内科学进展：强大获益-ACS患者他汀治疗决策思考.ppt

* * 2012 FDA解除他汀常规检测肝功能的限制指出他汀肝脏安全无需顾虑 * * 综合以上ACS患者他汀治疗早、严、长的原则，以及中国患者的实际情况，霍勇等著名专家提出ACS患者他汀续贯治疗新方案，对于急诊或择期PCI的患者建议 Patients with ACS have heightened focal inflammation within the vessel wall as well as evidence of a systemic inflammatory response (summarized in Table 3). In particular, T-lymphocytes present in the plaque produce a number of inflammatory proteins (cytokines), including interferon (IFN)-gamma, which lead to a decrease in collagen production by vascular smooth muscle cells. Activated macrophages produce large quantities of matrix metalloproteinases and elastases, which degrade collagen and elastin, resulting in a weakening of the fibrous cap. In the systemic circulation, evidence of immune activation also can be observed (Fig. 4) (36–40), resulting in the production of proinflammatory cytokines (Table 1). Suppressing the activity of inflammatory cells therefore represents an important therapeutic target for the management of ACS (Fig. 4). Acute coronary syndrome is associated with an increase in non-specific markers of systemic inflammation, such as CRP, and those with the highest levels have the worst clinical outcomes (41). Hepatic production of CRP is largely driven by increased release of cytokines, e.g., interleukins (IL-1, IL-6, IL-18) and tumor necrosis factor-alpha, which themselves also predict cardiovascular risk (42–45). Hence, cardiovascular risk could be reduced by treatments that have direct antiinflammatory effects. In contrast, ACS is associated with low circulating levels of the anti-inflammatory cytokines, e.g., IL-10, and recent observations suggest that high IL-10 levels attenuate the risk associated with an elevated CRP (46), reflecting a dynamic relationship between pro-inflammatory and anti-inflammatory processes. Another emerging prognostic marker also elevated in ACS is CD40-ligand (47), which has been shown to regulate plaque stability (48), and its potential modulation could be an important target for future syste