Implications of antibodies to heat-shock proteins in ischemic heart disease

Experimental studies illustrate that priming with infectious agents, like Chlamydia pneumoniae, is involved in plaque formation and progression based on molecular mimicry with host heat-shock proteins (HSP). We have here evaluated the hypothesis that C. pneumoniae contributes to atherosclerotic disease progression via anti-HSP antibodies.

The blood circulation of 151 consecutive patients with ischemic heart disease was screened for antibodies against human and Chlamydia HSP60 and C. pneumoniae IgG. Antibody levels were associated with the angiographic extent of coronary atherosclerosis, with clinical symptoms of ischemic heart disease and with biochemical and functional endothelial dysfunction markers.

Positive serology to human (11%) or Chlamydia HSP60 (22%) was not associated with the presence and extent of atherosclerosis, neither was it related with endothelial dysfunction. Patients with acute myocardial infarction had significantly lower Chlamydia HSP60 antibody levels (median OD 0.12, range: 0.02-0.75) than patients with stable (median OD 0.22, range: 0.02-2.67) or unstable angina pectoris (median OD 0.24, range: 0-2.48) (p=0.032). Subjects with positive C. pneumoniae IgG serology (if measured at a titre of 1:128) showed reduced flow-mediated vasodilation (p=0.024), but vasodilation responses did not differ in single-, two- or three-vessel disease.

Overall, antibody responses to C. pneumoniae IgG, human or Chlamydia HSP60 are not associated with endothelial dysfunction and presence and severity of coronary artery disease, arguing against the suggestion that infection contributes to disease progression and supplying additional proof that C. pneumoniae is an unlikely major risk factor of coronary atherosclerosis.