[WCC2010]急性冠脉综合征的病理生理机制与炎症因子标记物——Prof. Libby专访
<International Circulation>: The Optimized Coronary Artery Disease Treatment Strategy has made rapid progress. Could you share with us the latest developments in exploring the pathogenesis of the acute coronary syndromes, and especially their implications for management?
<International Circulation>: The Optimized Coronary Artery Disease Treatment Strategy has made rapid progress. Could you share with us the latest developments in exploring the pathogenesis of the acute coronary syndromes, and especially their implications for management?
Prof. Libby: We have learned a great deal about the way in which atherosclerosis — which is a very chronic disease — transitions from its stable or asymptomatic phase to its thrombotic complications. The first insight is that it is not always the critical stenoses that cause the acute coronary syndromes. The second recognition is that instead, a physical disruption of the atherosclerotic plaque causes most thrombotic occlusions that lead to fatal coronary events. The third insight is that inflammation promotes the fragility of the plaque that predisposes it to rupture. In our basic science laboratory, we have studied the way in which inflammatory mediators and inflammatory cells can promote the weakening of the collagen that strengthens the plaque’s fibrous cap and protects it from rupture. We have also contributed to understanding of the mechanisms by which inflammatory mediators can increase the thrombogenicity of the plaque once it ruptures. So we believe inflammation is a fundamental process that drives the thrombotic complications of atherosclerosis, both by effects on the structure of the plaque and by the capacity of the plaque to generate a trigger for thrombosis — its thrombogenicity. These points have considerable clinical implications. Contemporary cardiology has recognized that ischemia due to stenoses is appropriately addressed by revascularization strategies, and of course, appropriate revascularization is extremely effective in relieving angina. But unfortunately our revascularization approaches, be they surgical or percutaneous, do not decrease myocardial infarction or prolong life in broad categories of patients. In contrast, systemic therapy that can reduce inflammation — including lifestyle changes and lipid-lowering therapy, particularly with statins — can result in fewer coronary events and prolong life in appropriately powered studies. I think our patients deserve the best of revascularization for relief of their symptoms, as well as systemic therapy and lifestyle change to decrease the inflammatory burden and provide them with the best outcomes.