What is Coronary Artery Disease?
It was originally thought that coronary artery disease (CAD) was the result of narrowed arteries interfering with blood flowing through them depriving the heart of blood, oxygen and nutrients. This became the popular explanation when physicians began injecting contrast agents into the lumen of the arteries - the area where the blood flows - and noticed narrowings (stenosis) in people who had chest pain (angina).
This long held belief - a belief that unfortunately too many still hold onto despite presentations by myself and others at nationally and internationally acclaimed conferences, including but not limited to the American College of Cardiology - was disrupted in 1987 when a Russian pathologist by the name of Glagov, discovered that a number of patients who died from CAD did not have these narrowings. He discovered this after doing autopsies of these individuals and published the results in the New England Journal of Medicine.
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Prior to actually narrowing the lumen of the artery, InflammoThrombotic Immunologic material is deposited into the wall of the artery. This material then distended the wall of the artery outward - inteferring with the ability of the artery to relax and dilate to carry more blood when needed by the heart.
Later, when the wall of the artery can no longer stretch outward, or when the resistance to inward movement of the InflammoThrombotic Immunologic material is less due at the combined effect of the tunica intima (innermost part of the artery) and the resistance offered by blood flowing through the lumen of the artery than the resistance of the tunica externa (outer part of the wall of the artery), the InflammoThrombotic Immunologic material extends into the coronary lumen.
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When calcification occurs due to the death of cells leaking out calcium, the area becomes calcified. Under these conditions and these conditions only coronary artery calcium scoring provides information on the calcium being present.
If the plaque develops a fibrous cap, it is referred to as stable - less likely to rupture.
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When the material is mostly softer InflammoThrombotic Immunologic material, the resulting plaque is referred to as unstable (soft unstable plaque) which is more likely to rupture as the buildup of this material continues. Such a rupture inside a coronary (heart) artery, like a rupture outside an artery, will result in the body trying to stop the bleeding by forming a blood clot. When this happens, like all blood clots, blood flow stops.
When this happens inside an artery, the blood flowing inside the artery, can not extend past the area of the blood clot, preventing the area of the heart down (blood)steam from the clot, from receiving any blood. When this happens for an extended period of time, the heart begins to die (myocardial infarction, MI, heart attack). The death, as you will see in my following flow reserve graphic begins at the inner layer of the heart (endocardium) and over time, it will extend outward to the outer wall of the heart (epicardium). This takes approximately 4-hours as we demonstrated in our animal studies when I was a cardiology fellow.
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Prior to full thickness myocardial infarction (detectable on electrocardiogram; i.e. Q-wave MI, transmural MI, et cetera), the damage is detected by finding cellular damage leaked out from the dead heart tissue into the blood stream. The changes in the blood - cardiac enzymes - can be measured and change over time with the smaller molecules leaking out of damaged cells first, followed by the larger molecules when the holes in the damaged cells expand.
Cells Within The Wall of (Coronary) Arteries
Microscopic (Histology) View of an Artery
First Outward Extension of InflammoThrombotic Immunologic material - Then Inward
This buildup of InflammoThrombotic Immunologic material within the wall of the artery, interferes with the ability of the artery to relax - dilate - inhibiting the coronary artery from being able to increase the amount of blood flowing through it when the heart becomes more metabolically active.
It is this regional build up of InflammoThrombotic Immunologic material that interferes with the ability of the coronary artery in that region of the heart - compared with other regions of the heart which do not have this same build up of material - to increase its blood flow to meet the metabolic needs of a given area (region) of the heart that produces the chest pain we call angina. This regional difference in blood flow (Q) as well as regions of non-impaired blood flow, can be measured by FMTVDM.
The ability of the coronary arteries to increase blood flow is called flow reserve. Under normal circumstances, without coronary artery disease (CAD) - the accumulation of InflammoThrombotic Immunologic material impairing relaxation of the artery - or when the material is found only in the wall of the coronary artery but not the lumen, this ability to increase coronary blood flow is refered to as Coronary Flow Reserve (CFR).
When the InflammoThrombotic Immunologic material within the wall of the artery extends into the lumen of the artery, this is then referred to as Stenosis (narrowing) Flow Reserve (SFR) or Fractional Flow Reserve (FFR).
The proprietary equations explaining the relationship between SFR/FFR and coronary artery disease in people was developed by me in 1990. As demonstrated in the following graphic, this is different from the flow reserve equation produced by Gould, which described flow reserve in dogs. Every species is different and the Gould model only applies to dogs.
The results of my research on people is graphically shown below with the first comparisons with early FMTVDM made in 1991.
The InflammoThrombotic Immunologic factors that contribute to this buildup of material within the walls of the coronary arteries producing CAD were first presented by me three years later in 1994 at the American Heart Association Conference in Dallas. This were later published in a Cardiology textbook along with a chapter on SFR in 1999.
These factors were also briefly discussed during a 20/20 segment recorded in 2004; a clip from which is included below discussing some of what has been discussed above.
FMTVDM measures changes in regional metabolic and blood flow differences; i.e. flow reserve changes, resulting from InflammoThrombotic Immunologic material depositing in the walls of the arteries and when it occurs, within the lumen space. Like Cancer, COVID infections and other ITIRD, flow reserve can be augmented or reduced by many of the same chemical messengers including vascular endothelial growth factor (VEGF, IGF-1), interleukin-6 (IL-6) and others.
FMTVDM measurement of CAD takes advantage of it's unique ability to measure these changes in regional metabolism and blood flow by enhancing coronary blood flow from baseline to measure the flow reserve of each artery.