Role of cytokines in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty.
BACKGROUND
Inflammatory cytokines play an important role in mediating inflammatory/proliferative responses including atherosclerosis. However, their role in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty (PTCA) remains to be clarified.


OBJECTIVE
To determine plasma levels of inflammatory cytokines as well as cytokine-generation capacities of monocytes before PTCA and after the follow-up period.


METHODS
Plasma levels of cytokines in 34 consecutive patients before and 3-6 months after PTCA were measured by enzyme-linked immunosorbent assay. We measured the plasma levels of macrophage-colony-stimulating factor (MCSF) and transforming growth factor-beta. Cytokine-generation capacities of monocytes were also measured by a whole-blood induction method with lipopolysaccharide. The levels of cytokines measured for assessment of the capacities included those of interleukin-1alpha, interleukin-1beta, interleukin-6, granulocyte-colony-stimulating factor, tumor necrosis factor-alpha and interferon-gamma.


RESULTS
Plasma levels of MCSF in patients without restenosis (n = 20) decreased significantly (from 1460+/-138 microg/ml before PTCA to 1039+/-125 microg/ml after the follow-up period, P < 0.01), whereas those in patients with restenosis (n = 14) increased significantly (from 1107+/-105 microg/ml before PTCA to 1039+/-125 microg/ml after the follow-up period, P < 0.05). We noted a positive correlation between the increase in plasma levels of MCSF and the extent of loss of lumen by restenosis. Cytokine-generation capacities of monocytes for interleukin-1alpha and interleukin-1beta of patients with restenosis significantly increased but those of patients without restenosis did not. Furthermore, plasma levels of C-reactive protein decreased significantly only in patients without restenosis after the follow-up period.


CONCLUSIONS
These results suggest that inflammatory changes mediated by cytokines may be involved in the pathogenesis of restenosis after PTCA.
Division of Cardiology, St Mary's Hospital, Kurume, Japan.
H
H
Tashiro
H
H
Shimokawa
K
K
Sadamatsu
T
T
Aoki
K
K
Yamamoto
D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D002097:C-Reactive Protein / Q000378:metabolism; D003327:Coronary Disease / Q000209:etiology* / Q000628:therapy*; D016207:Cytokines / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D016173:Macrophage Colony-Stimulating Factor / Q000097:blood; D008297:Male; D009000:Monocytes / Q000378:metabolism; D012008:Recurrence; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000097:blood
D016207:Cytokines; D016212:Transforming Growth Factor beta; D016173:Macrophage Colony-Stimulating Factor; D002097:C-Reactive Protein