thanks to those who got back to me.....
angiogram came back fine so we are looking at arterial muscle spasms. have put him on tablets but no effect yet... still ischaemic and has chest pain.stress test tomorrow.....thanks so much for your replies.xxxx
FINALLY someone who knows about the existence of cardiac syndrome x! My wife was diagnosed with it yesterday after an angiogram. The cardiologist had fully expected significant blockage (failed stress test, and the elimination of chest pains when we'd do our daily walks esp. on inclines - using a nitroglycerine spray.
BUT, her coronary arteries were "totally clear", and her left ventricle test showed no anomalies.
Diagnosis: "Cardiac Syndrome X" - which might better be called "faux angina", but I'm a theologian Dr. not a medical one. :O)
Here's part of a brief description, the web link to it, and some very detailed links to the Mayo Clinic take on it -- the latter of which DEBUNKS the idea that its cause is
microvascular dysfunction (which is commonly assumed as the cause)!
What is it?
The term cardiac syndrome X was first used in 1973 to describe a condition that to this day remains a bit of a mystery.
Patients with the syndrome suffer the same chest pain as those with angina
For example, patients with the syndrome suffer the same chest pain as those with angina. In angina, this pain is often triggered by exercise and is caused by a narrowing of the arteries allowing insufficient blood to the heart. In cardiac syndrome X, the pain may also be triggered by exercise. When a treadmill or stress ECG test is performed to investigate the cause of the pain, the result is positive. However, when an angiogram - an x-ray dye test of the coronary arteries - is performed, no narrowing or hardening is found.
There's still no agreed definition of cardiac syndrome X. However, it's generally thought that to make a diagnosis the following criteria need to be fulfilled:
angina chest pain
positive stress test
completely normal coronary angiogram
(article continued on the web page).
For the MAYO CLINIC take on the subject, see:
which virtually rules our microvascular dysfunction which is commonly assumed
to be the cause.
I would think the way to determine microvascular ischemia (cardiac syndrome X) is with a nuclear stress scan. Thus even if the large vesssels relmain open as they do in angiography the tiny vessels will interfere with the blood flow to certain parts of the heart and thus be clearly visible.
THe upside is that CSX isn't life threatening.
Variant angina, or the unexplainable clamping down of vessels, sometimes major, ones usually at rest, can be a killer.
I would think that agressive lipid lowering treatment might be very wise in cases of CSX in order to clear as much of the microvascualture as possibe, as is hard exercise to force the formation of additional tiny blood pathways.
Is there evidence that "hard" exercise forces the formation of secondary blood pathways? I mean as distinct from minimal exercise which is a lot easier, and, for some like me, a lot less painful too.
The concept is attractive, but I wonder whether an enlarged heart is more likely.
My GP mentioned other pathways and scrutinised my angiograms (for minor blood vessels) but did not mention exercise as contributing. When asked, my cardioligist said exercise did not help the problem specifically.
The other point is that if hard exercise helps by creating and maintaining vascular pressure then it seems possible that vascodilators like nitrates and difedipine might negate the effect by making blood flow easier.
I would appreciate your comments on this.
I think the evidence is very good, if not overwhelming, for the formation of collateral circulation in response to the combination of exercise and occulsion. Less so for those with normal circulation. BUT how much exercise is necessary for a certain person to gain maximum benefit must be highly variable. Probably a person in heart failure with numerous nearly total occlusions will get benefits even by walking up a single flight of stairs daily but an active person who has one or two partial occlusions might need a 5 mile run.
I prefer to err on the side of "hard" aerobics so I am certain to be making collaterals. I have angiographic evidence that I have promoted a gargantuan microcirculation around my formerly clotted RCA...enough to eliminate pain from NEARLY all phases of my life in spite of a 100% blockage of the main trunk of the artery only a couple centimeters "South" of my aorta.
Of course NOTHING will stress the upstream of an artery better thhan a blockage...and that is an exercise stress on that artery 24/7.
It's hard to differentiate what is the effect of enlarging a damaged heart with exercise is. I really think that even the "experts" talk around the whole issue of heart remodelling from exercise vs. heart remodelling from myopathy. I see them as rather similar responses...after all, what else does a heart "see" but a wall of resistance to it's beat, i.e., blood pressure and it tries to accomodate the body, whether the body is resting in bed or at mile 15 in a marathon.
Yes indeed, I think that nitrates (long acting,) beta-blockers, and calcium channel blockers will all negate the positive effects of exercise...often even the ability to GET any . Their effect may be not unlike the effect of the "old-time" treatment for heart attack...stay in bed for 6 weeks, or for heart disease...stay in bed FOREVER. That was probably the worst medical advice ever given.
Of course, if one's heart is so badly damaged that exercise presents a sizeable risk of death, then exercise is off the table.
What I TRY to do, right or wrong, is to exercise aerobically to the point where I feel the very beginnings of chest discomfort...3 times a week. This usually is something like 40 minutes on equipment that gets me to 90% of my maximum heart rate. At that point I KNOW I am pushing on any occlusions as hard as possible and at that point I KNOW that the stress above the blockage is at maximum safe level and exerting the greatest force possible to perforate/drill/burrow new vasculature around the partial occlusion and to increase the width of those arterioles formed from earlier exercise.
How much less stress can do this would be sheer conjecture (or SHEAR conjecture ) on my part but at this maximum effort I can be sure that I am doing all that is humanly possible for me.
(psst, Just in case I keep a bottle of nitrates in my shorts...I haven't needed them yet! )
BTW, When I started this routine, I was able to do only 5 minutes on the elliptical trainer in spite of years of weightlifting which I do on alternate days...I exercise 5 or 6 times a week, not always to capacity but I do what I can for an old farte!
And, of course, all this is with the aid of statins, niacin, and reasonable fat limitation to limit additional plaque formation with an LDL of 62 and an HDL of 40. This is to take care of the "several other blockages of 40-60%" that cluttered up my coronary vasculature 3 years ago.
I agree with Lenin's opinion regarding one's metobolic and circultory system acting and reacting, in on-going basis, to stimuli to create a chemical balance and functional integrity. It should go without saying it would be necessary to have a proper diet, etc. to help adjust and compensate for any dificiencies. Introduction of chemical treatment or an operation may interrupt the natural process as the system may not recognize the orginal problem but now reacts to a different set of variables.
But there are situations that require medical intervention as a last resort. I have a totally blocked LAD at the apex area, but the system had/has adjusted by a natural bypass. If I had had angina before the complete blockage, there wouldn't be any natural bypass or angiogenesis, but there would have been a stent implant for pain relief. I did have a RCA implant that was 98% blocked. Learned by angiogram from my pulmonary edema dx. but I stll have MVR.
That address did not work for me, but I logged on to bmjjournals.com, linked to heart and searched with the keyword angiogenesis. It will take some time to read all the interesting information. Thanks.
I'm sorry that link diidn't work for you. I think a long time ago I might have been asked for my British postal code and I looked up one from a London hotel...perhaps it's stored in my cookie?
The intro starts with Heberden (of the Heberden's nodes of gout) back in his 1802 tract: Commentarii de morborum historia et curatione (Commentaries of the History and Cures of Disease). London, 1802 in which he found a man who had eventually cured his angina by going out first thing in the morning and chopping wood. That first attack, later called "walk through angina" allowed him a day without pain. It seems that there was a "morning stretch", if you will for his coronary arteries that opened them up.
I can definitely relate to that phenomenon and, in my own way, is what I have been trying. I think Cobalt Blue (wherever he is) does similar with his daily hard runs.
Previously, my only knowledge of Heberden was a gouty lump on my right thumb...he would have been a good doctor to stumble on in the 18th Century, no?
Thanks mate for the very helpful and inspiring reply. The reference you gave worked fine for me so it must be something wrong on KK's PC.
You might recall the so-called morning "stretch" is something I discovered for myself and mentioned on here - I think I called it "preconditioning". I found out about it by noticing that if I jogged downhill (the easiest way I could jog) I could turn around and then walk uphill without much pressure at all and without stopping - something I could never do if I just walked down the hill and up again. Furthermore, I found that the stretch lasts for some hours but not as long as overnight (it might if I stretched late at night but have not tried that yet). I found a morning jog for a km or so would allow me to walk up quite steep hills even 5 or 6 hours later in the day. (Also I felt better during the day.)
I now use this stretch technique to improve my exercise performance in a sport I play - it allows me to play harder and longer.
I also notice in my sport I can "break through" the angina barrier (something my GP told me NEVER to try to do). What I mean is that after the stretch I sometimes experience some (slight) angina when I start my sport, but I keep at it and it seems to gradually fade and I end up completing the sport without any angina. One thing I do notice is the next day I am physically very exhausted and when I am stuffed like that, with my body aching, the angina barrier well and truly returns.
The stretch seems to be something that can be used fairly reliably and I push it very hard. When I come home from a jog I have quite a bit of chest pain, and I am trying to do that hard jog twice a day. How wise this is is something I worry about, but it seems to work for me.
Although we can stretch the arteries (I assume this is what is happening) I can't find any evidence of an improvement in my condition. This is why I raised the question about exercise and angiogenesis with Lenin above. Perhaps I am expecting too much too soon but it's damn frustrating to go out each day and belt yourself at a wall that seems so solid and totally immoveable. (I've been at it for about 6 months so far and I have gone from jogging downhill (easy) to jogging on level ground with a bit of uphill - that's tough for me.)
I would appreciate your comments guys.
"It's hard to differentiate what is the effect of enlarging a damaged heart with exercise is. I really think that even the "experts" talk around the whole issue of heart remodelling from exercise vs. heart remodelling from myopathy. I see them as rather similar responses...after all, what else does a heart "see" but a wall of resistance to it's beat, i.e., blood pressure and it tries to accomodate the body, whether the body is resting in bed or at mile 15 in a marathon".
I don't quite understand, it seems to me a differentiation between a well-conditioned heart that beneficially enlarges to a pathologically heart increase is evident.
The evidence would be a pathologically size increase is heart that is decompensating and that would be confirmed by an inefficient pumping measured and recorded as an abnormal EF. When the heart is overstretched it loses its contractility, but when compensating it increases in size marginally and that increases contractility. Decompensation will result if the underlying cause goes unabated, i.e. MVR, afterload resistance, etc.
The well-conditioned heart increases muscle strength and size just as that of a skeletal muscle. The EF will be in the upper range. This result is a lower resting heartbeat as volume/stroke adequately meets oxygen/blood demand.
I have no problems in seeing the similarities of a heart growing in size to accomodate the increasing exercise needs of the body and the increase in size to compensate for it's own and the vacular system's destruction with disease.
I think there are more similarities than differences.
In fact, I can easily envision, as one poster recently alluded to, a woman with a deficient ejection fraction training for the half-marathon. Her heart will increase in size. From what, exercise, a failing heart or both? See what I mean?
The heart tries to survive stress and it does it by strengthening and increasing muscle mass. Even for a person dying of heart failure, the heart will TRY to strengthen and preserve its function by every means possible...even if the end result is less than stellar.
I AM having success in training away my angina and I don't mean with the "stretch" effect but rather a slow progression to more and more resistance to the level of exercise at which I can produce angina. It is SLOW in the extreme but there is a definite trend towards more and more "difficulty" in producing that certain chest discomfort. I think that anecdote of the man chopping wood implies that the man EVENTUALLY cured his angina though it wasn't specifically spelled out. That has to imply angiogenesis.
I think it's a matter of longer and longer at higher and higher heart rates and pressures to force more and more collaterals.
But I think tight lipid controls are also necessary so that we aren't clogging more vessels all the while we are circumventing the old clogs.
The evidence is so solid and well documented that a clog causes an alternate flow, collateral circulation. Arteries aren't smart...all they see, like a river, is a blockage that causes a pressure differential and like water seeking a lower level, blood will force new channels, as will dammed or clogging rivers. Raise that pressure diffential by whatever means and you increase the likelihood of more channels. Exercise raises that pressure differntial.
Alas, a lot of BP meds lower the pressure.
I hope someday to report that I can work out at 80% of my maximum heart rate for an hour without pain...I think that, for me, would define having CURED ANGINA.
QUOTE: "I have no problems in seeing the similarities of a heart growing in size to accomodate the increasing exercise needs of the body and the increase in size to compensate for it's own and the vacular system's destruction with disease.
I think there are more similarities than differences."
We know compensation enlargement of LV is a natural phenomenon to regulate a balance between the heart's right side and left side. It is a continuous function with each heartbeat. It becomes a problem when the LV cannot maintain a balance due to its inablity to effectively pump to meet system's demand. The problem can be due to impaired heart wall motion, MVR, etc.
To train and condition a heart requires an aerobic exercise routine both in terms of time and degree of exertion. The physical structure of the heart's muscle changes and size increases as does the strength of contractions.
On the other hand a pathologically sized heart is almost always due to heavy workload (ie, vascular contriction, excessive fluids, etc.) with little or no rest. The natural phenomenon to regulate overcompensates and stretches the heart wall and a physical change of the tissue itself. The overstretched heart loses its contractility (wall motion defect referred to ...Starling effect**) and heart failure ensues.
QUOTE:"In fact, I can easily envision, as one poster recently alluded to, a woman with a deficient ejection fraction training for the half-marathon. Her heart will increase in size. From what, exercise, a failing heart or both? See what I mean?"
A deficient EF almost always indicates an impairment in wall motion and any farther increase in size causes further decompensation and compounds the problem albeit exercise, whatever. The EF can rapidly drop to the heart failure range and death under a given circumstance.
**For more on the FRANK-STARLING Law. "The basis for compensation of low cardiac output is explained by the Frank-Starling Law which states that myocardial force at end-diastole compared with end-systole increases as muscle length increases generating a greater amount of force as the muscle is stretched. Overstretching, however, leads to failure of the myocardial contractile unit. The compensatory mechanism leads to further myocardial injury, dysfunction, and geometric remodeling."
Could be microvascular disease...formerly known as Syndrome 'X'. I was diagnosed in May....Calcium channel blockers are helping as well as nitro spray for chest pressure/pain when needed. Coronary arteries are completely clear...calcium score is zero...no stenosis...blood pressure is low and cholesterol excellent...Although there is a long history of heart disease, this seems to have been brought on by stepping up my workout at the gym...experienced symptoms similar to heart attack...was in ER 3 times and had numerous heart tests...took a long time to get a diagnosis but am regaining my life. I just turned 52. The first cardiologist said I was fine heart wise...a second one diagnosed me... Am also taking hawthorne, coQ10, cayenne, garlic, etc. to help with vascular health.
I hope you get to the bottom of this and that it's good news!