What has emerged from the trials is support for related lipid endpoints (such as apolipoprotein B and the number of LDL particles)  and inflammatory markers (such as high-sensitivity C-reactive protein)  and noninvasive plaque imaging. In many cases these can augment the risk that has been documented in patients with metabolic syndrome and diabetes. The studies have identified a large number of patients who may have been inaccurately felt to be at low risk and are subsequently identified to potentially profit from lower LDL levels. In addition, the perception that HDL is a routinely beneficial biomarker and one that should be targeted with specific therapy has been challenged by several large trials. This is due to our understanding that HDL functions as a “garbage truck” that facilitates the transfer of LDL from cholesterol-laden macrophages that are resident in plaque, to the liver where disposal occurs. However, these studies have questioned the wisdom of adding fibrates or niacin to statin therapy [8, 34]. An explanation for this dilemma has been offered in a recent publication in JACC showing that while niacin raised HDL-C it did not improve reverse cholesterol transport .
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