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41yo Male 15 stents RCA 100% for the 3rd time
From age 34 to 41 I have received 15 stents. My blockages happen rapidly and severe. My right coronary artery has been completely stented from top to bottom twice and my right coronary artery is 100% blocked again for the 3rd time. My cardiologist informed me that we can not fix it anymore. I now feel constant chest pain, shortness or breath, no energy. I can't live this way. In Vegas I've encountered doctors who say they can help and then throw their hands up. I've gone out of state and have had little success. I have blockages in my circumflex and LAD. Is it true that there is nothing else to be done with my RCA. Do I have to live without my RCA from now on? Believe me, there is nothing I haven't tried. I even contacted Cleveland Clinic when the study was going on to inject the good cholesterol. I was not a candidate. The blockages that should take many years to cause me trouble, end up causing my serious trouble within months.
maybe im wrong in my dynamics for flow/pressure.
If the LAD blocks, it isn't like theres nowhere for the blood to go, it isn't a dead end
because further up there's the circumflex, further up still there's the Aorta. If I had a hose pipe which was blocked at the end, pressure would build up. If there were thousands of holes in the hose pipe, then I block one, the water can still easily escape. Pressure would increase because the hose has no way to regulate the pressure but the flow rate
would remain the same as long as the tap isn't adjusted.
The body however has complicated ways and efficient ways to adjust pressure and keeping flow rate the same or increasing it. If the heart pumps faster or harder then pressure and flow rate increases. If the LAD blocks then the body will quickly adjust for the difference in pressure which would be tiny anyway. With 66,000 miles of blood vessels in the body, one small section of LAD will be negligeable. The flow rate will not change either. The only section affected by pressure/flow is the section not receiving blood due to the blockage. So again, how can collaterals be affected by pressure/flow?
Pressure and flow is changed by the body virtually every minute of every day, so how can this promote collateral growth? I'm still at a loss of understanding here.
If the LAD blocks, it isn't like theres nowhere for the blood to go, it isn't a dead end
because further up there's the circumflex, further up still there's the Aorta. If I had a hose pipe which was blocked at the end, pressure would build up. If there were thousands of holes in the hose pipe, then I block one, the water can still easily escape. Pressure would increase because the hose has no way to regulate the pressure but the flow rate
would remain the same as long as the tap isn't adjusted.
The body however has complicated ways and efficient ways to adjust pressure and keeping flow rate the same or increasing it. If the heart pumps faster or harder then pressure and flow rate increases. If the LAD blocks then the body will quickly adjust for the difference in pressure which would be tiny anyway. With 66,000 miles of blood vessels in the body, one small section of LAD will be negligeable. The flow rate will not change either. The only section affected by pressure/flow is the section not receiving blood due to the blockage. So again, how can collaterals be affected by pressure/flow?
Pressure and flow is changed by the body virtually every minute of every day, so how can this promote collateral growth? I'm still at a loss of understanding here.
It seems if the heart is pumping against resistance causing high blood pressure, why isn't that the accepted resistance keeping blood pressure the same with the entire circulatory system as has been suggested in another post? How does the vessel know what direction to go?
QUOTE;'Even if the pressure is now lower in this vessel due to the blockage, the pressure in all the other vessels is unchanged and so cannot be a trigger. Pressure should be the same all over. over the body. Also, let's look at a simple scenario. Let's assume that the LAD is blocked which is common and so very little blood flows into this vessel. It has significantly reduced in size and there is a real danger the occlusion will grow to cause a 100% blockage, killing the person.
QUOTE;'Even if the pressure is now lower in this vessel due to the blockage, the pressure in all the other vessels is unchanged and so cannot be a trigger. Pressure should be the same all over. over the body. Also, let's look at a simple scenario. Let's assume that the LAD is blocked which is common and so very little blood flows into this vessel. It has significantly reduced in size and there is a real danger the occlusion will grow to cause a 100% blockage, killing the person.
Hi Kenkeith,
You are in a similar predicament that I was in for two years until recent stenting. Your LAD is 75% blocked at the top and mine was 100% blocked for about 30mm. My collaterals were formed also, but due to a 100% blockage, they didn't have the same beneficial effect for me, although, they were enough to keep tissue alive. It is obvious in both our cases that the collaterals must have been growing for some period of time because they are slow growing. It is also obvious that they must start at the right time or I would certainly be dead. Now my LAD is fully patent, I wonder if the collaterals will close down as they are not needed and blood flow through the LAD could interfere with the flow through the collaterals. I'm sure back pressure must cause a problem. Maybe this is why my symptoms didn't improve much after surgery and I'm gradually showing benefits day after day. It seems slow, but I do notice a difference. It is now 3 weeks after surgery and I can breath cold air without feeling angina. I can now walk for miles on a flat surface but walking up inclines still causes shortness of breath. I can now eat after 3 weeks without getting angina whereas before I had to eat often but small. Lots of changes are coming into play each day, but small changes. I expected instantly to become an athlete, but I realise this is not going to be the case.
You are in a similar predicament that I was in for two years until recent stenting. Your LAD is 75% blocked at the top and mine was 100% blocked for about 30mm. My collaterals were formed also, but due to a 100% blockage, they didn't have the same beneficial effect for me, although, they were enough to keep tissue alive. It is obvious in both our cases that the collaterals must have been growing for some period of time because they are slow growing. It is also obvious that they must start at the right time or I would certainly be dead. Now my LAD is fully patent, I wonder if the collaterals will close down as they are not needed and blood flow through the LAD could interfere with the flow through the collaterals. I'm sure back pressure must cause a problem. Maybe this is why my symptoms didn't improve much after surgery and I'm gradually showing benefits day after day. It seems slow, but I do notice a difference. It is now 3 weeks after surgery and I can breath cold air without feeling angina. I can now walk for miles on a flat surface but walking up inclines still causes shortness of breath. I can now eat after 3 weeks without getting angina whereas before I had to eat often but small. Lots of changes are coming into play each day, but small changes. I expected instantly to become an athlete, but I realise this is not going to be the case.
Hi Max
I think you misunderstand me. I'm not saying collaterals don't form, in fact I have them myself. What I am saying is I cannot see how a difference in blood flow or pressure can suddenly activate a switch to encourage growth of those vessels. If we have low blood pressure for a few weeks, then suddenly it spikes due to stress or whatever, then we would all be growing them, but not everyone does. In fact, many people end up with severe tissue damage on the left side of the heart because they don't have this luxury. There is nothing in a blood vessel which can promote growth when blood
pressure in another vessel develops a differential. Let's think of this logically step by step.
Let's say your LAD develops an occlusion at the top and this grows each year, slowly. Eventually it reaches 75% or more and you have a different pressure in the lower LAD compared to the upper, either side of the occlusion. How can vessels that are not connected to the LAD know there is a lack in pressure? A 'signal' would have to be sent to instruct the collaterals to promote growth. A drop in blood pressure in the lower LAD will not increase blood pressure in other vessels of the heart. The only vessel affected will be the LAD. Blood pressure everywhere else will be the same as the upper LAD.
You say there is no Troponin in Arteries but I know that and I didn't say there is.
Coronary vessels lay against heart tissue and it's the heart tissue that contains Troponin 1. As cells begin to suffer lower Oxygen levels, Troponin starts to release. As the Oxygen lowers more, more Troponin is released. I was just trying to say that this would be a brilliant signal when felt by the collaterals to know there is a problem. I can't think of any other kind of signal which exists that will switch the growth on.
Some things observed are not so obvious. When fat was seen in coronary arteries for the first time in an autopsy, it was assumed, and still is by many, that this disease must therefore be caused by too much cholesterol. However, many studies are proving this is not the case. Cholesterol is simply one stage but not the major cause. To see collaterals forming in patients with a blocked LAD will cause the initial thought that the blockage must be causing it to happen directly, by a difference in pressure. When tissue is forming in a feotus, the tissue gives a demand for oxygen and capillaries/arterioles form to ensure all tissue is fed. There has to be a signal saying "hey im lacking oxygen here, grow this way". They don't simply grow for the sake of it because we only have a limited amount of blood and our heart only has a certain capacity. Tissue would be absolutely smothered with capillaries if this were the case and this would require more arteries and more veins to handle the extra demand. The research you quote is very basic and doesn't explain how the trigger for growth is activated. It doesn't state the chemical processes involved in the collaterals. With so much data missing, I have to remain sceptical.
I think you misunderstand me. I'm not saying collaterals don't form, in fact I have them myself. What I am saying is I cannot see how a difference in blood flow or pressure can suddenly activate a switch to encourage growth of those vessels. If we have low blood pressure for a few weeks, then suddenly it spikes due to stress or whatever, then we would all be growing them, but not everyone does. In fact, many people end up with severe tissue damage on the left side of the heart because they don't have this luxury. There is nothing in a blood vessel which can promote growth when blood
pressure in another vessel develops a differential. Let's think of this logically step by step.
Let's say your LAD develops an occlusion at the top and this grows each year, slowly. Eventually it reaches 75% or more and you have a different pressure in the lower LAD compared to the upper, either side of the occlusion. How can vessels that are not connected to the LAD know there is a lack in pressure? A 'signal' would have to be sent to instruct the collaterals to promote growth. A drop in blood pressure in the lower LAD will not increase blood pressure in other vessels of the heart. The only vessel affected will be the LAD. Blood pressure everywhere else will be the same as the upper LAD.
You say there is no Troponin in Arteries but I know that and I didn't say there is.
Coronary vessels lay against heart tissue and it's the heart tissue that contains Troponin 1. As cells begin to suffer lower Oxygen levels, Troponin starts to release. As the Oxygen lowers more, more Troponin is released. I was just trying to say that this would be a brilliant signal when felt by the collaterals to know there is a problem. I can't think of any other kind of signal which exists that will switch the growth on.
Some things observed are not so obvious. When fat was seen in coronary arteries for the first time in an autopsy, it was assumed, and still is by many, that this disease must therefore be caused by too much cholesterol. However, many studies are proving this is not the case. Cholesterol is simply one stage but not the major cause. To see collaterals forming in patients with a blocked LAD will cause the initial thought that the blockage must be causing it to happen directly, by a difference in pressure. When tissue is forming in a feotus, the tissue gives a demand for oxygen and capillaries/arterioles form to ensure all tissue is fed. There has to be a signal saying "hey im lacking oxygen here, grow this way". They don't simply grow for the sake of it because we only have a limited amount of blood and our heart only has a certain capacity. Tissue would be absolutely smothered with capillaries if this were the case and this would require more arteries and more veins to handle the extra demand. The research you quote is very basic and doesn't explain how the trigger for growth is activated. It doesn't state the chemical processes involved in the collaterals. With so much data missing, I have to remain sceptical.
For insight on collateral vessel development involves some preliminay setting so we all can be on the same page. The term "stenosis" can refer to an abnormal narrowing of an artery, usually of a discrete segment. Stenosis can also refer to a reduced cross-sectional area of a heart valve when it opens. In the case of an artery, stenosis most commonly most commonly occurs in large distributing arteries such as coronary, renal, cerebral, iliac and femoral arteries. The narrowing commonly results from a chronic disease process - atherosclerosis. Sometimes a vessel can become acutely stenotic due to focal vasospasm. But in general, stenosis results from chronic vascular disease.
Stenosis increases the vascular resistance as described by Poiseuille's equation, which says that resistance is inversely related to the radius to the fourth power. Therefore, if the radius (or diameter) of a vascular segment is reduced by one-half, the resistance within that narrowed segment increases by 16-fold. If this vascular segment were being perfused in isolation, the flow would be decreased 16-fold if perfusion pressure is held constant. However, in vivo this degree of stenosis would have relatively little effect on flow because the vessel is coupled in-series with other resistance vessels (CLICK HERE for more information). If we consider the renal artery and kidney circulation, the renal artery contributes to only a small fraction (<1%) of the total renal vascular resistance. Therefore, the renal artery needs to be narrowed considerably before overall renal vascular resistance is increased enough to significantly decrease renal blood flow. This is also true for other organ circulations such as the heart, limbs and brain.
The term "critical stenosis" refers to a critical narrowing of an artery (stenosis) that results in a significant reduction in maximal flow capacity in a distal vascular bed. A critical stenosis may or may not reduce resting flow depending on the organ's capacity to autoregulate its blood flow and the development of collateral blood flow, both of which serve to reduce the overall resistance in the smaller resistance vessels. Clinically, a critical stenosis typically is thought of in terms of a 60-75% reduction in the diameter of the large distributing artery. This explains why interventional measures such as balloon angioplasty, stent placement, or arterial bypass surgery are not usually conducted in patients until there is at least a 75% reduction in vessel diameter
The term "stenosis" can refer to an abnormal narrowing of an artery, usually of a discrete segment. Stenosis can also refer to a reduced cross-sectional area of a heart valve when it opens. In the case of an artery, stenosis most commonly most commonly occurs in large distributing arteries such as coronary, renal, cerebral, iliac and femoral arteries. The narrowing commonly results from a chronic disease process - atherosclerosis. Sometimes a vessel can become acutely stenotic due to focal vasospasm. But in general, stenosis results from chronic vascular disease.
Stenosis increases the vascular resistance as described by Poiseuille's equation, which says that resistance is inversely related to the radius to the fourth power. Therefore, if the radius (or diameter) of a vascular segment is reduced by one-half, the resistance within that narrowed segment increases by 16-fold. If this vascular segment were being perfused in isolation, the flow would be decreased 16-fold if perfusion pressure is held constant. However, in vivo this degree of stenosis would have relatively little effect on flow because the vessel is coupled in-series with other resistance vessels (CLICK HERE for more information). If we consider the renal artery and kidney circulation, the renal artery contributes to only a small fraction (<1%) of the total renal vascular resistance. Therefore, the renal artery needs to be narrowed considerably before overall renal vascular resistance is increased enough to significantly decrease renal blood flow. This is also true for other organ circulations such as the heart, limbs and brain.
The term "critical stenosis" refers to a critical narrowing of an artery (stenosis) that results in a significant reduction in maximal flow capacity in a distal vascular bed. A critical stenosis may or may not reduce resting flow depending on the organ's capacity to autoregulate its blood flow and the development of collateral blood flow, both of which serve to reduce the overall resistance in the smaller resistance vessels. Clinically, a critical stenosis typically is thought of in terms of a 60-75% reduction in the diameter of the large distributing artery. This explains why interventional measures such as balloon angioplasty, stent placement, or arterial bypass surgery are not usually conducted in patients until there is at least a 75% reduction in vessel diameter.
I have a totally blocked LAD with good collateral flow, so the subject has my interest for the past 5 years, and I apologize to those with less interest.
Stenosis increases the vascular resistance as described by Poiseuille's equation, which says that resistance is inversely related to the radius to the fourth power. Therefore, if the radius (or diameter) of a vascular segment is reduced by one-half, the resistance within that narrowed segment increases by 16-fold. If this vascular segment were being perfused in isolation, the flow would be decreased 16-fold if perfusion pressure is held constant. However, in vivo this degree of stenosis would have relatively little effect on flow because the vessel is coupled in-series with other resistance vessels (CLICK HERE for more information). If we consider the renal artery and kidney circulation, the renal artery contributes to only a small fraction (<1%) of the total renal vascular resistance. Therefore, the renal artery needs to be narrowed considerably before overall renal vascular resistance is increased enough to significantly decrease renal blood flow. This is also true for other organ circulations such as the heart, limbs and brain.
The term "critical stenosis" refers to a critical narrowing of an artery (stenosis) that results in a significant reduction in maximal flow capacity in a distal vascular bed. A critical stenosis may or may not reduce resting flow depending on the organ's capacity to autoregulate its blood flow and the development of collateral blood flow, both of which serve to reduce the overall resistance in the smaller resistance vessels. Clinically, a critical stenosis typically is thought of in terms of a 60-75% reduction in the diameter of the large distributing artery. This explains why interventional measures such as balloon angioplasty, stent placement, or arterial bypass surgery are not usually conducted in patients until there is at least a 75% reduction in vessel diameter
The term "stenosis" can refer to an abnormal narrowing of an artery, usually of a discrete segment. Stenosis can also refer to a reduced cross-sectional area of a heart valve when it opens. In the case of an artery, stenosis most commonly most commonly occurs in large distributing arteries such as coronary, renal, cerebral, iliac and femoral arteries. The narrowing commonly results from a chronic disease process - atherosclerosis. Sometimes a vessel can become acutely stenotic due to focal vasospasm. But in general, stenosis results from chronic vascular disease.
Stenosis increases the vascular resistance as described by Poiseuille's equation, which says that resistance is inversely related to the radius to the fourth power. Therefore, if the radius (or diameter) of a vascular segment is reduced by one-half, the resistance within that narrowed segment increases by 16-fold. If this vascular segment were being perfused in isolation, the flow would be decreased 16-fold if perfusion pressure is held constant. However, in vivo this degree of stenosis would have relatively little effect on flow because the vessel is coupled in-series with other resistance vessels (CLICK HERE for more information). If we consider the renal artery and kidney circulation, the renal artery contributes to only a small fraction (<1%) of the total renal vascular resistance. Therefore, the renal artery needs to be narrowed considerably before overall renal vascular resistance is increased enough to significantly decrease renal blood flow. This is also true for other organ circulations such as the heart, limbs and brain.
The term "critical stenosis" refers to a critical narrowing of an artery (stenosis) that results in a significant reduction in maximal flow capacity in a distal vascular bed. A critical stenosis may or may not reduce resting flow depending on the organ's capacity to autoregulate its blood flow and the development of collateral blood flow, both of which serve to reduce the overall resistance in the smaller resistance vessels. Clinically, a critical stenosis typically is thought of in terms of a 60-75% reduction in the diameter of the large distributing artery. This explains why interventional measures such as balloon angioplasty, stent placement, or arterial bypass surgery are not usually conducted in patients until there is at least a 75% reduction in vessel diameter.
I have a totally blocked LAD with good collateral flow, so the subject has my interest for the past 5 years, and I apologize to those with less interest.
Apparently you are rejecting the study by Yoshiyuki Takami, MD*, Hiroshi Masumoto, MD., Division of Cardiovascular Surgery, Kasugai Municipal Hospital, Kasugai, Japan who title their study to be "Angiographic Fate of Collateral Vessels After Surgical Revascularization of the Totally Occluded Left Anterior Descending Artery." It is worth repeating:
"Coronary collateral circulation may play an important role in maintaining viable myocardium after abrupt coronary occlusion (that is a blocked vessel) [1]. The potential of individuals to develop coronary collateral circulation is of major importance in myocardial vulnerability [2]. Collaterals develop as a result of a pressure gradient across the occlusion that recruits preformed interarterial connections [3]. Percutaneous coronary intervention (PCI) serves as a useful model investigating development and REGRESSION of collateral circulation [4, 5]. Collateral vessels can REGRESS with sufficient coronary perfusion during a relatively short period of time after successful PCI."
Troponin is a marker in the blood for heart muscle damage up to 14 days, nothing thereafter. Collateral vessels are a slow growing phenomon and does not produce troponin as there is no tissue damage.
Different resistance and pressure are present throughout the circulatory. Without the differences, blood flow would not happen, and there would be blood clots. A good example is the returning blood flow from lower extremities.
Thank you for your input, but the study in Japan makes more sense, however, I will pose the question to the experts. I don't want my father to lose collateral flow if a stent is implanted as the Japan study indicates.
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