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Calculating CVD risk in older patients

Estimating cardiovascular risk is an area that has received much attention of late and the subject of risk scoring systems is a keenly debated area.

The Framingham risk score was originally validated for people aged up to 75 years but is often used in much older populations despite concerns about its accuracy in this setting. Indeed newer risk algorithms such as QRISK2 are similarly limited by validation in populations under the age of 75.

The Leiden 85-plus Study1 aimed to address this issue. The authors investigated the performance of the classic risk factors as well as newer biomarkers in predicting cardiovascular mortality in an elderly population with no history of cardiovascular disease.

The Dutch observational prospective cohort study enrolled 215 women and 87 men aged 85 years or older, between 1997 and 2004, with no history of cardiovascular disease. Participants were followed for mortality for 5 years.

Cardiovascular risk factors were assessed at baseline. Traditional risk factors were included such as sex, systolic BP, total and HDL cholesterol, diabetes, smoking and ECG evidence of LVH. Novel biomarkers were also measured such as homocysteine, folic acid, CRP and interleukin 6.

The authors calculated a modified Framingham risk score and developed several unique risk prediction models using combinations of the classic risk factors and newer biomarkers. A linear predictor score was developed for each combination to represent an individual's predicted risk of cardiovascular mortality during the 5-year follow-up. Participants were assigned to a high-, intermediate-, or low-risk group on the basis of tertiles of the calculated scores for each model.

The results showed that 108 of the participants died during the study period with 35 of these deaths due to cardiovascular causes. Of these 35 cases the Framingham risk score had identified 12 people as being at high risk whereas the homocysteine based model identified 20. The Framingham risk score did not appear to predict five-year cardiovascular mortality with no difference observed in outcome between the high- and low-risk groups (RR 1.2, 95% CI 0.5-2.6). Of the novel biomarkers only homocysteine accurately predicted five-year cardiovascular mortality with a 3.4 times greater risk (95% CI 1.4-8.1) in the assigned high-risk group compared with the low-risk group.

The authors concluded that in very old people with no history of cardiovascular disease, concentrations of homocysteine alone can accurately identify those at high risk of cardiovascular mortality, whereas classic risk factors included in the Framingham risk score do not.

However, this was a small observational cohort study and these findings should be interpreted with a degree of caution. It is also important to note that although the study showed a higher CVD risk with higher levels of homocysteine it was unable to establish a cut-off point above which treatment would be recommended and this would limit its usefulness as a decision-making tool.

Furthermore actively lowering homocysteine has been shown to have no impact on CVD outcomes although this does not necessarily detract from its use as a predictor of risk.

What this study has done is further illustrate the limitations of the Framingham risk charts (modified or otherwise) in elderly patients. However this point is acknowledged by the Joint British Societies [JBS], who note that all patients over the age of 69 will have their risk underestimated by the JBS2 charts2, which are based on the modified Framingham score. In this group the advice is to use clinical judgement in combination with the charts to decide on the appropriateness of intervention. This is a highly sensible approach and I would advise against measuring homocysteine levels routinely in the elderly until more robust evidence is available to confirm that it is a reliable marker of CVD risk. Certainly there is no evidence to suggest that homocysteine levels per se should be a target of therapeutic intervention.

There is no evidence to suggest that homocysteine levels per se should be a target of therapeutic intervention


Dr Peter Savill
GPwSI cardiology, Southampton

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