To do such a test would could be devastating or lethal. If you block your arteries, you feel a lot of chest pain, as you do with ballooning during an angioplasty. This is because your heart muscle is being deprived of oxygen. To close your arteries for a few minutes may or may not be adequate time for collaterals to form. In some people they never do, and in some people collaterals form too late, when the MI has destroyed much valuable tissue. In most cases, collateral development is gradual, when the pressure gradients in the coronary arteries begin to alter to a certain level. This could even occur when blockages are 70% or more, but less than 100%. You could already have collaterals, given that you only feel symptoms at great exertion. As your blockage increases, maybe you will form more. As each person is different, you cannot predict such things, and there is no accurate simulation apart from actually causing the event in real time. But at what cost.
Please let me know your LVEF.I too was adviced bypass as angio showed all vessles blockages at beginning and at ends about from 60 % to 90%. I do not have chaste pain even on exersion. On second openion I managed with medicine only. Now it is almost ten months. I too have developed colaterals. I fail how colaterals are not accounted during angio.I personally feel this is commercial exploitation by noble profession. Due to risk involved as far as ossible avoid angiography, angioplasty and bypass surgery. My LVEF is 50%.
"I fail how colaterals are not accounted during angio"
Because the majority of them are just too small to see
Thanks for your comments.
C1 - "To close your arteries for a few minutes may or may not be adequate time for collaterals to form." Some misunderstanding... I am not seekeing to increase collaterals with this procedure, but merely to test the adequacy of existing ones to cope with an increasing or total blockage.
Thanks for the advice.
Dont have a LVEF, but the following notes are taken from the letter of my cardiologist commenting on my recent angiogram:
1. Ischaemic heart disease
2. Two vessel coronary artery disease (significant LAD diagonal disease with occluded RCA)
3. Good left ventricular function.
Non LV was performed as he has quite tortous coronary arteries... to be assessed pre-op with echocardiography"
I am 68 and very fit and active for my age.
If you fully block an artery to see how existing collaterals are coping, then you will end up with damaged tissue. The collaterals will have formed to cope with the amount of blockage already existing, not more, because it's all pressure related.
To see how effective collateral feeds are, there is a nuclear perfusion scan. This shows how well oxygen is distributed to all areas of the heart muscle.
Looking at your report, your RCA is blocked, but it must have formed good natural bypasses or you will be very ill. My RCA is blocked solid halfway down but the collaterals which have formed are large enough to see on an angiogram, and there are lots of them. My lower RCA is fully patent. Nobody can predict how much collateral growth you will develop, but exercise will certainly encourage it.
Posted by 05/08/2011
I am a 50 year old female that had restenosis following a balloon angioplasty and would appreciate your perspective on my case to determine if my treatment will limit restenosis and any options I have if further restenosis occurs.
When I found I had high thyroid problem last 2 years ago except Niacin. Before 5 days I have sever heart attack . My LDA is 100% blockage was found in my LAD. All other arteries were open.
Angioplasty was done. Please any problem in my future life is it dangerous or not ?
And what precaution is needed please reply me .
My informed me
My E-amil add.(1) Persis_jilla2000***@****- (2) ***@****
Q: "The collaterals will have formed to cope with the amount of blockage already existing, not more, because it's all pressure related."
....Collateral vessel developmenI IS pressure related and additiional pressure will not will Not have an adverse effect..how and from what else would the system respond as an occlusion progresses?. In fact additional pressure will have a beneficial effect, and that is the fact for vessel growth and expansion.
As an example EECP to develop collaterals is a process that expands diameter of and the opening of new viable channels and counter pressure is the driving force.
Also, collaterals is compensatory and a natural process when occlusions reduced the diameter of a vessel and as the increasing gradient pressure increases collateral vessels start and as the gradient pressure chronically progresses so does the collaterals bypass over a slow period of time. The result is one often does not know there is progressive occlusion! There is some evidence that an acute occlusion i.e. heart attack can have heart cell damaged reduced with collateral vessels that have started or already existing but not viable at the time.
I have a completely blocked LAD diagnosed about 8 years ago with tests for another condtion.. Others who have posted have a totally blocked LAD as well and do fine with the system's compensatory mechanisms and therapy. If the balloon angio does not sustain an opening enough to provide sufficient blood flow to heart cells then there can be a stent implant. If there is restenosis of a stent implant, there can be another stent implant, etc.
You may have better results if you start your own post (thread) or go to the expert forum (page down and to your right you will see the expert forums).
However, thank you for your question, and I can identify with your anxiety when I too first heard I had a completely blocked LAD. If you did or do not have other vessels feeding into the area normally supplied blood by your LAD you would not be around to post a question..so that indicates your system is working for you and not against you and you can be successfully treated and have many good years to go. Don't worry, you will be OK.
Have you had an echocardiogram? Is there any hypokinesis (heart wall movement disorder)? How low is your EF (amount of blood pumped with each heartbeat)
Is your heart enlarged? Heart valves normal? If you have your echo report and list an answer we can provide some information that can help you understand. Take care,
"....Collateral vessel developmenI IS pressure related and additiional pressure will not will Not have an adverse effect..how and from what else would the system respond as an occlusion progresses?. In fact additional pressure will have a beneficial effect, and that is the fact for vessel growth and expansion. "
Did you read the original question? Are you saying that closing each vessel in turn to test for collaterals can only be beneficial?
"Mechanical stimulation of angiogenesis is not well characterized. There is a significant amount of controversy with regard to shear stress acting on capillaries to cause angiogenesis, although current knowledge suggests that increased muscle contractions may increase angiogenesis. This may be due to an increase in the production of nitric oxide during exercise. Nitric oxide results in vasodilation of blood vessels."
The above is a quote from Wikipedia. In other words: don't know yet whether pressure differentials actually cause angiogenesis.
In addition what has been said, shear stress inducing endothelium stimulation for angiogensis is not the same as collateral vessel growth. A differential for angiogenesis is that it has its own blood source, and if out of control can be carcigenic. It is true, the theory suggests that angiogenesis is initiated by other factors in addition to shear stress.
Developed collateral vessels are a pathway that bridges the occlusion or collateral pathways to other vessels that feed the area deficit of oxygenated blood. The driving force to open new vessel growth is the high pressure gradient of the occlusion, comparable resistence of contributory vessels to be overcome by the higher resistence , blood flow velocity, etc.
Q:. Did you read the original question? Are you saying that closing each vessel in turn to test for collaterals can only be beneficial?
.....There is myocardial contrast echcardiograpy and Rentrop scoring for an estimate. Briefly, there is a pressure gradient with an agent for evaluation of the perfusion to areas of blood deficit areas, that information assessed with heart wall movement impairment provides information relative to collateral perfusion and can be categorized with a value...doesn't require each vessel closing as you suggested....
"The development of collateral vessels is triggered by the pressure gradient between the coronary beds of the arteries, caused by obstruction and myocardial ischaemia.3 It was found that patients with angiographically documented coronary artery disease, who develop collateral vessels, had a higher prevalence of myocardial ischaemia than those without collateral vessels, indicating that the presence of myocardial ischaemia is associated with the growth of collateral vessels".etc. etc. Additional info distinguish between angiogenises (network smaller vessels, capillaries, etc.) and arteriogenesis (larger vessels that increase in diameter for collaterals)...however, there may be some overlapping in development.
But the web site you copied and pasted that text from is regarding diabetic patients, which are known to have endothelium and monocyte dysfunction.
So what is your point? To quote what you allude from my prior post: "The development of collateral vessels is triggered by the pressure gradient between the coronary beds of the arteries, caused by obstruction and myocardial ischaemia.3 It was found that patients with angiographically documented coronary artery disease, who develop collateral vessels, had a higher prevalence of myocardial ischaemia than those without collateral vessels, indicating that the presence of myocardial ischaemia is associated with the growth of collateral vessels". Yes, my quotation marks provided for credibility and for your benefit there is authority as a basis for my comments (something you always cannot do when asked) :) I presented the information to provide a wider perspective to negate your misunderstanding especially for you so you know that collateral vessels and angiogenesis is different from arteriogensis for collateral vessel development and it is pressure related, but there is some overlap...go back to your thread "collaterals" and review..I thought you understood! Also, on this thread you incorrectly stated collateral vessels cannot be evaluated and measured....that is not true either.
I miss you point, we know there is endothelium cells dysfuntion for those with diabetes, and there may be some inhibition to open collateral vessels for those individuals... but "monocytes" relate to white blood cells and the immune system ?...and I am at a loss to know how that pertains to pressure related collateral vessel development. Do you mean myocytes?...that relates to heart cells!
"Do you mean myocytes?...that relates to heart cells!"
No, I mean MoNocytes. Yes they are related to the immune system, but the rest of that document explains the problem in diabetic patients.
What does this thread have to do with diabetes. Collateral vessels are developed from pressure, blood flow velocity and resistence to blood flow. If you have rational answer to my previous post then please answer. I don't have time for your nonsense and rambling to different subjects. An intelligent discussion is welcome, nonsense wastes my time and your time that you appear to have in abundance.:) Take care,
Who is an intellect? My knowledge comes through osmosis going on 8 years of compiling information through research almost 24/7 :) I occasionally save time by cutting and pasting so I can deal with more posts. Quotation marks around the posted comment indicates it is sourced...and it supports my understanding from other matrerials I have read. So now you are attacking me because I didn't provide the source of the quoted material? And are you saying I don't have prior knowledge of the subject matter in my thousands responses.... Search collateral vessels on this site's archives and you will not see any lack of knowldege. Unfortunately, YOU should quote the material on the internet you read because what you put in your own words is very often incorrect indicating you don't understand what you are talking about and it shows.
So you would rather change the subject and call me someone who steals materiaL..IS THAT WHAT YOU ARE SAYING! Is that what you are saying now to justify your ignorance of the subject being discussed :) You're a coward to unjustly attack me, and I believe you are covering your feelings of inadequacy by not answering in a respectful manner and you take a cowards way out....Someone like you hides behind a computer and feels safe to insult...you have done that many times and in my experience you may have the record...I've never seen such an ill mannered and disrespectful person, but then you are a coward.
The post providing Monocytes is a non sequitur as a dabetic patient and their medical condtion inhibits collateral vessel developmemt not enhance!
I've already been over that.
For the benefit of the archieves .
I think that when one is using quotes from the Internet, we should all give the source in order to be able to read the information. Not trying to cause any hard feelings, but it would be great to read the quote in it's intended context to help better understand the point being made.
Just my two cents:)
Hi...my father has the same problem he is 65 year old...doctor said after angiography that his RCA is totaly blocked and bridges collaterals. Doctor said that this not a case of operation..he will have to be on medicines..his blood pressure is fluctuating I am very worried about him. Can he survive on medicine...pls suggest bypass surgery is possible in this case or not ?