Yes, there is a difference. Angiogenesis is the development of small vessels mostly small arterioles, capillaries and venules. It has a connection to generate small vessels from epithelium cells (lines the vessel), blood flow, etc. Angiogenesis happens as an example from a wound. Out of control, it can be cancerous tumor.
But when an exsisting artery is occluded the development of blood flow from existing collaterals may be activated. There is evidence, mechanisms leading to the development of collaterals capable of conducting blood efficieniently differs from those usually involved in angiogenesis. I have read arteriogenesis is "state of art" term that includes both angiogeneis and collateral growth recognizing the difference between the two processes.
If you have other questions...what has been stated is not very much detail, and I hope it is not confusing!
Is there any physiological basis that can be relied on to develop collateral vessel bypass? It seems some people or at least most people that have heart issues have stents or by-pass. The short answer may be people that have a natural bypass don't participate on health forums as they don't have a heart a problem. Are there autopsy reports or something? I read autopsy reports state military personnel autopsies showed significant blockage in many young people! No mention of any natural bypass.
The development of collaterals doesn't occur in everyone. During one of my many stays in hospital, I was talking to a man who had a 95% occlusion in his LAD but no collaterals were forming. His Cariologist told him that the collaterals don't seem to always form in people and this is why it is still believed by some experts to have a genetic element. Collaterals are good if they form in that they can keep heart tissue alive. However, in many people they only provide enough Oxygen backup to be at rest or very slight exertion. So many people have the luxury of collaterals keeping them alive until a better solution can be decided.
I am still unsure what effect on collaterals a bypass or stent has. How does the increase in pressure in the LAD affect these newly formed vessels and the vessel providing them. Surely back pressure will be created. Collaterals in the bottom of my LAD were pushing blood UP the vessel and keeping me alive. However, now my LAD is fully patent, and high pressure is pushing DOWN the LAD, how is this affecting other vessels in my heart through the collaterals. I have an outpatients appointment with my cardiologist soon, I will ask him such questions and let everyone know. I also have a working Lima grafted to the LAD and this must also play around with pressure/flow as blood also streams in through the left main stem.
Max, if I understand your question, you are asking if there are any attributes or identifiable characteristics that are reliable to predict if one will have collaterals for their blocked vessels.
No, there is no way to know prior. If your father has CAD, and collateral blood flow and you are concerned there may a genetic component for CAD, you need to take precautionary measures to prevent CAD such as control your cholesterol, blood pressure, proper diet, exercise, etc.
However, my notes on the subject from a few years ago indicate there is evidence why some people with diabetes do not have adequate blood supplying collaterals. There is a biological component associated with diabetes and the cardiovascular system.... and my notes indicate there is evidence supported by lab experiments and general knowledge of fluid dynamics (or hemodynamics) that more than one occlusion in the same vessel prevents an adequate flow of blood from collaterals....may require interventional therapy.
This a Cleveland Clinic doctor's response: Stents, if patent, are likely to decrease collateral flow to the arteries in which they are in, thye will not affect distant arteries. This is not a problme because forward flow (throught the stent) and collateral flow are both driven by a pressure difference, so as long as there is forward flow, the collateral flow is no longer necessary. Again, stents do not inhibit collateral flow to the unstented arteries. EECP is done to alleviate chest pain from disease in arteries that are still diseased (unstented), therefore it is not contraindicated. Finally, stents have struts in them so they do not cover the openings of the diagonals, thereby, permitting continuous flow to those segements.
>>>I agree with the doctor's post [except some spellings] :) I will go into detail from my years of researched notes and prior forum posts to answer your questions. This is Max's thread, and I will wait to see if he has any questions first!
Thank you for that information kenkeith, much appreciated. Do you know what happens with regards to my Lima pumping blood into the LAD along with the flow through the main left stem? I assume that there shouldn't be a problem because the LAD will only accept the flow/pressure it requires?
Thanks again :)
No one has ever stated collaterals develop with everyone from what I have read on this forum. What has been said is that everyone has collateral vessels and the focus of this discussion it seems to me should be what underpinnings open and remodel collateral vessels for people with CAD or development after an acute myocardium infarction. I spent some time searching the internet regarding collaterals and found nothing that reports anything other than everyone has collateral vessels.
Ed, how do we know what you describe actually occurred? Could be a mistake!. Maybe if you start a thread someone can help you that had a similar experience. I would like to know more about what causes collaterals to develop and if there is anything I can do now because my father has CAD and I understand there is a genetic factor for CAD that can occur to a person at a young age. I wouldn't like to have my chest cracked open. Thank you in advance. Maybe I should have titled my post "collateral bypass" and not "angiogenesis bypass"; that seems to be irrelavant.
well max these things are determined and witnessed by a history of angiograms.
In my case, in Feb 07 there was a 90% occlusion in the top of my LAD and small vessels were seen on the Angiogram grouping around the base of the LAD. I had very bad angina at that time, but stenting a blockage in the mid circumflex cured that. No
collaterals were seen trying to feed the circumflex.
In aug 07 I suddenly felt very strong bouts of angina and was admitted back into hospital because they included chest pains. A new angiogram showed that the LAD was 100% blocked at the top and the group of vessels gathered at the bottom of the LAD had now anatomised to it, giving it a small feed. The feed was very small indeed and just enough to keep the heart tissue alive when at rest. A bypass was then performed and three months this failed as the 2 veins closed up. Strangely enough the collaterals hadn't receeded, which is a good thing because otherwise I would likely have died. They were still there as a backup and feeding into the LAD. I don't know how long they stay in place but they are still there two years later. Now my LAD is fully opened, it will be interesting to see what happens to those collaterals in the future.
Hi Max, you are doing the right thing by learning as much as you can about heart disorders...I have found it very helpful to decrease anxiety, apprehension, and it does motivate to exercise, maintain a healthful diet, etc.
I will depend on my notes going back several years and it hasn't been updated with current information, if any, on the subject (collateral vessels), as I have felt the issues are settled. It seems stress induced vessel remodeling (change in size, development) is altered by pathological conditions such as diabetes, hypertension and artherosclerosis (hardening of vessels).
Now, my take and certainly open for discussion as no one has all information, and starting with the facts that are not professionally disputed. It is recognized that gradient pressure is perfusion force "F" and resistance "R" times blood flow "B" are directly proportional to F. R is the resistence due to fluid shear stress (friction of blood flow against vessel walls) and B blood flow...both R and B are low when conduction through a healthy vessel is not impeded.
We analyze a segment from the opening "a" to "b" the end of the segment. When the vessel (segment a to b) becomes occluded, R increases and that is directly proportional to F causing an increase of perfusion force across the gradient....this the beginning of a single-vessel blockage. As the occlusion increases, the diameter of the vessel decreases and F increases until F overcomes the resistence of the smaller collateral vessels. As F increases B (blood flow) will increase and collateral vessels will provide sufficient blood supply, and probably no heart issue is every known.
Now consider a second occlusion begins downstream in segment a to b. This will change the fluid dynamics within the segment of the upstream collaterals that is proportional to the driving pressure (ie, the pressure gradient) between these 2 points a and b. After occlusion, a pressure gradient between the upstream and the downstream part of the segment results in increased blood flow in the collateral network. However, because this blood pressure gradient is limited by the resistance vessels lying downstream of the occlusion, and is further diminished as collateral flow increases, the remodeling of the collateral vessels is restrained. This would explain why only about 40% of the maximal physiological conductance is restored after arterial occlusion....May require intervention with two or occlusions even if there is some collateral flow.. It is my understanding collateral flow is not picked up with an angiogram until there is 99to 100% blockage.
**""An experiment developed by Eitenmüller and colleagues associated both femoral occlusion and femoral arteriovenous fistula, bypassing that downstream resistance arteries. The pressure gradient between the upstream and downstream segments of the occluded femoral was therefore quite significant, representing 60 to 70 mm Hg, driving a pronounced increase in collateral artery blood flow. The authors used this clever surgical model to demonstrate downstream resistance arteries to demonstrate that higher blood flow in collaterals results in more extensive remodeling such that maximal limb conductance reaches normal values or is even surpassed. This experimental process could be compared with events occurring during muscular exercise: there are several lines of evidences suggesting that the molecular mechanism of exercise-induced upregulation of vascular eNOS expression are closely related to the changes in fluid shear stress in the vasculature. Exercise increases heart rate, which in turn increases blood flow and vascular shear stress, leading to enhanced NO production". May help explain why exercise is helpful and when a cardiologist decides to stent or bypass procedure for multi-vessel occlusions and not to open an occluded vessel with good collateral blood flow.
Sorry for the long explanation....and that is the skinny on the subject. :)
Thanks for your time. To understand and referring to the model (segment 'a' to point 'b', and occlusion1 and occlusion2), if occlusion 2 (downstream lesion) is stented, that will increase collateral flow from occlusion1, and if occlusion1 is stented, that will regress collateral flow!! If that is true, my father's collaterals will be sufficient if there is no blockage down stream. Would that be correct? .
I am not associated with the medical profession however, I have read many, many papers and studies on the subject matter and, have had 4x CABG in July 2008. Once again in my lifetime I consider myself to be among the luckiest of lucky. My understanding is that everyone does not grow collateral arteries around their blockage. Furthermore, "Expert Reviews" suggests . . . "transferring the promising experimantal results into clinical practice has been more cumbersome than initially anticipated" Several of the papers I have read refeer[sp] to this process as fluid dynamics. Point A to point B. At point B a blockage has developed @ 100%. Fluid continues to flow in the direction of point B in which the artery begins to develop a collateral. To determine the size and magnitude of the collateral(s), testing must take place.
In my case, my EF remained within normal range. My first cardiac catherization revealed "a lot of collaterals" back in 1995. I clearly had CAD.
I am going to go back to the lab's who performed the testing and get copies of the test notes to check what exactly my EF was.
It is my understanding the vessels (can be microvessels as well) are in place and remodel (develop) based on hemo dynamics or fluid dynamics if you chose.