Great post, and painfully true for me; my father had to undergo his 2nd coronary bypass operation this past April 2007, and despite the strangely 'status-quo' or 'business as usual' attitude of both the surgeons and assisting doctors and nurses involved in my dad's procedure (yes, the whole thing seemed like such a regular day at the beach to them because Holy Cross in Fort Lauderdale performs so many of these operations on a daily basis, with success, of course) did nothing really to quell my family's fears of the severity of this operation; this is still a monstrous operation that not only takes a heavy toll on the patient, but on the family sitting in that waiting room as well.
I still cry at the memory of having to tell my dad, "hey Pop, you need another CABG" after an invasive angiogram revealed disaster after disaster in his arteries.
And this is why your message is so important, and why it needs to get out every day, and loudly.

I'm rooting for you. And I'm thankful you're here.

A few thoughts about this post:
The first is a question. What do you think about ultrasound screenings for carotid artery plaque, abdominal aortic aneurysm, and peripheral arterial disease? A company called Life Line offers these, saying that they show evidence of plaque build-up in the arteries. Are they useful in conjunction with a heart scan, or can they indicate risk similar to a heart scan? It sounds like they are intended to be early detectors of stroke risk. Are they worth the investment?

The second comment is an observation. Those of us not in the medical field tend to assume that anyone who is knows what he or she is talking about on the subject of the human body and illness. However it is apparent that those with M.D.'s can come to very different conclusions about what causes us to get sick and what we should do to prevent illness. Dr. Dean Ornish is an M.D. You are an M.D. Dr. Atkins was an M.D. Yet the dietary advice differs noticeably, so how do we know who is right and who to listen to? I've learned not to believe something just because a doctor says so, because when I followed the low-fat high-carb advice I got fat and felt horrible, but now that I am following a low-carb plan with plenty of protein and fat, I've lost 25 lbs. and feel great. My bloodwork also supports your claims: low triglycerides, high HDL, and low fasting blood sugar. It's kind of sad in a way that I actually get better medical advice from doctors whose blogs I read on the internet (I'm also a Dr. Eades fan) than from my personal physician. And finally, a thank-you: since reading your advice about Vitamin D, my flower garden is in the best shape it's been in in years, since I have a new knowledge about why it's so important spend some time in the sun and a new motivation, therefore, to be outside pulling the weeds.

And concerning your recent post  about breakfast cereals,congratulations are in order: I've broken my husband's cereal for breakfast habit. (I broke my own years ago.)

I have had good results with the Lifeline service, but only when used in conjunction with a heart scan. It cannot replace a heart scan. This is because, while atherosclerosis is a body-wide process, this disease does not perfectly track in parallel in all arteries of the body. You can, for instance, have lots of plaque in the carotid arteries while having only a modest amount of plaque in the coronary arteries, and vice versa.

I agree with your second comment. In fact, I have posted on this Blog about this.

We are all swimming in a sea of information and mis-information, and blind alleys along the way to the truth. We can only educate ourselves as best as possible and then come to our own judgements about the value of this or that argument.

I have a comment too: I think one reason there is so much confusion is because dietery connection with heart disease hasn't been sufficiently studied. We only saw some partial studies by Drs Ornish, Agatston, Atkins, Hayes but not much independent verification, AFAIK. For example there are some studies done by now on the effects of a high fat low carb nutrition in diabetes and epilepsy but virtually nothing that I know of for cardiac patients.  The only one such study I heard of was halted half way through (after showing very promising results) when the funding was cancelled, 27 years ago.
Stan (Heretic)

A somewhat updated comparison of old care versus new care: I was on American Airlines this week, and looked through their magazine. There was a full page ad from the Cooper Clinic in Texas; a 46 year old woman pictured said "I had no idea I had heart disease, but had a family history...an EBT scan and four stents later, with some lifestyle changes, I'm a new woman".

I understand you can't generalize from one case, and while this seems to represent cutting edge treatment, it also gives me the creeps thinking about the obvious drive for revenue here. Couldn't they have tried your approach for awhile before invading? Thanks.

I think that they tell the stories that have a "WOW!" factor. The Cooper Clinic does indeed engage in a low-level grade of preventive care (AKA Lipitor, etc.)

But I really hate those stories, too.

Saw a lady at shul today, she is convinced of Dr. Esselstein's more carbs- is- better method. Ornish, Esselstein.....hard to refute the drumbeat of eat carbs, cut meat and fat.

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.