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Do You Really Need More Lipoprotein Tests? By Simeon Margolis, M.D., Ph.D. - Posted Tue, Jan 09, 2007, 8:19 am PST

Provided by: Johns Hopkins University

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  • 1. Posted by A Yahoo! Health User on Tue, Jan 16, 2007, 7:58 am PST

    Dr. Margolis is way off...due to lack of information I am sure. Please provide this information for all to see and at least update your files with correct information. There are well over 1 million VAP test done annually next to 100,000 NMR test. Evidence for Using the VAP Cholesterol Panel for Comprehensive Coronary Artery Disease Risk Assessment and Treatment Planning The VAP cholesterol test is recommended for comprehensive assessment of the risk for Coronary Artery Disease (CAD) and the Metabolic Syndrome in all new patients. This recommendation rests on the inadequacy of the ordinary lipid panel to identify patients at risk for myocardial infarction,1 and similarly, the inadequacy of fasting glucose and insulin testing to identify many patients with the Metabolic Syndrome.2 Through direct measurement of the five major lipoprotein classes: HDL, Lp(a), LDL, IDL and VLDL, as well as LDL size and density pattern and key HDL/LDL/VLDL subclasses, the VAP panel increases detection rates to 90% of all patients who will have coronary atherosclerotic disease, up from 40% with the ordinary lipid panel.3 In addition, the presence of the lipid triad of high triglycerides, low HDL2 and small/dense LDL particles is a very specific and early indicator of insulin resistance.4 The VAP cholesterol panel provides this additional information at a cost comparable to the ordinary lipid panel and is nationally available through both diagnostic laboratories. Almost half of all patients who have heart attacks have “normal” cholesterol and only 25% of patients with premature coronary artery disease have abnormal LDL levels.1 Premature CAD is not rare, in fact 25% of acute myocardial infarction in community hospitals occurs in men under 55 and women under 65.5 In fact, 58% of these patients had LDL cholesterol 200 mg/dL versus 400 mg/dL in ATPII.7 In fact, as early as 1995, the NCEP Working Group points out that “patients with fasting triglyceride concentrations above 250 mg/dL warrant further evaluation in any case (NIH Consensus Conference 1984, 1993), which at least in some would usually require more extensive analytical procedures than use of the Friedewald equation.”8 Significantly, LDL has not been directly measured in today’s ordinary lipid panels; rather it is estimated using the Friedewald equation: [LDL] = [Total Cholesterol] – [HDL] – [Triglycerides/5] Thus, the calculated LDL is speciously low in patients with elevated triglycerides (TG).9 Although calculated LDL levels in healthy patients correlate well with directly measured LDL, they do not correlate well in patients with diabetes, coronary or other atherosclerotic disease.10 A second problem with the estimated Friedewald LDL is that it was never intended to be used in persons with LDL-C below 100 mg/dL, which is now our treatment target for high risk persons. Friedewald LDL-C is up to 18.5% falsely low when directly measured LDL-C is below 100 mg/dL, thus we systematically under treat high risk persons to their LDL targets when we rely on Friedewald.11 Another strong reason to get a direct LDL is that a large percentage of patients sent for ordinary lipid panels do not fast correctly, so their calculated LDL will be falsely low. In contrast, the directly measured LDL cholesterol in the VAP is accurate in these inappropriate, non-fasting persons. Again, with the new guidelines calling for LDL-C 200mg/dL should have the LDL-C directly measured using a CDC-NHLBI certified method. The development of this method, to calculate LDL-C, was done 17 years before the publication of the first NCEP Guidelines.

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  • 2. Posted by A Yahoo! Health User on Fri, Jan 19, 2007, 6:14 pm PST

    I am a 34 yo woman w multiple miscarriages, moderately elvated hypercoagulopathy results and a patent foramen ovale and low BP's no HTN at all and three stroke in 2 months, which caused them no one can figure it out. the cardiologist says the patent ovale is not the cause, the hematologist says maybe its a hypercoagulable state and in the mean time I was treated for vasculitis with high dose steroids, plavix aspirin and coumadin all at the same time. it seems like these drs need to cover all thebases without finding out what is the root of the problem. could the fact that I was on IM progesterone shots weekly through my recent pregnancy have caused the strokes no one will even ponder the thought

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  • 3. Posted by A Yahoo! Health User on Mon, Feb 04, 2008, 6:23 pm PST

    I'm taking Crestor again, after going off of it for 2 months....My chol. went up to 350, and my lipids were 250. what can i do to lower it even more? dr. didn't increase my doseage of 10mg. I do have family history of it, but went off of it for a short time, because of leg cramps all the time, and thought it was causing it. I am female, 59, 157 pounds...otherwise healthy, with the exception of arthritis in my hands, and fingers...

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  • 4. Posted by A Yahoo! Health User on Mon, Feb 04, 2008, 6:44 pm PST

    I'm taking Crestor again, after going off of it for 2 months....My chol. went up to 350, and my lipids were 250. what can i do to lower it even more? dr. didn't increase my doseage of 10mg. I do have family history of it, but went off of it for a short time, because of leg cramps all the time, and thought it was causing it. I am female, 59, 157 pounds...otherwise healthy, with the exception of arthritis in my hands, and fingers...

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  • 5. Posted by A Yahoo! Health User on Wed, Jun 17, 2009, 8:47 am PDT

    Why is apo B valuable in patients with normal LDL cholesterol but whose LDL particles are very small, but the NMR, which is the direct measurement of these particles and their sizes, is not?

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