Association of antibodies to heat-shock protein-65 with percutaneous transluminal coronary angioplasty and subsequent restenosis.
Heat-shock protein (HSP)-65 of mycobacterial origin has been implicated in the mediation of atherosclerosis by immune mechanisms. Any role of HSP-65 in mediating restenosis is however not clear. We determined the anti-HSP-65 antibodies in 28 patients, 25 male and 3 female, aged 35 to 78 years, with coronary artery disease (CAD) and undergoing percutaneous transluminal coronary angioplasty (PTCA). Of the 28 patients, 12 suffered restenosis five to seven months later. The serum levels of antibody were measured at baseline, immediately after PTCA, before discharge from the hospital, and at 6 weeks, 3 and 6 months after the performance of PTCA. The antibody levels were expressed in OD U/log titre, as explained in the text, and termed estimated OD or EOD. The control group consisted of 29 healthy volunteers, 16 male and 13 female, aged 24 to 59 years. The mean EOD of the patients at baseline was higher than that of the controls (0.60 +/- 0.12, SD; 95% CI 0.56-0.64 compared with 0.53 +/- 0.13; 0.48-0.58; p < 0.01). There were no correlation between age and EOD of patients, controls or both taken together, ruling out the influence of age on the EOD changes in the given age range. The mean antibody levels of the patients with CAD were similar whether or not they suffered subsequent restenosis (0.61 +/- 0.15; 0.53-0.69 in the patency group, and 0.60 +/- 0.10; 0.54-.066 in the restenosis group). However, the patients who did not develop restenosis had a drop in their antibody levels immediately after PTCA (0.51 +/- 0.14; 0.48-0.55; 2-tailed p = 0.029), and at discharge from the hospital (0.52 +/- 0.15; 0.44-0.60; p = 0.036) as compared with the baseline. This decrease of antibodies was not observed in the restenosis group. Furthermore, the anti-HSP-65 antibody levels remained slightly low throughout the 6-month follow-up in the patients with patent coronaries as compared with patients who restenosed, but the decrease was statistically not significant at 5% level at any stage. Besides the anti-HSP-65 antibodies, the levels of anticardiolipin (ACL) antibody were also measured in all the patients. The levels of the ACL antibody were found to be within the normal range before and at all stages after PTCA, ruling out the PTCA-associated change in the anti-HSP-65 antibody as a non-specific occurrence. Thus, a drop in the level of antibody against HSP-65 after PTCA seemed to be associated with a favourable outcome, and may serve as a useful prognostic marker of coronary angioplasty.
Mukherjee
M
M
Thrombosis Research Institute, Chelsea, London.
De Benedictis
C
C
Jewitt
D
D
Kakkar
V V
VV
D000328:Adult; D000367:Age Factors; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000886:Anthropometry; D000907:Antibodies, Bacterial / Q000097:blood*; D000942:Antigens, Bacterial / Q000276:immunology*; D001161:Arteriosclerosis / Q000276:immunology / Q000628:therapy*; D001426:Bacterial Proteins; D015415:Biomarkers; D018834:Chaperonin 60; D018833:Chaperonins / Q000276:immunology* / Q000502:physiology; D003327:Coronary Disease / Q000276:immunology / Q000628:therapy*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006949:Hyperlipidemias / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D009169:Mycobacterium tuberculosis / Q000276:immunology; D009765:Obesity / Q000453:epidemiology; D011379:Prognosis; D012008:Recurrence; D012307:Risk Factors; D012907:Smoking / Q000453:epidemiology; D017211:Treatment Failure
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D015415:Biomarkers; D018834:Chaperonin 60; C074119:heat-shock protein 65, Mycobacterium; D018833:Chaperonins