Lipid profile in patients with microvascular angina.

Abstract

Lipid, lipoprotein and apolipoprotein levels, as well as the susceptibility of low-density lipoprotein (LDL) to oxidation, were studied in patients with micro-vascular angina in comparison with patients with coronary artery disease (CAD) and normal subjects. Total cholesterol, LDL-cholesterol and apolipoprotein B levels in microvascular angina patients (235 +/- 46 mg dL-1, 135 +/- 33 mg dL-1 and 146 +/- 32 mg dL-1 respectively) were significantly higher than in control subjects (204 +/- 40 mg dL-1, 116 +/- 35 mg dL-1 and 129 +/- 29 mg dL-1 respectively, P < 0.01). These parameters were also significantly higher in CAD patients than in control subjects. By contrast, high-density lipoprotein (HDL)-cholesterol levels in microvascular angina patients were no different from those in control subjects, although both were significantly higher than in the CAD patients (48 +/- 16 mg dL-1 and 45 +/- 12 mg dL-1 compared with 40 +/- 10 mg dL-1, P < 0.01 and P < 0.05 respectively). Similar results were obtained for the apolipoprotein AI levels. Furthermore, the atherogenic risk ratio, LDL-cholesterol/HDL-cholesterol, in microvascular angina patients was significantly lower than in the CAD patients (3.4 +/- 1.2 vs. 4.1 +/- 1.5 respectively, P < 0.01). Median (range) serum lipoprotein (a) [Lp(a)] levels in microvascular angina patients and CAD patients [13 mg dL-1 (0.8-92) and 16 mg dL-1 (0.8-96) respectively] were significantly higher than in control subjects [7 mg-dL-1 (0.8-44)], P < 0.01 and P < 0.005 respectively. Sigmoidal curves and electrophoretic mobility of the Cu(2+)-oxidized LDL in both microvascular angina and CAD patients were not significantly different from those of control subjects. Finally, no significant differences were found between groups in total triglyceride levels or in very low-density lipoprotein (VLDL), LDL and HDL triglyceride levels. Our results show that the microvascular angina patients exhibit lipid abnormalities similar to those observed in CAD patients, with the important exception of the HDL-cholesterol and apolipoprotein AI levels, which are significantly higher in microvascular angina patients. We suggest that the abnormal cholesterol and Lp(a) levels may be involved in the pathophysiology of microvascular angina by affecting endothelial function and endothelium-mediated vasodilator responses, whereas the higher HDL levels may be a factor contributing to the absence of angiographically documented CAD in microvascular angina patients.