Summary
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% Cl 0.56-0.64 compared with 0.53 ± 0.13; 0.48-0.58;
p < 0.01). There was 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; 0.54-0.66 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 reste-nosed, but the decrease
was statistically not significant at 5% level at any stage. Besides the anti-HSP-65
antibodies, the levels of anticardio-lipin (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
