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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.
I still fail to see how it has anything to do with pressure. Pressure should be the same all 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. 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. There is no way a message can be sent from the LAD to other vessels to promote growth and in particular which direction to grow in. The only way I can see this working is if the 'tissue' affected by lower Oxygen tells the collaterols to grow in its general direction. The tissue under the arteriole or capillary must be giving out chemical stimulants to promote the growth and they will always grow over the deprived areas. I still believe troponin must be the key here because it is known to inhibit angiogenesis. When heart tissue is stressed, the troponin is released, hence higher elevations detected in blood samples, and the lack of troponin in the tissue will allow unhibited growth of the vessels again. I find the so called research of blood pressure/flow hard to swallow.
Ed, it appears you are referring to angiogenesis. Collaterals are independant vessels that provide a natural by-pass of blocked arteries. Angiogenesis is the process of providing a network of small vessels with more perfusion. If you want to learn
about the subject, then acquaint yourself with turbulence, blood flow velocity, those are a few of the factors involved affecting the epithelium and endothelium cells that trigger the phenomonon. I don't know if this is the correct procedure, but I make a request:
.
Is there a doctor that happens to visit this forum on weekends, and if so, is there an opinion regarding the total blockage of the LAD and a good collateral feed by-passing the blockage. My father has had 100% blockage of the LAD. The LAD is known as a "widow maker" so it is important to have a competent doctor with a good understanding what happens when the total blockage is somehow stented without rupturing the vessel wall.
My father's cardiologist states to open a totally blocked vessel "*****" the blood out of the collaterals as the blood flows through the opened blocked vessel. Another risk is that after years of developing collaterals there may not be viable vessels on the other side of the blockage! Thank you in advance, and if anybody has a source to rebut the source in the previous post.
about the subject, then acquaint yourself with turbulence, blood flow velocity, those are a few of the factors involved affecting the epithelium and endothelium cells that trigger the phenomonon. I don't know if this is the correct procedure, but I make a request:
.
Is there a doctor that happens to visit this forum on weekends, and if so, is there an opinion regarding the total blockage of the LAD and a good collateral feed by-passing the blockage. My father has had 100% blockage of the LAD. The LAD is known as a "widow maker" so it is important to have a competent doctor with a good understanding what happens when the total blockage is somehow stented without rupturing the vessel wall.
My father's cardiologist states to open a totally blocked vessel "*****" the blood out of the collaterals as the blood flows through the opened blocked vessel. Another risk is that after years of developing collaterals there may not be viable vessels on the other side of the blockage! Thank you in advance, and if anybody has a source to rebut the source in the previous post.
QUOTE:" I've been following the research for quite some time. It actually doesn't promote
collaterols in everyone, but it is hoped it will highlight the triggering mechanism. However, it does far more than this, it realigns the cells along the artery lining so they
lay in the direction of the blood, making it smoother".
__________________________________________
Sorrry I didn't supply my source** sooner, but it has been asked for...it is lengthy though! There is much more but my point it made. >>>The trigerring mechansm is resistance. As a vessel becomes occluded there develops a gradient pressure. The blocked side of the occlusion has high pressure and the other side of the occlusion has low pressure. The progression of the lesion continues to create a higher divergence and the higher pressured collaterals gravitates to the lower pressure side until there is a natural bypass. This is the fluid dynamics.
Not on the table: Collateral vessels are not the process of angiogenesis (as I read and may be confusing). There appears to be a reference to angiogenesis (shear stress, blood velocity, turbulance causing clots, biological interaction coding whatever, etc.) and it is associated in part with is a physiological process involving the growth of new blood vessels from pre-existing vessels. Though there has been some debate over this, vasculogenesis is the term used for SPONTANEOUS blood-vessel formation, and intussusception is the term for new blood vessel formation by splitting off existing ones.
Angiogenesis is a normal and vital process in growth and development, as well as in wound healing. However, it is also a fundamental step in the transition of tumors from a dormant state to a malignant one. The identification of an angiogenic diffusible factor derived from tumors was made initially by.....as described in a prior thread...there is a thin line for a cancer tumor development and angiogenesis as priviously stated in another post!
For some insight, the endothelial cells proliferate into the surrounding matrix and form solid sprouts connecting neighboring vessels. As sprouts extend toward the source of the angiogenic stimulus, endothelial cells migrate in tandem, using adhesion molecules, the equivalent of cellular grappling hooks, called integrins. These sprouts then form loops to become a full-fledged vessel lumen as cells migrate to the site of angiogenesis. Sprouting occurs at a rate of several millimeters per day, and enables new vessels to grow across gaps in the vasculature. It is markedly different from splitting angiogenesis, however, because it forms entirely new vessels as opposed to splitting existing vessels.[2]
**Source: Science Direct...there is no connection with cancer!
Collaterals are a common clinical occurrence after branch vascular OCCLUSIONS in humans and laboratory animals, yet the etiology and functional significance of these vessels is uncertain. A hypothesis is presented which attempts to explain the difficult problem of arterial collateral circulation. This theory is consistent with microcirculatory hemodynamic research which demonstrates that microcirculatory flow determinants are primarily guided by RESISTANCE..
_______________________________________________
**Original Articles: Cardiovascular
Angiographic Fate of Collateral Vessels After Surgical Revascularization of the Totally Occluded Left Anterior Descending Artery
Yoshiyuki Takami, MD*, Hiroshi Masumoto, MD
Division of Cardiovascular Surgery, Kasugai Municipal Hospital, Kasugai, Japan
Accepted for publication August 16, 2009
"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." This is not a new subject for me!...but it can be confusing if angiogenesis is not differentiated from collaterals.:)
Troubleheart: Collaterals are developed from EECP according to my cardiologist, but I don't have the time and I am somewhat asymptomatic so I don't wish to commit at the present time.
collaterols in everyone, but it is hoped it will highlight the triggering mechanism. However, it does far more than this, it realigns the cells along the artery lining so they
lay in the direction of the blood, making it smoother".
__________________________________________
Sorrry I didn't supply my source** sooner, but it has been asked for...it is lengthy though! There is much more but my point it made. >>>The trigerring mechansm is resistance. As a vessel becomes occluded there develops a gradient pressure. The blocked side of the occlusion has high pressure and the other side of the occlusion has low pressure. The progression of the lesion continues to create a higher divergence and the higher pressured collaterals gravitates to the lower pressure side until there is a natural bypass. This is the fluid dynamics.
Not on the table: Collateral vessels are not the process of angiogenesis (as I read and may be confusing). There appears to be a reference to angiogenesis (shear stress, blood velocity, turbulance causing clots, biological interaction coding whatever, etc.) and it is associated in part with is a physiological process involving the growth of new blood vessels from pre-existing vessels. Though there has been some debate over this, vasculogenesis is the term used for SPONTANEOUS blood-vessel formation, and intussusception is the term for new blood vessel formation by splitting off existing ones.
Angiogenesis is a normal and vital process in growth and development, as well as in wound healing. However, it is also a fundamental step in the transition of tumors from a dormant state to a malignant one. The identification of an angiogenic diffusible factor derived from tumors was made initially by.....as described in a prior thread...there is a thin line for a cancer tumor development and angiogenesis as priviously stated in another post!
For some insight, the endothelial cells proliferate into the surrounding matrix and form solid sprouts connecting neighboring vessels. As sprouts extend toward the source of the angiogenic stimulus, endothelial cells migrate in tandem, using adhesion molecules, the equivalent of cellular grappling hooks, called integrins. These sprouts then form loops to become a full-fledged vessel lumen as cells migrate to the site of angiogenesis. Sprouting occurs at a rate of several millimeters per day, and enables new vessels to grow across gaps in the vasculature. It is markedly different from splitting angiogenesis, however, because it forms entirely new vessels as opposed to splitting existing vessels.[2]
**Source: Science Direct...there is no connection with cancer!
Collaterals are a common clinical occurrence after branch vascular OCCLUSIONS in humans and laboratory animals, yet the etiology and functional significance of these vessels is uncertain. A hypothesis is presented which attempts to explain the difficult problem of arterial collateral circulation. This theory is consistent with microcirculatory hemodynamic research which demonstrates that microcirculatory flow determinants are primarily guided by RESISTANCE..
_______________________________________________
**Original Articles: Cardiovascular
Angiographic Fate of Collateral Vessels After Surgical Revascularization of the Totally Occluded Left Anterior Descending Artery
Yoshiyuki Takami, MD*, Hiroshi Masumoto, MD
Division of Cardiovascular Surgery, Kasugai Municipal Hospital, Kasugai, Japan
Accepted for publication August 16, 2009
"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." This is not a new subject for me!...but it can be confusing if angiogenesis is not differentiated from collaterals.:)
Troubleheart: Collaterals are developed from EECP according to my cardiologist, but I don't have the time and I am somewhat asymptomatic so I don't wish to commit at the present time.
i feel your pain i had a heart attack 3 yrs ago and had 4 stents put in and now i have 9 stents my cholesterol is good and all levels are fine my arteries just close up fast i would just like to know why and how to stop it i have stents in my lad and rca the circumflex i have them everywhere i think bypass is probley next for me though let me know if you find out why your artieries plugging so fast im curious
Cholesterol is used by the body to make new cells and repair damaged ones. When I had very high cholesterol before my heart trouble, I would heal very quickly indeed. People used to comment on how quickly a gash would heal and hardly leave any scar. I think this was due to the high cholesterol. Now it takes ages.
One thing which has always bugged me regarding cholesterol is why it has only affected
my coronary arteries. Ive had scans of nearly all my arteries and the only ones in trouble are the coronary ones. Strange. Im sure there must be a reason why cholesterol would
be used in just three arteries and not the rest of my 66,000 miles of blood vessels.
Personally I think it's high blood pressure, relating to stress. The Aorta is the first blood
vessel to receive blood from the left side of the heart and has to endure a pounding. It
calms blood flow down so the smaller vessels aren't so stressed. However, the coronary
arteries hang directly off the aorta and so feel the full force of each heart beat. Tiny in comparison to the aorta they must endure huge amounts of stress. I think this is why they are more prone to damage and hence a collection of cholesterol to try and repair
them. Maybe in people with heart disease they should remove the coronary arteries from the aorta and graft them onto a kinder vessel with less stress. As long as it's a major artery, they should still receive enough oxygen.
One thing which has always bugged me regarding cholesterol is why it has only affected
my coronary arteries. Ive had scans of nearly all my arteries and the only ones in trouble are the coronary ones. Strange. Im sure there must be a reason why cholesterol would
be used in just three arteries and not the rest of my 66,000 miles of blood vessels.
Personally I think it's high blood pressure, relating to stress. The Aorta is the first blood
vessel to receive blood from the left side of the heart and has to endure a pounding. It
calms blood flow down so the smaller vessels aren't so stressed. However, the coronary
arteries hang directly off the aorta and so feel the full force of each heart beat. Tiny in comparison to the aorta they must endure huge amounts of stress. I think this is why they are more prone to damage and hence a collection of cholesterol to try and repair
them. Maybe in people with heart disease they should remove the coronary arteries from the aorta and graft them onto a kinder vessel with less stress. As long as it's a major artery, they should still receive enough oxygen.
Hi,
I am well aware of my lipid levels. You will be shocked. My cholesterol was over 700 and my tryglicerides were in 1800's. And we checked this many times, the doctors believed it couldn't be accurate. It was accurate. Today, while on medication, my cholesterol hasn't gone below 300 and tryglicerides haven't gone below 400. Immediately flowing angioplasty my cholesterol is always around 250.(no idea why) Here is another thing I find very odd. I am on high dosages of blood thinners and a ful asprin every single day, yet I hardly bleed...or I can say if I do bleed, it's not much and stops right away. Another strange thing is these cholesterol deposits that I have had for years, even before I knew of my condition. I have had large ones on my elbows and fingers these xanthomas that are common among people with unusually high lipids. But I have multiple on my sholders and more interesting is that on my back, arms, and chest they form tiny rock like pieces that I can scratch and they come out. I told my doctors about the fact that I hardly bleed and also about the cholesterol deposits, they didn't seem to think much of it. In my opinion, these different things add up to something.
Any ideas or comments?
I am well aware of my lipid levels. You will be shocked. My cholesterol was over 700 and my tryglicerides were in 1800's. And we checked this many times, the doctors believed it couldn't be accurate. It was accurate. Today, while on medication, my cholesterol hasn't gone below 300 and tryglicerides haven't gone below 400. Immediately flowing angioplasty my cholesterol is always around 250.(no idea why) Here is another thing I find very odd. I am on high dosages of blood thinners and a ful asprin every single day, yet I hardly bleed...or I can say if I do bleed, it's not much and stops right away. Another strange thing is these cholesterol deposits that I have had for years, even before I knew of my condition. I have had large ones on my elbows and fingers these xanthomas that are common among people with unusually high lipids. But I have multiple on my sholders and more interesting is that on my back, arms, and chest they form tiny rock like pieces that I can scratch and they come out. I told my doctors about the fact that I hardly bleed and also about the cholesterol deposits, they didn't seem to think much of it. In my opinion, these different things add up to something.
Any ideas or comments?
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