Very interesting.

The article also contains this potential nugget:

Dr. Daniel S. Berman M.D., chief of Cardiac Imaging and Nuclear Cardiology at Cedars-Sinai reports that the danger in not testing for non-calcified blockages is great. These plaques, he says, are “more prone to rupture than calcified plaques. The new procedure, which does test for these, provides “better risk assessment.”

Any thought about these "non-calcified blockages"?  This is somewhat related to a question I asked a while back about "reducing plaque as measured by calcium score" and reducing risk by reducing risk of rupture in the artery.  You had a good answer to the question but it seems like there is more to explore here.

Thanks for the info.

Here is a similar study using ct to diagnose degree of stenosis:

Dual-source CT non-invasively detects coronary stenoses

15 October 2007

MedWire News: Dual-source multi-slice computed tomography (DSCT) angiography can accurately detect coronary stenoses in patients with an intermediate likelihood of coronary artery disease (CAD), even in the presence of arrhythmias and raised heart rates (HRs), researchers say.

Alexander Leber (University of Munich, Germany) and team explain in the European Heart Journal that using multi-slice CT to detect coronary stenoses can be limited by the appearance of motion artefacts.

The researchers tested the newly-developed DSCT technique in 90 patients with an intermediate pretest likelihood of CAD referred for invasive coronary angiography. They obtained data sets providing image quality sufficient for analysis in 88 patients.

The image quality was diagnostic in six of seven patients with atrial fibrillation, and in 46 out of 48 patients with HR >65 beats per minute (bpm).

In 1165 of 1174 segments, significant (>50% stenosis) disease was correctly ruled out using DSCT.

All patients (n=9) with at least one stenosis >75% (sensitivity 100%) and 11 of 12 (sensitivity 88%) patients with at least one stenosis ranging from 50-75% were correctly identified by DSCT.

Meanwhile DSCT-angiography correctly excluded a lesion >50% in 60 of 67 patients (specificity 90%, positive predictive value 74%).

The accuracy to detect coronary stenoses >50% was similar in patients with HR >65 bpm and those with HR =65 bpm (sensitivity 92 and 100%, specificity 88 and 91%, respectively).

The researchers conclude: "DSCT is a non-invasive tool that allows to accurately rule out coronary stenoses in patients with an intermediate pretet likelihood for CAD, independent of the HR."

Eur Heart J 2007; 28: 2354-2360

I thought I'd take another shot at stating the question I have about the relationship of a declining calcium score and plaque rupture risk.

If the calcium within plaque is reduced at greater rate than the plaque it had calcified, hence leaving that plaque non-calcified, then, does that recently non-calcified plaque qualify as being a type of plaque that, as Berman puts it, is "more prone to rupture than calcified plaques"?

There are a lot of different ways to state the question I guess.  Here's another try.

Does the process of calcium/plaque reduction per se result a type of instability that is "more prone to rupture"?

Perhaps it does not.  But if it does, then, it seems as if it would be important to understand how to increase stability per se.

In that case, aren't BOTH plaque reduction and plaque stability important?

How is plaque stability promoted?

Hope all this make sense.

Thanks.

Great questions. Not all answers are available.

However, there are several things we do know, mostly from intracoronary ultrasound studies, autopsy studies, and extrapolations from animal studies. (Real, live human data is not generally available, since few people would allow us to remove plaque.)

We know that:

--The lipid components of atherosclerotic plaque are fairly readily regressible, e.g., LDL cholesterol reduction. Lipid resorption precedes calcium extraction.

--Plaque instability is determined less than calcium presence or absence than by the presence of high-rupture risk markers, like collections of lipid near the surface, so called "lipid pools" and think fibrous "caps" at the surface-to-lumen interface, as well as inflammatory cell collections and enzymatic activity, e.g., matrix metalloproteinase.

--Calcium is probably the least resorbable factor in plaque. If you resorb calcium by x percent, you've probably resorbed the lipid and inflammatory elements hugely. However, given the rarity of profound regression in studies, these observations are scant.

--The trend towards substantial reductions in cardiovascular events in people who have not progressed heart scan score (or other measures of coronary atherosclerotic burden) vs. those who progress confirm that progressively increasing scores are accompanied by increasing risk of events, "plaque rupture."

--There are not enough data on event rates in people who drop their score substantially because: 1) Nobody except our program has achieved this, and 2) Events in people who reduce their score are, for all practical purpose, non-existent. We are collecting our data for publication in the coming year, as well as assembling the pieces for subsequent studies for full validation of these concepts.

Dr. Davis,

Thanks for an answer right on point.

You continue to amaze with your knowledge that speaks to an issue and makes common sense while at the same time you acknowledge that sometimes "we just don't know".

I know I've already said thanks for the answer but I thought I'd make one last point here.

There is a clear distinction between plaque reduction and plaque rupture risk reduction.

I think your last comment contained solid evidence, to the extent we now have it, that plaque reduction doesn't increase plaque rupture risk but in fact decreases it.

This has settled my mind on the issue (until there is more evidence to evaluate).

I understand that this is a needling kind of point but it seems to me an important one and I think the answer you gave is a great start on a new TYP Program Special Report.

You probably have a long list of these kinds of reports to write.  I'd recommend adding this topic to that queue.

Thanks again for everything you do.

Eventually, I'd like to see a two armed study comparing the Track Your Plaque appraoch to a control group using statins and an American Heart Association diet. My prediction is that there will be no comparison. However, I doubt a drug company would sponsor such a study that likely would cost several million dollars, given the large numbers of people required for conclusive outcome (i.e., cardiovascular events) data.

A more practical approach would be to do side-by-side serial heart scans with intracoronary ultrasound. I think this may be more achievable in the foreseeable future, but will require a great deal of planning. Believe it or not, I tried such a study nearly 12 years ago but encountered tremendous resistance, since such a study needs to be performed in a hospital setting.

Another thought: With the tremendous experience we are developing on line, this could be construed as a "virtual clinical trial" that allows us to quantify events among a growing number of people. Not as "clean" but still persuasive.

A pdf file with a more detailed description of how they do the mini-dose CCTA is at the cedars-sinai website here.

They reduce the radiation dose by using x-rays produced during only 1/10th of the cardiac cycle.

Thanks for the lead.

I looked at the press release but it leaves me puzzled. Many scan centers "gate" to the EKG. I'm not sure what they are doing differently. I'll do some digging.

No smart drug company will do a drug trial versus the TYP plan. (if they're smart!!) In the PROVE-IT trial, Bristol Myers conclusively demonstrated that their drug (pravastatin) sucked...  maybe you can use your favorite colleague's patients for the control-arm? *wink wink*

You definitely need to publish a 'metabolic' arm, including any T2DM patients. I think by distinguishing the difference, you may demonstrate even more accelerated plaque regression compared with non-metabolic.  Perhaps most pts are 'metabolic?'.  

remember if you have Asians or Indo-Asian patients, the BMI >= 27.5 is considered 'obese' and waist circumference > 35.5 inches for men is 'metabolic'...  hope that helps!

I agree.

Our first release of the data this coming spring will lump together people with metabolic syndrome and diabetes along with everybody else. As the experience grows, I believe that a subset analysis will be possible.

Following the advice of Dr Mirkin, I was  already pretty much on your recommended diet, whole intact grains, fruits, veggies, and a little oily fish.  At your urging, I very rarely eat a wheat product.  Have switched from olive oil to canola. http://tinyurl.com/JACC-OliveOil

I don't doubt you but I'm terribly curious as to why this should be. I'd always thought that cereals--rice, barley, rye, wheat, millet, quinoa--were basically natural foods that have been enjoyed by humans for hundreds of years. Are other grains also dangerous? If not, what's so special about wheat? And how about grains similar to wheat, such as spelt?

Ah, I wish I dropped my weight as easily by eliminating wheat. I have eliminated wheat 95% and no weight loss.
Dr. Davis, I also had a question for you. Is it safe to take Niacin while you are pregnant or trying to get pregnant?

P

"While some advocate the notion that only calories count and diet composition makes no difference, I offer this possibility: Whether or not weight is lost by diet, there can be enormous health effects independent of weight based on the composition of diet."

Well said! That is an absolutely crucial point, and one that is brought out well in the recent EJCN study: http://www.nature.com/ejcn/journal/vaop/ncurrent/abs/ejcn20094a.html

Health improved dramatically without weight loss.

I tell this to young people all the time. What you eat matters, and it matters beyond simply getting fat or not getting fat. Sure, they might be able to drink 12 coca-colas every day and stay thin for now, but what kind of long-term damage is being done beneath the surface?

i will attest that elimination of wheat and for that matter all grains and starches does work.  My small particls dropped from nearly 1800 to 1300 and HDL increased from 40 to 54. TRG dropped to 20 from 41.  So, in my case with no other dietary changes, the elimination of wheat worked.  At a good weight and still lost 4 pounds.

If you're curious as to evidence of the badness of wheat (or rather, gluten) there's a wonderful collection of peer reviewed studies here:
htpp://theglutenfile.com

Although I don't doubt the improvements you've seen regarding removing wheat from diet, what about those who don't see any difference?

I'm not talking about those who would eat muffins, cakes, pastries, tons of carbs, etc. As removing junk food would improve lipids in of itself.

But in my case, I reduced wheat products, and noticed a minor improvement in lipids, but nothing radical.

I eliminated wheat completely, and saw no difference. I didn't lose any extra weight, lipids were the same, and I didn't feel any different. But I wasn't overweight to begin with and didn't eat a lot of junk food anyway.

Are the improvements seen then mostly in those who overindulged in carbs/wheat, then went to a healthy diet (no wheat)? Is it the fact that some people have an almost wheat addiction, and when they eat any wheat products at all, they go overboard? Just wondering if there is any difference between a low carb, low wheat diet vs a diet with no wheat at all.

In my case, I don't see a big difference between them.

I'm also curious as to the explanation as to how the Italians and French get away with all the wheat products they eat, yet they have a lower rate of heart attack than Americans. Vitamin D? Better diet in spite of wheat intake? Wine/grape intake?

What about rice?

Dr Davis,

This is related to some of the other questions on this post, but I'm wondering to what extent this is a purely American thing? When people eat mainly packaged foods, and they all contain wheat and/or high-fructose corn syrup, then eliminating these foods is likely to have a major effect. When on a non-American diet, I wonder if it really matters?

Also, although you have lots of posts where wheat is mentioned, many of them seem to assume that readers already broadly share your view. But the idea that even wholewheat products are bad goes against everything I've learned over many years; it's such a radical idea that it would be nice if you could go back to first principles and take us through it really slowly. Why should something that we've all seen as healthy and natural be so bad for us?

I'm just coming to the end of your Track Your Plaque book, and this issue doesn't really figure, so I'm guessing you've experienced a fairly recent conversion? If so, perhaps you could share your experience so that we can see where you're "coming from"?

Sorry, forgot to mention one big reason why the anti-wheat message is difficult to understand: We're often told that the Mediterranean diet is one of the best for heart health. But I understand that pasta, usually made from wheat flour, is a staple there.
Similarly, the staple in Japan is white rice, but it's said that heart attacks are relatively few there.

A small but significant number of Type 2 diabetics report extra high glycemic reactions specific to wheat. Even some Type 1s have problems dosing insulin correctly which don't occur with other grains. I wonder just how widespread this actually is and if some of the symptoms are an effect of the insulin required to process the wheat.

Wheat is originally a transgenic cross, and has been greatly modified by plant breeders in recent decades so I wonder what effect such modifications (to increase yield, reduce straw length and improve disease resistance) have had on the actual biochemical content of the grains. Similar work on other grains may not have increased their toxicity along with the yield.

This would be an interesting field of study (pun intended) a friend still grows old varieties for thatching straw and they are over twice the height with far skinnier heads than his modern varieties in the next field, you'd be hard pressed to believe they were the same species

Rick: I'd always thought that cereals--rice, barley, rye, wheat, millet, quinoa--were basically natural foods that have been enjoyed by humans for hundreds of years. Are other grains also dangerous? If not, what's so special about wheat? And how about grains similar to wheat, such as spelt?

The key phrase is "hundreds of years" -- as opposed to what we were eating before that for much, much longer. Grains (agriculture) have only been around for the blink of an eye on the evolutionary timeline. Wheat and corn cause the most problems overall, especially when the harm they do is too subtle to notice, but I'm convinced that most people would be far healthier if they avoided grain entirely, or only consumed it in sprouted or fermented form.

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I always end up very worried when reading this type of stuff, sometimes I think that everything we eat is bad for health and it would be better not to eat at all and live out of serums.

NO I know who the real Enemy is... Wheat. The way you putted wheat is food's Antichrist. I really get a little upset when i read this stuff, at one point you regret all you have eaten in your life.

Weight loss⎯Patients have told me that they were actually frightened when they eliminated wheat, meaning weight dropped so rapidly that they thought something was wrong. Nothing is wrong. The weight loss simply represents the removal of this bizarre, unphysiologic trigger of appetite, blood sugar, insulin, and weight gain.

Very good, have a healthy future, a reasonable mix of vegetables, will be able to give us a healthy body. Thank you to share