Using simply age to screen for cardiovascular disease is as effective as more complicated methods using blood pressure and serum cholesterol, concludes a study published in PloS One in May by Nick Wald, Mark Simmonds, and Joan Morris. (1) Can this really be right and if so what does it mean?

The authors used a Monte Carlo simulation with 500 000 people aged 0-89 to reach their conclusion. Taking being 55 or over as a positive test will detect 86% of cardiovascular events with a 24% false positive rate. This simple assessment is compared with screening everybody from age 40 at five yearly intervals using the standard Framingham risk score until people reach the risk of a 20% chance of a cardiovascular event in the next 10 years, the cut off for treatment recommended by the National Institute of Health and Clinical Excellence (NICE). For the same 86% detection rate the false-positive rate is 21%. In other words, the two methods are effectively the same, almost nothing is gained from a series of visits to doctors, measurements, and blood tests.
Can this be right? It is. I write this after reading the comments of 24 reviewers of the paper. None of them seriously disputes the conclusion. Indeed, many say that the finding is unsurprising because within the Framingham score of risk age is so dominant.

The finding is, however, counterintuitive and contrary to current perception. Can people’s family history, smoking status, blood pressure, serum lipids, and weight—all recognised risk factors for cardiovascular disease—not make much difference?  As the paper says, “Causal CVD risk factors, even in combination, are poor CVD screening tests.” Risk factors and screening tests are different.

Many will also wonder why it is that we have a whole industry of screening tests—not only  Framingham but also the Reynolds risk score (2) or QRISK2 (3)—if age alone is just as good. There is also substantial research effort being applied to using genetic and other biomarkers to try and predict more accurately who will have heart attacks and strokes, research that has had disappointing results. (4)

Should we then abandon screening people for risk of cardiovascular events using the various scores and use simply age? People wouldn’t have to visit doctors for screening assessments. They wouldn’t have to have blood tests. They wouldn’t have to try and understand what their Framingham score meant, and they wouldn’t be divided into healthy sheep and unhealthy goats.

Complicated risk assessments might end, but risk reduction—encouraging and helping people to stop smoking, lose weight, increase physical activity, eat healthier diets, and drink less alcohol—should continue. Others apart from doctors and nurses can do this work.

Risk reduction is sensible for everybody, but the point of risk assessment is to limit treatment to those above a specified risk. It’s well recognised now that it is a person’s overall risk (so called “global risk”) that should be assessed and not simply raised blood pressure or serum lipids. One implication of the new study is that everybody might begin treatment at 55. This fits with the strategy advocated in 2003 by Wald and his colleague, Malcolm Law, of everybody who wants to beginning to take a polypill containing blood pressure lowering drugs, a statin, and possibly aspirin and folic acid. (5) This remains a controversial idea, although less controversial than when first described. Several companies in India have manufactured polypills, and two trials have been published showing their effect on measures like blood pressure and serum lipids. (6 7)

So will complicated risk assessments be abandoned? Perhaps not in the short term as we know that there is a long lag between evidence and action and as there is too much vested interest in both conducting the assessments and trying to devise new ones. Both are industries with markets to protect.

The new evidence, although not surprising, does strengthen the case for the strategy of offering the polypill to everybody at 55, but this strategy also threatens vested interests and traditional thinking. Pharmaceutical companies see lucrative markets being destroyed. Doctors, particularly cardiologists, are sensitive to the implicit criticism that their strategy of assessing risk and treating is unnecessarily complex and overlooks the fact that many cardiovascular events occur in people without high risk factors, the “prevention paradox”. (8)

Public health practitioners fear the polypill offers a licence to people to avoid healthy lifestyles, although there is every reason for people to combine the polypill with healthy lifestyles and no reason not to. Finally, some worry about medicalisation, although, as I’ve argued elsewhere, giving people the pill without tests is the opposite of medicalisation in that those who take the polypill can avoid falling into the hands of doctors. (9)

This is slightly edited portion of an editorial that appears in the Journal of Medical Screening and can be accessed for free at http://jms.rsmjournals.com/content/18/3/113.full
 
Competing interest: RS was the editor of the BMJ and the chief executive of the BMJ Publishing Group, which once owned the Journal of Medical Screening, and was until September a member of the board of the Public Library of Science. He’s also a long established enthusiast for the polypill and takes it every night.

1 Wald NJ, Simmonds M, Morris JK, 2011 Screening for Future Cardiovascular Disease Using Age Alone Compared with Multiple Risk Factors and Age. PLoS ONE 6(5): e18742. doi:10.1371/journal.pone.0018742

2 Ridker PM, Paynter NP, Rifai N, Gaziano JM, Cook NR (2008) C-reactive protein and parental history improve global cardiovascular risk prediction: The Reynolds risk score for men. Circulation 118: 2243–2251.

3 Hippisley-Cox J, Coupland C, Vinogradova Y, Robson J, Minhas R, et al. (2008) Predicting cardiovascular risk in England and Wales: prospective derivation and validation of QRISK2. BMJ 336: a332.

4 Wang TJ. Assessing the role of circulating, genetic, and imaging biomarkers in cardiovascular risk prediction. Circulation.2011; 123: 551-565doi: 10.1161/CIRCULATIONAHA.109.91256

5 Wald NJ, Law MR (2003) A strategy to reduce cardiovascular disease by more than 80%. BMJ 326: 1419–25.

6 Yusuf S, Pais P, Afzal R, Xavier D, Teo K, et al. (2009) Effects of the polypill (Polycap) on risk factors in middle-aged individuals without cardiovascular disease (TIPS): a phase II, double-blind, randomised trial. Lancet 373: 1341–51.

7 PILL Collaborative Group 2011 An International Randomised Placebo-Controlled Trial of a Four-Component Combination Pill (“Polypill”) in People with Raised Cardiovascular Risk. PLoS ONE 6(5): e19857. doi:10.1371/journal.pone.0019857

8 Rose G (1981). Strategy of prevention: lessons from cardiovascular disease. BMJ 282:1847-1851

9 Smith. R. The polypil is about demedicalisation not medicalisation. https://blogs.bmj.com/bmj/2009/05/01/richard-smith-the-polypill-is-about-demedicalisation-not-medicalisation/