41yo Male 15 stents RCA 100% for the 3rd time

[troubledheart]

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.  

[Arthur541]

I don't know if you are still following this site. I have some major blockages myself. I had a triple bypass 13 years ago, and now 2 of the 3 bypasses are blocked, along with some other arteries, just within the last year, probably from excessive stress.  I am trying out l arginine for my chest pain and my skin color.  I take 1,000 mg in the morning and at night. It's amazing!  I can see more pink in my face, hands, and arms.  I seem to feel the difference in my chest pain. Others I know take up to 5,000, but it seems to drop my blood pressure a bit much.  Look up l'arginine. It supposedly relaxes and opens arteries and several other things for the heart.  

[ed34]

"There can be added systolic blood pressure to the RCA and circumflex, but I don't see how pressure in one particular segment effects a distance segment.  If the pressure was that strong to back up, the vessels would burst.  RCA is on the right side of the heart  and has diffferent pressure gradients. "

This is my point exactly. My collaterals didn't start growth from the blocked LAD, they started growth from near the circumflex, off a diagonal vessel and grew across to the LAD. So pressure wouldn't have increased in them when the LAD was forming a blockage. If the collaterals started in the LAD, then I could understand, but mine didn't.
I have an early angiogram in feb 2007 which shows the collaterals near the LAD and the occlusion was around 90%. A second angiogram in Sept 07 shows the occlusion at 100% and the collaterals connected to be bottom of the LAD.

[kenkeith]

It is true electronics has series and parallel circuits, but both have a voltage drop....parallel less.  There are parallel vessels going to the heart and other organs, and there is less gradient pressures involved than with in series pressure drops.

There is higher resistance to blood flow going from the arteries to arteriolar and then caps.  The diameters decrease and that increases perfusion pressure and that is necessary to have blood flow.  That is an example of in series drops.

Potential collaterals can be attached to openings to the LAD but unopen.  If they weren't attached the Japan study could not have concluded a quick regression of collateral flow when the gradient pressure to the LAD after opening the blocked LAD.  You probably have collaterals ready to go if your LAD starts to occlude.

I used a garden hose analogy on another post where the hose had perforations through the casing to the inner lining, and there would be no water flow from the perforations.  But begin to block the flow of water at the end of the hose the water will begin to flow out of the holes...more occlusion more flow from the holes.  Fluid dynamics, hemodynamics, gradient pressures, resistence and fluid flow are all associated for an analysis.  

I have considered diffusion of fluid through a semipermeable membrane of vessels and that could be possible when enough pressure is applied within the LAD.

There can be added systolic blood pressure to the RCA and circumflex, but I don't see how pressure in one particular segment effects a distance segment.  If the pressure was that strong to back up, the vessels would burst.  RCA is on the right side of the heart  and has diffferent pressure gradients.

[ed34]

but blood vessels in electronic terms are not in series, they are in parallel. Many arteries in the body connect through capillaries into veins which feed back to the heart. Each
link through artery-capillary-vein can be referenced as a light bulb etc. If the circulatory system was in series, one blockage would stop the whole thing.
This is my point with regards to the blockage forming in a LAD. As the blockage increases, the pressure increases, but this pressure change is local to the LAD and the
collaterals concerned are not even attached to the LAD, they grow towards it from another source. So, again I'm struggling to see how a pressure variation in the LAD would affect the pressure in other vessels in the heart. If pressure increases in the LAD
for example due to a forming blockage, this doesn't increase pressure in the Circumflex or RCA. I'm still at a lostt how this could possibly work. There has to be another factor involved.

[kenkeith]

I don't understand your question regarding blood pressure.  Maybe you are referring to  systemic blood pressure?.  

If you are, and you have some understanding electronics, you can relate to a electronic circuit with cardiovascular system.  We know that an electronic circuit can have elements that require current to perform (accent lights, etc.)  Those elements have a voltage drop, and when in series with a INDEPENDANT source in volts,  the voltage drops are totalled and the total can't exceed the voltage of the source, or it will fail.  Systematic blood pressure (systole) is a DEPENDENT source and the individual pressure drops of gradient pressure segments are added together and there may or may not be a change of the system's blood pressure.  Normally the system can compensate by dilating or constrict vessels and other neurohumoporal effects and maintain a normal blood pressure.  

[kenkeith]

You may have to recall your elementary physics to understand what is happening with cardiovascular physiology (CVP). For review,  hemodynamics can be defined as the physical factors that govern blood flow. These are the same physical factors that govern the flow of any fluid, and are based on a fundamental law of physics, namely Ohm's Law, which states that current  equals the voltage divided by resistance.. In relating Ohm's Law to fluid flow (hemodynamics), the electro-voltage is the pressure difference (force and sometimes called  the DRIVING pressure, PERFUSION pressure, or PRESSURE GRADIENT, the electro-resistance is the resistance to blood flow  offered by the blood vessel and its interactions with the flowing blood, and the  electro's current is the blood flow. Hemodynamics resistance is based on length and diameter of that which is measured.  An occlusion would present resistance on degree of blockage and length of the stenosis.
________________________________________________

It is true some experts believe there may be a factor X involved in triggering collateral growth, but there is also the belief that gradient pressure is enough to grow collaterals.  That belief is based on acknowledging some individuals already vessels in place with poor blood flow or none.

We know from the formula that vessel blockage increases resistance to the lesion in discussion.  The vessel's resistance increases as the diameter is reduced, and from the formula we know gradient pressure increases, but the gradient pressure at certain level is not able to flow to the smaller collateral vessels already in place as the resistance is higher,  but the higher resistance is gradually overcome as the occlusion's diameter is reduced, and it now as a gradient force enough to penetrate the collateral vessesl.  As the gradient force increases at the site of the blockage more blood flows into the collateral vessels.>>>>>>
What happens if the occlusion is opened?>>>>  The gradient force drops as there is no longer any resistance, and collaterals will now lose the perfusion force and no blood will flow.  Will the newly opened occlusion supply blood to the area that had become accustomed to collateral blood supply? Will some heart cells be stunned ?  Will some cells hibernate? etc. The Japan study indicates there could be a problem.

QUOTE: "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".

>>>>"Autoregulation is a manifestation of local blood flow regulation. It is defined as the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure. For example, if perfusion pressure (same as gradient pressure) is decreased to an organ (e.g., by partially occluding the arterial supply to the organ), blood flow initially falls, then returns toward normal levels over the next few minutes. This autoregulatory response occurs in the absence of neural and hormonal influences and therefore is intrinsic to the organ".   This can also relate to your question regarding a spike.

[ed34]

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.

[Max_123]

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.

[ed34]

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.

[ed34]

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.

[kenkeith]

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.

[Max_123]

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.  

[ed34]

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.

[Max_123]

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.

[kenkeith]

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.

[cblmn7]

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

[ed34]

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.

[troubledheart]

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?

[ed34]

Thank you. I just got sick and tired of all the contradictions and nothing made real sense.
If they're not blaming cholesterol they're blaming smoking. If someone has normal cholesterol and doesn't smoke it's quite amusing to see the shocked look on a doctors
face because they have no explanation.

[Crewchief67t]

I just wanted to say i really loved your post!  Very interesting "take" on the deal.  I think you may be on to something.  

[ed34]

Lipid Apheresis

Personally I think it would be throwing good money after bad. Atherosclerosis is a disease which forms in different stages and the lipids getting used to repair arteries is
just one stage in that process. If there was absolute proof that high cholesterol was the
reason for atherosclerosis, or indeed there was a link between high cholesterol levels and
heart disease, then I would be more optimistic. However, this simply is not the case. There are high volumes of people with normal/low cholesterol who develop heart disease.
Think about it, if cholesterol was the problem, we would all be dead of atheroscerosis by
the age of two or three. We ALL have cholesterol, we would die without it and just because fats are found clogging arteries doesn't mean it is the major cause. In the UK
we have something called the French Paradox. The French population eat far more saturated fats than the english, have higher cholesterol in the average person and yet
suffer far less heart disease. First they blamed the Wine they consume. Nothing found. Then they blamed the grapes/grape skins in the wine, nothing found. Then they decided it must be due to the fresh ingredients they cook with, no proof found. They consume
tons and tons of cheese every year and seem to get away with it.  In the UK it was found that heart disease was more abundant in poorer areas, so it was automatically ASSUMED by the so called experts that the reason is bad diet, because they eat more
take aways and less fresh food because they cannot afford it. I just wish they would wake up and see the real link.
Poorer areas contain people with higher stress levels because every day they have to struggle to survive. They have to find rent money, food money and clothing money. Utility
bills are more problems and most families in poorer areas have more than two young children to care for. We have a welfare system which doesn't pay enough money for those people to survive and so crime rises. Our society is closely related to that in America and other countries are now becoming similar, and guess what, heart disease is
increasing in those countries. Stress is a killer over long periods of time, the body cannot handle it. How many people feel fine and then when suddenly have a stressful
moment have a heart attack? Society needs to change if we want healthier people.
I have hypercholesterolemia and believe me, my cholesterol was very high. I was incredibly fit until the age of 44, people used to say I was like a young lad. As soon as
my wife was diagnosed with cancer and nearly died, B A N G, that was it. All my problems started. She had inensive radio/chemo treatment, and was given the all clear
after three years. I had a triple bypass and felt great. Three months later, she was diagnosed with cancer again and BANG my bypass grafts closed up. Now she is in
the clear again having had it removed with surgery. Stress is the problem believe me.
You can lower your cholesterol as much as you like, the body will always find enough in the blood to start atherosclerosis under those conditions.

[troubledheart]

Well you have me thinking more about the EECP therapy.  You brought up important facts.  Here is something I have been wondering about.  If there is no blood getting through my right coronary artery, how can blood get to collaterol arteries that branch off of the RCA. As for your question regarding collaterols having the ability to know when a stent/artery is blocking. My cardiologist has informed me that as my arteries block it forces collaterols because the blood has no other place to go.  I wonder if they will eventually block as well.  I've been told that they do not usually block.  However in the 6 years that I have known about my condition, I have never had the "usual" happen to me.  My blockages occur 100 times faster than usual.  My medicated stents blocked within 1 year, that's not the usual. There are many other things we tried and things we expected based on what usually happens and it never is my outcome.  It makes me wonder why after all of this time my doctors still talk to me as if I might have the usual anything.  
Have you heard of Lipid Apheresis? I've looked into that.  It appears to be a non FDA approved treatment that has worked miracles in other people like me.  However, it's not a covered expense with insurance. It's incredibly expensive and must be done every 2 weeks and no longer.  The closest place that offers this is 4 hours away.  

[ed34]

I wonder if collaterols have the ability to know a stent is blocking the way to anastomose
to a vessel or whether it would still try in vain anyway. EECP does seem like a good
system, 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.
A technology Im still waiting for, one which I believe will be the utopia to all the problems, is a chemical which will break down plaque/fats built up in arteries. The biggest problem will be the extraction of the fats because blood is made up mostly from
water and fat will not dissolve in water. Maybe it will need nanotechnology to have molecule sized machines to grab the fat and never let go, eventually being filtered out through the kidneys into the lavatory.

[troubledheart]

Thank you for your post.  I know all about EECP.  In fact, I did start that treatment until I had to go out of state to an amazing cardiologist.  The EECP treatment is to help create collateral arteries.  I have been working out which create collateral arteries even faster than EECP. The problem is that as my RCA has closed again, I have a very hard time working out.  I have to stop ALL the time.  I don't believe I can commit to EECP. If I cannot commit to 7days a week for 12weeks (that's what I have been told) then I wont benefit from it.  The location isn't nearby, where I would have to go. I am just shocked that at my age, the cardiologists are okay with me losing my RCA completely.  I just keeep hoping that someone out there knows another option.  They should have done bipass surgery, yet they didn't.  Now what?