Screening patients for cardiovascular risk factors is often an opportunistic affair that can miss those at highest risk, such as socioeconomically deprived groups and middle-aged men, who often try to avoid the GP at all costs. Another approach is to screen all patients over a certain age, but the workload implications for primary care would be considerable and this approach is unlikely to be cost-effective in the long term. There is clearly a need to improve the efficiency of such screening and targetting patients with a family history may be the answer.

First-degree relatives of patients with premature CHD (<55 years in men and <60 in women) are at increased risk of coronary events. When compared with the general population, siblings of such patients have at least double the risk, with risk varying according to age at presentation and number of relatives affected. This is likely to be caused by both shared lifestyle risk factors and genetic predisposition. Naturally, offspring are also at increased risk and spouses and partners often share the same lifestyle risk factors as the index case.

A recent study, published in the BMJ,¹ found that 10-16% of first-degree relatives of patients with premature CHD had the disease. A paternal history of MI under the age of 50 carried a relative risk (RR) of 2.3 in siblings compared with a RR of 1.7 with a paternal presentation under the age of 70 (RR 3.6 and 2.2 respectively for maternal history). The risk increased as more first-degree relatives were affected.

What is not clear is how much of this increased risk is caused by genetic factors and how much results from shared lifestyle factors. The researchers in the BMJ study found that the offspring of patients with premature CHD had higher levels of modifiable risk factors than age- and sex-matched controls, so the lifestyle component must not be underestimated. This fact is further illustrated by the significantly higher levels of modifiable risk factors found in unrelated family members, such as the wives of patients who have had an MI, compared with the spouses of healthy men.

Therefore a robust process to target such people is to be welcomed. Chow et al suggest that relatives could be identified whenever someone is admitted to hospital for premature MI. They could then be offered screening and counselled about lifestyle issues with appropriate intervention. They estimate that by screening and treating middle-aged people with a family history of CHD 42% of premature MIs and 8% of all MIs could be prevented.So, if increased risk in the relatives of such patients is evident, are we acting on this knowledge in practice? EUROASPIRE II showed that 54% of siblings and 71% of offspring had not been screened.² Other studies have shown that siblings of such patients were less aware of cardiovascular risk factors than the general population and if problems such as hypertension or hyperlipidaemia were identified they were often suboptimally treated. If screening had occurred, it was usually opportunistic. It is not clear why relatives were not being screened, but I suspect lack of awareness and limited resources play a part, as well as the lack of an optimal screening strategy.

This is an impressive statistic and should prompt us to develop mechanisms to target and treat this group of high-risk patients. Perhaps integrating the index admission or first outpatient review with the early phases of a cardiac rehabilitation programme would facilitate the screening process, with the subsequent involvement of the relevant GP practice. At the very least risk calculations should incorporate family history, either as an adjusting factor if based on the Framingham dataset or by adopting newer risk scores such as QRISK,³ which integrate a family history of premature CHD into the algorithm.