Coronary arteries aren't what they seem

12. November 2007 William Davis (5)
Why do stress tests so often fail to detect coronary atherosclerotic plaque? Why do even heart catheterizations--the "gold standard"--fail to disclose the full extent of plaque within the walls of coronary arteries?

We owe much of the explanation of these phenomena to Dr. Seymour Glagov, retired professor of pathology at the University of Chicago.



When studying the coronary arteries of people who died, he observed that people commonly had plenty of atherosclerotic plaque lining the artery wall, yet it did not necessarily impinge on the artery "lumen," or the internal path for blood to flow.

The only time the lumen became obstructed by plaque was when either 1) plaque grew to overwhelming levels and was severe and extensive, or 2) when a plaque had "ruptured," meaning its thin covering had been penetrated and eroded by the underlying plaque tissue like a volcano emerging from the surface and erupting.

This groundbreaking observation, now dubbed "the Glagov phenomenon," explains why someone can have a normal stress test on Tuesday but erupt a plaque on Wednesday.

The Glagov phenomenon also explains why heart scans can detect plaque when both stress tests and heart catheterizations fail to do so. Many physicians will then interpret this to mean that the heart scan was wrong. With the Glagov phenomenon in mind, you can see that the heart scan is not wrong, it is simply detecting coronary atherosclerotic plaque at a stage that is not yet detectable by the other methods.

In the illustration, you can see that the lumen of the vessel is maintained--despite the artery on the left having minimal plaque, the artery on the right containing moderate plaque. If either artery were examined by a test that relies on blood flow--stress test or heart catheterization--both would appear normal. But a test that examines the artery wall, such as a heart scan, would readily detect the artery on the right and probably even the artery on the left.




I am very grateful to Dr. Glagov and his insight into this important process. Otherwise, we might still be floundering around trying to understand the apparent discrepances between these tests that simply provide different perspectives on the same problem.
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Comments (5) -

  • Anonymous

    11/13/2007 1:04:00 AM |

    I saw a new small 2 pound ultrasound machine for detecting plaque in neck arteries just hit the market place.  Article was at: http://www.newstarget.com/022212.html

    It sounds exciting that something like this would be easily accessible - as the author speculates.  Do you think this new small devise will be helpful - if one has plaque in neck arteries does that typically also mean plaque in the heart?

  • Dr. Davis

    11/13/2007 2:54:00 AM |

    Actually, I purchased one of these devices about 7 years ago. The data is reasonably well worked out: carotid ultrasound for a measure called intima-media thickness is a reasonable second choice to coronary plaque measurement. It can be useful to augment information from direct coronary scoring, or when heart scanning is impossible, e.g, some people after bypass surgery.

  • Anonymous

    11/13/2007 7:11:00 PM |

    You've been concentrating a lot on coronary arteries, and the effect of plaque build up. What about the valves of the heart? Can plaque build up on, or otherwise affect them?

  • Dr. Davis

    11/13/2007 10:08:00 PM |

    This blog and the accompanying website, www.trackyourplaque.com, are intended to focus on coronary issues.

    However, I have been seeing aortic valve disease actually improve with vitamin D. Please see my blog post, Valve disease and vitamin D at http://heartscanblog.blogspot.com/search/label/Valve%20disease%20and%20vitamin%20D.

  • buy jeans

    11/3/2010 10:15:10 PM |

    When studying the coronary arteries of people who died, he observed that people commonly had plenty of atherosclerotic plaque lining the artery wall, yet it did not necessarily impinge on the artery "lumen," or the internal path for blood to flow.

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Heart disease = statin deficiency

Heart disease = statin deficiency

10. May 2007 William Davis (1)
Judging from the conversations I hear from colleagues, what I hear from the media, and drug company advertising, you'd think that heart disease has one cause--a deficiency of statin drugs.

As their thinking goes, if you have coronary disease, you need a statin drug (Lipitor, Zocor, Crestor, pravachol, etc.). If you have progressive coronary disease, you need more statin drug. If you have a heart attack while on a statin drug, you need even more statin drug.

Some "experts" have even proposed that we do away with LDL cholesterol and we just give everybody a statin drug at high doses.

Does this make any sense to you?

Doesn't it make better sense that if someone has progressive heart disease or heart attack while on a statin drug, then target the other causes largely unaffected by a statin drug? Perhaps if LDL cholesterol remains high on the statin drug, then a higher dose is justified. But more often than not, it's not a high LDL on statin drugs that responsible, it's other causes. And there's many of them: low HDL, VLDL, IDL, Lp(a), deficiency of omega-3 fatty acids, inflammatory processes, vitamin D deficiency, among others. (An important exception to this is when the conventional calculated LDL substantially underestimates true LDL as measured by LDL particle number by NMR, apoprotein B, or 'direct' LDL.)

Imagine someone has pneumonia. After 2 weeks of antibiotics, they are only partly better. The solution: a higher dose of the same antibiotic--but never question if it was the right antibiotic in the first place. That's what is going on in heart disease.

The doctors have been brainwashed into believing this $22 billion dollar per year bit of propaganda. The drug companies actively try to recruit the public into believing the same. Don't fall for it.

The statin drugs do indeed have a role. But they are not the complete answer. More of the same when disease progresses makes no sense at all.
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Comments (1) -

  • Anonymous

    5/10/2007 5:57:00 PM |

    This is so true!! The drug companies just keep pushing the statins, and most doctors have bought into this.

    Thanks for this article.

    Marilyn, RN,BSN

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To B or not to B

To B or not to B

5. December 2010 William Davis (11)
Apoprotein B (apo B) is the principle protein that resides in LDL particles along with other proteins, phospholipids, triglycerides, and, of course, cholesterol.

There's a curious thing about apo B. Just like one child per family in China or one television per household in 1950s America, there is only one apo B for every LDL particle.

So measuring apo B, in effect, provides a virtual count of LDL particles. (Actually, VLDL particles, the first lipoprotein to emerge from the liver, also have one apo B per particle but LDL particles far outnumber VLDL particles.) While apo B structure can show limited structural variation from individual to individual, the effect on measured apo B is negligible.

One apo B per LDL particle . . . no more, no less. What about the other components of LDL particles?

The other components of LDL particles are a different story. Cholesterol and triglycerides in LDL particles vary substantially. Diet has profound effects on cholesterol and triglyceride content of LDL particles. A diet rich in carbohydrates, for instance, increases triglycerides in LDL particles while reducing cholesterol. This means that measuring cholesterol in the LDL fraction will be misleading, since cholesterol will be falsely low. LDL cholesterol is therefore a flawed means to assess the behavior and composition of LDL particles. In particular, when LDL particles become enriched in triglycerides, they go through a process that transforms them into small LDL particles, the variety most likely to cause atherosclerosis.

In other words, when the worst situation of all--an abnormal abundance of small LDL particles develops--it is usually not signalled by high LDL cholesterol.

Because apo B is not sensitive to the composition of LDL particles--high cholesterol, low cholesterol, high triglycerides, etc.--it is a superior method to characterize LDL particles. While apo B doesn't tell you whether LDL particles are big, small, or in between, it provides a count of particles that is far more helpful than measuring this deeply flawed thing called "LDL cholesterol."

(Even better: Count LDL particles and measure LDL size, since size gives us insight into sensitivity to oxidation, glycation, adhesiveness, ability to trigger inflammatory pathways via monocyte chemoattractant protein, various interleukins, tunor necrosis factor and others. This is why cholesterol panels should go the way of tie dye shirts and 8-track tapes: They are hopelessly, miserably, and irretrievably inaccurate. Cholesterol panels should be replaced by either apoprotein B or lipoprotein measures.)
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Comments (11) -

  • arnoud

    12/5/2010 2:53:08 PM |

    The NMR Lipoprofile test provides LDL particle counts, and the VAP test provides Apo-B measurement.
    Is there a direct conversion factor to determine Apo-B for a given total LDL count, and vice versa?

  • Anonymous

    12/5/2010 2:55:39 PM |

    Hi Dr. Davis,
    Is there an advantage to ordering the VAP along with the NMR Lipoprofile?  Does the information from one or both of these two tests greatly improve on measuring the apo B and apo A ratio?
    Thanks,
    John

  • Dr. William Davis

    12/5/2010 2:56:28 PM |

    Hi, Arnoud--

    Apoprotein B and NMR LDL particle number are roughly correlated with a difference in units by a factor of 10. An LDL particle number of 1000 nmol/L is approximately equal to 100 mg/dl apo B.

    By the way, apo B is calculated on VAP, not measured.

  • Martin Levac

    12/5/2010 4:18:26 PM |

    LDL does not cause atherosclerosis. Thus, there is no possible gradient such as "most likely". It might look like a semantics argument but I'm really just exposing the flawed hypothesis behind the semantics.

    What is truly most likely, is that whatever causes atherosclerosis also causes small LDL.

    Carry on.

  • Eugene

    12/5/2010 5:39:07 PM |

    Hi Dr. Davis,
    Is there an advantage to ordering the VAP along with the NMR Lipoprofile? Does the information from one or both of these two tests greatly improve on measuring the apo B and apo A ratio?
    Thanks,
    E. John

  • Travis Culp

    12/6/2010 4:20:19 AM |

    I was previously unaware of this information; thanks for the heads up.

  • Anonymous

    12/8/2010 7:54:55 AM |

    Dr. Davis,

    I've been following your dietary advice for a few years (low carb, little to no wheat, lots of nuts and flax) and all my biomarkers are excellent... Except.. my serum phosphorus, which tends to be either above the normal range or at the very high end of the normal range... this isn't an issue with my kidneys since all other markers are optimal... I wonder if you've seen similar results before with this nut/flax rich diet?

    Thanks,
    David

  • Anonymous

    12/8/2010 10:04:41 PM |

    I had an ApoB of 43 mg/dl, an LDL particle number on NMR of 593 nmol/L, and an LDL on NMR of 78 mg/DL with particle size of 21.6 nm.  My ApoB seems much lower than my LDL particle number (even after adjusting for the factor of 10). Weird?

  • Might-o'chondri-AL

    12/9/2010 3:24:37 AM |

    Glycosaminoglycan (dermatan sulfate form, a bi-glycan) and ApoB together make the type of plaque that is rupture prone.

    The enzyme hyaluronidase increases glycosaminoglycan synthesis when lack ApoE. In animal models the aorta collagen increases, plasma volume drops, proteinuria rises, endothelium degrades and atherosclerosis begins.

    The poly-anion hyaluronate is available (water soluble) in a pectic polysaccharide as hyaluronic acid in fruit of Abelmoschus esculentus; "okra" is the plant in English.

    This may partiallly explain the autopsy analysis of the differences seen in arteries of Africans (who eat okra) & Westerners. Maybe the okra hyaluronate "uses up" the excess enzyme hyaluronase, which effectively "neutralizes" the Apoliprotein risk factors (ApoE deficiency & hypothetically here the ApoB excess).

  • karl

    12/17/2010 9:48:44 PM |

    My hunch is apo-b is correlated with oxLDL, but I've seen no papers that show that small LDL or apo-b count is more predictive than oxLDL.

    We know that high carb yields high blood sugar and that alone is oxidative of LDL. What if apo-b is correlated with oxLDL because both are driven by high BG?

    Unless this is separated out,  we might be wasting money on expensive apo-b tests instead of cheap oxLDL tests or even cheaper postprandial BG testing.

  • Adriana

    10/5/2011 12:23:43 PM |

    This is interesting as there are reports of okra water reducing some people's fasting blood glucose.

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