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[WCC2012]升高HDL-C降低心血管剩余风险——Dr.Chapman专访

作者:  Chapman   日期:2012/5/2 15:09:04

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《国际循环》:您在WCC大会上做了关于升高HDL-C新策略的演讲。您能否就升高HDL-C重要的性略谈一二?

  <International Circulation>:In treating populations, do you think it would be most important to only treat people with atherogenic dyslipidemia or should we be trying to treat people without atherogenic dyslipidemia with the fibrate trials?

  Dr Chapman: The clear message from the subgroup analyses of FIELD, ACCORD, the message from VA-HIT, the message from the Helsinki Heart Study, is that the individuals with the lipid triad are the individuals who benefit clinically to the greatest degree from fibrate treatment. In a sense, the intervention trials with fibrates which have been conducted until now, have been somewhat misguided. They have not focused patient recruitment on the patients who would potentially benefit the most. Unfortunately, this is a major error. Therefore, we still find ourselves in the situation where we are not sure because we don’t have the appropriate clinical trial to really substantiate that fibrate intervention on top of a statin in individuals with atherogenic lipid triad, be they diabetic or non-diabetic, is beneficial.

  <International Circulation>:What about the data from ACCORD that suggested that fibrates were helpful for microvascular outcomes especially retinopathy regardless of atherogenic dyslipidemia?

  Dr Chapman: I think that these are very provocative data. They are hypothesis-generating data. From the ACCORD trial, there is data that supports the hypothesis that there may be a reduction in the frequency and degree of retinopathy in this instance with fenofibrate treatment. But there is also data from that trial suggesting that the degree of renal insufficiency or the rate of degradation of renal function may be attenuated. In other words there may be some improvement in nephropathy with a fibrate in the ACCORD trial and I think there is a suggestion of similar data in the FIELD trial. There is also data suggesting that the translation clinically of improvement in the microvasculature (or in other words, microangiopathy) affected by the fenofibrate at least in the FIELD trial is reflected in an overall benefit in target organ damage in diabetics to the degree that there was a reduction in amputations in the FIELD trial. So these data are very provocative and potentially very important but we come back to the same question. Do we need a new intervention trial to respond to these questions? Many of us in the field feel that we do and if such a trial were positive, it could be tremendously important for many patients around the world.

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