April-May 2008 Copyright 2008, Track Your Plaque, LLC 

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Track Your Plaque shows how to use CT heart scans as the 1st step in a proven program to slow, stop, even REVERSE heart disease!

In this issue:

 

Hello, Plaque-Trackers!

Cholesterol was the buzz word for heart health for the past 20 years.

But circumstances are due for a change. In future, I predict that the buzzword will be “plaque.” With mainstream reports like Dr. Steve Nissen’s ASTEROID Trial (showing regression of plaque using the high-dose cholesterol drug, Crestor), pop-media doctors like Dr. Stephen Sinatra’s recognition of the concept of measuring plaque, along with the Track Your Plaque program, more and more people will come to recognize, as we have, that it’s not cholesterol that counts, it’s the disease itself: atherosclerotic plaque!

Plaque can grow; plaque can shrink. Each day that goes by, we get better and better at stopping and reducing plaque.

In this issue of the Track Your Plaque Newsletter, I talk about two issues that can impact on heart scan scores: distribution of coronary calcium—“inside” or “outside” the artery--that is measured by heart scans, and the question of whether the blood thinner, warfarin, rapidly gaining a reputation for disrupting normal calcium metabolism, may increase heart scan scores.

Track in health!


Dr. Davis
 


Another Track Your Plaque Success Story: Track Your Plaque saves the day!

Mel is a 62-year old retired college professor. A “young” 62, Mel was having a great time in retirement, traveling with his wife, visiting his four grown children and his many grandchildren. All in all, life was good.

But Mel’s heart scan score was the one thing that marred his otherwise wonderful life. An initial scan in 2003 showed a score of 341.

Mel’s family doctor did the usual thing and prescribed a statin drug for a moderately elevated LDL cholesterol. A little over one year after the first scan, a second scan showed a score of 391, representing an 8% annualized rate of increase. No change in Mel’s program was suggested by his family doctor.

A third scan about 3 ½ years later showed a score of 649, a 13% annualized rate of increase. That’s when Mel came to us.

Despite taking a cholesterol drug, Mel proved to have a very high LDL cholesterol (measured, not calculated) that consisted almost entirely of small LDL particles, a severe pattern. As most participants starting out in the Track Your Plaque program, Mel also proved deficient in vitamin D, and had an elevated C-reactive protein representing a hidden inflammatory response.

We showed Mel how to correct all of his patterns. The one abnormality he struggled with was to make a large impact on small LDL. Mel was only modestly overweight to begin with, suggesting that small LDL was largely a genetically-programmed effect. Nonetheless, a repeat heart scan another year later revealed a score of 648, representing no change from the previous scan.

Dr. Davis:

Mel provides yet another great example of how the statin drugs, when used in isolation, may slow the expected increase of heart scan scores of 30% per year, but rarely stop the process. The Track Your Plaque program asks a simple question: Why did Mel have coronary atherosclerotic plaque in the first place?

A simple analysis answered the question. In Mel’s case, several previously unrecognized patterns emerged that we then proceeded to correct.

Mel’s case also highlights another interesting phenomenon: small LDL particles. While they are easy to identify, they can also be easily corrected when worsened by lifestyle factors, such as poor choice in foods. However, sometimes we do encounter a roadblock after we’ve corrected all lifestyle factors, added appropriate supplements like niacin, yet are left with a substantial proportion of small LDL. Here’s where we still could use some better tools. Perhaps, when tools to better deal with small LDL, we can see people like Mel not just stop his score, but drop it like some of our other success stories.
 

Calcium on the inside or calcium on the outside?

A reader writes:

“I had a heart scan and my score was 131. When I told my doctor about it, he said, ‘I’m not sure what that means. The calcium could be on the inside of the artery or it could be on the outside. Let’s do an angiogram to find out.’

“I’m confused. The heart scan report said nothing about calcium being on the ‘inside’ or the ‘outside.’ It just said that women with heart scan scores in this range were at risk for heart attack and that further testing might be considered. What should I believe? Is there really a difference between calcium being on the ‘inside’ vs. the ‘outside’?”

Arterial calcium can indeed be either in the inner lining of arteries (the “’intima”) or the deeper muscular layer (the “media). It’s calcium in the intima that we’re most interested in, but heart scans cannot distinguish intima from media.

However, this is rarely a practical issue. In the vast majority of people, calcium is in the intimal lining of arteries and truly signifies atherosclerotic plaque.

There are three situations in which calcium may occur in the media and not necessarily represent run-of-the-mill atherosclerosis:

1) People with kidney failure
2) Very elderly people—e.g., over 75 years old
3) Disorders of calcium metabolism—e.g., hyperparathyroidism

However, despite calcium developing in the medial layer, studies have shown that risk for heart attack and other cardiovascular events is no different than if it was in the intima. Most of the time, in fact, medial calcification occurs in concert with intimal calcification.

So, in all reality, rarely is this a real issue. For all practical purposes, calcium signifies atherosclerotic plaque; the more calcium there is (the higher the heart scan score), the greater the risk for heart attack, etc.—regardless of whether it’s intimal (“inside”), medial (“outside”), or a combination.

Then why the enthusiasm for CT angiograms or conventional coronary angiograms (heart catheterization)? In my experience, the most common reasons are:

1) Your doctor doesn’t understand the above issues and truly does not know that calcium of any sort correlates closely with risk.
2) Angiograms make more money and lead to “downstream” procedures.
3) Defensive medicine—i.e., the fear of “missing something” that could lead to risk of a lawsuit.

In my view, it is silly to advise anyone who has a heart scan score that the “inside” vs. “outside” distinction needs to be made. There are clear-cut reasons to justify angiograms, such as symptoms of heart disease, abnormal stress tests suggesting poor coronary flow, ongoing unstable symptoms of heart disease, or follow-up after heart attack. But definitely not to tell whether calcium is “inside” or “outside.”
 

Does warfarin (Coumadin®) increase heart scan scores?

(Reprinted from The Heart Scan Blog)

Gilbert is a 58-year old high school science teacher.

When I first met Gil, he'd been having bouts of atrial fibrillation and had required various medications to suppress recurrences of the rhythm. However, because his rhythm proved somewhat difficult to control, his electrophysiologist (heart rhythm specialist) prescribed warfarin to reduce the risk of stroke. With atrial fibrillation, because of blood stagnation (in the left atrial appendage) in the heart, there is a stroke risk of approximately 8% per year. Warfarin reduces this risk substantially, to about 2%.

I met Gil because he had a cholesterol disorder. In my practice, the first step in gauging the implications of a lipid or lipoprotein disorder is to obtain a heart scan. If the heart scan score is zero, great. It means that we have plenty of time to treat the disorder since risk for cardiovascular events is near zero; it means less intensive efforts are necessary. But if the heart scan score is, say, 1200, then an aggressive approach in short order is required, since risk for heart attack may as high as 20-25% per year, even in the absence of symptoms.

Gil's heart scan score: 787—high and posing a risk for heart attack of about 5–10% per year without preventive efforts. Gil did indeed prove to have a complex lipoprotein disorder, as well as high blood pressure, vitamin D deficiency, and several other potential contributors to coronary plaque.

Gil did just about everything right: He exercised, followed the recommended diet, achieved better than the Track Your Plaque 60-60-60, lost 18 lbs of abdominal fat.

Gil's rhythm stabilized for several months, only to have atrial fibrillation break through again. So Gil's electrophysiologist re-prescribed warfarin.

18 months later, Gil's 2nd heart scan score: 1410—a near doubling. Unsettling to Gil and to me, to say the least.

How can this happen in the face of perfect lipids/lipoproteins, correction of hidden causes like lipoprotein(a) and inflammation, along with a vigorous lifestyle effort?

I fear that the culprit might be warfarin.

Warfarin, better known by its brand name, Coumadin®, may have some effects that intersect with the Track Your Plaque mission of reducing coronary plaque.

It is no secret that, beyond the obvious risk of bleeding from blood thinning, warfarin also may:

  • Accelerate aortic valve calcification
  • Accelerate calcification of the framework of the mitral valve (the mitral "anulus")
  • Accelerate osteoporosis (i.e., removal of calcium from bones)
  • Induce an artificial situation of vitamins K1 and K2 deficiency.

Why calcium deposition in some organs (valves and perhaps arteries), but calcium removal in other areas (bone)? Vitamin K2 maintains normal and ordered calcium metabolism; the artificial deficiency created by warfarin can disrupt both processes, though manifested in different ways.

The vitamin K1 deficiency is the route by which blood thinning is achieved. However, the K2 deficiency may have undesirable consequences, among which are seen in the above list of various pathologic calcifications.

I therefore wonder if warfarin dramatically accelerates the coronary calcium that we track to gauge the progression of coronary atherosclerosis. One experience is hardly sufficient reason to sound the alarm. It is also difficult to pinpoint the cause of the explosive growth in Gil's coronary calcium specifically on warfarin.

That all said, I am quite certain it was the warfarin.

Unfortunately, some people are unavoidably committed to warfarin, such as those with specific genetic blood clotting disorders, prosthetic valves, prior deep vein thromboses and pulmonary emboli, etc.—serious reasons. Until an alternative emerges, warfarin remains a necessity for some people. (No, nattokinase is NOT an alternative, at least not one that would permit survival.)

My personal policy is that warfarin be used only when absolutely necessary and the gains markedly outweigh risks—including that of possible accelerated calcification of multiple sites.

Whether we will be able to get Gil off warfarin and potentially gain control over his coronary disease/plaque/calcium remains to be seen. I sure hope so.

References

Caraballo PJ, Heit JA, Atkinson EJ et al. Long-term use of oral anticoagulants and the risk of fracture. Arch Intern Med 1999; 159 (15): 1750–6. PMID 10448778.

Pilon D, Castilloux AM, Dorais M, LeLorier J. Oral anticoagulants and the risk of osteoporotic fractures among elderly. Pharmacoepidemiol Drug Saf 2004;13(5): 289–294.PMID 15133779.

Gage BF, Birman-Deych E, Radford MJ, Nilasena DS, Binder EF. Risk of osteoporotic fracture in elderly patients taking warfarin: results from the National Registry of Atrial Fibrillation 2. Arch Intern Med 2004; 166(2):241–246.PMID 16432096
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Complete Handbook of Vitamin D and Heart Health
Vitamin D is among the most exciting new developments to appear on the landscape of
heart disease prevention. It has leapt from relative obscurity to the top of the list of useful
strategies for plaque control. It has certainly earned a place in the Track Your Plaque program.

The Ups and Downs of Blood Pressure: What it all means.



Copyright 2008, Track Your Plaque