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Old 06-30-2006, 08:48 AM   #1
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Lightbulb Angina threshold - why does it change?

Can anyone help on this?
I find that when I exercise there is a point where chest pressure becomes quite noticeable - for me that's when pressure becomes pain and I halt the exercise. However, the amount of exercise I can do up to that point varies greatly from day to day (or every few days - not sure exactly). Some days I can do say 1000 steps on my treadmill and I have to stop and other days I can do 2 or 3 times as many and even then the pressure/pain is not that bad that I have to stop. (They are my "great" days.)
I wondered if it was stress or exercise (ie my fitness on the day) that varied it - I just can't fathom it at all. From what I can see stress doesn't seem to be doing it, or diet either, as my diet is more or less steady. (But I do mix in a few different herbs from time to time.)
I can't believe my plaque levels are going up and down every few days.
But it comes down to this - either the artery walls are flexing differently, or the response of my heart to the blood in the arteries is different.
I think it must be my blood chemistry (liver function maybe?) because nothing else adds up.
Maybe someone has tried things like CoQ10 or Carnitine, or even a herb, and noticed a similar effect. (I wondered about Vitamin C, or niacin.)
If we could get an idea of what's doing it, it might be a start to exercising more and feeling better. Am I the only one?
Beefsteak

Last edited by Beefsteak; 06-30-2006 at 09:04 AM.

 
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Old 06-30-2006, 10:57 AM   #2
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Re: Angina threshold - why does it change?

My thought is that you have ingested something that is altering the vasoelastic properties of your arteries, and that it is acting differently day to day when you exercise. You say your diet is steady and you "mix in a few herbs"....well, those details might be at play here. Various supplements act as vasodialators, I know because I am taking them all....fish oil, magnesium sulfate, bromelein. Others may not dilate but may relax arterial walls. Maybe a more careful logging of intakes and correlate with the differences you see in exercise would tell you something.

Just guessing here....

 
Old 07-01-2006, 09:22 AM   #3
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Re: Angina threshold - why does it change?

Ken - thanks for the reply.
Amongst the things you mention I am taking just a couple of fish oils a day - plus a couple of garlic caps. That's every day so nothing new there. I doubt my magnesium would be changing enough to cause it but I will try a mag. supplement just in case I am deficient.
At first I thought I might have had an improvement through exercise + lipitor + my diet, but since it went back to the old angina threshold after a few days it does not appear to be that.
Since your post I have read up more on the magnesium effect - I recall you mentioned it once before.
What other stuff is there that could be classed as a vasodialator?
I want to track this damn effect down because it was sure useful to me - and would be to others.
Beefsteak

 
Old 07-01-2006, 11:06 AM   #4
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Re: Angina threshold - why does it change?

Beefsteak: first comment: just because you are ingesting the same amount of things each day, does not mean your body is absorbing identical amounts after each intake. Stomach emptying time, amount of fat in the mean/snack, other foods, etc., all can contribute to the amount (rather the concentration) of the key item as it travels along the tract. If different amounts are absorbed, the effects on your arteries may be variable.

Other items I just found after some searching are anything containing nitrites (hot dogs, bologna, pepperoni), garlic (which you say you are already taking) [actually, the list of beneficial characteristics of garlic for helping heart disease is really neat and I may add this to my list], cocholate (really a vasocontrictor from the caeffine)...many of the site hits relate to migraines.

 
Old 07-03-2006, 10:14 AM   #5
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Cool Re: Angina threshold - why does it change?

Ken,
I have done some tests and think I have worked it out. Partly at least.
It's due to exercise.
Let me explain -
I do small sessions on a stepper - 500 steps - several sessions in the day for about 5 minutes each, before I get on the treadmill.
I never get angina of any significance on the stepper.
Then, later in the day, I do a longer treadmill workout - that's my main daily workout, when I hit the angina barrier.
What I've done is to double my small stepper sessions from about three or four to eight, or ten. Then, when I do the treadmill I find I can go much longer before the angina becomes a problem (ie chest pain) and I have to stop. So the "pre-conditioning" (I'll call it that) from the stepper boosts my treadmill performance. Importantly, in my case, it seems to boost it a lot and I can go for 3 or 4 times longer on the treadmill and even then I pull up feeling a lot better than I ever did with the shorter "preconditioning".
Another thing I've found is that if I boost my treadmill performance by "preconditioning", and I try the treadmill again the next morning it's still there. Great! That is, the improved resistance to the angina carries over and remains there the next day. So it does not drop back immediately. Great too!
I am still coming to grips with this - working out what the pattern is.
What I plan next is to try and keep it at the high treadmill perfomance level by using the treadmill both in the morning and the afternoon.
That way I reckon I can stop from dropping back. (It's a lot of excerise though. )
The question that remains is even if I keep up the exercise and push the angina threshold higher - will it remain there and what do I have to do to keep it up there? If it quickly drops back after say no exercise for 24hrs that may mean I have flexed the arteries out a bit, got some better blood flow, but they quickly go back again. I pretty well know that will happen from my experience now. Maybe I need to keep them "open" for a month or so to get something permanent.
This is all hopeful thinking and just my crude ideas on it. But the facts stand and I am in there fighting!
Thanks for reading the post, and I welcome comments from you - or anyone in fact who might be interested.
Beefsteak.

 
Old 07-04-2006, 06:11 AM   #6
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Re: Angina threshold - why does it change?

Beefsteak,

That's a WONDEFUL question.


There are many many vasodilators and vasoconstictors circulating at any time, some caused by food, by exercise, by temperature, by mood and god knows what else. A normal person might not notice most of the ebb and flow but a person with angina who aches with any degree of vasoconstiction might. What I'm saying is that you might not ever be able to quantify with any precision what is doing what, WHEN.

On the "preconditioning", I think you are very much on the right track. I've noticed the samne thing. Even within an exercise I sometimes have some discomfort at minute 5, say, that goes away by minute 7 and doesn't return for the next half hour even though I'm taking my heart rate higher and higher.
I put it down to stiff vessels that take some time to accommodate to exercise...it might be correllatable to blood pressure changes, but as a sample of one, I doubt that I could work it out.

On your wondering about how long the "preconditioning effect" lasts, it may be hard to pin down but it seems logical that with more and more exercise the effect can be made to last longer and longer. Maybe at the level of trained athlete (please God! ) it would be permanent.

Sometime this week, I'll play with your idea and do a 4 minute workout on the elliptical and then wait 15 minutes and then "KILL MYSELF" on the elliptical trainer. I'll try for a personal second-best at up to 90% maximum HR. (My best was an hour because I got hooked on a TV show on the plasma screen attached to the trainer...snazzy gym! I could hardly walk for 2 days after that...no more hour-long ellipticating! )

As a corollary to all this, I think the WORST thing a person with angina could do is to gear a lifestyle towards NEVER suffering any pain or discomfort. The level of exercise will becoome less and less and less, and the drugs more and more, until one is completely incapacitated and bed-ridden...I saw this progression in my mother. Personally, I think pushing to the level of discomfort EVERY day is the very best way to battle the beast...it's what I try. For me the exercise capability is still great, but even for someone who gets pain at 6 steps, I think he should go for SEVEN every day...and then EIGHT.

Last edited by Lenin; 07-04-2006 at 06:23 AM.

 
Old 07-05-2006, 07:42 AM   #7
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Re: Angina threshold - why does it change?

Great discussion, and I can't disagree with anything either of you has said. The thing I am concerned with--for myself--is angina at rest rather than while exercising. Clearly, spasm is involved (my brief encounters are almost always at night when I am asleep). So I am left wondering how overlaying exercise (greater O2 demand for the heart) on the propensity to spasm can either help or hurt further narrowing of whatever blockage is occuring. Searches on "spasm" have not produced anything I deem useful and I conclude in part that the medical community does not know that much about it--especially spasms right at the edge of the stent.

I am now 20 days post third angio/2nd stent and am just now noticing an increasing frequency of mild (very mild) angina at rest....not a hopeful sign.

I have not exercised in almost four weeks and really feel it, so I concur with Lenin's comments. I wonder if exercise would tend to dampen out spasms or increase them. Any speculation on anyone's part??

Ken

 
Old 07-06-2006, 04:46 AM   #8
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Re: Angina threshold - why does it change?

Ken,
Would you call your condition "unstable angina?" How long do the bouts with pain/discomfort last? Is there anything that relieves them?

 
Old 07-06-2006, 02:23 PM   #9
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Re: Angina threshold - why does it change?

Lenin: after lots of reading on this, I conclude that right now, I do not have 'unstable angine' but rather arterial spasm. Here is what I understand the difference(s) to be. Spasm is a localized constriction of the arterial wall, which can occur with or without the presence of plaque buildup. The few articles I found suggest that this can occur right at the leading edge of newly placed stents. One interesting angiograph showed a full diameter vessel (where the stent was) and right in front of it, a 90% reduced diameter section formed days (weeks perhaps) after stent placement.

There is a very rare form of angina called Prinzmetal's or variant angina which is caused by a somewhat spontaneous spasm of the arteries, absent any localized stimulus like a stent edge or even plaque.

Unstable angina, which is what I believe I had when I started on this adventure back on May 1, is the rupture of a plaque that has built up significantly. The plaque actually hemorages (sp?) and the thing most cardiologist worry about is localized thombosis, leading to MI or death.

In all of the cases, classic angina pain appears at rest and not during exertion. Curiously, research has suggested that most unstable or spasm induced angina episodes occur at night or early morning, usually while asleep. This has been my experience, although I found that episodes occured regularly while reclining on the sofa watching TV.

I also think that the PATTERN of the episodes is an important thing to watch. In my case, the frequency and the intensity increased in spite of a drastic increase in fish oil and vitamins as I tried to stave off the inevitable. Now that two stents are in place, I believe I am fighting a) spasm from the edge effects of the stent; b) increases tendency for platlets to gather at the leading edge of the stent (and perhaps within the cracks of the struts of the stent); and c) along any wounds formed between the stent struts and the walls of the artery. Of course, I am on the regime of plavix and aspirin but to it, have added as many supplements as I can to help reduce platlet stickiness and promote arterial vasodilation (fish oil, bromelein and quecertain, garlic tablets, and newly added--promegranate--see below). It is quite a complex mechanical and chemical model and all of the research in the world can not tell them exactly what is going on at the detailed level.

Curiously and happily , I added a new supplement to my toolbag--pomegranate capsules, just yesterday. It is way too early to know if I am just experiecing the placebo effect, but I have learned that I can tell with high reliebility when "my heart is feeling bad". I mentioned in a previous post increasingly mild episodes of angina, yet since beginning yesterday a rather high intake of pomegranate capsules (250mg x 6-8 daily), I have experienced no further angina episodes and I "feel great". Again, probably a placebo effect going on but I plan to continue. Searches for pomegranate and heart disease produced a lot of small sample studies, all positive.

Ken

 
Old 07-07-2006, 06:13 AM   #10
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Re: Angina threshold - why does it change?

Just a little brainstorming.

As per your mental illustration about the leading edge phenoomenon:

Quote:
Spasm is a localized constriction of the arterial wall, which can occur with or without the presence of plaque buildup. The few articles I found suggest that this can occur right at the leading edge of newly placed stents. One interesting angiograph showed a full diameter vessel (where the stent was) and right in front of it, a 90% reduced diameter section formed days (weeks perhaps) after stent placement.
I would think that a leading edge problem like the one described is not uncommon but gives no evidence at all of spasm, but rather the commonplace accretion of plaque at an "irritant" point or point of chaotic fluid flow. I'd think that such a 90% blockage would be most evident on exercise...hence "stable" in spite of its rapid progression (I know, sounds paradoxical!).

I also don't like that definition of UNSTABLE ANGINA as including plaque rupture. There are many people who suffer such angina night after night and the probability of surviving multiple plaque ruptures night after night seem remote to me.

I think the definitions of these three angina variants limp and that more overlap is present. For example, I doubt that many people suffer Princemetals with clean arteries and I doubt that many with unstable angina would fail to show ischemia on a stress test so I see a lot of gray area here.

How do YOU do on a treadmill for 20 minutes at 130 BPM? That will tell a lot.

I think you might be right on the money with your leading edge theory but I think you are restenosing there rather than causing spasm. Perhaps both. Or else you had SEVERAL areas in your coronary circulation that were causing problems and they missed one?

Quote:
I am now 20 days post third angio/2nd stent and am just now noticing an increasing frequency of mild (very mild) angina at rest....not a hopeful sign
Forgive me for saying this but is it POSSIBLE that you might be looking too hard.
(I DO understand how very worried you must be.)

Let me try to comiserate: When I got my stent and complete relief from angina I was thrilled and felt like a kid again. But several months later, running for a train, I got hit with the unmistakable heartburn. I could have sat on the subway platform and cried my eyes out. The second time, a month later running for a bus AGAIN, I got a doozy and tears of grief actually streamed down my cheeks (on a crowded bus.) It's been 2 1/2 years and I've suffered maybe 20 bouts of discomfort, maybe 3 of them quite painful. I realized FINALLY, I'll never be 18 again, but Hell, I am the ablest and best built of the sixth decaders at my gym and I am going to make that ENOUGH for me.
What I am saying is that if all you get is a LITTLE angina at rest maybe all is well.

EVENTUALLY I plan on having another angio with the hope of cleaning out any detrius in my stent and angioplastying anything else that needs it...but if I can put this off for 10 years, HOORAY for me.

Ken,
How low are you keeping your LDL? You seem to have a propensity for laying down plaque and thus I think the <<70 guidline is written just for you. I don't share your jejune view of supplements and cutesy foods like pomegranate for heart health...although I LOVE Grenadine!

Last edited by Lenin; 07-07-2006 at 06:36 AM.

 
Old 07-07-2006, 03:14 PM   #11
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Re: Angina threshold - why does it change?

Quote:
Originally Posted by Lenin
I would think that a leading edge problem like the one described is not uncommon but gives no evidence at all of spasm, but rather the commonplace accretion of plaque at an "irritant" point or point of chaotic fluid flow.
I think this is right but the accretion of plaque (actually clumps of platlets) stimulates the release of constricting chemicals right at the site.

Quote:
Originally Posted by Lenin
I also don't like that definition of UNSTABLE ANGINA as including plaque rupture. There are many people who suffer such angina night after night and the probability of surviving multiple plaque ruptures night after night seem remote to me.
You may not like the sound of it, but search "unstable angina" and rupture is included in almost every page that pops up. My primary and the ER doc also said the same thing. I also think a more precise description is spasm induced by the buildup which runs the HIGH risk of rupture.



Quote:
Originally Posted by Lenin
I think the definitions of these three angina variants limp and that more overlap is present. For example, I doubt that many people suffer Princemetals with clean arteries and I doubt that many with unstable angina would fail to show ischemia on a stress test so I see a lot of gray area here.

How do YOU do on a treadmill for 20 minutes at 130 BPM? That will tell a lot.
You probably are right that there is some overlap and conditions probably mix to a degree. I think the entire thing has a lot of "grey area". In 1980, I had three stress tests in a two month period, NEVER experienced pain, and yet was 95% blocked when they finally decided to do an angiogram (I HAD showed altered wave form on the 3rd stress test but not pain). One thing I have learned is that there are no absolute and hard rules that apply to everyone.

I have not had a stress test since 1995. The symptoms I presented with suggested unstable angina to everyone and cath showed 85% blockage.


Quote:
Originally Posted by Lenin
I think you might be right on the money with your leading edge theory but I think you are restenosing there rather than causing spasm. Perhaps both. Or else you had SEVERAL areas in your coronary circulation that were causing problems and they missed one?

Forgive me for saying this but is it POSSIBLE that you might be looking too hard..
You are right on the money. Today was my 2 week followup with the cardio and he said about the same thing---he thinks I am worrying too much and overanalyzing. He also said that numbers of his patients experience some spasming for weeks maybe months after stenting. The mild symptoms I reported did not worry him at all. His chief worry is from "stent closure"---which he described not as mechanical stent collapse (the stent is stronger than any spasming artery around it), but rather sudden and catestropic thombosis/clotting shutting off almost all flow. He said this was unlikely with the antiplatlet medicines (plus my other supplements).


Quote:
Originally Posted by Lenin
What I am saying is that if all you get is a LITTLE angina at rest maybe all is well.
Again, right on target. I have made up my mind that things have to get somewhat more severe and more frequent before I start to worry much more.


Quote:
Originally Posted by Lenin
How low are you keeping your LDL? You seem to have a propensity for laying down plaque and thus I think the <<70 guidline is written just for you. I don't share your jejune view of supplements and cutesy foods like pomegranate for heart health...although I LOVE Grenadine!
"Jejune: 1. Lacking in nutritive value.
2. Displaying or suggesting a lack of maturity; childish.
3. Lacking interest or significance; dull; meager; dry. "

Hmmmmm. Had to look it up. Seems like a poor choice of word, not fitting the situtation (esp number 2-- ) Proven clinical studies from many countries show the physiological benefits of many of the things I am taking. "Cutesy"?? The pomegranate stuff is admittedly new and small sample, so maybe more speculative---but "cutesy"??? ; the others not so. My LDL was 75 a week before my last hospitalization and the hospital lab measured 65 so I am in the ballpark for trying to avoid depositing more LDL, maybe even regressing any other blockages (I did have a 50% and 30% lesion elsewhere but nothing was done with them).

Ken

Last edited by Ken289; 07-07-2006 at 03:17 PM.

 
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Old 07-08-2006, 05:33 AM   #12
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Re: Angina threshold - why does it change?

You are absolutely right...COMPLETELY wrong word choice (must be plaque in my carotid )

The word I was going for was most definitely not the rather insulting JEJUNE, but the much more pleasant HALCYON.
Forgive my temporary mental block; I didn't mean to be rude.


I think with your LDL's where they are you'll lose plaque at a good clip...and I hope for the same for myself with my 69 LDL. (Now if I could only change my genes and stop making the Lp(a) molecule (LDL + plasminogen.)

Last edited by Lenin; 07-08-2006 at 05:38 AM.

 
Old 07-08-2006, 08:02 AM   #13
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Re: Angina threshold - why does it change?

Quote:
Originally Posted by Lenin
I would think that a leading edge problem like the one described is not uncommon but gives no evidence at all of spasm, but rather the commonplace accretion of plaque at an "irritant" point or point of chaotic fluid flow.

Answer:
"I think this is right but the accretion of plaque (actually clumps of platlets) stimulates the release of constricting chemicals right at the site".

I consider a sudden muscular contraction of a vessel in this discussion to be usually idiopathic (but possibly due to chemical imbalance), involuntary and of short duration...the condition that is referenced seems to be a block or stenosis! What is the source that clumps of platelets stimulate the release of constricting chemicals? Of interest as plavix helps prevent blockage, and it may be the chemical mechanism that helps prevent restenosis!?...

 
Old 07-09-2006, 02:10 PM   #14
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Re: Angina threshold - why does it change?

Kenkeith--the more I talk the more I sound like I know what I am saying---but probably not.

What are the causes of spasm (yes of short duration) right at the entrance to the stent? That mechanical entrapment of platlets occurs (or can occur) seems somewhat obvious, no matter how slippery they are from the plavix. A not insignificant related question is: if they are mechanically trapped there, how would they cause irritation leading to constricting chemical release? Seems hard to imagine. Perhaps the mechanical edges of the stent, "poking" into the wall of the artery, not unlike someone poking a stick in your side, is enough to irritate nearby cells and they protest by pouring out these vasoconstrictors. This in turn spasms the artery wall.

How's that for a theory.

Whatever the mechanism (who can know?), my idea is to overwhelm any vasoconstricting chemicals with vasodilators and antioxidents--hence my megadose intake of jejune....er....halcyon....supplments. I have also tried to take less per dose and more doses per time. Another variable (we need more yes?) is the clearing effect of the kidneys and liver, so it seems like keeping the (antioxident) fires stoked frequently will be more beneficial to the stent site than will massive doses once or twice a day.

Make sense?

 
Old 07-09-2006, 02:37 PM   #15
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Re: Angina threshold - why does it change?

Beefsteak and Lenin: what is the status of your experimentation with "preconditioning" exercises before starting vigorous exercise? Have you done more experiments and continue to see the same effect?

I am interested as I start cardiac rehab this week and want to talk about your "theory" with the exercise technicians at the lab and to perhaps build some warmup/preconditioning into my routine.

We got a little off the topic of the thread with my digression into unstable angina (although the discussion was very useful). What about the "angina threshold" question??

Thanks.

 
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