It has been suggested in an article published in the open –access journal PLoS Medicine that there is a relation between coronary heart disease and levels of interleukin-6(IL-6) initiated by inflammation that pulls immune system cells towards injured part. John Danesh (University of Cambridge) and colleagues also mention that new drugs designed to fight vascular disease may also target the IL-6 protein.
Coronary heart disease (CHD) is one of the biggest causes of death in adults in developed countries. When deposits of plaque, calcium, and other cellular waste products harden against the arterial walls (atherosclerosis), there is a discontinuity of blood flow through the body and these blockages in the coronary arteries result in CHD
The research by Danesh and colleagues centers atherosclerosis as an inflammatory condition. They work on the grounds that the immune system responds to injury by developing an area of redness and swelling (inflammation), a process which contains the production of cytokines. Cytokines are proteins that pull immune system cells to an injured site, such as an artery wall that has been damaged by atherosclerosis. Inflammation of the damaged artery, due to these cytokines, may further increase in the growth of atherosclerotic plaques. Thus, the researchers set out to observe if a relation could be formed between prolonged moderate increases in a cytokine called interleukin-6 (IL-6) and CHD. If they find such a link, new therapies could be developed that target cytokines in order to reduce inflammation and slow down atherosclerosis.
Danesh and colleagues examined two large-scale studies made during 1967 and 1991 that added almost 25,000 healthy middle-aged people – the Reykjavik Study (RS) and the British Regional Heart Study (BRHS). Over a 20-year period, 2,138 had a first nonlethal heart attack or died from CHD. The researchers had access to the baseline IL-6 levels in these participants and in 4,267 participants who did not have CHD. Adjusting for a year-to-year consistency of IL-6 levels, the researchers found that increased long-term IL-6 levels were associated with a doubling of the risk for CHD. In a brief meta-analysis, the authors point out that their finding is consistent with findings from 15 previous relevant studies.
“Long-term IL-6 levels are associated with CHD risk about as strongly as are some major established risk factors, but causality remains uncertain. These findings highlight the potential relevance of IL-6-mediated pathways to CHD,” conclude the authors.
In a joining perspective by Bruce Neal (George Institute for International Health, Sydney, Australia) included the same issue of the journal. Neal writes:
“It is now widely recognized that 90% or more of vascular disease can be explained on the basis of known risk factors, so these new data about IL-6 probably have relatively little to add in terms of our understanding of causation. There are also multiple interventions that modify these known risks and avert premature death and disability from vascular disease at low cost. Therefore there is little need for a new and probably costly drug that acts via IL-6. The better application of proven risk stratification methods and the more efficient delivery of proven management strategies could already cut a swathe through the current vascular disease burden. These proven strategies should remain the priority, particularly in developing regions of the world where most vascular disease now occurs. A focus on the identification of practical strategies for the delivery of existing interventions could deliver highly cost effective global health step.”
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