Nicorandil has a protective effect on the ischemic rabbit spinal cord, and the beneficial effect seems mediated through the activation of adenosine triphosphate-sensitive potassium channels.

FK506 and chronic administration of cyclosporine A, but not rapamycin, protect the spinal cord from transient ischemia. Although these results are compatible with inhibition of calcineurin in the mechanism of neuroprotective action of these drugs, other effects through different pathways cannot be excluded before further study.

No abstract

Purpose: To determine the predictive value of serum lipid levels on the development of later cardiovascular events after abdominal aortic aneurysm (AAA) surgery. Methods: A total of 101 patients under 70 undergoing an elective AAA surgery were divided into the following two groups: 1) those who developed later cardiovascular events after AAA surgery, including cerebral infarction (n = 4), catheter intervention (PCI) or surgery for coronary artery disease (CAD) (n = 9) and other vascular disease. (CVE group; n = 19); 2) those without later events (NoCVE group: n = 82). Preoperative atherosclerotic risk factors including serum lipid levels were subjected to univariate and multivariate analysis. Results:The CVE group showed a significantly lower high-density lipoprotein cholesterol (HDL-C) level (32.9 ± 6.6 vs 41.6 ± 12.1 mg/dL; p <0.001), higher low-density lipoprotein cholesterol (LDL-C) / HDL-C ratio (4.30 ± 1.01 vs 3.24 ± 1.15; p = 0.001), and higher prevalence of mild CAD (without an indication of PCI) (p = 0.029) preoperatively. Cox hazard analysis indicated that preexistent mild CAD (hazard ratio 4.70) and preoperative HDL-C <35 mg/dL (hazard ratio 3.07) were significant predictors for later cardiovascular events after AAA surgery. Conclusion: Patients at high risk for later cardiovascular events should require a careful follow-up and may also require an aggressive lipid-modifying therapy.

Lowered post-therapeutic LDL-C levels can decrease the risk of later, local vascular events after PAD treatment. These results may support the rationale for aggressive lipid-modifying therapy for PAD.