Detection of the "midband" lipoprotein in patients with coronary artery spasm.

Abstract

Dyslipidemia in patients with coronary vasospasm has been characterized by a low level of high-density lipoprotein (HDL) cholesterol without elevation of low-density lipoprotein (LDL) cholesterol, distinct from patients with organic coronary artery disease. Disordered triglyceride-rich lipoprotein metabolism may be linked to the genesis of coronary artery spasm. The incidence of the "midband" lipoprotein observed between very low-density lipoprotein (VLDL) and LDL bands in the polyacrylamide disc gel electrophoretic analysis was determined in 48 patients with coronary spastic angina (CSA), in 50 patients with stable effort angina and a significant fixed coronary stenosis (SEA), and in 40 control subjects without coronary artery disease (Control). The incidence was significantly (p<0.05) higher in CSA (71%) than in SEA (50%) and Control (25%). Smoking was significantly (p < 0.05) more prevalent in CSA (77%) than in SEA (50%) and Control (50%). In SEA, serum levels of triglyceride and apoproteins C-II, C-III, and E were all significantly higher, and the serum level of HDL cholesterol was significantly lower in the midband-positive than in the midband-negative subgroup. In CSA, no significant differences were found in these serum levels between the midband-positive and -negative subgroups, except for a significantly (p < 0.05) lower level of HDL cholesterol in the former. However, a significantly (p < 0.05) higher incidence of diabetes mellitus or impaired glucose tolerance was noted in the midband-positive (41%) than in the midband-negative subgroup (7%) in CSA. The incidence of the detected midband lipoprotein was significantly decreased in the blood samples obtained from 20 of CSA after a > 6-month angina-free period (70-->25%, p < 0.05). The midband lipoprotein was frequently detected in patients with coronary vasospasm, suggesting that dyslipidemia with disordered triglyceride-rich lipoprotein metabolism may be linked to the genesis of coronary artery spasm.