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Episode #26: Dissecting the controversy around JUPITER with Dr Paul Ridker

Aug 20, 2010 14:30 EDT


Hailed as a landmark trial by many, JUPITER has spawned a vociferous cadre of detractors whose assertions have stirred debate and some controversy throughout the cardiovascular community. Dr Paul Ridker joins the show to review key areas of criticism pertaining to the design and execution of the trial, putatively skewed results from halting the trial early, data inconsistency, and the involvement of industry in JUPITER.

What are your thoughts on the JUPITER trial? Do you find the criticism of JUPITER constructive or virulent?

See:

JUPITER gets a battering, but Ridker fights back

JUPITER hits New Orleans: Landmark study shows statins benefit healthy individuals with high CRP levels

JUPITER casts a large shadow: Moving from efficacy data to the big picture

AHA 2008: The AHA Flies to JUPITER





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Your comments
Episode #26: Dissecting the controversy around JUPITER with Dr Paul Ridker
# 1 of 2
August 28, 2010 01:08 (EDT)
W.E. Feeman, Jr, MD

1)  When did Paul Ridker change his mind?  It was only a short time ago that he stated that inlammation in atherothrombotic disease (ATD) was due to well-known ATD risk factors and he gave the example of the high rates of inflammation in subSaharan Africa, and yet the low ATD rates.  He now says that  the baseline LDL level is immaterial because people with high hsCRP received benefit from rosuvastatin even when LDL<60 mg/dl at baseline.  In fact statins lower hsCRP rapidly--even within a day or so--and hence must interfere with their synthesis.  My point is that he has wihdrawn his earlier comment of "What a bastard child I have created," has now placed inflammation above lipid risk factors, and has turned 50 years' research on its head ( epidemiology of ATD ).  While I have no objection to abrupt changes of thinking and I agree that people, including physicians, are resistant to changing long held beliefs, those who would herald such reolutions must be free of an appearance of conflict--and Ridker's holding of the hsCRP patent has the appearance of impropiety.                

 2)  I have an age-sex database of 1009 people who have developed some form of clinical ATD in the 1974-2003 timeframe.  This data has been published.  I can tell you that few patients have ATD events with LDL<60 mg/dl--certainly less than 1% of the ATD population.  Moreover, no one aged 80 years or older in my general population database has an LDL<60 mg/dl.  Ridker has bindly followed the tunnel-vision approach of the NCEP and focused on LDL.  He would do better to use a lipid ratio, because it detects the population at risk of ATAD much better than does LDL.  (For my approach, please see Amer J Cardiol, 2008, August 1 issue, "Treating Lipids in the General Population.")  I would bet you that if Ridker were to plot Jupiter pataients' CRF-SBP plots on my graph, those with end of trial plots below the threshold line did not have, in the absence of cigarette smoking, any ATD events, irrespective of hsCRP.  I would further bet that those with LDL levels below 80 mg/dl were cigarette smokers with/without high TG.  The average LDL at which patientws in my practice sustain an ATD event is 145 mg/dl in men and 154 mg/dl in women--and these are people of al ages.

 3)  What I am saying is that we can identify the population at risk of ATD very well, and we don't need hsCRP to do it.  In my opinion, hsCRP in conjunction with lower LDL levels is simply a surrogate for a low HDL.  Let Ridker do what I have suggested above and he will see why I at least look at his findings with a jaundiced eye.

 
# 2 of 2
August 31, 2010 05:07 (EDT)
W.E. Feeman, Jr, MD
I forgot to add a couple of items to my previous comments.  First, Wang and Chang (in a 2004 aricle in J Clin Endo Metab, 2004;89:4762-4767) showed that in diabetics who were treatment-naive, hsCRP correlated with the CRF and nonHDL cholesterol, but not with LDL cholesterol.  Second, CRF and non-HDL cholesterol were very highly correlated (r=0.68, p-value<0.0001.

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