The American Society for Preventive Cardiology 30 Years and Counting

ASPC CVD PREVENTION

July 30, 2015 marks the start of the ASPC’s Annual meeting, taking place once again at the spectacular Boca Raton Resort. This year, in addition to our world-class faculty, new elements will be added to the meeting – poster presentations to be published in Clinical Cardiology as well as a Level 1 Expert’s Course in Preventive Cardiology. Over the next three months I will certainly write more about the conference and I hope many of you will avail yourselves of its offerings. (For more complete information please visit www.aspconline.org).

Today however, on the heels of the Dallas Cardio-Metabolic Health Congress (CMHC) I am compelled to write this brief note about the ASPC. The reason is simple. As I sat in the speaker’s row with my friends and colleagues Drs. Jamie Underberg, Amit Khera, and Michael Miller it became clear that the thirty-year-old organization is now firmly entrenched in mainstream education. You see, Dr. Underberg sits on the ASPC’s Board of Directors while Dr. Khera is the Secretary; I am the President Elect, and Dr. Miller is a Past President. It was truly heartwarming to have us all gathered together for the sole purpose of helping to educate our colleagues about issues such as Familial Hypercholesterolemia (FH), Hypertriglyceridemia, Lipid and Cholesterol Guidelines, and the future of HDL research and therapies.  The ASPC is growing at a gratifyingly rapid rate, as more and more physicians, ARNPs, and other healthcare practitioners embrace the doctrine that cardiovascular disease prevention must preempt intervention in order for our nation and the world at large to be able to truly enjoy optimal health. If you are not already a member of the ASPC, please consider becoming one. Also, I encourage everyone interested in prevention to join us in July. I promise you will not be disappointed.

Learn more about preventive cardiology at www.preventivecardiologyinc.com.

For more information about the supplements and vitamins critical to your everyday health visit www.vitalremedymd.com.

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Cholesterol and Vascular Disease Part 5: Non-Statin Cholesterol Medications

September is National Cholesterol Education Month. In support of this important educational initiative we are republishing our six part series on cholesterol and the role it plays in cardiovascular disease.

Note: Seventy-one million American adults have high cholesterol, but it is estimated that only one-third of them have the condition under control.

Previously, in Part 4 of this blog series on cholesterol we spoke about the statins. This week we will look at other cholesterol medications. Another very effective method for decreasing LDL is by combining a statin with other drugs.

Medications

  • One of the most effective add-on medications is Ezetimibe. This medicine works by blocking cholesterol absorption in our small intestine. It’s not just the cholesterol we eat that is blocked; more importantly it’s the enormous amount of cholesterol that is recycled daily between our liver and intestine. At this point, clinical trials have failed to demonstrate a reduction in heart attack and stroke by using Ezetimibe. Still, many lipid specialists (me included) believe that future trials will demonstrate its importance in particular patient populations.
  • Another important class of cholesterol-lowering drug is called the bile acid sequestrants. Welchol is the most commonly utilized of these medications. By blocking the reabsorption of bile acids in our intestine our liver is forced to produce more bile acids from their precursor, cholesterol. Interestingly, WelChol also has the added benefit of lowering blood sugar and increasing HDL. Patients with very high triglycerides should be careful of this medication because it can increase triglycerides further. Like Ezetimibe, WelChol is best used in combination with a statin. Read More…

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Cholesterol and Vascular Disease: Part One – The History of Cholesterol

September is National Cholesterol Education Month. In support of this important educational initiative we are republishing our six part series on cholesterol and the role it plays in cardiovascular disease.

Note: Seventy-one million American adults have high cholesterol, but it is estimated that only one-third of them have the condition under control.

For over twenty years I have practiced and taught Cardiology. Starting in the invasive and hospital-based world (performing angioplasties, stents, atherctomies, lasers, and electrophysiologic procedures) and then segueing into prevention, cholesterol abnormalities, and cutting-edge non-invasive imaging of the carotid and coronary arteries, I have had the unique and great fortune to participate in exceptionally diverse aspects of cardiovascular health and illness. I have learned a great deal along the way and some of these experiences have been shared in articles and books I’ve written. Now I’d like to clarify one of the murkiest issues I’ve encountered in all my years of practice – the cholesterol conundrum. This post is the first of a series that will hopefully clarify the cholesterol debates that currently perplex numerous patients and physicians.

In the early 1900s a young medical student named Anitschkow made the initial association between cholesterol and vascular disease. He fed unsuspecting rabbits a high cholesterol diet. After they had enjoyed a number of tasty meals he sacrificed them in order to examine their aortas (the very large blood vessel that runs from our heart to our legs). What he found was revolutionary. The rabbits that consumed their normal low fat diets were just fine, but the cholesterol-fed rabbits had all developed severe plaques in their aortas. Of course none of the rabbits was lucky (they were all killed) but had they been allowed to live, the ones with normal diets would have done great, while those who had consumed large quantities of cholesterol would have suffered from heart attacks, strokes and premature death. Read More…

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CoQ10 Levels – Another Example that Knowledge is Power

I have always believed it is better to know than not to know. In Medicine such a philosophy often translates into performing tests in order to acquire data. Novel blood tests represent a safe and effective way to better understand subtle perturbations in our patients. About eight months ago the Cleveland Heart Lab added CoQ10 levels to its offerings and since then I have monitored them in my patients. The results have been eye opening. Ironically, although a long-time advocate of appropriate supplementation (in 2002 I founded an ultra-conservative nutritional supplement company www.vitalremedymd.com) I have grossly under-appreciated the prevalence of low CoQ10. Yes, statins can lower these levels, but my contention had been that the absence of statin-related symptoms assured the adequacy of body stores of this nutrient. Quantifying my patients’ CoQ10 levels disproved my prior conviction as I have witnessed a surprisingly high number of asymptomatic people harboring low CoQ10 levels. And, understanding that low CoQ10 might be associated with larger heart attacks and lower levels of HDL, I now feel compelled to correct this problem through supplementation.

Although many years back I had formulated StatinGuard® to maintain normal CoQ10 levels, I had never recommended it to asymptomatic individuals, my aim being to always minimize the ingestion of anything superfluous (supplement or medicine). Since the revelation produced by utilizing the CoQ10 blood test, I’ve recommended StatinGuard far more frequently. A CoQ10 measurement is just one of many innovative windows now available for physicians to peer through in order to inspect the metabolism of individual patients. Each test holds its own distinctive place in the practice of patient-centric medicine. The lesson once again: it is always better to know than not to know.

Visit vitalremedymd.com for more preventive healthcare solutions.

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Knowledge Reveals Profound Ignorance: the Hallmark of Medicine

I’ve said this many times before, Medicine Is a process, one that replaces old ideas with new understanding. HDL offers a perfect example. We all know HDL to be “the good cholesterol”. Simple, correct? HDL is the cholesterol that protects us from heart attacks and strokes; that’s its job. Low HDL implies risk while high HDL, protection. Enter the science of the past decade. Everything has changed. We’ve discovered that raising HDL in patients already on statin medications does not (as we previously believed) necessarily equal risk reduction. Far more profound than this realization is the fact that HDL is NOT “the good cholesterol”. Yes, it is a carrier of cholesterol, and yes it helps reduce the risk of heart attack, but NO it is NOT cholesterol.

It turns out that HDL is an extraordinarily complex structure with many phases of life and many forms and functions. HDL can be a disc and it can be a sphere. It can be very large or very small. Its surface can carry over 200 different types of fats and about 200 various forms of proteins. And, specific combinations of these fats and proteins will imbue the HDL particle with specific functions. HDL particles can help us fight infections, carry vitamins and nutrients throughout our bodies, protect LDL particles from oxidation, and shuttle proteins around the body to be given to more needy recipients. The list goes on. HDL is amazing. And the more amazing we know it to be the more we must admit how little we understand HDL. So if HDL is so complex, imagine how intricate our entire bodies are. The bottom line, please be patient with your doctor. He or she is trying desperately to understand and work with an ever-expanding field of information. Please understand that what may seem to be mistakes in science are often simply the byproducts of growth and development. We all aspire to the same goal, the expansion of health and reduction of illness. We really are all on the same team.

Visit vitalremedymd.com for preventive healthcare solutions.

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Cholesterol and Vascular Disease Part 5: Non-Statin Cholesterol Medications

Last week, in part 4 of this blog series we spoke about the statins. This week we will look at other cholesterol medications. Another very effective method for decreasing LDL is by combining a statin with other drugs.

Medications

  • One of the most effective add-on medications is Ezetimibe. This medicine works by blocking cholesterol absorption in our small intestine. It’s not just the cholesterol we eat that is blocked; more importantly it’s the enormous amount of cholesterol that is recycled daily between our liver and intestine. At this point, clinical trials have failed to demonstrate a reduction in heart attack and stroke by using Ezetimibe. Still, many lipid specialists (me included) believe that future trials will demonstrate its importance in particular patient populations.
  • Another important class of cholesterol-lowering drug is called the bile acid sequestrants. Welchol is the most commonly utilized of these medications. By blocking the reabsorption of bile acids in our intestine our liver is forced to produce more bile acids from their precursor, cholesterol. Interestingly, WelChol also has the added benefit of lowering blood sugar and increasing HDL. Patients with very high triglycerides should be careful of this medication because it can increase triglycerides further. Like Ezetimibe, WelChol is best used in combination with a statin.
  • Niacin, vitamin B3, is also often used in cholesterol management. It’s best known for its impact on raising HDL and lowering triglycerides. Niacin also has an effect on LDL however. It increases LDL particle size, and by so doing, can actually decrease LDL particle number. Niaspan is the pharmaceutical version of niacin that is most commonly utilized by the physicians. It’s method of action is poorly understood and quite complex. Like WelChol and Ezetimibe, niacin is also best used in conjunction with a statin.
  • Fenofibrates represent yet another class of medications that is used for cholesterol management. Their dominant effect is to lower triglycerides and raising HDL. At this point clinical trials have not found them to be effective in decreasing cardiovascular events, but they are improving lipids and lipoproteins.
  • The active ingredients in fish oil, DHA and EPA, can also have an effect on lipids and lipoproteins. They can lower triglycerides, increase HDL, and sometimes increase particle size and by so doing decrease particle number. In patients with very high triglycerides, fish oils can at times increase LDL cholesterol. Their method of action is also quite complex and beyond the scope of this blog.

Diet and Exercise

In managing cholesterol abnormalities we should never neglect the value of diet and exercise.  A healthful diet will unquestionably improve your lipid and lipoprotein profile. Even when taking a statin, a healthful diet must be maintained.  In fact, there is a specific dietary program called the Portfolio Diet that is geared specifically to lower cholesterol. Exercise can also benefit your lipid and lipoprotein profile. Daily exercise for 30-60 min. can significantly decrease your LDL particle number, increase your HDL, and lower your triglycerides. The bottom line, if you’re physically capable, exercise every day.

A few other cholesterol management strategies are either in the pipeline, or utilized only in very high risk patients. They will be the subject of next week’s blog, part 6 in this series, Cholesterol and Vascular Disease.

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Cholesterol and Vascular Disease: Part 2: LDL-Cholesterol is Important, but LDL-Particle Number is Far More Revealing

We left off with part 1 of the Cholesterol and Vascular Disease blog concluding that the two key assumptions made by cholesterol scientists in the 1940s and ‘50s were wrong. These assumptions were: 1. All LDL particles are the same size and 2.  All similarly-sized LDL particles have the same cholesterol content. Had these assumptions been correct there would have been no need to evaluate any other LDL parameter beyond LDL cholesterol. Given the fact that they are wrong however, means that looking simply at LDL cholesterol allows for the persistence of significant and dangerous “hidden risk”.  And risk that is hidden is risk that will not be corrected. Therefore we must dig deeper into this issue and how it can translate into a higher risk for developing arterial plaque.

First, let’s deal with the size issue. We now know that many individuals have very small LDL particles, while others have large, normally-sized particles. The larger the LDL particles, the more cholesterol they can fit within them. Smaller particles on the other hand cannot carry nearly as much cholesterol as their larger brethren. (That is simple enough. A large bucket holds far more water than a tiny cup.) Therefore, if you have very tiny LDL particles, you need many more of them to generate an LDL cholesterol content (LDL-C) than someone with very large particles. (Back to the water analogy –  If you need to carry a quart of water and you have one quart-sized bottle, you can carry all the water in one bottle. If you have only cups available, you will need four of them to carry the same amount of water.) The result of this disparity in LDL size is that two people with the same LDL-C (130 mg/dL for example) will have very different LDL particle numbers when their LDL particles are very different sizes.

The second erroneous assumption was that similarly-sized LDL particles always carry the same amount of cholesterol within them.  This too has turned out to be false.  Under certain metabolic conditions – diabetes, obesity, overweight, high triglycerides, low HDL– LDL particles tend to be under-filled. Once again in these patients in order to generate a particular LDL-C level, more particles are required.  (Back to the water analogy – if you have only cups available to fill, but are permitted to fill them only half way, it will take twice as many cups to carry the same amount of water as your friend who is allowed to fill the cups to the very brim.) Therefore, two individuals with precisely the same LDL-C can have vastly different LDL-Ps. So the bottom line is that LDL-C is NOT a good surrogate for LDL-P after all. OK, you buy that, but you might now be asking yourself,” Does it really matter if I have a lot of LDL particles?” A common and excellent question with a simple answer – YES! This is because more particles translate into a higher risk for developing plaque.  And the reason this is so, is actually quite intuitive. The more LDL particles a person has bouncing around in the blood stream, the more likely the particles are to encounter and penetrate the walls of his/her arteries. (The shotgun vs. the pistol is another helpful analogy. Even if you are an expert marksman, you are much more likely to hit your target with a shotgun than a single-shot pistol.) This is important because the penetration of our arteries by LDL particles initiates the process of atherosclerotic plaque formation. Yes, it all begins with a single particle. Next week we will discuss how such simple LDL particles can initiate a process that still kills more Americans than any other disease.

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