Search

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.

Intra-aortic balloon (IAB) counterpulsation can augment the cardiac output. However, the effect of different IAB volumes on cardiac performance has not been adequately evaluated in humans. Eighty-two patients (52 males [63%]; mean age, 65 +/- 12 years; mean body surface area [BSA], 1.8 +/- 0.2 m(2)) had IAB counterpulsation for cardiogenic shock, refractory angina, and preoperatively for high-risk cardiac surgery. Cardiac hemodynamics were prospectively studied during IAB with inflation volumes of 32 vs. 40 cc. Hemodynamic data collected included aortic pressure, pulmonary artery pressure, systemic and mixed venous oxygen saturations, and cardiac output (by Fick). Transthoracic echocardiography (TTE) was used to obtain both velocity time integrals (VTIs) and the area of the left ventricular outflow tract (LVOT). Left ventricular stroke volume was then calculated as LVOT area x VTI. Cardiac output (CO) determined by the Fick method and VTI did not differ significantly (P = NS) between the two inflation volumes (y = 0.002 + 0.97x). In a subgroup of 33 patients with BSA