People who have a reduced lung capacity may have a greater risk of heart attack and stroke because they show evidence of inflammation, reveals a study published online ahead of print in Thorax.

This association is not related to smoking, respiratory diseases or obesity.

The New Zealand researchers took measurements of lung capacity and inflammation in 1,000 adults aged between 26 and 32 years.

To measure inflammation, they looked at the amount of C-reactive protein (CRP), an inflammatory marker, circulating in the blood. Higher levels of CRP were found in the blood of those with smaller lung capacities.

Although increased levels of markers for inflammation have previously been found in the blood of older people with reduced lung function and chronic obstructive pulmonary disease (COPD), the authors say: ‘To our knowledge, this is the first report of an inverse association between lung function and CRP in young adults.’

The results showed that this association was not related to smoking or lung disease, because the relationship existed even in people who had never smoked and had no respiratory disease. It was also not explained by obesity, which is often associated with raised inflammatory markers.

It has been suggested that an increased risk of cardiovascular disease may exist in older adults with COPD because inflammation is a risk factor for hardening of the arteries or atherosclerosis.

However, this study found an association between higher serum CRP and lower lung function in adults as young as 26 years, who the authors say are very unlikely to have developed either clinically significant atherosclerosis or COPD.

They say: ‘These findings indicate that the association between lower lung function and increased inflammation predates the development of either chronic lung disease or clinically significant atherosclerosis.

‘Establishing whether systemic inflammation leads to reduced lung function or whether lower lung function leads to inflammation is difficult, but this research suggests that the association between poor lung function and cardiovascular disease may be mediated by an inflammatory mechanism.’

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