How sad.  A physician of Dr. Goldhaber's credibility doing such a disservice to medical science by promoting a technology as useless in the screening population as HS-CRP.  

 

It is continually ignored by Harvard that in MESA, the subset of patients who had heart attacks during  the study had on average a lower baseline HS-CRP than the patients who had no heart attacks during the study.  In the St. Francis Heart Study, HS-CRP added little to baseline risk assessment and added nothing after atherosclerosis imaging. 

 

In addition, the highly touted Jupiter study demonstrated benefit of Crestor only in the population with at least one risk factor.  HS-CRP alone was not predictive of benefit.

 

It is clear that this Emperor has no clothes. 

 

Is Dr. Goldhaber  truly that ignorant of the DATA or is he the marketing arm of the HS-CRP syndicate? 

 

It does not bother me to see Harvard make a little money.  It bothers me when Harvard uses its bully pulpit to promulgate bad information! 

There is a fundamental misconception about the Jupiter trial that Dr. Goldhaber and many others demonstrate by saying "these patients have more vascular risk with elevated CRP than those with with elevated lipid levels" (Goldhaber quote here).  The Jupiter trial was as much a trial involving patients with dyslipidemia as it was about inflammation--and yet this fact has been lost on many who interpret a low LDL-C to mean a "normal" lipid level in Jupiter.

As Allan Sniderman repeatedly mentions, LDL-C does not equate to LDL (total atherogenic burden--Apo B or LDL-P).  

In Jupiter, LDL-C was indeed low (26th %ile compared to Framingham population), but Apo B was very high (60th percentile for men, 70th percentile for women).  This discordance (typical in insulin resistance) was clinically significant---yet largely ignored.

 Jupiter patients were largely unhealthy, metabolic syndrome patients (41%)--with a major dyslipidemia that belied the "normal" LDL-C that gave casual observers the false impression they had low LDL.

 The predictive value of either Lp(a) or hsCRP are moderate...they are both markers for possible elevated vascular risk and demand further examination of the patient (e.g. coronary calcium scans, advanced lipid analysis)----not a reflex treatment with either rosuvastatin (jupiter) or niacin (EAS).  To put a patient on a statin from an elevated CRP level is absurd---what if it is elevated because of an inflammatory condition in a knee?

 Biomarkers are useful to alert one to a POSSIBLE issue--further testing is needed before action.  Again, Jupiter is a trial involving DYSLIPIDEMIA as well as inflammation as a marker for risk.

A state of dyslipidemia exists when the balance between the pro-atherogenic lipids (mainly LDL) and the anti-atherogenic lipids (mainly HDL) favors the accumulation of LDL in the subintimal space.  This can occur even when the lipid profile is "normal."  Were Dr Goldhaber to look at LDL-HDL ratios he would not need to look at either hsCRP or Lp(a); neither are necessary to predict the population at risk of atherothrombotic disease (ATD).  To predict the populatiuion at riskof ATD, may I refer you to letters published in the Ameridcan Journal of Cardiology (1 August 2008 and 1 September 2010).  This predictive tool, using only the Cholesterol Retention Fraction (CRF, or [LDL-HDL]/LDL), systolic blood pressure (SBP), and cigarette smoking status, was presented at the 2010 annual symposium of the National Lipid Association in Chicago, along with its validation.  The data has been presented for publication and such consideration is in progress.