I originally posted on this topic 16 months ago after the untimely death of Tim Russert. Since that time, thousands of people have died from cardiovascular disease. It is the number one killer in the USA and approximately over 2600 people die each die from it each day.

Last week, the book that I co-authored with Tom Dayspring M.D. and William Cromwell M.D., two noted lipidologists, was published. It is titled Lipid and Lipoprotein Disorders: Current Clinical Solutions. I thought it was apropos to try and draw attention again to this most important topic.

Hyperlipidemia is the most modifiable risk factor leading to atherosclerosis, yet traditional lipid testing may miss up to 50% of people who have abnormal lipids. Prevention includes identifying people at risk and providing the best treatment individualized to their specific problem. Atherosclerosis results from a buildup of cholesterol-laden macrophages in the arterial intima. This occurs when atherogenic lipoprotein particles (principally low-density lipoprotein [LDL]) enter the arterial wall, become oxidized, and are subsequently ingested by macrophages.

It is with this background that I will discuss advanced lipoprotein testing and its role in identifying all patients at lipid related risk and as a tool for management of abnormal lipid levels. I often ask myself how is it that healthcare providers do not understand this type of testing? I honestly believe that if all people are identified as being at risk, and then if treated appropriately, we would significantly change the face of cardiovascular morbidity and mortality. As physicians, we are taught in medical school that it is all about total cholesterol, HDL-C, LDL-C, and triglycerides, yet few really understand the limitations of traditional lipid testing. I hear everyday physicians say that if it is so important how come everyone is not doing it? I believe the answer is that one does not want to change from old patterns of thinking, and according to other physicians, it is too much trouble to learn and understand.

Recently, the ADA/ACC released a Joint Concession Statement on lipoprotein management in patients with cardiometabolic risk (CMR). The full text is available on my website www.lipidcenter.com. I believe it is mandatory reading. It states that patients with CMR in the moderately high, high, and very high risk groups, it is now the standard of care to quantitate lipoproteins by performing ApoB or LDL-P on all patients to ascertain risk and as a goal of therapy.

As many of us in healthcare know, since sterols are insoluble in the blood, they need to be driven around the body in lipoproteins. These include HDL-P, VLDL-P, and LDL-P among others. HDL particles are also known as ApoA and all the particles that cause atherosclerosis are known as ApoB. Although NCEP (National Cholesterol Education Panel) recommends calculating the non-HDL cholesterol, this value only can alert the physician that there may too many lipoprotein particles despite having a normal LDL-C. Approximately 90-95% of the circulating ApoB particles are LDL-P, which have a half-life of around 3 days. As varying amounts of triglycerides and cholesterol are driven around the body, in what I tell my patients are "cars", the ApoB particles enter the arterial wall if there are too many of the "cars" circulating in the bloodstream. By simple diffusion, all the bad particles flow from inside the artery and move into its wall and are "eaten" by macrophages, which become foam cells and are the hallmark of atherosclerosis.

In eight published studies of over 11,000 subjects, using LDL-P and other lipoprotein concentrations remained the most significant and independent predictor of cardiovascular morbidity and mortality over any other lipid parameter including the usual ratio that all physicians and patients talk about. In a nutshell, it is the number of LDL particles that matter most... it is the number of cars that cause a traffic jam not the people in the cars[TM]. For example, what if a person with moderate risk has met NCEP guidelines and has a LDL-C of 110mg/dl. How do I know that there are not 100 cars with one person driving or two big buses with 55 people? The answer is that I do not unless I measure LDL-P directly by using NMR or as a second option measuring ApoB with Gel Electrophoresis. Traditional testing measures the passengers and lipoprotein testing measures the cars, and it is the number of cars (LDL-P) measured by NMR (Nuclear Magnetic Resonance) that are the most numerous ApoB particles in the body and matter most in the development of atherosclerosis.

Although a comprehensive review of each of the methodologies to perform lipoprotein testing is beyond the scope of this blog post, I feel that measuring LDL particles directly using NMR is the best way to ascertain someone's true risk and then use that number as a guide to management. As I said in my posting about Alex Trebeck, the CDC states that 50% of people who have heart attacks have "normal" cholesterol. I hope you now understand why this can happen, having a normal LDL-C but high LDL-P, and be proactive and demand that your physician performs advanced lipoprotein testing.

[TM]-US Trademark No. 77/693074, The Center For Cholesterol Management

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Labels: cholesterol, lipoprotein, testing

Labels: angiograms, atherosclerosis, cholesterol, coronary artery disease, CT, heart disease, testing

Part 1: CIMT

Cardiovascular disease remains the number one killer of both men and women. Does knowing this fact make it obligatory for health care providers to provide some type of warning system to possibly prevent a cardiovascular event or death? Let's look at the various techniques that are currently in use to potentially identify early atherosclerosis which would then permit early aggressive treatment. I do understand that many people who read my blog have different levels of understanding of these difficult medical issues. While I will try to keep it simple, I believe it is important to do it in such a way as to not trivialize such an important topic.

Invasive coronary angiography (angiogram or cardiac catheterization) is still the gold standard to identify clinically significant coronary artery disease. Like all invasive procedures, there are inherent risks associated with the procedure - risks that include heart attack, stroke, death, damage to the artery in the arm or groin used as the puncture site, and kidney failure to name a few.

I believe that many cardiologists indiscriminately perform angiograms of the heart arteries for reasons that are clearly not supported by the literature. With this said, I prefer to perform noninvasive testing in order to identify patients at risk. If after following a treatment algorithm, it is felt that coronary angiogram becomes necessary; it then can be done in accordance with well-accepted indications.

Noninvasive Methods
Let's first look at carotid intima-media thickness, also know as CIMT. This involves measuring the thickness of two concentric (circular) layers of the neck arteries using duplex ultrasound. To be more precise, it measures the thickness of the first two layers of the mid-portion of the common carotid artery. CIMT was first reported as a surrogate or substitute marker for atherosclerosis in 1986. This was a comparison between autopsy studies and what was found in B-mode ultrasound studies. There was a measurement error of less than 20% in 77% of the subjects studied. In a follow up study, they found that patients with high cholesterol had increased CIMT augmented by including traditional risk factors. Fourteen years later, the American Heart Association deemed CIMT the only acceptable noninvasive method for assessment of cardiovascular risk. It is thought that any increase in CIMT is a reactive process secondary to shear stress and pressure within the artery from hypertension and plaque formation.

The ARIC trial is the largest CIMT observational cardiac endpoint trial to date. In 13,870 middle-aged adults, CIMT measurements were increased in those patients with coronary artery disease. Quantification studies showed that a .2mm increase in CIMT yielded a 33% relative risk increase in heart attack and 28% for stroke. Similarly, in both the CHS study and Rotterdam study, increased CIMT correlated with subclinical atherosclerosis. Since CIMT is a recognized marked of cardiovascular risk, it is used as a primary endpoint in clinical trials. The beneficial effects of cholesterol lowering on CIMT progression have been demonstrated in ARBITER, ASAP, and ACAPS. In the ENHANCE study, the results were not accurately portrayed by the media and I have previously written about the actual results on my blog. Additional studies using different blood pressure medicines are ongoing in order to see their effect on CIMT.

The main problem with measuring CIMT is that there has been significant inter-observer variability. Technical advancements in B-mode ultrasonography have reduced this problem.

To be continued...

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• Low Heart Disease Risk? Test May Show Otherwise
• Cholesterol Management Message Board with Michael F. Richman, MD, FACS
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Labels: angiograms, atherosclerosis, cholesterol, CIMT, coronary artery disease, testing