Angiogenesis a bypass

[Max_123]

My father has blocked arteries, but it appears there is adequate blood flow around a completely blocked left-side large vessel.of the heart.  I'm concerned and interested because this may happen to me so I have done some reading on the subject.  I read angiogenesis is the process and posts on this forum indicate the process is collateral vessel?  Thank you in advance.:)

[HeartTwo]

Had Nuclear Imaging Study - Exercise Stress about 3 weeks prior to 4x CABG. Went and received the results yesterday. My EF was 60% !
Ok, so now luck is my new best friend. My opinion is that I attribute this to my body developing collateral arteries over a period of 30 to 40 years. First detected in 1995, these 'collaterals" continued to grow at a pace > my arteries deterioration. I was very active and had almost NO symptoms. These collaterals suplied more than sufficient blood as is evidenced by the EF of 60% just prior to my CABG.
Interesting to note that I had conversations last night with over 50 years of medical experience of the BSRN, BS, MS RN type and,opinions seemed to be scattered all over the place. Is there a reader out there who would argue against me having CAD and Ischemic Heart Disease? I appreciate your input. Thank You.  

[kenkeith]

I experienced the same phenomonon over a period of years....Not everyone seems to be a good candidate and that appears to be diabetics (vascular disease), and aging individuals who may have some hardening of the vessels and loss of flexibility of vessel walls.  My thoughts are as a vessel begins to occlude, hemodynamics (arterial pressure, blood flow velocity increases, etc.) begins to remodel vessels  and has the occlusion increases so does the hemodynamics.

My theory has been when there is medication and/or stents to treat CAD the hemodynamics change and the system does not see an occlusion problem to react. I have read there is a school of thought that does not agree.

[ed34]

"My thoughts are as a vessel begins to occlude, hemodynamics (arterial pressure, blood flow velocity increases, etc.) begins to remodel vessels  and has the occlusion increases so does the hemodynamics. "

I find it hard to swallow this, not that I'm arguing with expert, but simply that I can't see any plain logic in it. I have seen patients with no collateral developement who are in their 40's and without diabetes, I wouldn't class these as old. I was 46 when collaterals were seen forming so I assume that the age limitation factor much be further upstream.
My real struggle with this idea is that blood pressure is high in many patients who develop CAD and it has been high for many years. So if blood pressure was an issue, one would expect to see everyone develop collaterals (in my opinion anyway). Flow velocity is really going to achieve nothing because it's the pressure which matters.
What intrigues me is that according to my history of angiograms, my collaterals started to form when I began experiencing angina discomforts. I still cant help but wonder whether a chemical process triggers collaterals to begin forming. Has research been done for example to see what happens when collaterals (undeveloped) sense the presence of Troponin I ?

[kenkeith]

QUOTE: "My real struggle with this idea is that blood pressure is high in many patients who develop CAD and it has been high for many years. So if blood pressure was an issue, one would expect to see everyone develop collaterals (in my opinion anyway). Flow velocity is really going to achieve nothing because it's the pressure which matters".

>>>>I don't have the knowledge of molecular science related to the anatomy of arteries, nor the a complete understanding of the physics  related to hemodynamics as that also involves neurohormones in the blood that is a chemical mediator, etc., etc.  

But one cannot dismiss velocity when referring to hemodynamics. For reference the study of the causes of motion is called "dynamics" and that would include  "dynamical" variables: momentum, force, potential energy, pressure and power. Each of these quantities will directly or indirectly involve the mass of the object.  Mass is defined dynamically in terms of force and acceleration (velocity).

Start with anastomosis: When blood vessels connect to form a region of diffuse vascular supply it is called an anastomosis (pl. anastomoses). Anastomoses provide critical alternative routes for blood to flow in case of blockages.  

Then understandingly, force (pressure) is required to change momentum; alternatively, a change of momentum ("impulse") causes a force to be felt.  Since momentum has dimensions of mass times velocity, force has dimensions of mass times acceleration.  But  not all of that energy goes into moving the blood. Some of it is stored as potential energy in the increased blood pressure, some is stored as elastic energy in the walls of the vessel (inner lining of vessel),  and some is lost to dissipation. Regarding the age that would more accurately refer anatomically and not chronologically, and age can break down the inner lining and a loss of elasticity.  This would inhibit vessel remodeling.

As you know hemodynamics also involves macroscopic turbulence (You may know about turbulance of the major vessels and its significance) for anastomosis . But the relevant turbulance are eddies (smaller turbulance)  This is due to the assumption that viscous dissipation is proportional to the velocity gradient.  I don't believe one can dismiss velocity any more than any other factor for hemodynamics.

[ed34]

After doing some more research in EECP, I think I am getting a bit closer to understanding why collaterals form. EECP simply opens existing arteries and it isn't the pressure/flow or mass that creates collateral growth, I read this....

"There is preliminary data suggesting that EECP can help induce the formation of collateral vessels in the coronary artery tree, by stimulating the release of nitric oxide and other growth factors within the coronary arteries. "

So, it looks as though certain chemicals are required which excite the collaterals into developing which makes much more sense to me.

[kenkeith]

I agree with what you have stated except your conclusion is partially incorrect.  To add what has been said, collateral arteriolgenesis starts with endothelium cells (inner most cells that line the vessel),  but it is the physical forces that is the primary stimuli.  It is FLOW that increases size, and PRESSURE determines wall thickness of the vessel and are the mechanisms of transduction of the mechanical stimulus into collateral vessel growth  response (don't confuse angiogenesis growth factors with arteriogenesis, arteriogenesis has another dimension).  This in part is the basis of my theory that a stent implant inhibits collateral growth because there is damage to the endothelium cells and smooth muscle mitosis is affected as well.  And when the stent dilates the vessel that will also affect the pressure and velocity of blood flow. And studies have identified a host molecules whose endothelium production is mediated by shear stress (velocity).  That may be what you are referring to (NO, growth factors, etc), but velocity is the stimulus and the variable factor.  EECP increases pressure, pressure increase velocity, and velocity increase shear stress.

It is known blood flow velocity is inversely related to the cube of the collateral  vessel radius...so increased blood flow (velocity) directly results in an increase shear stress.  Since growth increases collateral vessel diameter, shear stress falls quickly.  This maybe the reason ateriogenesis stops prematurely and restores only 35-40% of the maximal condition of the replaced artery.  Also, large vessels with low blood flow tend to close or reduce their lumen (vessel channel), but small vessels with chronically (possibly years) increased flow tend
to get wider.