© July 2004
Whole Foods Magazine
Coenzyme Q-10 and Heart Health
An interview with Dr. Stephen Sinatra: Part 5
Monitoring Your Cardiovascular Health
By Richard A. Passwater, Ph.D.
In the February issue, we chatted with cardiologist Stephen Sinatra about the real risk factors in cardiovascular disease and learned how Dr. Sinatra became involved with coenzyme Q-10 in his cardiology practice. We also discussed the actions of coenzyme Q-10 that especially benefit heart and vascular health. Dr. Sinatra described how he uses coenzyme Q-10 in his cardiology practice. In the March issue, we looked into why coenzyme Q-10, the nutrient Dr. Sinatra calls "the fertilizer for the heart," is becoming used as an adjunct treatment by more and more cardiologists, and we discussed the studies behind this acceptance. We also covered congestive heart failure (CHF) and mitral valve prolapse, and we talked about a couple of dramatic cases.
In the April issue, Dr. Sinatra discussed what he calls the "twin pillars of heart health," and we learned that his clinical experience now suggests that even better heart health can be obtained with a third nutrient, ALPHA-LIPOIC ACID, to form what Dr. Sinatra sees now as the "triad" that may become the new frontier for metabolic cardiology. In the June issue, Dr. Sinatra chatted with us about using nutrients to help lower high blood pressure. Now, in this next-to-last segment, Dr. Sinatra will discuss with us the new non-invasive tools that can be wisely used to monitor our risk for heart disease.
Stephen T. Sinatra, M.D., F.A.C.C., F.A.C.N., C.N.S., is a board-certified cardiologist and a certified bioenergetic psychotherapist. He has more than 25 years of experience in helping patients prevent and reverse heart disease. He also is certified in anti-aging medicine. He is a fellow of the American College of Cardiology and former chief of cardiology at Manchester Memorial Hospital where he was director of medical education for 18 years. Dr. Sinatra is also assistant clinical professor of medicine at the University of Connecticut School of Medicine.
At his New England Heart & Longevity Center in Manchester, CT, Dr. Sinatra integrates conventional medical treatments for heart disease with complementary nutritional, anti-aging and psychological therapies that help heal the heart. He is uniquely qualified to give advice on nutritional supplements and the heart, since he is one of the few medical doctors who formulates his own vitamins. He knows how to pick quality ingredients and is expert in dosage, absorption and the effects of combining supplements with cardiac medications.
In addition, Dr. Sinatra has authored and/or co-authored several books on heart disease and is the editor of the monthly newsletter on heart health, The Sinatra Health Report. His most recent book, co-authored with his wife, Jan Sinatra A.P.R.N., is Lower Your Blood Pressure in Eight Weeks (Ballantine Books, 2003). Additional information can be found on his website at www.drsinatra.com.
Passwater: Earlier in this series, we discussed that inflammation is a major risk factor in artery disease, even more so than blood cholesterol level. What is the difference between "silent" inflammation (SI) and "classical" inflammation? What should people be monitoring as an inflammation index?
Sinatra: Inflammation is the "first-alert" mechanism that calls into action the cells responsible for surveillance and protection, heralding them to go to work and limit the damage. These cells attack and destroy the invaders, and clean up the damaged cells, repairing and clearing as they go until a healthy state is restored. This "classical" inflammation is a beneficial process. We often see it as a wound turning red and swelling.
Researchers now recognize another type of inflammation called "silent" inflammation (SI). This type of internal inflammation is the culprit behind many chronic diseases, including coronary heart disease. The chronic and continuous low-level demand that SI places on the body’s defense systems results in immune system dysfunction. In SI, there is no regulated progression of a normal inflammatory response; instead, there is immune system chaos.
Some of the factors that trigger SI are free radical damage, excessive insulin levels, tobacco smoking, obesity, periodontal disease, emotional stress, and bacterial and viral infections.
The markers or indicators of SI are elevated c-reactive protein (CRP), homocysteine, IL-6 and Lp(a). When these indicators are elevated, they have been found to be more predictive of heart disease than traditional risk factors such as elevated blood cholesterol levels.
A seminal study showed that people with high blood levels of CRP, one of the cardinal markers of inflammation, were over four times more likely to have heart attacks than those with low levels of CRP.
Passwater: It has been an important breakthrough to recognize SI as an important risk factor in heart disease. Are there any other major breakthroughs that we should know about?
Sinatra: When I started cardiovascular training some 30 years ago, we were confronted with the awful syndrome of sudden cardiac death. And the problem is that about 50% of the time, coronary artery disease (heart disease) presents itself with death as its first symptom. And 90% of the time, heart disease is asymptomatic. So what I am talking about, the dilemma of heart disease for a contemporary cardiologist, is that you’re dealing with a disease that is 90% asymptomatic and in which 50% of the time death is the first symptom. Obviously, there is a major problem here.
Passwater: So you need to pick out these people who are at risk for sudden cardiac death before their first clinical symptom, which may be death.
Sinatra: Yes. Well, years ago, all that we had was the electrocardiogram, the stress test, and then the stress nuclear test. Angiography: became the gold standard.
If we saw high-grade lesions (plaque commonly, but inaccurately called cholesterol deposits), then we would bypass the lesions, and more recently we are doing angioplasty and stents.
Passwater: Well, these are household words now. Angioplasty being a procedure using a balloon-tipped catheter which is inflated at the site of plaque to enlarge a narrowing in a coronary artery. Stents are tubes designed to be inserted into a vessel or passageway to keep it open. Stents are inserted into narrowed arteries to help keep them open after angioplasty.
Sinatra: The problem is that although some people have diminished blood flow due to large plaques reducing blood flow by as much as 95% or 99%, that is a problem that we can fix. However, there are lots of people out there who have comparatively small lesions that reduce blood flow by only 20% to 40%, but these plaques can rupture and almost instantly form a clot that completely shuts off all blood flow in the artery which can result in sudden death. Small, vulnerable soft plaque is more likely to rupture than large calcified plaque.
Passwater: OK, rupture is the key. Most serious heart attacks seem to be caused by clots forming at the site of a rupture of plaque rather than a clot forming in a very narrow (but unruptured) place in the artery.
What causes soft plaque to rupture? It sounds as if this is a sudden physical event rather than a biochemical event. Does it involve stress hormones that cause an artery to suddenly constrict and then crack?
Sinatra: There are five common reasons; 1) The patient isn’t getting enough essential fatty acids such as the omega-3s in fish oil. 2) The patient doesn’t exercise, or the patients exercises too strenuously after not exercising for long periods, causing a sudden strain. 3) The patient’s blood vessel is bent. 4) The patient has high blood pressure, smokes tobacco or is exposed to a lot of second-hand smoke. 5) The patient has a fit of anger or rage in the settings just mentioned.
Passwater: I hope I didn’t interrupt your train of thought, you were telling us about how we now are recognizing the dangers of these smaller vulnerable plaques.
Sinatra: Well, now we know that these diffuse plaques that can be found in multiple coronary arteries that are prone to rupture can cause major problems. Back in the 70s and 80s, when I was doing angiography and by-passes, it would be common for us to see a patient in the emergency room who had a 95% lesion in the left anterior descending artery we would by-pass that lesion. Stents may not be very effective with the small plaques, and we can’t stent everything. So, we would leave the 20% or 30% lesion alone. What would happen is that we would see that same patient back in the emergency room a year later—with a heart attack that would be due to that slight lesion.
So, clearly, what we have learned over the last 30 years is that vulnerable plaque in the coronaries is a very serious issue. Because when they do rupture, even a small plaque can cause sudden cardiac death.
Passwater: Is the message that no plaque is good plaque, but small soft plaque is worse than older plaque that may even be partially calcified? Is there any relationship/correlation between calcium in the artery and soft plaque?
Sinatra: If plaque is calcified, it is less likely to rupture.
Passwater: So while it is not good to have calcified plaque—any calcium in the blood vessels at all—it is worse to have vulnerable soft plaque?
Sinatra: Non-calcified plaque is more serious because it has a little fibrous cap that is more prone to rupture. But calcified plaque ruptures as well—just not as easily.
You’ve heard of people who in a fit of anger, or people who aren’t accustomed to exercise and are then forced to wrestle with changing a flat tire or moving a refrigerator or furniture or shoveling heavy snow, suddenly have an acute myocardial infarction (heart attack). Well, that’s usually due to plaque rupture. So emotional factors or sudden bouts of anger or rage can cause plaques to rupture.
If you have calcified plaque, it is certainly a risk factor, but if you have soft plaque, it is more serious than calcified plaque.
Passwater: So we now know that smaller soft plaques are vulnerable to rupture, which can lead to sudden death. Can you detect soft plaque easily? Just how do you diagnose heart disease now in the year 2004 as opposed to say, 1974?
Sinatra: There’s much more sophistication. The first thing we can do is draw blood samples and look for the toxic "footprints" such as blood levels of homocysteine, Lp(a), fibrinogen, fibrin degradation products that tell us how hypercoaguable the blood is, oxidized-LDL, and serum ferritin (too much iron in the blood is a risk factor). That part is easy. Then in that same blood sample, we can look for silent inflammation markers such as CRP, tumor necrosis factor, -all of these cytokines. The higher they are, the more vulnerable someone is to SI. We know now that SI is a root cause of heart disease.
We have all of these more meaningful indicators now as opposed to just having blood cholesterol numbers. A good blood screen can pick out a lot of risks. Then we can target these high vulnerabilities with nutraceuticals. A good blood assessment, way beyond cholesterol, is what is really needed—especially with people having a family history of heart disease.
Passwater: Yes, that’s certainly a major improvement over the years. It took a long time to overcome the biases of those who believed in the old approach--"cholesterol is the only thing"—whether it be dietary cholesterol or blood cholesterol
This cholesterol-phobic group controlled research funding, dissemination of information and essentially the advertising of foods for decades, thus impeding research into the major causes of cardiovascular disease. For decades, all that the establishment preached was cholesterol, blood pressure and smoking. What other innovations are available to us now?
Sinatra: There are several important innovations. A second innovation is the Electron Beam Computed Tomography (EBCT) of the heart. This, too, increases our prognosis reliability. The third thing we can do now, is measure Intra-Medial Thickness (IMT) of the carotids. The fourth thing we can bring to the table is cardiovascular genetics. This is really exciting.
Passwater: These innovations sound very helpful. Let’s talk about them in more detail in our next installment. Dr. Sinatra, thanks for sharing your life-saving information with us. WF
© 2004 Whole Foods Magazine and Richard A. Passwater, Ph.D.
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