The most common pathogenesis of coronary artery disease is atherosclerotic plaque formation in the coronary arteries leading to narrowing of the blood vessel and impairment of blood flow.1 ,2 Therapeutic measures are aimed at revascularisation and increased blood flow. While coronary angioplasty is widely used today, one shortcoming of this procedure is the occurrence of restenosis in which the lesion regenerates in approximately 30% of patients within three months, necessitating reoperation.3 Although the pathogenic mechanisms of restenosis have been extensively studied in recent years, the underlying mechanisms are still not fully understood but are thought to be associated with neointimal formation as part of an inflammatory response to vascular injury.

Of the inflammatory mediating substances, the interleukins are the most well characterised. Interleukin 6 (IL-6) is the predominant determinant for production of acute phase proteins (for example, C reactive protein), and shows proinflammatory properties in addition to cellular effects (for example, smooth muscle hyperplasia) which are associated with restenosis. IL-6 concentrations which are raised in unstable angina are also raised after angioplasty, suggesting that IL-6 may therefore be a sensitive marker reflective of the postprocedure initial inflammatory response, and also a possible predictor of later restenosis.4 ,5 A relation between IL-1 concentrations and luminal renarrowing has been shown.6 We conducted a prospective study to assess whether circulating IL-6 concentrations are associated with restenosis.

In 20 patients with stable angina pectoris undergoing elective coronary angioplasty, IL-6 concentrations were measured before, immediately after, and at one and six hours postprocedure by an enzyme immunoassay (Fujirebio, Tokyo, Japan); a coronary angiogram was done six months postprocedurally to assess the presence of restenosis (> 50% lumen loss).

Of the 20 patients examined, nine showed restenosis. Mean (SD) circulating baseline IL-6 concentrations did not differ regardless of presence of restenosis, being within the normal range for either group (3.3 (2.9) v 1.9 (0.7) pg/ml for non-restenosis v restenosis, respectively; normal reference 2.8 (1.6) pg/ml). Patients with restenosis, however, showed significant (p < 0.05) increases in IL-6 concentrations at one hour (p = 0.03) and six hours (p < 0.01) postprocedure with 3.6 and 4.4-fold increases, respectively. Circulating IL-6 concentrations at six hours postprocedure for the group with restenosis also exceeded the normal range (> 2 SD). In contrast, the non-restenosis group did not show significant increases at any time point (fig 1). There was no significant difference in prevalence of coronary risk factors, including hypertension, hyperlipidemia, diabetes mellitus, and gout as well as previous myocardial infarction and past coronary bypass, between the groups with and without restenosis.

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Figure 1

Circulating IL-6 concentrations in patients with and without restenosis. Graph shows fold increases of IL-6 concentrations at measured time point against baseline. Error bars show SEM. *p < 0.05 against baseline; **p < 0.01 against baseline.

The finding that postprocedure IL-6 concentrations are increased in patients with restenosis following coronary angioplasty suggests that IL-6 may be a predictive marker of ensuing restenosis. Although the number of patients examined was small and the specificity of the IL-6 response to the coronary artery unclear, based on our preliminary findings targeted anti-inflammatory treatment may be warranted as an adjunct for patients with raised IL-6 concentrations following angioplasty. Further large scale studies should clarify the role of IL-6 concentrations as a predictive and therapeutic marker of restenosis.