bypass, no thanks?

[oldie]

I have coronary artery disease just diagnosed. I'm offered three routes: medication and change lifestyle, catherterisation, bypass surgery. Each one to be done if the previous one doesn't work. 2 and 3 are way out of my league.  Has anyone gone ahead with stage one, medication, and recovered or even just gets along with life?

[erijon]

Depends, can you tell us a little more about the severity of your blockages?

Jon

[ed34]

If you have stable angina, then medication can help to some extent but I really wonder about long term effects of some drugs. You end up taking drugs to keep your heart from working hard, keep your blood pressure low and anthing else necessary such as nitrates
to open the arteries. Your body adapts to these drugs and I found after two years it's
difficult to let go of them. I've been off beta blockers for 24 hours and Im listening/feeling my heart every second to see if it might be affecting me. I had this drug to keep my heart
safe and now I'm scared that Im not taking it. Like erijon says, it depends on the severity of your blockages and how much discomfort you are in. They have to weigh up risk against quality of life. The thing to realise though is that medication will not remove artery disease. This has to be a physical thing using tools, or bypassing it with other vessels from your body.

[oldie]

I had an echocardiogram with Dobutamine injection to put my pulse up to 120, a range suitable to an 80-year-old. The conclusion: the test 'suggests trivascular disease'. To confirm it  I'd have to do catherisation with a dye. Stents would presumably follow this though the cardio says three is too many and a by-pass should be done.  I have no angina. I have shortess of breath running up stairs (but not every time) and four times in three months when lying down. He is proceeding on this symtom alone seting aside the dizziness, nausea, fatigue, confusion etc that have pursued me for 25 years after ten years of severe stress, and have been acerbated by a amiodarone-induced hypothyroidism and its controlling medicines. All a  bit complicated? Please don't be put off. I need to hear from you.

[ed34]

If you have a cardiologist worth the money he earns, you will already be on medication that will be the best for your symptoms. What you have to weigh up is your quality of life.
If you are happy with your ability to do things, then you can just carry on with medication until it comes to the time when things get worse. If you want to look a bit
more to the future and want to have something done now, I would opt for the bypass as
a first option if you have very bad disease. Rather than having a truck load of stents fitted, you will be better off with a bypass. At a later stage, if necessary, the occassional stent can be fitted. That's the way I look at it anyway :)

[oldie]

thanks for coming back so fast. Yes I have three new medications. All look good for my situation. You opt for bypass 'if I have very bad disease'. The cardio hasn't said this. I suppose he is waiting for me to choose the cath and dye test. A good part of each day I feel fine.  I have no angina. Breathless episodes have only once been alarming (when lying down).  When the demons descend I feel rotten but get over it.You've made things clearer for me with your phrase 'quality of life'. I take it this means I'd feel better after a bypass than on medication alone. Trouble is a $20,000 bypass is not an option especially as it doesn't guarantee longer life expectation. I'm now reading the Courage report with avid attention. Thanks for the tip

[kenkeith]

As I stated on your other post, I am on meds only for a 72% blocked circumflex and totally blocked LAD.  I don't have any limitations on the quality of life, and the quality is as expected.  It doesn't make sense to risk an intervention especially CABG as it would not increase my quality of life, and the risk of something less that what I know experience.  There can be a memory problem, recurring pain, occlusion of the by-pass vessel, etc.  Also, heart treatment is quickly advancing and future options may be very patient friendly replacing current procedures.

[ed34]

The majority of bypass operations now do give a prolonged boost to quality of life. The
reason being, they tend to use arteries rather than veins when grafting to the worst affected areas. Arteries last the natural life of the patient whereas the veins used tend to
last between 10-15 years on average. My two grafted veins lasted three months which is
uncommon, but the grafted artery is still working after two years with no problems and
shows no signs of disease. You can't put a price to life, I've always said that. How can
you possibly determine what a life is worth, we can't even create it in a lab which shows how precious it is.
I get the feeling that Kenkeith is hanging on as long as possible for the miracle cure.
The favoured progressing branch of research is of course stem cells. These seem to
be progressing in some ways and yet miserably failing in others. Stem cells programmed
to become heart tissue or arteries are not doing anything when injected into diseased
hearts. However, organs grown from scratch in labs are working. I believe a fully grown,
fully functioning rabbits heart was recently created in a lab and it took just a few days
to grow it to adult size. It was hoped that injecting stem cells would remove the need to
transplant, but this isn't working. If however, a new heart for my body could be created in
a lab, free of disease, I wouldn't hesitate having it transplanted and put up with the
discomfort. There would be no special drugs needed because obviously rejection would
not be an issue. I believe this technology will be available in around 10 years time, but
I can't help but wonder how the costs will be reflected. Lots of money has been spent on
this research and they will want it all back in just a few years plus a huge profit.
But to summarise what I said to you, IF your quality of life is not good then I would opt
for a bypass if disease is severe. IF your quality of life is acceptable for you, then I would
just stick to medication.

[cblmn7]

I totally agree with ed34 your heart is not anything to mess around with no matter what the cost you cant put a price on your life get the bypass work out the cost later

[kenkeith]

No, I'm not waiting for any easy cure!  Presently, I am symptom oriented...no symptoms, no problem as it relates to coronary occlusions.  What would a CABG do medically when the known ICX blockage is successfully dilated with medication?  With a nitrate the coronary vessel dilates to >2.25 mm (that is larger than the smallest stent size) and obviously that is sufficient as there is angina relief (condition is getting better and may not need the med...haven't tried to workout without a nitrate...will try). Doc states because my HDL is greater than LDL there can be some reversal.

Also, stent or CABG will/can have an adverse or a negating effect on the natural development of collaterals and posibly its suscepibility to properly and effectively perfuse an area it has established.  What little is known, it is known that collaterals go to the area that is in need for a blood supply.  Also, stenting or CABG forever removes the possibility for natural healing...one can always turn to an interventional procedure if and when it is required, and that would occur when medication fails to adequately dilate the vessel, and there is angina.    

>>cblm, you may have money problems, I don't.  Listen to your body, it may enlighten you.  If a person does not feel well, see a doctor, if (s)he dismisses your complaints be persistant until there is a proper dx.  or see a different doctor.  If one feels healthy, don't look for a solution!  If it isn't broke, don't fix it as the saying goes.  Don't mess around and shop for a doctor to fix something that doesn't exist, because if you do, you may find a doctor that agrees with you!

[cblmn7]

no i dont have money probs i also have excellent insurance i told oldie to go get his work done because he said bypass is$ 20,000 and he cant afford it i have no idea what your talking about i see mt heart dr all the time

[ed34]

Not everyone has the luxury of developing collaterals. It depends on your genetic make up. There is also the problem that collaterals have no guarantee in supplying an adequate supply of oxygen, especially for exertion. My LAD was totally blocked at the
top but was fed by collaterals. The LAD was so thin you could hardly see it on an angiogram. This isn't an adequate fix in my opinion. But what really concerns me is the
long term effects of medication, especially nitrates. When you take this medication, it
doesn't magically aim just at the coronary arteries, it dilates ALL arteries in the body to
some extent. In some people this causes blood pressure to drop too much and is damaging long term to the brain and other major organs. So I wonder what long term
sacrifices are made with medication. I had a Stent in my circumflex 2 years ago and
it is still fully patent with new tissue grown through it, forming a new artery lining. When
you look at the latest angiogram it's very hard to locate it visually. You say you are happy with taking nitro before going to the gym, but I would be seeing it a different way.
There is a lump of plaque in your circumflex, just waiting to fracture and break off. This
will obviously be very life threatening and can happen at any time. Dilating the vessel
with nitro is also having an effect on the plaque, stretching it. It's like waiting for a bomb
to go off and personally I would rather defuse it.

[itdood]

Just a suggestion, for moderate stenosis and plaque buildup, statins have been shown to reverse it up to 10%.  The study I read was called the ASTEROID trial.  It was a bit extreme on the reductions, getting LDL down around 60.  I think Crestor actually claims this, but Crestor is also called the "gorilla" statin because it's about the strongest one and therefore has greater propensity for side effects.

Couple statin therapy with life style changes you may be able to reduce the plaques.

I remember my Grandmother always fretting over her heart.  Going to the ER, couldn't find anything wrong.  SHe's now 95 and hasn't complained about it in a while :-)

I find it odd about the sleeping part of your SoB (I could be wrong).  Have you had a Holter study done to make sure the symptoms you are feeling aren't rhythm related?  

ANother option, and from what I've heard a better diagnostic tool, is cardiac MRI instead of the CATH.  If you aren't a candidate for stents anyway, might as well get the MRI.  The MRI can detect CAD and a host of other issues as-well.

[oldie]

Would someone who went the medication route say how long the cardio told you to take them before coming back to see him? Mine says two weeks. I can't believe  they can take affect in so short a time. I want to give them a full chance in the hope they will put off surgery.
nb. I have 'suspected' trivascular obstruction. I have had a stress test (with dobutamine) but  not  a cath with dye.  I do not have  angina. All the other symptoms - imbalance, nausea, general malaise, fatigue, shortness of breath - come and go maybe two/three days a week.  sometimes I'm free of them for from five to ten days.

[kenkeith]

Ed: "Not everyone has the luxury of developing collaterals. It depends on your genetic make up. There is also the problem that collaterals have no guarantee in supplying an adequate supply of oxygen, especially for exertion".  

.>>>>..Somewhere and on more than one occasion, I believe, I have stated there are degrees of actualiztation.  There is no evidence that it is genetic, although almost every condition has an element component.  What is known is there are for most individuals pathways already etched for collaterals to develop, and development happens when there is a need for blood/oxygen in a depleted or depleting location.  It is a slow process of occlusion and a slow process of collateral development.  It seems to me, if a stent is implanted or a bypass of an occlusion that takes away the need for collaterals to develop or fully develop.

My occlusion of the LAD took may years took many years, and obviously the development of my collaterals took many years.  I never had any symptoms until CHF (caused by compromising my respiratory system).  If I had had a warning (angina)10 or more years ago, and a stent, it seems plausible collterals would not fully develop.

---Oldie, I have been seeing my cardio doc twice a year for 5 years.  No change in my condition except my lipids HDL is now higher than my HDL, trig and total choles. couldn't be better. I don't know how long it takes for medication to be effective, but it is no unreasonable to see a doctor within a short time to adjust the meds if necessary, and if the med is effective.  After that period tijme you will probably see the doctor twice a year for an echo, stress test, etc.

Sometimes, one has a serious heart condition without any angina...usually for a diabetic or an older individual.  Your other symptoms could be heart related...such as a heart valve regurgitation, low cardiac output due to weak heart muscle contractions, etc.  The shortness of breath should be professionally evaluated...there could be a respiratory problem, pulmonary hypertension, pulmonary embolism, COPD, etc.

[ed34]

Well they aren't already 'etched' but they are already there as blood vessels feeding
Heart tissue. There are two types of collaterols, one more beneficial than the other.
In some patients, the tiny capillaries extent across to feed into other deficient tissue/blocked native vessels. In some patients it is the Arterioles which obviously offer a
higher volume. In most patients this never happens. A study discovered that around 48% of people develope either form of collaterols under the age of 60. Above this age the figure
drastically reduces to 34-35%.
Research has been desperately trying to understand what triggers this so they can induce an 'natural bypass system' rather than surgery. However, it appears to be much
more of a mystery than expected. They are still unable to establish why arterioles
adapt in some people and capillaries in others. If this ability does exist, then hopefully
one day they will be able to trigger the heart to grow a whole network of Arterioles bypassing any restrictions. I wonder though, when the heart is covered completely with
adapted arterioles, with no room for more and these start to clog, what then?

[kenkeith]

There is a fine line between benign,helpful angiogenesis and a cancerous tumor...may be an enclosure with no where else to go!?   When the triggering mechanism is learned that may also be a cure for cancer.  

My understanding (my word etched) the vessel network is available but not open.

My theory and it is related to fluid dynamics.  As an anology when a river is blocked by a dam, the pressure that builds causes distributaries around the dam.  Or the "garden hose effect" .  If water is run through a hose that has tiny holes punctured into the casing, there will be very little water out of the holes unless there is blockage of the hose.  Blockage increases pressure and will force the water out of the holes and the greater the pressure the greater the flow.  The coronary vessel is the hose and collaterals are developed from the internal pressure buildup from the occlusion and I can't disprove that theory.

For 5 years I have read individuals distressed from occluded vessels and almost all have had an interventional procedure.  I have had no intervention except 98% lesion stented and LAD is totally blocked.  How many individuals are there in the general population that have developed collateral vessel bypass and have never been treated for a coronary event or any other heart problem...no knowledge of a heart problem...granted there are some individuals that have a heart attack, but that is almost always from a clot due to a rupture of the endothelium from soft plaque.

You show me documentation were collateral blood flow has developed subsequent to a stent implant or CABG.  Age considerations are not inconsistant with anything that has been said.

[ed34]

"When the triggering mechanism is learned that may also be a cure for cancer. "

Hmm, I'm not sure about that. When collaterols develop they seem to have a built in
'controlled' purpose. When they come across another vessel, they anatomise to it and
the growth stops. Cancer has no purpose, the cells simply multiply out of control and
have lost their reason for being there. I can't see it being a fine line myself. It seems
to me that they have some kind of stem cell functionality left in them and are already
programmed to be blood vessels but not yet complete in growth. Something seems to
tell them to stop growing but remain on standby. I do agree that if they find the mechanism for creating more growth, the benefits would be astrounding. Maybe drugs
developed could enable blood vessels to take on the same condition elsewhere in the
body, such as the brain. Research is very heavy on this topic at the moment because it is seen as a strong possibility to erradicate the need for bypass surgery.

[kenkeith]

I am referring to a cancerous tumor.  It is angiogenesis  where the tumor has its own supply of blood and vessels and continues to grow.  The triggering mechanism for that condition remains unknown!

The development of collateral vessels is triggered by the pressure gradient between the coronary beds of the arteries, caused by obstruction and myocardial ischemia....that is my reference and in a sense relates to fliud dynamics physiology.  additionally EECP uses pressure to develop collaterals....success rate is about 75%.  The presence of adequate collateral vessels feeding the myocardial area at risk may limit the infarct size following coronary occlusion and may even provide a survival benefit.

I don't understand your other remarks such as growth stops at a certain interval and it remains on "standby."  What is your source for that information, etc.?

However, mechanisms which  some patients with coronary artery disease develop coronary collaterals, while others do not, are not well established. The severity of coronary stenosis and duration of angina both affect degree of collateralization.  My contention is  if an individual is ischemic, interventional treatment decreases coronary stenosis and angina thereby limiting the degree of collateration.

[ed34]

If you look at how anything in the body develops, I won't go into all the technical details with regards to genes, hox genes etc, but suffice it to say, control genes tell cells what
to become, when to start multiplying and when to stop. Most areas of the body have an
ability to obviously heal itselt, but this is simply waiting for new cells to rebuild that area.
With regards to collaterals, this is totally different. The vessels seem to know which area
to head for, like they are being messaged to commence growing. If you look at my angiogram, I have grown many collaterals to the left ventricle area, but nothing to help
the right ventricle. My RCA has been totally occluded above the acute margin for many
years and there are many other occlusions up to 90%. Nothing triggered collaterals to
grow to this area, but something did to the left side.
So what I'm saying is, it is obvious that the capillaries and arterioles cease growth at
a certain level of development but then commence growth again when given a message
to do so.
Cancer cells are totally different with no similarities at all. A cancer cell doesnt even use oxygen, it ferments sugar for energy. Oxygen actually destroys oxygen cells. If cancer
cells are put into a high oxygen environment, they die. Being anerobic and no longer
aerobic means they are basically not relying on the body in the same way as normal cells. There are certain anti bodies which actually inject oxygen into a cancer cell to kill it. Cancer cells have lost the ability to control their growth rate due to an aleration in their
genes. So, they are not switched on for growth, switched off, then switched on again when required. They simply divide, divide, divide, divide out of control. So where are the
similarities you are referring to?

[kenkeith]

Are you pasting your post from a source outside the parameters of the "Post Comment"
box associated with the thread being answered?  Or do you have a computer problem with an inability to format margins?

I have thought about the question why the right side (RCA) doesn't develop collaterals as readily as the left side.  My RCA was 98% blocked and stented, and no collateral vessels NOTED. It is my opinion there never will be any collateral vessels at that site now as stent reduces the resistence of a blocked vessel.

It's usually the left side that's affected (collateral growth) because this side works much harder, as it contains the main pumping chamber of the heart. While the right side has only to pump blood to the lungs, the left side has to pump blood all around the body.  It may be the right side has very little priority, and there are other compensating factors that will feed the blood/oxygen deficit. After reading thousands of heart related posts, it is the left side that has the greatest number of collateral development and blockage and fewer for rightside by a very large margin.  

Why vessels seem to know where to go?  It is known vessels develop and blood goes where there is a need to vasculate.  Stent or by-pass takes away that need, and I doubt if there will ever be collateral development.  Fluid dynamics may partially answer....when a river's water flow is blocked it develops distributaries...distributaries will  go around the blockade and if the pressure is strong enough it will  spread.  The pressure on the distal side of a blockade will have reduced pressure and that will be an attraction for the higher pressured distributaries (collaterals) to return to the area of least resistance...it my opinion the defvelopment of collaterals is almost entirley pressure oriented...I don't beleive there is any mysterious code as it relates to fluid dynamics.  However, diabetes does inhibit collateral growth (usually) indicating a connection with the arteries and possibly the the endothelium cells having a role in communicating distress, etc.

[ed34]

we could go on guessing all year as to what causes the collaterals to jump into action but I seriously doubt if its pressure related. If that were the case, everyone with low blood pressure or high blood pressure would have developed collaterals everywhere over the heart tissue. As far as I know there is no particular feed back between pressure and
artery cells. If I had to have a stab at the mechanisms involved with collaterals, and using
nothing but logic I would conclude the following...
The Heart is an independant system in reality, although the brain can produce hormones
to alter the rate, it would happily continue to function if the brain was removed. I would
therefore conclude that the heart itself triggers the formation of collaterals. This would
only need to be achieved when the heart is in trouble, not receiving adequate oxygen.
When heart tissue is in stress, it releases troponin which maybe inhibits angiogenesis
when in heart tissue. When released from the heart cells, indicating stress, maybe this
then allows angiiogenesis to continue. This would be a logical system and one which
is totally controlled within the heart as an isolated organ. As the heart tissue is re oxygenated, the troponin will gradually be replaced in the tissue, stopping the angiogenesis again. Sound logical to you?