|
|
|
Apr 14th, 2006 - 15:12:46 |
Just a few short years ago, our perception of the coronary arteries and the atherosclerotic process that results in more deaths than any other disease in the Western world was entirely different from what it is today. As an active interventional cardiologist I performed thousands of angioplasties and inserted stents in blood vessels choked by tightly packed plaque. The hope back then was to avert the seemingly inevitable: a progressive encroachment of fatty and calcific debris that could ultimately lead to the complete closure of a coronary artery, causing a heart attack.
Now we know the arteries that are most susceptible to abrupt closure are actually those with less severe narrowing, typically blocked by under 50 percent. As counterintuitive as it may sound, the nasty-looking, heavily calcified, tightly narrowed arteries that in years past sent shivers up and down the spine of the interventional cardiologist actually fare much better than the soft, lipidladen, thinly capped plaques that minimally obstruct arterial blood flow-yet terrify today's cardiologist. Hand in hand with this sea change in our understanding of cardiovascular danger has come a vastly greater grasp of the biology of our blood vesselsspecifically, what makes some of them fall prey to aggressive and life-threatening coronary and cerebral vascular disease while leaving others free from its grip.
Inflammatory Risks
Inflammation is now understood to be the fuel that drives the atherosclerotic engine besieging our blood vessels. Our arteries are no longer inert bystanders of an invading army of fat. Instead, our blood vessels are active participants, integrally involved in the atherosclerotic process. In fact, in many ways they are themselves the perpetrators of their own demise.
Basically this is how it works. Our blood vessels, when at peace, are coated with a smooth, undisturbed, single layer of cells called the endothelium. When left unmolested, this Teflon-like lining remains serene and secure. An offending agent, however, can change all this. The "wrong substances" can initiate the process of destruction that will inevitably reshape the vascular landscape and lead to the development of advancing coronary artery disease.
What are these potential instigators of inflammation and atherosclerosis? LDL particles (especially when numerous, small, and oxidized) represent perhaps the greatest offenders. Then you have free radicals, which are enemies of many of our body systems, including our arteries. Elevated homocysteine levels also predispose our blood vessels to damage and plaque buildup.
Inside the Artery Wall
What do these offending agents do to our seemingly blameless blood vessels? The ringleaders of arterial decay, LDL particles are small packets that transport the lion's share of our body's cholesterol. Cholesterol does not float freely in our blood but is, instead, compartmentalized into tiny floating packets (like LDL and HDL), as blood and fat don't mix well. Small pores, or portholes, that dot the single-celled endothelial covering normally permit only a limited penetration of LDL particles into the blood vessel wall. But as the number of these particles increases (especially when smaller in size and more oxidized), the more readily they will penetrate the vessel barrier and come to rest beneath the vessels' surface.
There, inside an artery's wall, the process of inflammation begins its spiral of destruction. Specialized inflammatory cells engulf the cholesterol in an attempt to quell the problem, but the opposite often occurs. The cells themselves become transformed. They release a host of substances that summon other inflammatory cells, which in turn release more and more harmful products. Inflammation soars, plaque grows, and the artery reshapes itself in an attempt to preserve an adequate lumen (the inner diameter, as in a hose) to maintain an ample flow of blood. The more the artery is bombarded by offending agents like homocysteine, LDL, and free radicals, the more rapidly the progression of plaque buildup occurs.
It's similar to an emerging hurricane: When the elements are properly positioned-low and high pressure systems, warm ocean water- a raging storm can develop. So, too, in our arteries: When the inciters of destruction are left unchecked, a heart attack, possibly even a fatal one, can strike.
Natural Solutions
Most people recognize the role of lifestyle choices in health maintenance. Daily exercise, a diet rich in fruits, vegetables, legumes, fiber, and plenty of water, active management of life's stressors, and avoiding harmful substances such as tobacco are known to promote better health. But what else can we do to stave off vascular disease, that great slayer of human beings? How can we combat the inciting inflammatory process just discussed? Fortunately there are several weapons at our disposal.
First let's look at cholesterol. In order to shed a clearer light on your lipids, have your doctor perform specialized blood tests such as the LipoProfile from LipoScience labs in North Carolina. There is so much more to the cholesterol problem than most standard blood tests reveal.
In order to make more refined recommendations, cardiologists need to know the number and size of your LDL and HDL particles (as well as other more esoteric elements of your lipids). Please be open to the use of statins (if indicated). These pharmaceuticals have been shown in countless studies to convey huge reductions in cardiovascular events and death from heart disease.
A natural solution to the annoying side effects of muscle aches and weakness that accompany statin use is the combination of CoQ1O, L-carnitine, and lipoic acid. These three substances work within our cells' mitochondria, where statins are believed to cause problems. Taking this combination of nutritional supplements has helped many of my patients continue, symptomfree, on life-prolonging statin therapy.
Ask for a PLAC test to examine the level of inflammation in your arteries. The well-known Creactive protein (CRP) test demonstrates more widespread (or systemic) inflammation and, thus, will be elevated not only in patients with coronary disease but also in smokers, overweight individuals, and those with rheumatologic disorders. By contrast, the PLAC test reveals inflammation only when it exists within our arteries.
If you have evidence of inflammation, add a high-quality omega-3 fish oil supplement to your regimen. Omega-3 oils decrease the risk of cardiovascular events. These fats convey benefits on many fronts: They are anti-inflammatory, antiarrhythmic (i.e., diminish abnormal heart rhythms), and antithrombotic (i.e., decrease the ability of our blood to clot). Omega 3s also lower triglycerides and
may even lower your blood pressure. These fats are so beneficial that even the somewhat conservative American Heart Association (AHA) has made a formal recommendation for their use. If you have coronary artery disease or two or more cardiovascular risks (diabetes, high blood pressure, tobacco abuse, a family history of coronary disease), the AHA advises you to consume 1,000 mg of combined EPA/DHA daily. This 1,000 mg refers to the EPA/DHA, not the fish oil itself. (You need to read the labels carefully to see how much EPA/DHA is contained in a given product.) To avoid PCBs, mercury, and other adulterants, choose a highquality product.
Additional Testing
Then there's the issue of the free radicals, our enemies, and the antioxidants, our allies. Again, ask your doctor about specialized blood testing. Spectracell Labs in Houston, Texas, offers an excellent way to evaluate your individual antioxidant needs. By using this test I've found that many people are surprised to learn that they don't require the amounts and forms of antioxidants often considered appropriate. Through specialized blood tests, patients are better able to tailor their therapy to meet their own personal needs. After all, we are all individuals and must be examined and treated as such. Of course, when it comes to antioxidants, don't forget that food is your greatest ally. Fruits, vegetables, tea, and even chocolate offer a whole spectrum of antioxidants.
Finally, elevated homocysteine levels can damage our arteries. Homocysteine can lead to blood clotting, inflammation, and even DNA damage. High homocysteine levels increase our risk not only of heart attacks but also of osteoporosis, macular degeneration, strokes, and Alzheimer's disease. Solid trials evaluating the impact of lowering homocysteine levels have yet to be completed. But given the magnitude of destruction that high homocysteine imparts, I advise my patients to lower very high levels of homocysteine. To accomplish this, I recommend starting with a combination of vitamins B6, B12, and folic acid (the latter being the most important of the three). After three months, if levels are not where we'd like them, I add N-acetylcysteine (NAG) to the regimen. But don't forget that lifestyle factors also contribute to high homocysteine levels: Excess weight, sedentary behavior, tobacco abuse, and copious coffee consumption are a few of these modifiable factors.
Work with Your Physician
Health is best achieved when patients and doctors work together in a harmonious relationship. We are on the same side, with the same goal: the pursuit of optimal health. Enlist your physician in your quest for health. More than likely, you'll be pleasantly surprised by your doctor's response. If not, there are plenty of other physicians who will aid you in your quest.
SOURCES "Dietary Supplementation with n-3 Polyunsaturated Fatty Acids and Vitamin E after Myocardial Infarction: Results of the GISSI-Prevenzione Trial," Lancet, 8/7/99 • "The Effect of Pravastatin on Coronary Events after Myocardial Infarction in Patients with Average Cholesterol Levels" by F. M. Sacks et al., N Eng J Med, 10/3/96 • "MRC/BHF Heart Protection Study of Cholesterol Lowering Therapy and Antioxidant Vitamin Supplementation in a Wide Variety of Patients at Increased Risk of Coronary Heart Disease...," Eur Heart J. 5/99 • "Primary Prevention of Acute Coronary Events with Lovastatin in Men and Women with Average Cholesterol Levels" by I R. Downs, JAMA, 5/27/98
Top of Page
|
|
|
|
