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 implicate d in the mediation of atherosclerosis by immune mechanisms. Any role o f HSP-65 in mediating restenosis is however not clear, We determined t he anti-HSP-65 antibodies in 28 patients, 25 male and 3 female, aged 3 5 to 78 years, with coronary artery disease (CAD) and undergoing percu taneous 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 di scharge from the hospital, and at 6 weeks, 3 and 6 months after the pe rformance of PTCA. The antibody levels were expressed in OD U/log titr e, as explained in the test, and termed estimated OD or E(OD). The con trol group consisted of 29 healthy volunteers, 16 male and 13 female, aged 24 to 59 years. The mean E(OD) of the patients at baseline was hi gher than that of the controls (0.60 +/- 0.12, SD: 95% CI 0.56-0.64 co mpared with 0.53 +/- 0.13: 0.48-0.58: p < 0.01). There was no correlat ion between age and E(OD) of patients, controls or both taken together , ruling out the influence of age on the E(OD) changes in the given ag e range. The mean antibody levels of the patients with CAD were simila r whether or not they suffered subsequent restenosis (0.61 +/- 0.15; 0 .53-0.69 in the patency group, and 0.60 +/- 0.10: 0.54-0.66 in the res tenosis group). However, the patients who did not develop restenosis h ad a drop in their antibody levels immediately after PTCA (0.51 +/- 0. 13: 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 thr oughout the 6-month follow-up in the patients with patent coronaries a s compared with patients who restenosed, but the decrease was statisti cally not significant at 5% level at any stage. Besides the anti-HSP-6 5 antibodies, the levels of anticardiolipin (ACL) antibody were also m easured 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, ru ling out the PTCA-associated change in the anti-HSP-65 antibody as a n on-specific occurrence. Thus, a drop in the level of antibody against HSP-65 after PTCA seemed to be associated with a favourable outcome, a nd may serve as a useful prognostic marker of coronary angioplasty.