My life is easy

In the old days (the 1980s and 1990s), practicing cardiology was very physically and emotionally demanding. Since procedures dominated the practice and preventive strategies were limited, heart attacks were painfully common. It wasn't unusual to have to go to the hospital for a patient having a heart attack at 3 am several times a week.

Those were the old days. Nowadays, my life is easy. Heart attacks, for the most part, are a thing of the past in the group of people who follow the Track Your Plaque principles. I can't remember the last time I had a coronary emergency for someone following the program.

But I am reminded of what life used to be like for me when I occasionally have to live up to my hospital responsibilities and/or cover the practices of my colleagues. (Though I voice my views on prevention to my colleagues, the most I get is a odd look. When a colleague recently covered my practice for a weekend while I visited family out of town, he commented to me how quiet my practice was. I responded, "That's because my patients are essentially cured." "Oh, sure they are." He laughed. No registration that he had witnessed something that was genuine and different from his experience of day-to-day catastrophe among his own patients. None.)

I recently had to provide coverage for a colleague for a week while he took his family to Florida. During the 7 days, his patients experienced 4 heart attacks. That is, 4 heart attacks among patients under the care of a cardiologist.

If you want some proof of the power of prevention, watch your results and compare them to the "control" group of people around you: neighbors, colleagues, etc. Unfortunately, the word on prevention, particularly one as powerful as Track Your Plaque, is simply not as widespread as it should be. Instead, it's drowned out in the relentless flood of hospital marketing for glitzy hospital heart programs, the "ask your doctor about" ads for drugs like Plavix, which is little better than spit in preventing heart attacks (except in stented patients), and the media's fascinating with high-tech laser, transplant, robotic surgery, etc.

Prevention? That's not news. But it sure can make the slow but sure difference between life and death, having a heart attack or never having a heart attack.

My bread contains 900 mg omega-3

Phyllis is the survivor of a large heart attack (an "anterior" myocardial infarction involving the crucial front of the heart) several years ago. Excessive fatigue prompted a stress test, which showed poor blood flow in areas outside the heart attack zone. This prompted a heart catheterization, then a bypass operation one year ago.

FINALLY, Phyllis began to understand that her unhealthy lifestyle played a role in causing her heart disease. But lifestyle alone wasn't to blame. Along with being 70 lbs overweight and overindulging in unhealthy sweets every day, she also had lipoprotein(a), small LDL particles, and high triglycerides. The high triglycerides were also associated with its evil "friends," VLDL and IDL (post-prandial, or after-eating, particles).

When I met her, Phyllis' triglycerides typically ranged from 200-300 mg/dl . Fish oil was the first solution, since it is marvelously effective for reducing triglycerides, as well as VLDL and IDL. Her dose: 6000 mg of a standard 1000 mg capsule (6 capsules) to provide 1800 mg EPA + DHA, the effective omega-3 fatty acids.

But Phyllis is not terribly good at following advice. She likes to wander off and follow her own path. She noticed that the healthy bread sold at the grocery store and containing flaxseed boasted "900 mg of omega-3s per slice!". So she ate two slices of the flaxseed-containing bread per day and dropped the fish oil.

Guess what? Triglycerides promptly rebounded to 290 mg/dl, along with oodles of VLDL and IDL.

A more obvious example occurs in people with a disorder called "familial hypertriglyceridemia," or the inherited inability to clear triglycerides from the blood. These people have triglycerides of 800 mg/dl, 2000 mg/dl, or higher. Fish oil yields dramatic drops of hundreds, or even thousands of mg. Fish oil likely achieves this effect by activating the enzyme, lipoprotein lipase, that is responsible for clearing blood triglycerides. Flaxseed oil and other linolenic acid sources yield . . .nothing.

Don't get me wrong. Flaxseed is a great food. As the ground seed, it reduces LDL cholesterol, reduces blood sugar, provides fiber for colon health, and may even yield anti-cancer benefits. Flaxseed oil is a wonderful oil, rich in monounsaturates, low in saturates, and rich in linolenic acid, an oil fraction that may provides heart benefits a la Mediterranean diet.

But linolenic acid from flaxseed is not the same as EPA + DHA from fish oil. This is most graphically proven by the lack of any triglyceride-reducing effects of flaxseed preparations.

Enjoy your flaxseed oil and ground flaxseed--but don't stop your fish oil because of it. Heart disease and coronary plaque are serious business. You need serious tools to combat and control them. Fish oil is serious business for triglycerides. Flaxseed is not.

More Omnivore's Dilemma

Another irresistible quote from Michael Pollan’s book, The Omnivore’s Dilemma:

“In many ways breakfast cereal is the prototypical processed food: four cents’ worth of commodity corn (or some other equally cheap grain) transformed into four dollars’ worth of processed food. What an alchemy! Yet it is performed straightforwardly enough: by taking several of the output streams issuing from a wet mill (corn meal, corn starch, corn sweetener, as well as a handful of tinier chemical fractions) and then assembling them into an attractively novel form. Further value is added in the form of color and taste, then branding and packaging. Oh yes, and vitamins and minerals, which are added to give the product a sheen of healthfulness and to replace the nutrients that are lost whenever whole foods are processed. On the strength of this alchemy the cereals group generates higher profits for General Mills than any other division. Since the raw materials in processed foods are so abundant and cheap (ADM and Cargill will gladly sell them to all comers) protecting whatever is special about the value you add to them is imperative.”

A food manufacturer’s nightmare is when you and your family shop in the produce aisle in the grocery store. Produce is unmodified (aside from the pesticide and genetic-engineering issues), not added to, and therefore of no interest to the food manufacturer, since no additional profit can be squeezed out of it. If you pay 45 cents for a cucumber, there’s no room for a processor to multiply it’s return.

Vegetables and fruits have imperfections, no doubt, particularly pesticide residues and the “dumbing-down” of some foods to increase their desirability (e.g., green grapes, what I call “grape candy”). But vegetables and fruits are the closest you can get to foods that are essentially unmodified by a food manufacturer. Due to the absence of processing, they are not calorie-dense like a bag of chips; they include all the naturally-occurring healthy factors like flavonoids that food scientists have, thus far, struggled and failed to identify, quantify, and control; and they lack all the unhealthy additives that processed foods require for extended shelf life, palatability, and reconstitution (anti-separating agents, emulsifiers, sweeteners, etc.)

Vegetables, in particular, should be the cornerstone of your plaque control program. Not breakfast cereals, breads, bacon, sausage, mayonnaise, fruit drinks and soda, all the foods that worsen the causes of coronary plaque and raise your heart scan score.

If you would like to understand how the current perverted state of affairs in food have come about, Pollan’s book is must reading.

Pollan's The Omnivore's Dilemma


‘You are what you eat’ is a truism hard to argue with, and yet it is, as a visit to a feedlot suggests, incomplete, for you are what what you eat eats, too. And what we are, or have become, is not just meat but number 2 corn and oil.”

Author Michael Pollan offers unique, enlightening, and entertaining insights into the food we eat in his new book, The Omnivore’s Dilemma: A natural history of four meals.

Pollan draws parallels between the dilemma of the primitive human living in the wild, having to stumble through the choices of animals and plants that could nourish or kill, and the ironically modern return of this phenomenon in present-day supermarkets. While the dangers of food choices aren’t as immediate as in the wild (eat the wrong mushroom or herb, for instance, and you die), they can nonetheless be life-threatening, or at least health-threatening. Hydrogenated oils, high-fructose corn syrup, carageenan, guar gum. . .“What is all this stuff anyway, and where in the world did it come from?”

Among the issues Pollan discusses is that of modern cattle raising practices: the rush to fatten a cow from an 80 lb calf to a 1200-pound, bloated cow over a period of 14 months. Nature created this animal to mature over a 4 to 5 year period through grazing, thus it’s beautifully “engineered” ruminant system that allows it to digest cellulose in grasses, a process that humans and other mammals are incapable of. The pressures to bring greater quantities of beef to market at a reduced price and make more money have resulted in a farming industry that encourages the incorporation of unnatural, often inhumane practices like corn feeding (rather than grass grazing), refeeding of bovine body parts (thus “mad cow disease”), and widespread and chronic administration of hormones and antibiotics.

(I can't help but think that the rapid and perverse fattening of cattle by industrial "farming" is paralleled by the fattening of the eating American. After all, we are the hapless recipients of this flood of cheap, unhealthy, plasticized food.)

The industrialization of food has de-personalized the act of eating. You no longer have any connection with the green pepper in your salad (unless you grew it yourself), nor do you have any appreciation for the suffering of the cow in your hamburger. Worse, the distortion of livestock raising practices has modified the food composition of meat. Range-fed animals, leaner and richer in omega-3 fatty acids, have been replaced by the marbled, saturated fat-rich modern grocery bought meats.

This is a theme that Pollan reiterates time and again: how food processing adds value to the manufacturer, often starting with a healthy ingredient but modifying it, adding ingredients, taking out others, until it’s something decidedly unhealthy. Yet the manufacturer will trumpet the fact that a healthy ingredient is included. Breakfast cereals are the most blatant example of this. What the heck are Cheerios but an over-processed attempt to make more money out of the simple oat?

Pollan’s eloquent and unique insights into food are definitely worth reading.

As always, per our Track Your Plaque policy, I recommend Mr. Pollan’s book strictly on its merits. We obtain no “cut”, commission, or other financial gain by recommending his book. Track Your Plaque members pay their modest membership fee for truth. They do not pay for us to advertise something that provides hidden advantage to us. We do not advertise, editorialize to steer you towards a specific product or service. What we say, we truly believe.

The most frequently asked question of all

The most frequently asked question on the Track Your Plaque website:

"Can you recommend a doctor in my area who can help me follow the Track Your Plaque program?"

This is a problem. Unfortunately, I wish I could tell everyone that we have hundreds or thousands of physicians nationwide who have been thoroughly educated and adhere to the principles I believe are crucial in heart disease:

1) Identify and quantify the amount of coronary atherosclerotic plaque present. In 2007, the best technique remains CT heart scans.

2) Identify all hidden causes of plaque. This includes Lp(a), post-prandial disorders, small LDL, and vitamin D deficiency.

3) Correct all patterns.


But we don't.

You'd think that this simple formula, as straightforward and rational as it sounds, would be easily followed by many if not most physicians. But Track Your Plaque followers know that it simply is not true. My colleagues, the cardiologists, are hell-bent on implanting the next new device, providing a lot more excitement to them as well as considerably more revenue.

The primary care physician is already swamped in a sea of new information, going from osteoporosis drugs, to arthritis, to gynecologic issues, to skin rashes and flu. Heart disease prevention? Oh yeah, that too. They can only dabble in heart disease prevention a la prescription for Lipitor. That's quick and easy.

Nonetheless, I believe we should work towards identifying the occasional physician who is indeed willing to help people follow a program like Track Your Plaque. As we grow, we will need to identify some mechanism of professional education and we will maintain a record of these practitioners. But right now, we're simply already stretched to the limit just doing what we are doing.

If you come across a physician who practices in this fashion and you've had a positive relationship, we'd like to hear about it.

Do stents kill?

There's apparently a lively conversation going on at the HeartHawk Blog (www.hearthawk.blogspot.com). Among the hot topics raised was just how bad it is to have a stent.

I think that my comments some time back may have started this controversy. I've lately noticed that having a stent screws up your heart scan scoring in the vicinity of the stent. I was referring to the fact that I've now seen several people in the Track Your Plaque program do everything right and then show what I call "regional reversal": unstented arteries show dramatic drops in score of 18-30%, but the artery with a stent shows significant increase in score.

This is consistent with what we observe in the world outside Track Your Plaque when stents are inserted. Someone will get a stent, for instance, in the left anterior descending artery. A year later, there will be a "new" plaque at the mouth of the stent or just beyond the far end. This is generally treated by inserting another stent. Use of a drug-coated stent seems to have no effect on this issue.

Now, my smart friends in the Track Your Plaque program would immediately ask, "Does this mean you continually end up chasing these plaques that arise as a result of stents? Do you create an endless loop of procedures?"

Thankfully, the majority of times you do not. Rarely, this does happen and can lead to need for bypass surgery to circumvent the response. But it is unusual. The tissue that grows above and below stents does seem to be unusually impervious to the preventive efforts we institute.

Perhaps there's some new supplement, medication, or other strategy that will address this curious new brand of plaque growth. Until then, you and I can only take advantage of what is known. If it's any consolation, the plaque that seems to grow because of a previously inserted stent seems to lack the plaque "rupture" capacity of "naturally-occuring" plaque. It is, indeed, somehow different. It is more benign, less likely to cause heart attack. It's always been my feeling that this tissue behaves more like the "scar" tissue that grows within stents, causing "re-stenosis", a more benign, less rupture-prone kind of tissue.

Dr. Reinhold Vieth on vitamin D

A Track Your Plaque member brough the following webcast to our attention:

Prospects for Vitamin D Nutrition
which can be found at http://tinyurl.com/f93vl

Despite the painfully dull title, the webcast is the best summary of data on the health benefits on vitamin D that I've seen. The presenter is Dr. Reinhold Vieth, who is among the handful of worldwide authorities on vitamin D. In 1999, Dr. Vieth authored the first review to concisely and persuasively argue that vitamin D nutrition was woefully neglected and that its potential for health was enormous.
(See Vieth R, Am J Clin Nutr 1999 May;69(5):842-856 at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10232622&query_hl=1&itool=pubmed_DocSum.)

I predict that, after viewing Dr. Vieth's hour-long discussion, you will be as convinced as I am that vitamin D is crucial for health. Unfortunately, Dr. Vieth doesn't delve into the conversation about the potential effects on heart disease, since his audience was primary interested in multiple sclerosis, a disease for which vitamin D replacement promises to have enormous possibilities. Even in 2007, the data suggesting that vitamin D has heart benefits is circumstantial. Nonetheless, from our experience, I am thoroughly convinced that, with replacement to blood levels of vitamin D to 50 ng/ml, heart scan scores drop more readily and faster.

If you view Dr. Vieth's wonderful webcast, keep in mind that when he discusses vitamin D blood levels, he's using units of nmol/l, rather than ng/ml. To convert nmol/l to ng/ml, divided by 2.5. For example, 125 nmol/l is the same as 50 ng/ml (125/2.5 = 50).

Vitamin D on Good Morning America


Positive comments about vitamin D made it to a discussion on Good Morning America today about the new and exciting developments in nutrition and "functional foods".

I'm thrilled that the media is conducting these conversations. It sure is making my job easier, not having to persuade patients that taking vitamin D is truly and hugely beneficial for health. I still have to struggle with my colleagues, who tell patients to stop the "poisonous" doses we use.

But I worry that many of the details behind vitamin D don't quite make it to the media conversation. These are crucial, make-it-or-break-it issues, such as:

--Vitamin D must be vitamin D3 or cholecalciferol, not D2 or ergocalciferol. D2 is virtually worthless. Little or none is converted to the active D3, despite the fact that D2 is the form often added to some foods.

--Vitamin D3 supplements must be oil-based capsules, or gelcaps. Tablets are so poorly or erratically absorbed that it's simply not worth the effort. (We get ours from the Vitamin Shoppe.)

--The dose should be sufficient to eliminate the phenemena of deficiency, which is around 50 ng/ml. I take 6000 units per day. Dr. John Cannell of www.vitamindcouncil.com takes 5000 units per day. I give my wife 2000 units per day (she's not as deficient as I was), each of my kids 1000 units per day, except for my 180 lb. 15 year old who takes 2000 units.

I fear that, when people hear that vitamin D packs fabulous effects for health, they will take a 400 unit tablet--nothing will happen. They will not obtain the benefits such as reduction of blood pressure and blood sugar; increased bone density, reduction of arthritis, dramatic reduction in risk for fractures; reduction in risk for colon, prostate, and breast cancer; reduction in risk for multiple sclerosis; reduction in inflammatory processes such as those evidenced by C-reactive protein; and facilitation of reduction of heart scan score.

Would you bet your life on chelation?


Hugh's heart scan score was 1751, an awful score. Recall that, at this level of scoring, Hugh's heart attack and death risk is 25% per year.

Obviously, serious efforts need to be taken. In this situation, much as I despise drug companies and what they represent and their heavy-handed ways, I'm more inclined to resort directly to prescription agents, as well as our nutritional supplements and other strategies. The price of dilly-dallying could be his death.

Hugh and his wife asked about chelation. Now, there are five studies I'm aware of that have tried to examine the value of chelation. None showed any measurable benefit, though all were rather weak in design and small in number of participants. One study, for instance, looked at whether anginal chest pains were provoked any later after chelation. Another looked at whether calf claudication, or calf cramping while walking due to artery blockages in the leg arteries, was delayed on treadmill testing after chelation. No benefit was observed: no delay in provocation of angina, no delay in provocation of claudication.

However, the adherents of chelation have been vehement enough that the NIH has funded a large, multi-center study to settle the question once and for all. Best I can tell, the study has not been contaminated by any drug company involvement. It is meant to be an unbiased, objective study of whether chelation has any value.

My personal experience in patients who underwent chelation is that, despite spending hundreds or thousands of dollars, plaque grew at the expected rate--no effect at all.

None of this constitutes proof of efficacy nor proof of lack of efficacy. We will need to await the NIH trial to have better information.

Should Hugh bet his life on chelation? I advised him strongly against it. At this point, the only reason I can see to pursue chelation would be faith--that is, expectation based not on fact, but on hope.

The powerful forces preserving the status quo


An interesting quote from the book, Critical Condition: How health care in American became big business--and bad medicine:


Politics and Profits

To protect its interests and expand its influence, the health care industrial complex has done what all successful special interests do: It's become a big donor and a high-powered lobby in Washington. In the last fifteen years, HMOs, insurers, pharmacuetical companies, hospital corporations, physicians, and other segments of the industry contributed $479 million to political campaigns--more than the energy industry ($315 million), commercial banks ($133 million), and big tobacco ($52 million). More telling is how much the health care industry spends on lobbying. It invests more than any other industry except one, according to the nonpartiisan Center for Responsive Politics. From 1997 to 2000, the most recent year for which complete data is available, the industry spent $734 million lobbying Congress and the executive branch. Only the finance, insurance, and real estate lobby exceeded that amount in the same period, with a ttoal of $823 million. In contrast, the defense industry spent $211 million--less than one-third of the health care expenditure.


These telling statistics indicate just how vigorously profit-seeking forces in heart care are trying to preserve the status quo. Hospitals want to protect their valuable procedure-driven enterprise, the pharmaceutical industry wants to protect its enormous though little-known niche of procedure-based medications (like $1200 a dose ReoPro), and the medical device industry wants to maintain the multi-billion dollar-generating machine aided and abetted by the FDA's 501k rule (that makes entry to market a breeze).

The current procedure based formula for heart disease profits so many and they are desperate to preserve it. Resistance to the deep-pocketed efforts of industry and hospitals will come from people like you and me, trying to propagate a better way.

Remember: hospital procedures for coronary disease represent the failure of prevention. They are not--any longer--successes in and of themselves.

Read a scathing insight into some of these practices by reading investigative journalists' Donald Barlett and James Steele's book, Critical Condition. I found their descriptions painfully accurate. (But don't get too angry! Remember: only optimists reverse their plaque! We need to turn the conversation in a positive direction, not just in this Blog or the Track Your Plaque website, but nationwide.)

One of the new missions for the www.cureality.com website is to help you understand just how powerful, insidious, shrewd, and pervasive the efforts to maintain the current system truly are.
What does "Success" mean in the Track Your Plaque program?

What does "Success" mean in the Track Your Plaque program?

Say you begin with a CT heart scan score of 400.

You correct your lipoprotein pattterns, take fish oil, correct 25-OH-vitamin D3 to 50 ng/ml, correct your other hidden patterns, follow a diet suited to your patterns.

One year later, you get another heart scan. What score would constitute "success"?

With all of our recent talk about record-setting reductions in heart scan scores, is it really necessary to drop your score that much to succeed?

For instance, is our latest record-setting 63% drop in score better than "only" a 10% drop in score? Both represent reversal of coronary plaque. Both signify huge reductions in risk for plaque rupture, or heart attack.

You can read about how we view the various forms of success in the program by reading our latest Track Your Plaque Special Report, Winning Your Personal War with Heart Disease: The Track Your Plaque 5 Stages of Success.

We are making the Report available to everyone. Just go to the www.cureality.com homepage.

Comments (11) -

  • WCCAguy

    10/2/2007 11:22:00 AM |

    Hi Dr. Davis,

    This post touches on a point I've been wondering about.

    You write that a drop in CT heart scan score signifies a "huge reduction in risk for plaque rupture, or heart attack."

    As I understand it, strictly speaking, the score indicates a reduction in the volume of calcium/plaque in the arteries.

    In your books and articles you provide references to the studies which document the statistical correlation between FIXED scores and rupture/heart attack.

    My question is this (and you may have answered this question already elsewhere):  Have there been studies that document a statistically significant relationship between a reduction in plaque volume (as opposed to a fixed value) and risk of a CAD event?

    A follow up question:  Is the actual reason for the risk reduction due to score reduction actually known?  I can imagine that one reason might be that because the arteries have plaque reduced, they are actually larger in terms of blood flow supported than they were before the plaque was reduced.

    My belief, however, is that there could be additional reasons for a reduced plaque over time = less risk correlation.

    Thoughts about this?

    Thanks.

  • Dr. Davis

    10/2/2007 12:13:00 PM |

    Great questions.

    We do know that, if plaque is permitted to grow (by several measures including angiographic studies, carotid ultrasound, as well as heart scan scores), the likelihood of events escalates along with it. This is known with absolute confidence.  

    We also know that reductions in plaque burden are also correlated with reductions in risk, also by just about any measure, though the magnitude of reduction varies, since each approach provides a different persective on plaque composition, all differ on incorporation of the Glagov phenomenon ("remodeling"). More data on event reductions are needed, however. But until recently, genuine bona fide reversal had been elusive.

    Lastly, actual examination of tissue that has regressed is very limited. As you can imagine, if someone asked you, having regressed, to allow a sample of artery tissue to be removed, you'd likely not be interested. Thus, the observations are indirect and come from animal studies and observations like intracoronary ultrasound.

    Actually, reductions in heart scan scores are a surrogate for inactivation of plaque, removal of inflammatory cells, removal of fat-laden tissue, etc. The reduction  in calcium is a parallel phenomenon that we can see. I also wonder, given the wonderful effects of vit D and possibly K2, whether the reduction in calcium provides benefits of its own, independent of the inactivating effects.

  • Anonymous

    10/3/2007 3:56:00 AM |

    While everyone agrees that reduction of atherosclerotic plaque is a good thing, there are several clinical studies that suggest that reduction of calcium in the plaque may not be good. For example, this study found that culprit stenoses in arteries of patients with stable angina had more calcium than those of patients with unstable angina, which had more calcium than those with acute myocardial infarction. This suggests that plaque accumulation in a specific location may actually be beneficial if it stabilizes the plaque and makes it less likely to rupture.

    There is not much data on calcium score reduction because it is so rarely seen. What is needed are long-term studies showing that calcium score reduction does reduce the number of adverse coronary events.

  • Dr. Davis

    10/3/2007 11:53:00 AM |

    I disagree.

    There is a commonly offered argument that calcium stabilizes plaque. I think this is nonsense. There are studies by Renu Virmani and others that demonstrate that the shear and tension forces at the edges of calcified plaque are, in fact, areas of greater stress and thereby risk for plaque rupture.

    While intracoronary ultrasound will sometimes show that a small segment of a recently ruptured plaque will involve a non-calcified segment, we are NOT using calcium in a lesion-specific fashion. We use it as an index of total plaque.

    I also believe that emerging concepts, such as the influence of vitamin D3 on gamma-carboxyglutamic acid Gla protein in vascular tissue are pointing towards the fact that vascular calcification is part of a regulated, active process that influences plaque activity and rupture potential. (See Johnson et al, Vascular calcification: pathobiological mechanisms and clinical implications. Circulation Research 2006 Nov 2006;99(10):1044-59.)

    Increasing calcium scores have been conclusively associated with dramatic increases in coronary events. Likewise, emerging data, including our own, show reducing calcium scores is associated with virtual elimination of events.

    Do you have something better?

  • Anonymous

    10/3/2007 1:53:00 PM |

    No, I don't have anything better - I don't argue that an increasing calcium score is good, only that we have nothing more than anecdotal evidence to show that calcium score reduction is beneficial. And, there are other experts in the field that do not agree that it is. The recent torcetrapib clinical trial shows that not all ways of increasing a generally beneficial lipid such as HDL are theraputic. Have you considered documenting the results of your practice, i.e., what percent of your patients show calcium score change in each of several percentage ranges including reductions, and what their follow-up results are in terms of hard cardiac events? That might stimulate interest in a controlled clinical trial to verify your results.

  • Dr. Davis

    10/3/2007 2:21:00 PM |

    What experts "agree" that a reduction in calcium score is not beneficial? Can you specify who? I know the literature on calcium scoring quite well, and I don't ever recall such a study.

  • WCCAguy

    10/3/2007 9:27:00 PM |

    Dr. Davis,

    The wizard, hmmm, I mean, Dr. Oz says on Oprah that "we'd rather focus on the plaque itself—because the calcium actually might help stabilize the plaque and reduce the chance of it rupturing."

    http://www2.oprah.com/health/yourbody/youdocs/youdocs_faqs_io_10.jhtml

    So, there's the proof you asked for.  It was on the Oprah show.

    And by the way, Oprah's doc says that Ornish has the answer here:

    http://www2.oprah.com/health/yourbody/youdocs/youdocs_faqs_io_11.jhtml

    Seriously, this question of the Calcium Score relationship to risk reduction is a key issue and I appreciate your sharing your knowledge about the question.

    It will be interesting to see if Anonymous gets back to you with expert reference list you've asked for.

  • Anonymous

    10/3/2007 11:05:00 PM |

    I don’t think there is a study that shows that because calcium reduction is so infrequently seen. I have discussed it with the Director of Preventive Cardiology at a State University Hospital who is of the opinion that calcium reduction may not be beneficial. I suspect that most experts would say that there isn’t enough data to conclude that reduction of calcium is either beneficial or detrimental because most have never seen it.

    My point is that several studies show that plaque rupture tends to happen in arteries that have “spotty,” but not extensive calcium, and that coalescence of small calcium deposits into larger deposits reduces the surface area in contact with softer plaque, thereby reducing the extent of the stress risers that can lead to plaque rupture. Quoting from some of these

    “…double helical computerized tomography demonstrates that extensive calcium characterizes the coronary arteries of patients with chronic stable angina, whereas a first AMI [acute myocardial infarction] most often occurs in mildly calcified or noncalcified culprit arteries.” Shemesh et. al., American Journal of Cardiology, 1998 Feb 1;81(3):271-5, Comparison of coronary calcium in stable angina pectoris and in first acute myocardial infarction utilizing double helical computerized tomography.

    “Acute coronary syndromes are associated with a relative lack of calcium in the culprit stenoses compared with stenoses of patients with stable angina.” Joshua A. Beckman et. al., Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1618, Relationship of Clinical Presentation and Calcification of Culprit Coronary Artery Stenoses.

    “The relationship between calcification and clinical events likely relates to mechanical instability introduced by calcified plaque at its interface with softer, noncalcified plaque. In general, as calcification proceeds, interface surface area increases initially, but eventually decreases as plaques coalesce. This phenomenon may account for reports of less calcification in unstable plaque.” Moeen Abedin et. al.,  Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1161, Vascular Calcification - Mechanisms and Clinical Ramifications.  

    “In AMI patients, the typical pattern was spotty calcification, associated with a fibrofatty plaque and positive remodeling. In ACS [acute coronary syndrome] patients showing negative remodeling, no calcification was the most frequent observation. Conversely, SAP [stable angina pectoris] patients had the highest frequency of extensive calcification…To the best of our knowledge, the present IVUS study is the first to demonstrate the relationship between calcification patterns, arterial remodeling, and the morphology of plaques within the culprit lesion segment. The major finding is that there is a significant difference in the pattern of coronary calcifications at the culprit lesion segment, particularly with respect to size, number, and length of the deposits, among patients with AMI, UAP [unstable angina pectoris], and SAP. Small calcium deposits were significantly more frequent in the culprit lesion segments in ACS than in SAP patients.” Shoichi Ehara, et. al., Circulation. 2004;110:3424-3429, Spotty Calcification Typifies the Culprit Plaque in Patients With Acute Myocardial Infarction.

    Also, there is an MRI study of  the carotid arteries of CAD patients who had been given niacin, lovastatin, and colestipol for 10 years. In comparison with matched, untreated patients, the carotid plaque of the treated patients showed much less lipid but much more calcium than the untreated patients. Xue-Qiao Zhao, Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1623, Effects of Prolonged Intensive Lipid-Lowering Therapy on the Characteristics of Carotid Atherosclerotic Plaques In Vivo by MRI.

    It seems that reduction of the “spotty” calcium may reduce the likelihood of plaque rupture, but reduction of coalesced calcium such as is seen in stable angina patients may  increase the surface area of calcium (if the coalesced calcium reverts to spotty deposits) and therefore be detrimental. From the standpoint of evidence-based medicine, the only way to be sure of the effects of calcium reduction is to conduct a clinical trial of patients undergoing such reduction.

    In the meantime, Dr. Davis, since you are one of the few cardiologists whose patients are experiencing calcium score reduction, it would be of great benefit if you would document the results of your practice in a quantitative way.

  • Dr. Davis

    10/4/2007 12:30:00 AM |

    I believe that you are confusing two phenomena.  

    Tissue characterization of specific plaque locations that are prone to rupture (or have ruptured) examined by techniques such as intracoronary ultrasound, is distinct from the concept of using coronary calcium scoring as a surrogate measure of total plaque volume.

    I believe that lipid-laden, calcium-poor plaques do tend to identify sites more prone to rupture. I have witnessed this myself in many intracoronary ultrasound procedures personally performed.

    This is different from using calcium as an index of plaque. While we are uncertain of the relationship of calcium to total plaque in people who have experienced calcium score reduction, all circumstantial evidence points towards dramatic regression of lipid laden plaque, regression of inflammatory cell composition, replacement by fibrous tissue matrix, reduction of oxidative capacity, reduction of  matrix metalloproteinase content, in other words, all the factors that trigger plaque rupture.  

    Though just my suspicion, I believe that the initial relative composition of calcium to plaque of 20% is likely increased, meaning calcium occupies more of total plaque volume. In other words, my suspicion is that, if calcium regresses, total plaque volume has regressed even MORE.

    We plan to publish our data this spring. We had planned to publish our experience much sooner, but the addition of vitamin D to the program has boosted success so much that we decided to start over again around 2 years ago.

  • Anonymous

    12/13/2009 6:34:36 PM |

    hm... bookmarked style Smile)

  • Anonymous

    4/29/2010 4:00:38 AM |

    so great, your arteries are cleared up but you'll get cancer and die from all of those ct scans.
    lovely.

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