An international group led by University of Cambridge researchers found that an inflammatory protein called interleukin-6 receptor (IL6R) contributes directly to CHD development.
In a second study, researchers said the disease could be prevented by targeting IL6R using existing anti-inflammatory treatments.
Research has connected inflammation to atherosclerosis, which causes CHD. But it remained unclear whether this link was causal. Now, two meta-analyses published in The Lancet have shed light on this mechanism.
In the first study, researchers explored whether a genetic variation that reduces the effect of IL6R in some people also lowered their risk of CHD, comparing 82 studies of more than 200,000 participants.
Researchers found that for each copy of this variant inherited, a person’s levels of the inflammatory C-reactive and fibrinogen proteins fell by 7.5% and 1% respectively. Risk of CHD dropped by 3.4%.
In the second study, researchers led by a team at University College London looked at data from 40 studies of 133,449 participants. They found that this genetic variant had a similar effect on inflammatory biomarkers in the blood as tocilizumab, a rheumatoid arthritis drug that blocks IL6R.
Study co-lead Dr Adam Butterworth of the University of Cambridge said tocilizumab ‘might therefore be a viable drug for preventing heart disease’.
Professor Alan Silman, medical director of Arthritis Research UK, said: 'People with rheumatoid arthritis have a slightly greater chance of having a heart attack, which seems to be an effect of inflammation, and the risk is reduced by controlling the disease through drugs.
'It seems not unlikely, therefore, for a drug used to treat rheumatoid arthritis - tocilizumab, which blocks the inflammatory processes by blocking the Il6R - may also show promise in treating heart disease.'