Solving the HDL Mystery
Dysfunctional HDL is a relatively new concept in humans. Cardiologist Stanley Hazen of the Cleveland Clinic has been studying altered forms of HDL and surmises that this might explain the torcetrapib surprise. Hazen is eager to analyze blood samples from patients in the Pfizer study to look for dysfunctional forms of HDL, stressing that quality, not just quantity, matters. His colleague and head of cardiology at the clinic, Steven Nissen, believes he's really on to something. Nissen led a smaller torcetrapib study that measured plaque in the coronary arteries over time in some 1,200 patients, half on and half off the new drug, using a fairly precise imaging technique called intravascular ultrasound. As Nissen points out, this IVUS study, which he and the other investigators are analyzing, will tell if the drug reduced the plaque as it was expected to do. Coupled with Hazen's study of the patients' HDL, Nissen thinks we will have some crucial answers in just a matter of months.
Though it would be easy to toss off torcetrapib as a dud and move on without knowing why, that would be a huge mistake. The drug's failure points to mysteries of cholesterol and heart disease. In solving them, we are sure to find new avenues for drug discovery. In the process, Pfizer's current trials and tribulations may become a big win for patients.
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