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Can a blocked artery open without intervetion??

About two weeks back I was forced to physically exert myself to my limits while walking one kilometer ramp. Immediately after this incidence my pulse remained very high for 2-3 hrs while resting after the incidence, as compared to my normal routine . This happened on two consecutive days. Few days after these incidences, when I went for my normal walk, angina pain which I used to get during initial period of my walking time, disappeared. I distinctly feel more energetic than before. My pulse now remains much slower than it was before above incidence. Could it mean one of my blocked arteries have opened?? Otherwise how can these changes be explained?

As regard my disease background, I had MI in 2007 which resulted in stented LAD now open, LCx still 100% blocked, getting filled retrogradely, RCA 100% open. Other smaller arteries had blockage 60-80%. My EF is 30.

Wondering, if such exertions are performed in controlled environment, can they help improve circulation?

Thanks in advance.



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Avatar universal
Thanks All for the posts. Just to explore what could have happened after the insident I mentioned in my initial post, I went for an echo study. This is how my LV function compares with my echo before this incidence (the data within brackets are my echo results in November 2009) :

LV distaloic dia: 59 mm (60)
LV systolic dia: 50 mm (50)
Parasternal Long Axis Views:
- IVS is thin and akinetic (same)
- Posterior LV wall motion normal (Posterior LV wall motion hypokinetic)
Apical View:
- LV wall motion abnormality (Akinesia of mid distal and septum and apex)
Mild AR and MR. Trival PR (No MR)
LV EF 35% (33 +/- 3)

No major change except mild AR and MR as compared to No MR earlier. Posterior LV wall motion is normal as compared to hypokinetic earlier. I am not sure if any of this is significant.


Helpful - 0
367994 tn?1304953593
"Dislodged plaque that does not cause a heart attack may increase the size of the lumen and better blood flow...long shot but possible (my opinion). "  My point and it is an opinion not all plaque that dislodges will cause a heart attack (blockage).  Hard plaque that breaks off does not necessarily cause a clot.  In fact I doubt that it ever causes a clot!  Double whammy is something you incorrectly conclude...not true.  SOFT PLAQUE causes the greatest percentage of heart attacks.  

"Well of course. The less plaque there is, the less fat there is. However, hard plaque is a bigger risk for heart attack because it is brittle, whereas soft plaque is flexible".  Hard plaque is not the biggest risk for heart attack it is the soft plaque:

Undisputed facts by the medical community: There is a medically recognized difference...respectfully your view of the formation of plaque, where it exist, what is vulnerable plaque, etc. is nonsense.  The large, CALCIFIED plaque growing on the inside surface (lumen) of coronary arteries is not the cause of most heart attacks. Rather, the primary culprit is the soft, relatively small "vulnerable" plaque that forms within the vessel walls. Large, calcified plaque is actually relatively STABLE and, because of its hard calcified covering, less commonly cracks. The more DYNAMIC, less stable soft plaque is much more likely to suddenly rupture. As the body forms a clot to try to heal such a rupture, the result may be a total blockage of blood flow; in other words, a heart attack. The soft plaque is hidden INSIDE THE WALLS of the artery and often causes no obvious blockage or loss of blood flow until, of course, the often-fatal rupture.

There isn't anything to disagree with your research and knowledge of EECP.  I agree with the assessment valve disorder patients should not have EECP thereapy.  The hospital I go to has a recently acquired EECP equipment.  I don't know the profit margin, but my cardiologist seems has a positive opinion, but I have a valve problem and don't want to take any unnecessary risk...especially since medication works for me at the present time.  

There has been a reliable study that compares medicated heart patients and EECP for exercise tolerance.  The results were 31.4% for EECP and 13.1% for medication, and that is a 58% differential.
Helpful - 0
976897 tn?1379167602
"Dislodged plaque that does not cause a heart attack may increase the size of the lumen and better blood flow...long shot but possible (my opinion). "

This is where the problem of the double whammy occurs and why heart attacks kill. Once the plaque falls away, a clot will quickly form there. This is why anti clotting medication is immediately administered by paramedics. I doubt if any broken away plaque will not cause a blockage somewhere, it would have to be about the size of a red blood cell to get through the capillaries. So, one artery would be opened, at the expense of another.

"Next the body forms a plaque over the broken lumen to hold in the mess". >>> The lumen is the channel, the open space...plaque invades that space."

Yes I meant endothelium.

"That is true, if I understand, but plaque to hold it in escapes me."

Most of the fat is under the endothelium, trapped in the artery wall as foam cells. The plaque forms over the top of the damage in the endothelium to prevent it from escaping. This plaque starts off quite soft but hardens over time with the addition of calcium.

"I believe you are referring to soft plaque. That plaque does not physically extend into the lumen, but it will cause stenosis"

Plaque is plaque, whether hard or soft, it is plaque. Soft plaque simply hardens over time.
When my blockage was recently removed, the cardiologist had to remove the very hard plaque at the face. About 2-3mm into the hard plaque it became soft. Most likely because calcium could not be delivered to this area because it was embedded and there was no blood reaching it. Are you confusing soft plaque with fat?

"CT scan can detect as it views the entire anatomy of the vessel.  The less soft plaque the less risk of heart attack"

Well of course. The less plaque there is, the less fat there is. However, hard plaque is a bigger risk for heart attack because it is brittle, whereas soft plaque is flexible.

http://www.eecp.org.uk/
Snippet ....

Clinical Trials show that approximately 80% of angina patients experience significant symptom relief after EECP that may last up to three years.
Data gathered by the International EECP Patient Registry of over 5,000 patients showed:
after 24 months follow up 31% of patients recorded being angina free compared to 0% at the start of the study.

Now this site claims different statistics.

http://www.vasomedical.com/

In fact, clinical studies show, over 75% of patients benefit from EECP therapy and sustain improvement up to three years post- treatment.
It doesnt say WHAT clinical trials.

But every site you look at says the benefits stop after a few years, 3-5 seems average. You can then have the treatment all over again.

One thing which worries me is that eecp is in many private clinics and claiming cardiologist dont like the methods because they can't make a good enough return from it. So, I wonder if it's just a fancy gimmick.

If you have recently had a stent fitted, or a valve problem, then you cant have the treatment.
Helpful - 0
367994 tn?1304953593
Shear stress can dislodge plaque and about 3% of a heart attacks are due to rupture of hard plaque that resides within the lumen.  Dislodged plaque that does not cause a heart attack may increase the size of the lumen and better blood flow...long shot but possible (my opinion).

I would like to read what you read a couple of months ago.  Its been awhile but I provided
the math for gradient pressures (variable within the system pressure), velocity, shear stress and the results thereof.  When it works it can be explained...but when it doesn't work that can't be explained!  Apparently, there is an X factor.

"Next the body forms a plaque over the broken lumen to hold in the mess". >>> The lumen is the channel, the open space...plaque invades that space.
"The more mess under the lumen, the more trouble a person will get, this is the key".>>> I believe you are referring to soft plaque.  That plaque does not physically extend into the lumen, but it will cause stenosis.
"Now, if you imagine a small amount of material under the lumen, then the plaque will not have to be very thick to hold it in. This will not really restrict blood flow, there will be no angina and the patient will never know they exist".  >>>That is true, if I understand, but plaque to hold it in escapes me.  CT scan can detect as it views the entire anatomy of the vessel.  The less soft plaque the less risk of heart attack.
"It is stated that collaterals develop from eecp therapy, but what bothers me is they close up again".>>>Do you have authority sited for that proposition?

Have I misssed anything?  Take care.
Helpful - 0
976897 tn?1379167602
"I'm not completely convinced a partially blocked coronary cannot be cleared of some blockage in the lumen with an increase of pressure, thereby, resizing for better blood flow"

From what I have been reading, it doesn't work quite like that. There seems to be a few schools of thought on this, but I found one a couple of months ago which seemed to make the most sense. Initially it depends on how badly the lumen is damaged and how much material becomes trapped under it. White cells mutate into macrophages and attempt to gobble up the mess under the lumen and when they die they become foam cells, mostly fat. The more mess under the lumen, the more trouble a person will get, this is the key.
Next the body forms a plaque over the broken lumen to hold in the mess. This will have calcium added and make it quite a hard brittle substance, but also it will stiffen the artery in that area. Now, if you imagine a small amount of material under the lumen, then the plaque will not have to be very thick to hold it in. This will not really restrict blood flow, there will be no angina and the patient will never know they exist.
Now imagine a lot of material under the lumen. The artery wall is actually slightly pushed out under the pressure and a thicker layer of plaque is required. Blood flow is restricted and IF the artery can dilate further to compensate, then it will. However, the thick plaque could inhibit this action. However, IF the artery dilates then we hit a catch 22. The pressure increases and so the body builds up more plaque to hold back the fats. Blood is restricted again. The trouble is, the vessel has not dilated to its maximum so there's nothing which can be done and angina comes into play. If the patient continues to develop high blood pressure, the plaque keeps growing and can become a total occlusion.
When I look at my very first Angiogram from feb 07 and compare them to all the others I've had in the last three years, they are identical. No small or large blockages have changed size and that's probably because I reduced my stress levels in life which I believe was the cause of my disease. Even though the disease has not progressed, thank goodness, none of the blockages have shrunk, even with statins.
In another post, someone said how they managed to exercise through the angina, gradually progressing each time. Exercising became easier which is probably due to collateral development. I'm not sure if it's just down to flow or pressure, I think it has something to do with demand. I believe I developed collaterals to my LAD because I was working very hard in the building trade, really having a high demand on my heart. When I was in hospital last May, I was talking to a young man in the bed next to me. He was a physical fanatic who went jogging every day, went to the gym every day and did all kinds of aerobic stuff. He had a 98% blockage in his LAD but had no collateral development.
Now, if it was down to just flow and pressure, then he should have formed these adaptations, but from what I can gather, there are just as many who do not, that do.
I'm sure they are getting close to their understanding of this inbuilt bypass system, but I don't think they are quite there yet.
It is stated that collaterals develop from eecp therapy, but what bothers me is they close up again. If a patient NEEDS this extra supply to their heart and it makes them feel much better, then I have to ask a couple of simple questions....
1) why dont they form on their own
2) why dont they stay formed. Patients have to have top ups every few months.
Helpful - 0
367994 tn?1304953593
QUOTE broken pen: "No blocked coronary artery can be reopened spontaneously. If you can force yourself to exercise, collateral blood vessels will develop to supply the part of the muscle supposed to be supplied by the obstructed artery"

Just read you didn't believe collateral vessels can be exploited with EECP. If I understand, you are saying counter-pulsating pressure with EECP is in ineffective to develop collaterals, but the hemodynamics of excessive exercise can develop collaterals?

I'm not completely convinced a partially blocked coronary cannot be cleared of some blockage in the lumen with an increase of pressure, thereby, resizing for better blood flow.  Of course the take away of the plaque dislodged would have to be innocuous. But agreed there can be no spontaneous (without external cause) opening.
Helpful - 0
916737 tn?1243936842
No blocked coronary artery can be reopened spontaneously. If you can force yourself to exercise, collateral blood vessels will develop to supply the part of the muscle supposed to be supplied by the obstructed artery. The pain which used to appear when exercising will no longer be felt since the muscle is re-oxygenated again. I agree with ed34, if you repeat your angio, you will still find the obstruction.
Helpful - 0
976897 tn?1379167602
I have not seen any evidence that proves artery disease (atherosclerosis) can reverse.
I have seen cases where it has stopped progressing though.
What you have more likely done, is forced the formation of your collateral vessels, giving extra feeds into the deprived area of heart tissue. Everyone apparently has these vessels, already in place and ready to assist the heart obtain a greater feed of blood. However, not everybody seems to form them. I have heard of a number of people who were energetic form these vessels, so perhaps the fact that you are working your heart harder than it can cope with is forcing these vessels to open up. With the extra supply, your angina symptoms will diminish. Collaterals are like small bypass vessels already built into the heart. If you had another angiogram, I would be willing to bet that your original blockages still exist.
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Avatar universal
You raise a very interesting question!

I am becoming more and more curious about the body's ability to reverse heart disease in certain cases.  Of course i don't know that this is possible, but i do think that the 'mechanical' view of heart disease is becoming somewhat limited (although still very useful) and it may help to start to see the arteries and the heart as biological and physiological systems, not just pumps and tubes.

I used to think exercise was good for the arteries because it 'moved' the fat along and out of the way, like a running river clears silt.  Now i think that's an outdated view.  Rather it would seem that chemical processes take place, for example, exercise tends to increase HDL cholesterol, which mops up LDL cholesterol (or something like that, i'm not claiming any expert knowledge here).....it also seems to change the chemical structure of soft plaque, firming it up.  

I'm currently interested in the work of Dr Caldwell Esselstyn.....if you want to google this.  
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Avatar universal
I don't know, but you could ask your doctor about sending you to cardiac rehab.
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