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.

I would be very interested to know what you think of what he has to say about glutathione, which in my quick look at his web sites, leaped out at me.  As a fairly new TYP member, I don't recall coming across any discussion of it on TYP in what I've read so far, though I may have just overlooked it.

Thanks for the link to Dr. Dach. Good stuff there.

Dr. Dach's blog also references Nutrasal's phoschol product ... is it beneficial or a hoax? It might be akin to chelation therapy not supported by Dr Davis... but it's hard to resist the claim that phoschol returns cholesterol from plaques to the liver to be processed.

So iodine deficiency in early 20th century America was a big problem. How to solve this enormous public health problem in a large nation without television, few radios, no internet, with a largely rural and often illiterate population?

I've been reading a lot of articles about Dr. Jeffrey Dach... and I think he is one of the best exponents in this kind of programs, it's all about perspectives and his points has been shaping my thoughts.

Hi Dr. Davis:

I have been a follower of your blog for a number of years now.  It ha been an inspiration as i have fought to regain my health over the past 9 years.

After suffering a mild MI in 2002 and being diagnosed as diabetic, I was placed on the standard allopathic protocol of statins, Ace inhibitors/beta blockers and low-fat diet. Needless to say, they didn't help me.  I did manage to lose weight, but blood sugar and blood pressure remained problematic.

In 2005, I realized from doing extensive research on sites such as yours that eliminating all refined carbs, sugars and trans fats was the key to my success. I have lost 180 pounds and maintain a weight of 165 lbs. with a height of 6' 1". I am 53 years old, and definitely feel younger than I was in my 30's.

I supplement with fish oil and DHA, vitamin D and a number of other nutrients to provide a baseline of building blocks to help my cells regenerate and avoid chronic disease. Eliminating wheat is the most significant element in regaining my health and dramatically lowering risk form a second heart attack.

I would enjoy discussing my journey, and thank you for all your dedicated work.

Any updated information on heartscans in people who've already had a bypass, a 4x bypass?  Would a scan yield any useful info?

I am new to your website, and I am interested in it. I once weighed 800 pounds, and am now down to 215 pounds. You can check my website for more information. www.justinwilloughby.com

Hi, John--

Fabulous results!
Could you provide contact info here: http://typ.trackyourplaque.com/contact.aspx
I appreciate your help on this. It will make a fascinating story!

Hi, Justin--

Incredible!
However, I am looking for stories in which elimination of wheat was the principal strategy. Is this what you did to lose the 600 lbs (!!!)?

All I get is "500 Internal Server Error" when try to comment.

Web site server is no good at all ... previous thread rejected my comments more than twice on several days, so I tried this thread and post came right through.
Doc - you are not getting your moneys worth despite your page looking pretty .

Just went back to previous thread to try and post since see 2 above went through and got the same "server error"  boot a couple of minutes after my 2 above. Something not working right here.

Sorry, Might. Still working out glitches.
I will discuss with IT people.

Dr. Davis
I have been batling weight for my whole life and by the age of 45 I weighted 290 lbs and was a heavy drinker until I quited drinking and started exercising with a low fat mid protein and high carb diet and due to the fact that I stoped drinking I started to loose weight also as the weight droped I exerciced more till the point that I started to train for a half Ironman there is where the fat lost stoped and I plateaued at 230 lbs and no matter how hard I trained I couldnt lose more and aproaching the half Ironman I even gained weight so shortly after finishing the race my coach sugested me to visit your blog and sent me the link of your post on wheat belly,
that was like the turning poin of my life and shortly I was following your advices and trying to live a more primal life and practically becoming a caveman the results I lost 60 more pounds and gained a vitality like I have never experienced today after 6 more half Ironman races and 1 full Ironman I try to live wheat free and visit regularly your blog not to mention that I follow most of your blog roll!!!
Everytime that I find myself eating wheat I feel terrible my inmune function suffers and I almost get sick I say almost as I haven't get sick in almost 2 yers that I have been following a mostly primal life and as I feel a sickness coming I just get back to being wheat free and low carb all around!!

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

Well all best in this post is the image of Obesity!

You have to love the Germans.

One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched.

Dr Davis,

Please give us your take on KIF6.  I know that the data in some ways is preliminary.  All that I can seem to find is the 3 JACC articles in 1/08.  2 of them simply show a high prevalence of the arg/trp or arg/arg variant. But the study showing a statistical difference in MI/ Cardiac Death in as little as 30 months comparing 40 pravachol vs 80 lipitor is impressive.  Statins do save lives so they are ok with me.  It is just that the number needed treat/ number needed to harm ratio is too high.  KIF6 has the potential to cut the number needed to treat in half.

Co-incidentally I am about to go off my Crestor (40mg) for a "rest". I need to loose weight (5'7" and 195lb) but when I started my p90x program, I found that those annoying muscle aches in my left arm and right hand were such that I could not do a single pull up.  My Dr. asked that I stay on the higher dose of Crestor and supplement with CoQ10.  I will add CoQ10 to the fish oil, Niacin and vitamin D I am taking.  I'm going to start Vitamin K2 supplementation too (Canada does not allow high dose for some strange reason). But more than anything, recognizing some of the side effects I have read here, I think a break from Crestor is  overdue for me.

there is no shortage of criticism on this blog of statins and they certainly are over prescribed.  the real question is: when and only when should they be tried?  It would be helpful if you posted on this now that you have carefully gone in to some of the negatives of statins, but also, acknowledged their value.

What about women with high cholesterol without (overt) heart disease or a family history of heart disease? Some say that older women with high cholesterol live longer and better. This certainly has been true in my family. The women live to 90's without heart disease, total cholesterols 220-250 LDL certainly higher than the current "normal/optimal" but with high HDL and low triglycerides.

Hey there, Dr. Davis. Where are all the testimonials from people who have no side effects from statins and are doing just fine with lowered LDL levels?

Or does your profit incentive prohibit you from being fair and balanced, just like the pharmaceutical industry.

I dare you to publish this post. Not doing do will reveal your true intentions.

Steve and Bruce--

I am mindful of the fact that representatives of the pharmaceutical industry troll the blogosphere and internet in order to post comments to counter the rapidly growing rejection of the statin franchise. If you work for Pfizer, AstraZeneca, et al, I would kindly ask you to mind your own business.

If you do not, then please recognize that what I say is said because of the overwhelming influence of the drug industry. It is a David vs. Goliath world. The drug industry does not need to be defended. They would willingly take as much of your money and your insurer's money as possible. Their goals have little to do with health, but everything to do with profit.

If you have fallen victim to their brand of Kool Aid, then perhaps it's time for a little reality check.

Yet more scary but interesting stuff!

I was put on lipitor but had a (rare but reported) side effect that in retrospect was BG lowering over and above the reactive hypos I was already suffering

Switched to simvastatin and have been on it ever since, it appears to do exactly what it says on the tin, halves my LDL without affecting the lethal trigs and HDL (diet fixed them)

NOW I'm wondering if my apparent senility attacks are in fact not due to advancing age. In typing this I have already done several letter pair reversals. I actually forgot to make an appointment for my blood tests which ironically I am now going to blame on the statin (grins) I was going to drop them for a month prior to the next tests but maybe I am going to drop them now.

Why? I have also begun getting tinnitus. The trigger factor appeared to be NSAIDS, even ointment was bringing it on. Now I'm getting it even without these.

I suspect statin side effects are still rare compared to the percentage of people who don't get them BUT with an increasing statinised population there's a low percentage of a huge population now reporting in, hence the apparently increased incidence.

DR Davis:
i do not work for big pharma or any medical or health related profession, and am only interested when statins should be prescribed since my NMR results showed high small LDL despite my not eating wheat,using fish oils, taking D3 as you suggest. Since my Doc says statin time, i am only trying to get the best info in light of all negative publicity.
Perhaps you read my comment to fast; it was not advocating them, but asking since you in your post allude to possible cases when it should be used.  Your comment to me is therefore way out of line.

I fall on the side of believing that statins should never be prescribed.  From my understanding, while there's a slight indication that they can reduce cardiovascular events, they DO NOT reduce all-cause mortality.  This strongly suggests that they are mostly ineffective at doing what they're touted to do, and they introduce a new set of problems that can reduce the patients quality and length of life.

The purported benefits of statins, in all cases, can be beaten handily by a change of diet and supplements.

I think your personal practice is a testament to this, and yet you still leave several diet and supplement tactics on-the-table that could improve the results you could achieve. (I base this on reading every entry in your blog, and listening to your podcasts with Jimmy Moore.)

I love that you're well ahead of 99.999% of the other cardiologists.

I would like to know of any situation that you can quickly describe in which a statin makes sense.  I have an open mind about this, and perhaps you can convince me that such cases exist.

Stop press, dropped last night's statin and already the tinnitus is much reduced. It was never bad but was increasing and I thought its prevalence at night was due to quietness of the environment not to the fact I'd just taken the statin.

Now in the past I'd dropped the things for a month on month off trial which is why I am confident there were THEN no noticeable side effects.

SSRI poop-out is a well known phenomenon and the explanation used to be that while they upregulated serotonin, over time they would then downregulate dopamine in some individuals.

Most statin side effects I've heard of seem to be fairly instant, now I'm wondering if there's a similar temporal effect whereby some side effects don't develop for months or even years. This might explain why reports of problems are increasing over time even faster than the population is becoming statinised

Just wanted to report back on the break I have taken from 40mg Crestor.  Although I posted here on March 1st, I was really hesitant to stop since I was off on a business trip and not going to be too careful about diet.

Anyhow, full 10 days without Crestor and I have ZERO arm aches and have no issue doing chin ups (well, I can do some and all without the sharp "broken bone" pain).

I know I'm going to end up back on Statins as I really hate eating meat, but while I am trimming down, I will stay off them for maybe 3 or 4 months then get a blood test before asking the primary care phys for a dose recommendation.

An Appeal for Support and Conformation of MRI Results

My daughter has lived with ALS-like symptoms for almost 3 years. The worst of the symptoms began when her simvastatin was increased to 80mg in 2008.
Her MRIs show LESIONS in the brain stem, specifically in the PONS area of her brain.
Of course, her 4 physicians refuse to believe that a statin is involved. They are all satisfied with the diagnosis of “Ataxia”.

My Appeal is to all those who are/were on statins and have similar brain lesions as shown and documented in MRIs. Please reply here, or contact her father directly: Dr Stephen Arvay, stephenx11@cogeco.ca

What I am advocating is that statins be used carefully, after all efforts at correction of lipid/lipoprotein patterns have been made, with an assessment of true coronary risk (not such nonsense as the Framingham score). A more reasonable application of statin drug prescription would shrink the market from its current $27 billion to a tiny fraction of that.

when taking statins, follow doctors advice, take the drugs according to doctors prescription, the  drug carefully to be safe.

Finlaly! This is just what I was looking for.

Ya learn something new evreyady. It's true I guess!

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