Is low density lipoprotein apheresis effective for coronary artery disease?

Low density lipoprotein (LDL) apheresis is one type of therapy currently being used for coronary artery disease; however, there has been no study to compare the effectiveness of this therapy with the effectiveness of other treatments, such as coronary artery bypass grafting (CABG) and percutaneous transluminal coronary angioplasty (PTCA). In this study, we evaluated the clinical results of these three therapies to compare their individual effectiveness for the treatment of coronary artery disease. Forty-four patients with two vessel disease (plasma cholesterol levels > 250 mg/dl) were divided into three groups (L, LDL apheresis; C, CABG; I, PTCA). After 2 years' observation, the coronary artery findings were evaluated by quantitative coronary angiography (QCA), frequency of cardiac events, changes in plasma lipids, and subjective symptoms, and the cost was examined. The symptoms of patients in Groups C and I showed significant improvement when compared with those of Group L. In Group L, the frequency of cardiac events was low (L, 0%; P, 44%; C, 14%), and lipid reduction was marked (L, 48%; P, 13%; C, 14%); however, the cost of this therapy is much more than the other therapies. There was no difference in the minimal luminal diameter evaluated by QCA in the three groups. LDL apheresis may be a good strategy for coronary disease, if its cost can be improved.

Effects of brief glucocorticoid exposure on growth of vascular smooth muscle cells in culture.

While prolonged exposure of vascular smooth muscle cells (VSMC) to glucocorticoid has been shown to inhibit cell proliferation, the effect of a brief pulse exposure is not known. We studied the short-term effects of pulse exposure to dexamethasone (DEX) on DNA synthesis in cultured VSMC. VSMC were pulsed with DEx for varying time intervals and [3H]thymidine incorporation into cells after 24 h was measured. Exposure to DEX for 24 h decreased [3H]thymidine incorporation, while pulse treatments with DEX from 2 min to 6 h significantly increased [3H]thymidine incorporation. Maximal proliferative effect was observed with a 20-min exposure. The effect of a 20-min pulse was dose-dependent, with the half-maximal dose of DEX being approximately 10(-7) M. A selective glucocorticoid receptor antagonist, RU486, inhibited the proliferative effect of DEx. Concentrated conditioned medium from cells exposed to 10(-6) M DEX increased [3H]thymidine incorporation by other VSMC in a dose-dependent manner. These results suggest that short-term pulse DEX exposure is capable of producing one or more autocrine growth factors in VSMC via a glucocorticoid receptor action. This effect of glucocorticoid pulses may contribute to the pathogenesis of arteriosclerosis and hypertension.