Editorial
Interleukin 6: a message from the heart
| The first 150 words of the full text of this article appear below. |
The
idea that inflammatory processes are involved in the pathogenesis of
atherosclerotic coronary artery disease is not new,1 but
it has attracted renewed focus recently because of combined clinical,
epidemiological, pharmacological, and histological observations. Case-control studies have established consistent associations between
circulating inflammatory markers, in particular C reactive protein
(CRP), and the subsequent risk of cardiovascular events in healthy
people2 3 and in patients with established coronary heart
disease.4 5 CRP concentrations are often increased during
acute coronary syndromes and higher concentrations predict a worse
outcome in patients with unstable angina.6 Indeed, the
protective effects of aspirin3 and
pravastatin5 are greatest in patients with the highest
baseline CRP concentrations, in keeping with the anti-inflammatory
properties of both drug classes,7 while angiotensin
converting enzyme (ACE) inhibitors also prevent coronary events,
probably through anti-inflammatory activity.8 The pivotal
roles of monocyte derived macrophages and T lymphocytes as the
regulators of matrix degradation, apoptosis, cell replication,
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