Measuring Regional Coronary Artery Blood Flow -
True Coronary Artery Disease & Cause of Angina
To measure the amount of blood flow (Q) a coronary artery should be able to carry to supply the regional metabolic needs of the heart, you need to know how to calculate flow through a tube and you need to know the measurements of that tube - in this case the measurements of coronary arteries.
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Some of my work carried out in the late 1980s and early 1990s utilized Quantitative Coronary Arteriography (QCA) to obtain the actual measurements of coronary arteries. This research utilized more than 40% of the world QCA data. It resulted in both the actual measurements of coronary arteries and the proprietary equation that is part of FMTVDM. This proprietary equation makes it possible, through the use of AI, to derive anatomic information (structure of the arteries) from the physiologic (blood flow; Q) information obtained by FMTVDM; both of which are critical in decision making processes involving patient care.
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Simple tubes are essentially cylinders. Arteries are cylinders that become smaller and smaller as they move from beginning to end; however, if you focus on a small enough region of the artery - as we can with FMTVDM nuclear isotope imaging - the artery itself will not appreciably change in diameter and any reduction in flow through the artery is then the result of the InflammoThrombotic Immunologic material within the wall of the artery and the subsequent inability of the artery to relax to increase the blood supply in that region of the heart. As we have discussed previously, with time this buildup in InflammoThrombotic Immunologic material will eventually encroach upon the lumen of the artery where the blood is flowing.
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Calculating the Volume of Blood Flowing
Through a Region of a Coronary Artery
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The volume of blood flowing through the artery or tube =
Volume = (π) x (radius)2 x (length)
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Where π (pie) = approximately 3.14, and (radius)2 = radius squared or (radius x radius) of the tube (artery). The radius is one-half the diameter - the distance across the lumen of the artery. Length is the length of the artery under consideration.
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From my research with QCA I can tell you that non-diseased coronary arteries have the following lengths and diameters.
The term dominant merely refers to which artery - the right coronary (RCA) or the left circumflex (LCx; Cx) - supplies blood to the posterior descending artery (PDA) of the heart. This is the artery typically responsible for supplying blood to the inferior (bottom) 1/3rd of the interventricular (wall of the heart separating the right ventricle (pump) from the left ventricle (pump) - septum. This is the RCA most (80-85%) of the time.
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As my QCA research showed, by the time coronary artery disease (CAD) has progressed to the point of encroaching upon (narrowing) the lumen of the artery, the following length and diameter of diseased arteries are seen.
Using this information, including how to calculate the volume of blood within an artery, we can measure someone's regional blood flow differences using FMTVDM and then calculate both regional blood flow differences and the anatomic differences that give rise to these regional blood flow differences (CAD; heart disease).
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Time for Some Practice Examples -
Changes in Regional Blood Flow that will
Produce Regional Blood Flow Differences (RBFDs).
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With this information in hand, lets begin with a basic comparison of the ability of an artery to carry blood at baseline - rest.
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Using the information from the two tables, lets look at what happens when we begin with a left anterior descending artery (LAD) starting with a diameter of 3.5 mm and a length of 15 mm. We will then compare the volume of blood this artery can hold before CAD and after InflammoThrombotic Immunologic material has reduced the diameter of this same artery to 1.5 mm.
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When we calculate the volume of blood in the artery at any given moment of time before there is CAD, the artery will be able to hold 144.24 cubic millimeters of blood. This means there is 144.24 cubic millimeters of blood, containing the isotope which will be delivered to the heart for FMTVDM measurement. [If the diameter is 3.5 mm, one-half that (radius) is 1.75 mm.]
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Volume (144.24 mm3) = (3.14) x (1.75 mm)2 x (15 mm)
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In this artery, in this example, once the InflammoThrombotic Immunologic material has compressed the inner wall of the coronary artery into the lumen where the blood is flowing, the diameter of the lumen has been reduced to 1.5 mm. This represents a 57.1% diameter stenosis (% DS). The volume of blood along with the isotope to be measured with FMTVDM is now 26.51 cubic millimeters.
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Volume (26.51 mm3) = (3.14) x (0.75 mm)2 x (15 mm)
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When you compare the change in the diameters of the artery before and after narrowing, you can see that the length of the artery remains the same. However, when you look at the cross section of the artery and the reduced diameter resulting from the InflammoThrombotic Immunologic material, it is easy to see how this reduction in diameter results in reduced regional coronary blood flow.
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These changes in coronary lumen narrowing, which occur late in CAD, are the classic approach people have used to understand CAD.
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However, the coronary arteries, as discussed previously, are unique in that they are the only arteries in the human body that can increase their resting flow by five to six times to provide blood to the heart at peak demand - a requirement for the highly metabolically active heart responsible for pumping blood throughout the body.
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The difference in flow between a resting flow and peak flow of 5-6 times baseline, is equivalent to that which we just saw worked out in the above example. The difference between the ability to carry 144.24 mm3 and 26.51 mm3 is a factor of 5.4; in other words the example used to understand flow reduction caused by a narrowed coronary lumen is identical to changes in flow from rest to maximum blood flow. This maximum blood flow (flow reserve) is frequently tested by stressing the heart to see how much you are able to increase your blood flow. Can you increase your blood flow 5-6 times at peak flow as rest?
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The difference in blood flow is substantial as shown by the numbers we calculated using actual human coronary QCA data.
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The principle is the same; differences in blood flow from one coronary artery segment (region) compared to another, can be measured using FMTVDM.
These regional blood flow differences can be measured, using FMTVDM to first find those artery segments that cannot relax upon demand to carry more blood to the heart as needed and later as disease continues the narrowing of the coronary lumen (coronary lumen disease; CLD).
As discussed previously, it is this difference in regional blood flow, resulting from the inability of a portion of a coronary artery to relax and increase its blood flow due a buildup of InflammoThrombotic Immunologic material that defines coronary artery disease and causes angina!
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Once CAD begins exertional symptoms begin as the regional demand for blood flow is not met. But as I have discussed on 20/20 and elsewhere, the first symptom for half of all people with CAD is death.
As CAD continues and the InflammoThrombotic Immunologic material extends into the coronary lumen (CLD) - reducing event baseline blood flow, the person will most certainly notice symptoms of heart disease (chest discomfort/angina, dyspnea - shortness of breath due to failure of the heart to adequately keep up with pumping of blood with resulting accumulation of blood within the lungs, nausea - when the inferior (bottom) part of the heart is irritated stimulating the vagal nerve, referred discomfort to neck and (usually but not always) the left arm as the nerves coming from that part of the body are irritated, along with other symptoms) at rest.
This simple reduction in baseline regional resting flow is typically not appreciated by half the people until they have a heart attack and suffer permanent damage to their heart.
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Further Understanding The Importance of
Coronary Flow Reserve (CFR; SFR; FFR)
to Meet the Demands not only of the Heart but the Body.
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Lets begin by looking at an example of a normal healthy human heart without coronary artery disease. When the person becomes more metabolically active (physical activity, infection, cancer, et cetera) the heart needs to be able to increase its cardiac output (blood pumped from the heart) to meet the increased metabolic demands of the body.
To do this the heart must also increase the amount of blood it is receiving through the coronary arteries, to keep up with its increased metabolic demand. With a faster heart rate, there will be less time in between heart beats for the heart to receive this blood since the heart, unlike the rest of the body, receives its blood supply when the heart is relaxing (diastole), while the rest of the body receives its blood supply from the heart during contraction/pumping of the heart (systole). A faster heart rate means less relaxation (diastole) time and less time for the heart to receive blood - during the same time the heart must work harder. Hence, the uniqueness and importance of the coronary arteries being able to relax to fill with more blood during diastole - i.e. flow reserve.
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Fortunately, the heart can take advantage of its flow reserve as long as the walls of the arteries have not been damaged by the buildup of InflammoThrombotic Immunologic material.
​From a cross sectional view, a coronary artery at rest would have the diameter as shown on the left, while the relaxed coronary artery, would have a diameter similar to that on the right. The difference in the ability of these two different diameter coronary arteries to carry blood flow to the heart should be apparent.
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Through these coronary arteries isotopes will flow along with the blood. From here the isotopes will be taken up by the heart. The cells will then recycle (redistribute) the isotopes based upon metabolic activity of the heart cells (myocytes) and blood flow to those myocytes.
The greater the metabolic activity of the heart (stress - physical exercise like the Bruce Treadmill test; pharmacologic stress - drugs that relax the artery to increase its diameter) and metabolic activity of the heart, the greater the uptake and redistribution of the isotope for FMTVDM measurement.
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While the size of these red dots representing the lumen of the coronary arteries are of course much larger than actual coronary arteries, they serve to drive home the point that small changes in diameter yield significant differences in the volume of blood which can flow though a coronary artery.
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Reductions in Coronary Flow Reserve (CFR) = CAD = Angina
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Now that we have covered some of the fundamental changes seen with reduced regional coronary blood flow resulting from the buidup of InflammoThrombotic Immunologic material, it is time to look at how I was able to define these differences in flow reserve and scientifically demonstrate that these regional blood flow differences are the cause of angina.
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Lets begin by reducing the size of these red dots to the actual diameter size of human coronary arteries. As you can see, Artery "A" is 3.5 mm in diameter; roughly the size of a normal, healthy, proximal (beginning of) human left anterior descending artery (LAD).
Under resting conditions, Artery "A" has a diameter of 3.5 millimeters and carries through it, at least at this point in the artery, the normal amount of blood expected under resting conditions.
When that same artery sees deposits of InflammoThrombotic Immunologic material it can no longer relax and successfully achieve its flow reserve of 5-6 times baseline. The resulting limitations in its ability to relax and increase its blood flow to the heart is impaired and it may only be able to achieve a flow reserve of 2.0 - in other words, it can only increase its blood supply to the heart by a factor of 2 or twice what it carries at baseline.
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By comparison, another arterial region may have less InflammoThrombotic Immunologic material and have a flow reserve of 3.5 - making it possible for this arterial region to carry 3.5 times as much blood at peak flow as at rest.
Another artery segment may have NO InflammoThrombotic Immunologic material and may therefore be able to reach its flow reserve of 5-6 - making it possible for this arterial region to achieve its full flow reserve to meet the demands of that area of the heart.
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As you can see from the diagram, the difference in being able to relax (dilate) and increase flow reserve, can be measured in millimeters.
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While none of these examples show narrowing of the lumen of the artery (CLD), they each - except for the last one with no disease - are associated with insufficient blood flow (flow reserve), depending upon the demand place on the heart which determines the demand placed on the coronary arteries.
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FMTVDM Measures Regional Limitations in Flow Reserve, Demonstrating that Angina is Caused by Regional Blood Flow Differences
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In 2000, at the Joint Session for the European and American Colleges of Cardiology, held at the American College of Cardiology (ACC) Conference in Anaheim, CA, I presented research showing that angina, chest pain from insufficient blood flow to the heart, was the result of regional blood flow differences. These regional blood flow differences could be the result of coronary lumen disease (CLD); however, CLD was not necessary to produce these regional blood flow differences.
This presentation was part of a series of eight lectures held by the ACC. Each presentation was 1-hour long and was attended by approximately 5,000 physicians and healthcare providers. The presentations were recorded for others to listen to and receive CME credits following successful completion of questions to demonstrate understanding of the material presented. The results were later published in the Journal of the American College of Angiology.
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To prove the cause of angina I took 72 people, 39 men and 33 women with exertional CAD. At rest they were completely comfortable without angina. This meant that when they were laying on an imaging table - performing no exercise or exertion - they had no chest discomfort (angina).
While lying on the exam table, they were given an enhancing agent to relax their coronary arteries. This is known as pharmacologic stress. It relaxes the coronary arteries, increasing the flow reserve in their coronary arteries.
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As discussed above, the ability to increase coronary flow reserve is dependent upon the amount of InflammoThrombotic Immunologic material present in different arterial regions. In all instances; however, there was no limitation in baseline (resting) flow and there was no increased demand for blood flow being placed on their hearts as they were all lying comfortably on an exam table.
Coronary arteries with no disease and no flow reserve problems, like Artery "E" above, relaxed to carry 5-6 times the amount of blood during administration of the pharmacologic stressing agent. This was verified by FMTVDM measurement.
As measured with FMTVDM, all of the arteries, including those with disease, relaxed to varying degrees depending upon how much InflammoThrombotic Immunologic material was present to impair flow reserve. The more diseased, the more the reduction in flow reserve; but, any flow reserve above 1.0 means there was an increase in coronary blood flow, without an increase in workload on the heart or demand by the heart for more blood flow.
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The only differences, measured by FMTVDM, were the differences in regional flow reserve resulting from differences in the build up InflammoThrombotic Immunologic material impairing arterial regions from being able to relax and increase their flow reserve to the same extent as non-diseased coronary artery regions could increase their flow reserve in a setting where there was no increased demand upon the heart.
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Despite the increase in flow reserve - an increase that varied by region depending upon the amount of CAD present, an increase that was not needed by the heart to meet the needs of the heart because there was no increased cardiac workload - these patients experienced angina, in the presence of increased coronary blood flow.
The angina was reversed in all individuals by giving a second drug, which reversed the effect of the pharmacologic stressing agent; thereby reducing overall coronary blood flow.
Once reversed, the flow reserve decreased in all coronary artery regions. This reversal returned all blood flow back to baseline, which meant there was less blood flowing throughout the heart. Despite the reduction in blood flow, all angina went away.
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Therefore, reduction in blood flow is not the cause of angina. Angina is the result of regional blood flow differences. Differences which were measured using quantitative FMTVDM.
"When you have excluded the impossible, whatever remains, however improbable, must be the truth."
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As Galileo Galilei once said, "All Truths are Easy to Understand Once They are Discovered. The point is to Discover Them."
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Angina is the result of regional blood flow differences
in the heart.
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Once you think about it, it's obvious. Most, if not all of our medications, surgeries, and interventions, successfully reduce angina by redistributing coronary flow reserve from good flow reserve areas to poorer flow reserve regions. Thereby eliminating the disparities; but, not the underlying problem - the cause of the disease, the InflammoThrombotic Immunologic material that builds up in the arteries of our heart to produce deficiencies in blood flow reserve.
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This is the fundamental reason why I have devoted decades into determining what causes this buildup of InflammoThrombotic Immunologic material and what we can do about it.
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This same buildup of InflammoThrombotic Immunologic material occurs either as a result of, or in response to, the factors I have shown to be responsible for many other chronic diseases [https://www.flemingmethod.com/], including
cancer,
high blood pressure,
strokes,
diabetes mellitus,
obesity,
our response to many infectious diseases (e.g. COVID)
and much more.
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FMTVDM Quantitatively Measures the Regional Metabolic and Blood Flow Differences resulting from the deposition of InflammoThrombotic Immunologic material.
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On the next page, we will turn our attention to FMTVDM quantitative measurement of these differences in regional metabolism and blood flow.