a CHD risk of 15% equates to a cardiovascular risk of 20% [81].

Identification of individuals at high absolute risk is straightforward and can be undertaken accurately by using one of the available modalities mentioned above [17,83,84,85]. Quantification of the absolute risk assists in deciding upon the need for lipid lowering treatment, considered at present to decrease the risk of heart attacks and strokes without increasing other causes of mortality or morbidity. However, the increased understanding and widespread acceptance of the usefulness of lipid lowering treatment has brought into consideration the cost-effectiveness of such treatment. Current UK policy, for instance, recommends that lipid lowering treatment should be offered to anyone with an absolute annual risk of 3% or more [86], while others favor a 1.5-2% absolute risk threshold before beginning treatment [81,83]. Still others have argued that estimates of relative risk should form the basis for treatment guidelines [87]. Since age is the major determinant of absolute risk, treatment thresholds based on absolute risk will tend to postpone treatment to older age, whereas guidelines based on relative risk will tend to lead to treatment of younger people.

Using absolute risk for decision making on lipid lowering treatment raises the problem faced by practicing clinicians of what advice to give to younger people who are at substantially increased risk compared with their age group, but who nevertheless remain below the defined absolute risk threshold for treatment.

Common sense, of course, dictates that all such individuals should be offered appropriate advice on lifestyle modification at the earliest opportunity and that individualized decisions about treatment should be taken from case to case, based on the global risk profile of the particular individual.


Primary prevention programs aimed at reduction of risk behaviors on a population-wide basis and the identification, stratification, and selected treatment of high-risk individuals prior to their development of disease should be cornerstones of any approach to reduce the population's burden of CHD. Also, prevention strategies should begin in childhood. These two approaches should be complementary.

The healthcare system should benefit from population-wide efforts via health education, environmental intervention, or legislation to reduce the burden of deleterious health behaviors. This should facilitate risk-factor change in the clinical setting. Policy makers, employers, and community leaders look to healthcare providers to provide advice and leadership. Both the capacity to prevent CHD and the will to implement policies and programs will be necessary to reduce CHD and communities and physicians' offices [88].


  1. van Berkel TF, Boersma H, DeBquer D, Deckers JW, Wood D: Registration and management of smoking behaviour in patients with coronary heart disease. The EUROASPIRE survey. Eur Heart J. 1999, 20: 1630-1637. 10.1053/euhj.1999.1635.

    Article  CAS  PubMed  Google Scholar 

  2. The World Health Report:. Life in the 21st century: A vision for all. Geneva: WHO;. 1998

  3. Murray CJL, Lopez AD: Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. The Lancet. 1997, 349: 1436-1442. 10.1016/S0140-6736(96)07495-8.

    Article  CAS  Google Scholar 

  4. Sans S, Kesteloot H, Kromhout D: The burden of cardiovascular diseases mortality in Europe. Task force of the ESC on Mortality and Morbidity Statistics in Europe. Eur Heart J. 1997, 18: 1231-1248.

    Article  Google Scholar 

  5. Johanesson M, Jønsson B, Karlsson G: Outcome measurement in economic evaluation. Health Econom. 1995, 5: 279-296.

    Article  Google Scholar 

  6. Johannesson M, Jonsson B, Kjekshus J, Olsson AG, Pedersen TR, Wedel H: Cost-effectiveness of simvastatin treatment to lower cholesterol levels in patients with coronary artery disease. N Engl J Med. 1996, 336:: 332-336.

    Article  Google Scholar 

  7. Wood D: European and American recommendations for coronary heart disease prevention. Eur Heart J. 1998, 19(Suppl A): A12-A19.

    Google Scholar 

  8. Ellerbeck EF, Jencks SF, Radford MJ, Kresowik TF, Craig AS, Krumholz HM, Vogel RA: Quality of care for Medicare patients with acute myocardial infarction: a four-state pilot study from the Cooperative Cardiovascular Project. JAMA. 1991, 273: 1509-1514.

    Article  Google Scholar 

  9. Action of Secondary Prevention through Intervention to Reduce Events (ASPIRE) Steering Group : a British Cardiac Society survey of the potential for secondary prevention of coronary heart disease. Heart. 1996, 75: 334-342.

    Article  Google Scholar 

  10. EURO-ASPIRE Study Group : A European Society of Cardiology survey of secondary prevention of coronary heart disease. Eur Heart J. 1997, 18: 1569-1582.

    Article  Google Scholar 

  11. Jolly K, Bradley F, Sharp S, Smith H, Thompson S, Kinmonth AL, Mant D: Randomized controlled trial of follow-up care in general practice of patients with infarction and angina: final results of the Southampton Heart Integrated Care Project (SHIP). BMJ. 1999, 318: 706-711.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Bradley F, Wiles R, Kinmonth AL, Mant D, Gantley M: Development and evaluation of complex interventions in health service research: case study of the Southampton heart integrated care project (SHIP). BMJ. 1999, 318: 711-715.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Cohen MV, Byrne M, Levine B, Gutowski T, Adelson R: Low rate of treatment of hypercholesterolemia by cardiologists in patients with suspected and proven coronary artery disease.. Circulation. 1991, 83: 1294-1304.

    Article  CAS  PubMed  Google Scholar 

  14. Pearson TA, McBride PE, Houston-Miller N, Smith SCJ: Organisation of preventive cardiology service. J Am Coll Cardiol. 1996, 27: 1039-1047.

    Article  CAS  PubMed  Google Scholar 

  15. Sueta CA, Chowdhury M, Boccuzzi SJ, Smith SC, Alexander CV, Londhe A, Lulla A, Simpson RJ: Analysis of the degree of undertreatment of hyperlipidemia and congestive heart failure secondary to coronary artery disease. Am J Cardiol. 1986, 83: 1303-1307.

    Article  Google Scholar 

  16. Lowensteyn I, Lawrence J, Levinton C, Abrahamowicz M, Grover S: Can computerised risk profiles help patients improve their coronary risk? The results of the Coronary Health Assessment Study (CHAS. Prev Med. 1998, 27: 730-737. 10.1006/pmed.1998.0351.

    Article  CAS  PubMed  Google Scholar 

  17. Canadian Task Force on the Periodic Health Examination : Periodic health examination 1993 update: Lowering the blood cholesterol level to prevent coronary heart disease. Can Med Assoc J. 1993, 148: 521-38.

    Google Scholar 

  18. Pyorala K, De Backer G, Poole Wilson P, Wood D: Prevention of coronary heart disease in clinical practice. Recommendations of the Task Force of the European Society of Cardiology, European Atherosclerosis Society and European Society of Hypertension. Eur Heart J. 1994, 15: 1300-1301.

    CAS  PubMed  Google Scholar 

  19. Summary of the Second Report of the National Cholesterol Education Program NCEP) Expert Panel on Detection, Evaluation and Treatment of High BloodCholesterol in Adults. (Adult Treatment Panel II). JAMA. 1993, 269: 3015-3023.

  20. Grover SA, Coupal L, Hu XP: Identifying adults at increased risk of coronary heart disease. How well do the current cholesterol guidelines work?. JAMA. 1995, 274: 801-806.

    Article  CAS  PubMed  Google Scholar 

  21. Grover SA, Lowensteyn I, Esrey KL, Steinert Y, Joseph L, Abrahamowicz M: How accurately do Canadian physicians assess the coronary risk in their patients? The preliminary results of the Coronary Health Assessment Study (CHAS). BMJ. 1995, 310: 975-978.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  22. Kottke TE, Solberg LI, Brekke ML, Cabrera A, Marques MA: Delivery rates of preventive services in44 Midwestern clinics. Mayo Clin Proc. 1997, 72: 515-523.

    Article  CAS  PubMed  Google Scholar 

  23. Rose G: The strategy of preventive medicine. New York: Oxford University Press, Inc,. 1992

    Google Scholar 

  24. Kelly DT: Our future society: A global challenge. Circulation. 1997, 95: 2459-64.

    Article  CAS  PubMed  Google Scholar 

  25. Randomized controlled trials in cardiovascular disease: past achievements, futurechallenges. BMJ. 1999, 319: 564-568.

  26. Winocour P: Cost-effective strategies for reducing coronary risk in primary care. BMJ. 1995, 311: 573-

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. The World Health Report:. Life in the 21st century: A vision for all. Geneva: WHO;. 1998

  28. Kale R: Health information for the developing world. BMJ. 1994, 309: 939-942.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  29. Steering Committee on Future Health Scenarios:. Primary care and home care scenarios 1990-2005. Dodrecht: Kluwer Publishers,. 1993

  30. Musgrove P: World Bank. Investing in health: the 1993 World Development Report of the World Bank. Bulletin of the Pan American Health Organisation. 1993, 27: 284-286.

    CAS  Google Scholar 

  31. World Health Organization: The District Health Care System Geneva: WHO, 1987; White Kerr L:. Health services research: an anthology. Washington DC: PAHO,. 1992

  32. Wootton R: Telemedicine in the National Health Service. J Royal Soc Med. 1998, 91: 614-621.

    CAS  Google Scholar 

  33. Allen A, Wooton R, Loane M, Nair F, Moutray M, Harrisson S, Doolittle G, McLernan A: The potential for telemedicine in home nursing. J Telemedicine Telecare. 1998, 4: 214-218.

    Article  Google Scholar 

  34. Evidence-base Medicine Working Group : Evidence based medicine: a new approach to teaching the practice of medicine. JAMA. 1992, 268: 2420-2425.

    Article  Google Scholar 

  35. Swan HJC, Gersh BJ, Grayboys TB, Ullyot DJ: Evaluation and management of risk factors for the individual patient (case management). J Am Coll Cardiol. 1996, 27: 1030-1047.

    Article  CAS  PubMed  Google Scholar 

  36. Action of Secondary Prevention through Intervention to Reduce Events (ASPIRE) Steering Group : A British Cardiac Society survey of the potential for secondary prevention of coronary disease: ASPIRE. Heart. 1996, 75: 334-342.

    Article  Google Scholar 

  37. Wilson PW, Dàgostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB: Prediction of coronary heart disease using risk factor categories. Circulation. 1998, 97: 1837-1847.

    Article  CAS  PubMed  Google Scholar 

  38. The Pooling Project Research Group : Relationship of blood pressure, serum cholesterol, smoking habit, relative weight and ECG abnormalities to incidence of major coronary events. J Chronic Dis. 1978, 3: 201-306.

    Google Scholar 

  39. Pearson TA, Jamison DT, Trejo-Gutierrez J: Cardiovascular disease. In Disease Control Priorities in Developing Countries.Edited by Jamosson DT, Mosley WH, Measham AR and Bobadilla JL. New York: Oxford University Press, Inc,. 1993, 577-594.

    Google Scholar 

  40. British Cardiac Society working group on coronary prevention : Conclusions and recommendations. Br Hear J. 1998, 19: 1434-1503.

    Article  Google Scholar 

  41. Shepherd J, Betteridge DJ, Durrington P, Laker M, Lewis B, Mann J, Miller JP, Reckless JP, Thompson GR: British Hyperlipidaemia Association guidelines on strategies for reduction of coronary heart disease and desirable levels for blood lipid levels. BMJ. 1987, 295: 1245-1246.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Betteridge DJ, Dodson PM, Durrington PN, Hughes EA, Laker MF, Nichols DP, Rees JA, Seymour CA, Thompson GR, Winder AF: Management of hyperlipidaemia: Guidelines of the British Hyperlipidaemia Association. Postgrad Med J. 1993, 69: 359-369.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. Sever P, Beevers G, Bulpitt C, Lever A, Ramsay L, Reid J, Swales J: Management guidelines in essential hypertension: report of the second working party of the British Hypertension Society. BMJ. 1993, 306: 983-987.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  44. Alberti KGMM, Zimmet P: Definition, diagnosis and classification of diabetes mellitus and its complications. Part I: diagnosis and classification of diabetes mellitus. Provisional report of a WHO consultation. Diabet Med. 1998, 15: 539-553.

    Article  CAS  PubMed  Google Scholar 

  45. Wilhelmsson C: Coronary heart disease: epidemiology of smoking and intervention studies of smoking. Am Heart J. 1988, 115: 242-249.

    Article  Google Scholar 

  46. Hjermann I, Velve Byre K, Holme I, Leren P: Effect of diet and smoking intervention on the incidence of coronary heart disease. Report from the Oslo Study Group of a randomized trial in healthy men. Lancet. 1981, ii: 1303-1310.

    Article  Google Scholar 

  47. Rosenberg L, Kaufman D, Helmrich S, Shapiro S: The risk of myocardial infarction after quitting smoking in men under 55 years of age. N Eng J Med. 1985, 313: 1511-1514.

    Article  CAS  Google Scholar 

  48. Rosenberg L, Palmer J, Shapiro S: Decline in the risk of myocar-dial infarction among women who stop smoking. N Eng J Med. 1990, 322: 213-217.

    Article  CAS  Google Scholar 

  49. Gibbons RJ, Chatterjee K, Daley J, Douglas JS, Fihn SD, Gardin JM, Grunwald MA, Levy D, Lytle BW, O'Rourke RA, Schafer WP, Williams SV, Ritchie JL, Cheitlin MD, Eagle KA, Gardener TJ, Garson A, Russel RO, Ryan TJ, Smith SC: ACC/AHA/ACPASIM guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force of Practice Guidelines. JACC. 1999, 33: 2092-2197.

    Article  CAS  PubMed  Google Scholar 

  50. Daly L, Mulcahy R, Graham I, Hickey N: Long-term effect on mortality of stopping smoking after unstable angina and myocardial infarction. BMJ. 1983, 287: 324-326.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  51. Pietinen P, Vartiainen E, Seppanen R, Aro A, Puska P: Changes in diet in Finland from 1972 to 1992: impact on coronary heart disease risk. Prev Med. 1996, 25: 243-246. 10.1006/pmed.1996.0053.

    Article  CAS  PubMed  Google Scholar 

  52. Law M: Plant sterol and sterol margarines and health. BMJ. 2000, 329: 861-864.

    Article  Google Scholar 

  53. Burr ML, Fehily AM, Gilbert JF, Rogers S, Holliday RM, Swetnan PM, Elwood PC, Deadman NM: Effects of changes in fat, fish, and fibres intakes on death and myocardial reinfarction: diet and reinfarction trial. Lancet. 1989, 2: 757-761.

    Article  CAS  PubMed  Google Scholar 

  54. Tunstall-Pedoe H, Woodward M, Tavendale R, A-Brook R, McCluskey MK: Comparison of the prediction, by 27 different factors, of coronary heart disease and death in men and women of a Scottish heart health study: cohort study. BMJ. 1997, 315: 722-729.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  55. Paffenbarger RJ, Hyde R, Wing A, Jung D, Kampert J: The association of changes in physical activity level and other lifestyle characteristics with mortality among men. N Eng J Med. 1993, 328: 535-545.

    Article  Google Scholar 

  56. Wannamethee S, sharper A, Walker M: Changes in physical activity, mortality, and incidence of coronary heart disease in older men. Lancet. 1998, 351: 1603-1608.

    Article  CAS  PubMed  Google Scholar 

  57. Doll R, Peto R, Hall E, Whatley K, Gray R: Mortality in relation to consumption of alcohol: 13 years' of observation in male British doctors. BMJ. 1994, 309: 911-918.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  58. Rimm E, Klatsky A, Grobbe D, Stampffer M: Review of moderate alcohol consumption and reduced risk of coronary heart disease: is the effect due to beer, wine, or spirits. BMJ. 1996, 312: 731-736.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  59. Turner RC, Millns H, Neil HA, Stratton IM, Manley SE, Matthews DR, Holman RR: Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus. UKPDS. BMJ. 1998, 316: 823-828.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  60. Wood D, De Backer G, Faergeman O, Graham I, Mancia G, Pyorala K: Prevention of coronary heart disease in clinical practice: recommendation of the Second Joint Task Force of European and other Societies on Coronary Prevention. Ather-oscl. 1998, 140: 199-270.

    Article  CAS  Google Scholar 

  61. MacMahon S, Peto R, Cutler J, Collins R, Sorlie P, Neaton J, Abbot R, Godwin J, Dyer A, Stamler J: Blood pressure, stroke, and coronary heart disease. Part 1, Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet. 1990, 335: 765-774.

    Article  CAS  PubMed  Google Scholar 

  62. Shaper A, Wannamethee S, Walker M: Body weight: implications for the prevention of coronary heart disease, stroke and diabetes mellitus in a cohort study of middle-aged men. BMJ. 1997, 314: 1311-1317.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  63. Willet WC, Manson JE, Stampfer MJ, Colditz GA, Rosner B, Hennekens CH: Weight, weight change, and coronary heart disease in women. Risk within the "normal" weight range. JAMA. 1995, 273: 461-5.

    Article  Google Scholar 

  64. Scottish Intercollegiate Guidelines Network (SIGN):. Lipids and the primary prevention of coronary heart disease. 1999

  65. Wood D, De Backer G, Faergeman O, Graham I, Mancia G, Pyorala K: Prevention of coronary heart disease in clinical practice. Recommendations by the second joint task force of the European Society of Cardiology, European Atherosclerosis Society and European Society of Hypertension. Eur Heart J. 1998, 19: 1434-1503. 10.1053/euhj.1998.1243.

    Article  Google Scholar 

  66. Anderson KV, Odell PM, Wilson PWF, Kannel WB: Cardiovascular disease riskprofiles. Am Heart J. 1991, 121: 203-208.

    Article  Google Scholar 

  67. British Cardiac society, British Hyperlipidaemia Association, British Hypertension Society, British Diabetic Association : Joint British recommendations on prevention of coronary heart disease in clinical practice: summary. BMJ. 2000, 320: 705-708. 10.1136/bmj.320.7236.705.

    Article  Google Scholar 

  68. Grundy SM, Pasternak R, Greenland P, Smith S, Fuster V: Assessment of cardiovascular risk by use of a multiple-risk-factor assessment equations. Circulation. 1999, 100: 1481-1492.

    Article  CAS  PubMed  Google Scholar 

  69. Ramsay LE, Williams B, Johnston G, MacGregor G, Poston L, Potter J, Poulter N, Russel G: Guidelines for management of hypertension: report of the third working party of the British Hypertension Society. J Hum Hypertens. 1999, 13: 569-592. 10.1038/sj/jhh/1000917.

    Article  CAS  PubMed  Google Scholar 

  70. Wilsson PW, D'Agustino RB, Levy D, Belanger AM, Silberhatz H: Prediction of coronary heart disease using risk factor categories. Circulation. 1998, 97: 1837-1847.

    Article  Google Scholar 

  71. Wood D, Durrington P, Poulter N, McInnes G, Wray J: Joint British recommendations prevention of coronary heart disease in clinical practice. Heart. 1998, 80: 1-29S.

    Article  Google Scholar 

  72. Ulrich S, Hingorani AD, Martin J, Vallace P: What is the optimal age for starting lipid lowering treatment? A mathematical model. BMJ. 2000, 320: 1134-1140. 10.1136/bmj.320.7242.1134.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  73. Schulte H, Assman G: CHD risk equations, obtained from the Framingham study, applied to PROCAM study. Card risk factors. 1991, 1: 126-133.

    Google Scholar 

  74. Haq IU, Ramsey LE, Yeo WW, Jackson PR, Wallis EJ: Is the Framingham risk function valid for Northern European populations? A comparison of methods for estimating absolute coronary risk in high risk men. Heart. 1999, 81: 40-46.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  75. Keys A: Seven Countries: A multivariate analysis of death and coronary heart disease. Cambridge, Massachusetts: Harvard University Press;. 1980

    Book  Google Scholar 

  76. ERICA Research Group : Prediction of coronary heart disease in Europe. The 2nd report of the WHO-ERICA Project. Eur Heart J. 1991, 12: 291-297.

    Google Scholar 

  77. Menotti A, Puddu PE, Lanti M: Comparisons of the Framingham risk function-based coronary risk chart with risk function from an Italian population study. Eur Heart J. 2000, 21: 365-370. 10.1053/euhj.1999.1864.

    Article  CAS  PubMed  Google Scholar 

  78. Dyslipidaemia Advisory Group on behalf of the Scientific Committee of the National Heart Foundation of New Zealand : 1996 National Heart Foundation clinical guidelines for the assessment and management of dyslipidaemia. NZ Med J. 1996, 109: 224-231.

    Google Scholar 

  79. Wallis EJ, Ramsay LE, Ul Haq I, Ghahramani P, Jackson PR, Rowland-Yeo K, Yeo WW: Coronary and cardiovascular risk estimation for primary prevention: validation of a new Sheffield table in the 1995 Scottish health survey population. BMJ. 2000, 320: 671-676. 10.1136/bmj.320.7236.671.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  80. British Cardiac Society, British Hyperlipidaemia Association, British Hypertension Society, endorsed by the British Diabetic Association : Joint British recommendations on prevention of coronary heart disease in clinical practice. Heart. 1990, 80 (Suppl 2: S1-S29.

    Google Scholar 

  81. Pyorala K, De Backer G, Graham I, Poole-Wilson P, Wood D: Prevention of coronary heart disease in clinical practice: recommendations of the Second Joint Task Force of European and Other Societies on Coronary Prevention. Eur Heart J. 1998, 19: 1434-1503. 10.1053/euhj.1998.1243.

    Article  Google Scholar 

  82. Ramsay LE, Williams B, Johnston GD, MacGregor GA, Poston L, Potter JF, Poulter NR, Russel G: British Hypertension Society guidelines for hypertension management 1999: summary. BMJ. 1999, 319: 630-635.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  83. Jackson R, Barham P, Bills J, Birch T, McLenan L, MacMahon S, Maling T: Management of raised blood pressure in New Zealand: a discussion document. BMJ. 1993, 307: 107-110.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  84. Hingorani AD, Vallance P: A simple computer program for cardiovascular risk factor management and prescribing guidance. BMJ. 1999, 318: 101-105.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  85. Haq IU, Jaclson PR, Yeo WW, Ramsey LE: Sheffield risk and treatment table for cholesterol lowering for primary prevention of coronary heart disease. Lancet. 1995, 346: 1467-1471.

    Article  CAS  PubMed  Google Scholar 

  86. Campbell NC, Thain J, Dean HG, Ritchie LD, Rawles JM: Secondary prevention in coronary heart disease: baseline survey of provision in general practice. BMJ. 1998, 315: 1430-1434.

    Article  Google Scholar 

  87. Betteridge J, Shepherd J, Thompson G: Sheffield tables have shortcomings. BMJ. 1997, 315: 1619-

    CAS  PubMed  PubMed Central  Google Scholar 

  88. Pearson TA, Bales VS, Blair L: The Singapore Declaration: Forging the Will for Heart Health in the Next Millennium. CVD Prevention. 1998, 1: 182-199.

    Google Scholar 

  89. Martin MJ, Hulley SB, Browner WS, Kuller HL, Wentworth D: Serum cholesterol, blood pressure and mortality: implications from a cohort of 361662 men. Lancet. 1986, ii: 933-936.

    Article  Google Scholar 

  90. The President's Health Security Plan: The Clinton Blue Print. New York: Times Books;. 1993

  91. Stone EJ, Pearson TA, Fortman SP, McKinley JB: Community-based prevention trials: challenges and directions for public health practice, policy, and research. Ann Epidemiol. 1997, 7 (suppl): S113-S120.

    Article  Google Scholar 

  92. Blackburn H: Epidemiological basis of a community strategy for prevention of cardiopulmonary disease. Ann Epidemiol. 1997, 7 (suppl): S8-S13.

    Article  Google Scholar 

  93. Grundy SM, Balady GJ, Criqui MH, Fletcher G, Greenland P, Hiratzka LF, Houston-Miller N, Kris-Etherton P, Krumholz HM, LaRosa J, Ockene IS, Pearson TA, Reed J, Washington R, Smits S: Guide to primary prevention of cardiovascular diseases: a statement for healthcare professionals from the task force on risk reduction. Circulation. 1997, 95: 2329-2331.

    Article  CAS  PubMed  Google Scholar 

  94. Pearson TA, McBride PE, Houston-Miller N, Smiths SC: Organisation of preventive cardiology service. JACC. 1996, 27: 1039-1047.

    Article  CAS  PubMed  Google Scholar 

  95. Carleton RA, Dwyer J, Finberg L, Flora J, Goodman DS, Grundy SM, Havas S, Hunter GT, Kritchevsky D, Lauer RM: Report of the Expert Panel on Population Strategies for Blood Cholesterol Reduction. A statement from the National Cholesterol Education Program, National Heart, Lung, and Blood Institute, National Institute of Health. Circulation. 1991, 83: 2154-2232.

    Article  CAS  PubMed  Google Scholar 

  96. Martin MJ, Browner WS, Huylley SB: Serum cholesterol, blood pressure, and mortality. Lancet. 1987, i: 503-

    Article  Google Scholar 

  97. Wood D: National Heart and Lung Institute, Dovehouse Street, London SW3 6LY, U.K. Prevention of Coronary Heart Disease in Clinical Practice. Recommendations of the Second Joint Task Force of European and other Societies on Coronary Prevention. Eur Heart J. 1998, 19: 1434-1503. 10.1053/euhj.1998.1243.

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations


Corresponding author

Correspondence to Cornel Pater.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Pater, C. The current status of primary prevention in coronary heart disease. Trials 2, 24 (2001).

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • DOI:


  • cardiac
  • population
  • prevention
  • primary
  • risk