The Real Cause of Heart Disease? part 3 of 4

By Uffe Ravnskov MD

The new hypothesis
When the lipoproteins bind the toxic intruders to their surface, all of them - toxins, microorganisms and lipoproteins - aggregate, meaning that they lump together into microscopic clumps that circulate in the blood.

A contributing factor may be the anti-oxLDL antibodies. Antibodies have two arms and are therefore able to bind two oxidized LDL-particles at the same time. Also, if too much homocysteine is present in the blood, it reacts with LDL molecules and makes them lump together. In the view of Dr Kilmer McCully and myself, these particles play a crucial role in the creation of the vulnerable plaque.

I shall soon explain in which way, but first a question: What is a vulnerable plaque? Doesn't it look like something all of us know very well? Probably you have already guessed it, but here is what we think: the vulnerable plaque is a pustule, a small boil. Its interior looks like the interior of a boil, its temperature is higher than the surrounding tissue, just as is the case with a boil, and it may burst and empty its contents like a boil.

Boils and pustules are characterized by a special type of white blood cells called neutrophil granulocytes. In the inflamed atherosclerotic tissue some other types dominate, the so-called B and T-cells, those that belong to the antibody-producing system. Neutrophil granulocytes are rare except in the region around the vulnerable plaques,(17) a further indication that it is a pustule. Pustules are created by microorganisms. If the vulnerable plaque is a pustule, it should contain the responsible microorganisms as well, and when it bursts, they should enter the arterial blood and create symptoms similar to any other infectious disease.

Indeed, patients with an acute heart attack often have fever, chills and some sweating. They also have leucocytosis (too many white blood cells in the blood), and high levels of the same blood constituents that are elevated in infections, for instance CRP, and in about a fifth of patients with cardiogenic shock (life-threatening heart attacks) living bacteria are present in the blood.(18) It is also in accordance with our hypothesis that large numbers of neutrophil granulocytes are found almost always in the heart tissue about 24 hours after an acute heart attack.

The idea is not new. As far as we know it was first suggested by Sir William Osler, the Canadian pathologist and physician who became the Regius Professor of Medicine at Oxford and a leading physician of his time. In one of his papers he described the vulnerable plaque as an atherosclerotic pustule.(19)

But how is the boil created? Here is our explanation.

The mechanism
When blood is pumped into tissues by the heart it goes through a complicated mesh of vessels. The first one, the largest artery in the body, is the aorta. All organs in the body (other than the lungs), including the heart and the brain, are supplied by branches from the aorta.

When an artery enters an organ it splits up into smaller arteries named arterioles and each arteriole splits up into capillaries, the smallest vessels in the body, visible only with a microscope. The width of a capillary is so small that it forces red blood cells to fold in order to be able to pass through. The capillaries supply the tissues with oxygen and nutrients and after that they join as venules and veins that return the blood to the heart, from where it is pumped to the lungs.

Even the walls of the larger vessels such as arteries and veins are nourished through capillaries, the so-called vasa vasorum, which surround these vessels like an intricate meshwork. What we suggest is that the LDL clumps may become so numerous and of a size that they are able to obstruct the vasa vasorum. Consequently small parts of the arterial walls become malnourished, get too little oxygen and may even die.

You could say that they cause a small infarct of the artery wall. The toxic passengers of the obstructing clumps may now escape from the LDL prison and start multiplying in the dead tissue, which therefore becomes inflamed.

That too little oxygen is available, a condition named hypoxia, has been shown by intricate chemical analysis of atherosclerotic arteries. Hypoxia is most pronounced in the deeper parts of the inflamed arterial walls where the macrophages are dominant.(20)

If the immune system is OK, the surrounding white blood cells and the antibodies attack the microorganisms. Fibroblasts and new capillaries grow into the inflamed tissue and sooner or later it will be transformed into a scar, the fibrous plaque. If not, a pustule is created, its thin membrane may burst, the content of the plaque flows out into the blood, a clot is created at the margins and, if it becomes too large, the blood flow becomes obstructed and the tissue that is nourished by the artery dies.

If it happens in a coronary artery the result is a heart attack; if it happens in a carotid artery the result is a stroke; if it happens in an artery that goes to the eye, the victim may become partially blind.

Everything fits
There is much evidence supporting the idea that inflammation of the arteries is not the primary cause of heart attacks or strokes, but a secondary phenomenon caused by the microorganisms or their toxins. They are not settling in the atherosclerotic plaques because they are safe there; vulnerable plaques may occur anywhere, also in normal arteries, which explains why a heart attack may be seen also in people with completely normal arteries.

The primary cause is not the microbes either; it is the factors which stimulate their growth or make our immune system fail. It is not the water that causes the ship to go down; it is the iceberg that has staved in the keel.

That the microbes play an important role is obvious, and the evidence is right before our noses. For instance, mortality in myocardial infarction and stroke increases during influenza epidemics (21) and people with infected teeth (22) or with bacteria in the blood (23) are at greater risk than healthy people.

Further, about a third of all patients with acute myocardial infarction or stroke have had an infectious disease immediately before onset.(24) All kinds of infectious diseases may be responsible. Most common are respiratory diseases, but other types have been described as well, such as tuberculosis, HIV, tooth and urinary tract infections.

If a vulnerable plaque may appear in normal arteries, and if microorganisms cause stroke and myocardial infarction, then vascular disease may occur in all ages. This is true also. Finnish researcher Erkki Pesonen and his team noted that the coronary arteries were narrowed in children with infectious diseases, both in those who died and those who survived.(25) Stroke may even appear in early childhood. A Canadian research team found that about a third of these children suffered from chickenpox a few months before.(26)

If inflammation was primary, anti-inflammatory drugs should be of benefit, but they are not. On the contrary, the Vioxx scandal told us that such treatment increases the risk of heart disease, and other anti-inflammatory drugs have the same effect.(27)

Skeptics may object that statin treatment is of benefit and statins are anti-inflammatory. This is correct, but statins have many other effects; e.g. they inhibit the coagulation of the blood by enhancing a process called fibrinolysis and by slowing down the function of the blood platelets, and the platelets are necessary for the formation of blood clots.

Statins are also known to stimulate the production of nitric oxide (NO), and nitric oxide makes the arteries widen. Statins would probably have a much better effect if they didn't lower cholesterol and if they weren't anti-inflammatory, because inflammation is a necessary step for normal healing of infectious processes.

The Real Cause of Heart Disease? Part 4

Dr. Uffe Ravnskov MD
Author of "The Cholesterol Myths" and "Fat and Cholesterol are Good for You"
Creator and spokesman of THINCS, "The International Network of Cholesterol Skeptics"

17. Huemer HP and others. Intervirology 1988;29:68-76.
18. Superti F and others. Med Microbiol Immunol 1992;181:77-86.
19. Flegel WA and others. Infect Immun 1989;57:2237-45.
20. Cavaillon JM and others. Infect Immun 1990;58:2375-82.
21. Northoff H and others. Beitr Infusionsther 1992;30:195-7.
22. Flegel WA and others. Infect Immun 1993;61:5140-6.
23. Feingold KR and others. Infect Immun 1995;63:2041-6.
24. Netea MG and others. J Clin Invest 1996;97:1366-72.
25. Naruko K and others. Circulation 2002;106:2894-900.
26. Kohsaka S and others. Arch Intern Med 2005;165:1643-50.
27. Osler W. Modern Medicine: its practice and theory. Lea and Fibiger, 1908, p426-47.

September 2011 

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