Brief overview of the standard lipid profile

Brief Overview of the Standard Lipid Profile
With Advanced Understanding

Standard Lipid Profile:

Test
Values/Ranges
> or = 40 mg/dl (Male) > or = 50 mg/dl (Female) (Calculated)
Use the numbers above to calculate the numbers below. This will help you better understand your patient’s cardiovascular risk thereby helping to guide your treatment decisions. While we recognize that ApoB is the best marker of risk, it is not easily available, nor do many insurance’s pay for it yet, therefore, we believe that using Non-HDL is the next best marker. Non HDL Cholesterol = (Total Cholesterol – HDL) 210 Triglyceride to HDL Ratio = (Triglycerides / HDL) 250 Cholesterol to HDL Ratio = (Total Cholesterol / HDL) 210
Residual Risk = The additional risk of Cardiovascular Disease AFTER you have gotten
the Non-HDL to target. Specifically look at the HDL & Triglycerides.
In addition to the standard Lipid Profile, you may also consider looking at the following:
• hs C-Reactive Protein • Berkley VAP, NMR Lipid Profile, SpectraCell Lipid Profile, Boston HeartLab Profile – Pharmacological Armamentarium

Lescol XL, Pravachol, Mevacor, Zocor, Lipitor, Crestor • Other Cholesterol Lowering Zetia, WelChol • Fenofibrates Tricor, Trilipix, [Lopid (contraindicated w/Statins)]
Definition of terms used below:
Non-HDL Cholesterol = The cholesterol within all of the ApoB particles.
HDL-C = Cholesterol content within all of the HDL particles.
HDL-P = Number of HDL particles.
LDL-C = Cholesterol content within all the IDL and LDL particles.
LDL-P = Number of LDL particles. (large and small)
ApoB = Collective concentration of all the ApoB containing lipoproteins

Example of Two Patients

Patient # 1
Patient # 2

Discussion: Both patients have relatively the same Total Cholesterol level and both have
exactly the same LDL-C. Patient # 2 is at significantly higher risk of cardiac events
because the Non-HDL is higher and thus the number of particles is higher. Non-HDL is
a better surrogate marker of ApoB than is LDL-C. This patient’s TGs are also markedly
elevated.
CAD and Atherosclerosis are caused by a complex series of events in which lipoproteins play a major role. Lipoproteins are water soluble containers that carry cholesterol and triglycerides. Many complex body processes interact with lipoproteins decreasing their size and density. This conversion makes lipoproteins more likely to interact with the arterial wall where they can deposit their cholesterol and other lipid contents and initiate CAD or Atherosclerosis. The amount of cholesterol carried within these particles can vary between each pt. and even within a pt. This is why standard cholesterol levels can underestimate the number of LDL particles in some pts. Knowing the pt’s number of LDL particles can help in the diagnosis and management of cardiovascular disease risk. An easier way to think of it is to think of heart disease as a traffic jam. The cars represent
lipoprotein particles and the passengers in the cars represent cholesterol. It’s the number
of cars that cause the traffic jam, not the passengers. Just as cars cause the traffic jam,
excess particles cause heart disease.
References:

http://www.nhlbi.nih.gov/guidelines/cholesterol/index.htm (accessed 6.29.08)
Lipids, Apo lipoproteins, and Their Ratios in Relation to Cardiovascular Events
With Statin Treatment
Circulation 2008;117;3002-3009; originally published online Jun 2, 2008;
DOI: 10.1161/CIRCULATIONAHA.107.713438
Trig/HDL ratios in - AJC, 8/05 McLaughlin, p339
Trig/HDL Ratios in Blacks - Fasting Triglyceride and the Triglyceride–HDL Cholesterol
Ratio Are Not Markers of Insulin Resistance in African Americans Anne E. Sumner, et
al. Arch Intern Med. 2005;165:1395-1400
www.lipidsonline.org (accessed 9.26.09)
Pocket Guide – Lipid and Lipoprotein Disorders: Current Clinical Solutions
www.GuidelineCentral.com, 2009, (Cromwell, Dayspring, Richman)

Source: http://www.houdyslipidemiasociety.org/pdfs/boalp.pdf

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dentistry.cu.edu.eg

Cairo Dental Journal (25) Number (3), 323:328 September, 2009 The INflUeNCe Of MTAD IRRIgANT ON The ApICAl MICROleAkAge Of ObTURATeD ROOT CANAlS Mohamed M. Ibrahim;(1) Naguib M. Abul Enein;(2) Abdalla M. Shahin(3) and Amany E. Badr(4)1. Assistant lecturer, Conservative Dentistry Department, Faculty of Dentistry, Mansoura Univerisity. 2. Professor, Head of Endodontic Departme

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