血脂治疗敏新进展赵水平.pptVIP

A vicious cycle of vascular inflammation with recurrent injury results in the formation of a necrotic core and eventually vulnerable plaque. The initial step is entry and entrapment of LDL within the arterial wall, followed by entry of monocytes that take up the LDL and become foam cells. Crystals in the foam cells induce apoptosis, leading to further attraction of macrophages that forms an extracellular lipid pool within the arterial wall. This then constitutes the basic elements of a vulnerable plaque. * Mechanism of plaque rupture and/or erosion induced by cholesterol crystallization. In the case of a large necrotic core, the plaque cap is torn, leading to rupture, whereas in the case of a small necrotic core, it leads to erosion. Furthermore, trauma to the vasa vasorum by cholesterol crystals within the plaque causes intra plaque hemorrhage. Modified and reproduced with permission. * * Finally, we assessed the percentage of change in LCBI. We found dramatic reductions in percent LCBI between standard and aggressive treatment groups. LCBI was reduced by 27% per lesion, 25% per 10mm and 22% per 4mm. * * It is well established that achieving lower LDL-C levels results in a greater reduction in cardiovascular (CV) events; however, there has been uncertainty about the possible side effects that could be associated with achieving very low LDL-C levels This latest analysis from JUPITER showed that patients who achieved very low LDL-C ( 50 mg/dL) with CRESTOR 20 mg had significantly fewer CV events and a similar safety profile to patients not achieving such a low LDL-C. The risk of major CV events was also lower in those achieiving very low LDL-C ( 50 mg/dL) than those not achieving such a low LDL-C (HR 0.49, 95% CI 0.34-0.72, p=0.0003). Although the rate of myalgia was higher in the rosuvastatin group overall than in the placebo group (p=0.015), there was no difference in the rate of occurrence of muscle weakness, myopathy, mood disorders, peripheral neuropathy or