Differences in human antioxidized LDL autoantibodies in patients with stable and unstable angina.

BACKGROUND: Autoantibodies to oxidized LDL (anti-oxLDL) have been found in the serum of patients with coronary artery disease (CAD). This study was designed to compare the differences in anti-oxLDL titers and isotypes in unstable and stable angina patients and to correlate these results with known markers of active inflammation in CAD. METHODS: Thirty patients from a tertiary referral general hospital with documented CAD were studied. Anti-oxLDL IgG titers and its isotypes, high sensitivity C-reactive protein (hsCRP) and serum amyloid A (SAA) were measured. RESULTS: The anti-oxLDL IgG titer was lower (p=0.03) in the unstable angina group compared to the stable angina patients (0.084+/-0.102 OD versus 0.195+/-0.149 OD, respectively). The predominant IgG isotype in both groups was IgG2. IgG4 was significantly higher (0.270+/-0.146 OD, p=0.04) in the unstable angina group versus patients with stable angina (0.198+/-0.019 OD). There was a significant inverse correlation between anti-oxLDL and hsCRP and SAA in this sample population (R=0.37, p<0.05 and R=0.36, p<0.05, respectively). CONCLUSION: Patients with unstable angina have lower levels of anti-oxLDL IgG in the acute setting of CAD. Plaque instabilization does not seem to acutely modify the isotype subsets of anti-oxLDL IgG in these patients.

Increased Th1 activity in patients with coronary artery disease.

BACKGROUND: Atherosclerotic lesions are mainly composed of macrophages and T lymphocytes. Specific T helper type 1 (Th1) cytokines and interferon gamma (IFN-gamma) inducible chemokines have been shown to be present in these lesions, modulating the local immunologic response. To explore whether this increase in Th1 activity could also be detected in circulating cells indicating a systemic activation, we studied the peripheral expression of Th1 cytokines and chemokines in patients with coronary artery disease and controls. METHODS AND RESULTS: Fifty patients with coronary artery disease (25 with unstable angina and 25 with stable angina) and 10 controls were studied. Serum interleukin (IL)-12 and IFN-gamma and the expression of IFN-gamma inducible chemokines IP-10, Mig and their receptor CXCR3 in peripheral cells were analyzed. Serum IL-12 and intracellular expression of IFN-gamma were significantly elevated in patients with unstable angina. An enhanced expression of IFN-gamma chemokines IP-10, Mig and CXCR3 in patients with stable angina was also observed. CONCLUSIONS: This study demonstrates an increased systemic inflammatory activity in patients with coronary heart disease with a predominant Th1 response, particularly in patients with unstable angina, suggesting an important role played by this polarization in plaque formation and rupture.