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Stress Test Results
My test results where:
There is moderate fixed defect involving the apex and inferior wall. There is no convincing reversible ischemia seen. What exactly does this mean ?
There is moderate fixed defect involving the apex and inferior wall. There is no convincing reversible ischemia seen. What exactly does this mean ?
The locations of the heart wall (apex and Inferior) has impaired movement or contractility ability usually caused by lack of blood to the subject area. Reversible ischemia (lack of blood flow) means it can be treated effectively with a stent, etc. Do you have an echo report, and if so does it provide the left ventricles ejection fraction (EF))?
You say:' Reversible ischemia (lack of blood flow) means it can be treated effectively with a stent, etc.'
Just what I needed to hear and stated with your usual precision. What I cannot find is how long the new blood flow via the stent will take to revive the weakened muscle - weeks, months? Perhaps the time is not measurable?
the dubotomine stress test prior to the stenting said it showed positive for ischemia affecting heart wall in three places. EF was 70.19%.
What was notable about this test was that I am perfectly normal at low and medium dose of the dubotamine. Maybe I should lust live like that - low and medium pulse? All the grim looking stats came at high dose with pulse at 120. That's high for an 81-year-old? It would take me a fair sprint along the road to get it up to that level.
Just what I needed to hear and stated with your usual precision. What I cannot find is how long the new blood flow via the stent will take to revive the weakened muscle - weeks, months? Perhaps the time is not measurable?
the dubotomine stress test prior to the stenting said it showed positive for ischemia affecting heart wall in three places. EF was 70.19%.
What was notable about this test was that I am perfectly normal at low and medium dose of the dubotamine. Maybe I should lust live like that - low and medium pulse? All the grim looking stats came at high dose with pulse at 120. That's high for an 81-year-old? It would take me a fair sprint along the road to get it up to that level.
You say:' Reversible ischemia (lack of blood flow) means it can be treated effectively with a stent, etc.'
Just what I needed to hear and stated with your usual precision. What I cannot find is how long the new blood flow via the stent will take to revive the weakened muscle - weeks, months? Perhaps the time is not measurable?
the dubotomine stress test prior to the stenting said it showed positive for ischemia affecting heart wall in three places. EF was 70.19%.
What was notable about this test was that I am perfectly normal at low and medium dose of the dubotamine. Maybe I should just live like that - low and medium pulse? All the grim looking stats came at high dose with pulse at 120. That's high for an 81-year-old? It would take me a fair sprint along the road to get it up to that leve and I don't have to sprint at all..
Just what I needed to hear and stated with your usual precision. What I cannot find is how long the new blood flow via the stent will take to revive the weakened muscle - weeks, months? Perhaps the time is not measurable?
the dubotomine stress test prior to the stenting said it showed positive for ischemia affecting heart wall in three places. EF was 70.19%.
What was notable about this test was that I am perfectly normal at low and medium dose of the dubotamine. Maybe I should just live like that - low and medium pulse? All the grim looking stats came at high dose with pulse at 120. That's high for an 81-year-old? It would take me a fair sprint along the road to get it up to that leve and I don't have to sprint at all..
QUOTE: "What I cannot find is how long the new blood flow via the stent will take to revive the weakened muscle - weeks, months? Perhaps the time is not measurable?"
When there has been deprivation of blood/oxygen to a specific area of the heart due to ischemia (blocked vessels) the heart cells can become necrotic (dead) and/or go into hibernation or are stunned. The result will be hypokenisis or akinesis (dead) that decreases the contractility of the left ventricle. This could be of a minor to severe degree, and of variable size or extension. It is generally due to lack of blood supply to that area of the heart, but there can be other causes.
The hallmark of hibernation is that the muscle cells, and heart function itself, wake up when ischemia is relieved. Hibernation was first hypothesized to explain the rapid improvement in heart function observed in some patients after coronary bypass surgery. Stunning is a related phenomenon. Stunned heart muscle does not recover as rapidly as hibernating heart muscle. But in contrast with infarcted heart muscle, in which many muscle cells are dead, it does indeed recover. Function in the stunned heart muscle may not return for 10 to 16 days after the restoration of blood flow.
To answer your question of how long depends on whether the heart cells are stunned, hibernating or necrotic...or combination of the 3 variables.
I had hypokinesis due ischemia, and a stent implant to the RCA restored the heart cells and EF returned to normal. I don't know the exact time, but the later echo did not show any impairment of heart wall movement. I had hibernating heart cells and a heart attack.
"Stunned Myocardium
If blood flow is returned to an area of heart muscle after a period of ischemia (lack of blood supply), the heart muscle may not pump normally for a period of days following the event. This is called "stunned" heart muscle or myocardium. The most likely condition with just blocked vessels.
Hibernating Myocardium
After a heart attack, some areas of heart muscle do not pump as they should. Some areas will have permanent damage. Other areas are able to return to their normal function if blood flow is returned to that area (by medications or a procedure). Hibernating myocardium is heart muscle that is "resting" and may possibly return to normal function." May take longer or not completely recover from a heart attack.
When there has been deprivation of blood/oxygen to a specific area of the heart due to ischemia (blocked vessels) the heart cells can become necrotic (dead) and/or go into hibernation or are stunned. The result will be hypokenisis or akinesis (dead) that decreases the contractility of the left ventricle. This could be of a minor to severe degree, and of variable size or extension. It is generally due to lack of blood supply to that area of the heart, but there can be other causes.
The hallmark of hibernation is that the muscle cells, and heart function itself, wake up when ischemia is relieved. Hibernation was first hypothesized to explain the rapid improvement in heart function observed in some patients after coronary bypass surgery. Stunning is a related phenomenon. Stunned heart muscle does not recover as rapidly as hibernating heart muscle. But in contrast with infarcted heart muscle, in which many muscle cells are dead, it does indeed recover. Function in the stunned heart muscle may not return for 10 to 16 days after the restoration of blood flow.
To answer your question of how long depends on whether the heart cells are stunned, hibernating or necrotic...or combination of the 3 variables.
I had hypokinesis due ischemia, and a stent implant to the RCA restored the heart cells and EF returned to normal. I don't know the exact time, but the later echo did not show any impairment of heart wall movement. I had hibernating heart cells and a heart attack.
"Stunned Myocardium
If blood flow is returned to an area of heart muscle after a period of ischemia (lack of blood supply), the heart muscle may not pump normally for a period of days following the event. This is called "stunned" heart muscle or myocardium. The most likely condition with just blocked vessels.
Hibernating Myocardium
After a heart attack, some areas of heart muscle do not pump as they should. Some areas will have permanent damage. Other areas are able to return to their normal function if blood flow is returned to that area (by medications or a procedure). Hibernating myocardium is heart muscle that is "resting" and may possibly return to normal function." May take longer or not completely recover from a heart attack.
thank you for giving so much time and thought to my question. That is indeed at horough answer which I will re-read with care.
Is there a test which can accurately evaluate if cells are stunned/hibernating or dead?
If not, how do they evaluate if a bypass will be beneficial?
Very interesting post by the way :)
If not, how do they evaluate if a bypass will be beneficial?
Very interesting post by the way :)
Good question. I have researched the subject on several occasions, but unable to find anything. To test viability of damaged heart cells would involve knowledge of cell biology, cellular hypoxia and diagnosis, and some stem cell information gets into the subject, and I don't have any special information or knowledge on the subject. It seems the tests that are familiar for differential dx of cell viability are blood tests, EKG and ECHO. Severely damaged cells (negrotic) will develop scar tissue and the EKG will show (should) STEMI (ST interval Elevated from an MI), etc. The ECHO will show heart wall movement impairment, and blood tests for acute conditions.
A differential analysis of no scar tissue, hypokinesis, and acute or chronic condition are the factors to be considered.
A differential analysis of no scar tissue, hypokinesis, and acute or chronic condition are the factors to be considered.
I do know that after my MI and having discovered a blocked LAD they refused to do intervention on that vessel until evaluation of tissue condition had been conducted. My ECG
was normal but they proceeded with an Echo. This showed no problems but it was as though they refused to believe the results due to the known condition of the LAD. I was then sent for a nuclear perfusion scan which agreed with the Echo. This is when they seemed to realise that collateral formation must have occurred and I was presented with the diagnosis "no tissue damage".
It would seem they are not interested in hibernating or stunned cell differentiation, because both will recover over time. I believe they simply look for dead cells as you indicate, scar tissue, which of course is not treatable.
was normal but they proceeded with an Echo. This showed no problems but it was as though they refused to believe the results due to the known condition of the LAD. I was then sent for a nuclear perfusion scan which agreed with the Echo. This is when they seemed to realise that collateral formation must have occurred and I was presented with the diagnosis "no tissue damage".
It would seem they are not interested in hibernating or stunned cell differentiation, because both will recover over time. I believe they simply look for dead cells as you indicate, scar tissue, which of course is not treatable.
As a matter of fact, some reliable sources state it is stunned cells that have a time differential less than hibernating, and another source will say it is the hibernating cells. So it seems it doesn't make much difference how it is termed....just there is a time difference between the two as you state.
So there is no confusion, whether it is called stunned or hibernating heart cells, the significance is there is a short time period following a heart attack where the cells can be revitalized...a matter of hours or days?!
When there has been ischemia for a period of time, some heart cells may go into hibernation or have become stunned, whatever the terminology ..but not both.
The distinquishing factor is that damaged cells from an acute heart attack have a short time period to be revitalized. I had an ischemic silent heart attack, apparently over a period of time, and the hypokinesis was overcome with reperfusion therapy to the blood deficit area.
When there has been ischemia for a period of time, some heart cells may go into hibernation or have become stunned, whatever the terminology ..but not both.
The distinquishing factor is that damaged cells from an acute heart attack have a short time period to be revitalized. I had an ischemic silent heart attack, apparently over a period of time, and the hypokinesis was overcome with reperfusion therapy to the blood deficit area.
my stress test 10 months ago was positive for ischemia. I never had angina. at least in its painful versions. I therefore was not stress tested since 1989 when all was normal. This is the situation of the 20% of CAD patients who have no pain and therefore no warning of trouble. They can run one day and have a MI the next. With these patients there is no way of telling how long their heart walls have been without sufficient supply of blood and it must be harder sill to judge which of the three conditions - dead, hibernating, or stunned - their heart muscle cells are in. My stent was put in RCA six weeks ago so I already know that immediate cure for heart area discomfort (my version of angina or 30-year stress?) has not happened in my case .I know without trying that there is nothing to gain by bringing up the three conditions with my very experienced interventionist cardio (about 3000 caths in 20 years). He will ask is there any pain? No. Good. Come back in two months. That's why I need the opinions of lay experts like you.
My first cardilogist (interventional) expressed a pessimestic view that my EF 13-29% would never improve. Didn't consider hibernating heart cells...it is not a given! I don't have much to add that I have not already provided.
http://www.medhelp.org/posts/Heart-Disease/COREG-MEDICATION/show/496227
Journal of Nuclear Medicine Vol. 49 No. 3 399-413
A further understanding of CAD pathophysiology at the molecular and cellular levels will allow radionuclide imaging to evolve into a primary prevention tool by earlier detection of atherosclerosis as well as identification of vulnerable plaques and adaptations in myocardial metabolism.
Radionuclide tracers by their nature reflect physiologic processes at the cellular level. Nuclear imaging techniques are well suited for cardiac molecular imaging because of their relatively high intrinsic sensitivity and excellent depth penetration. Hence, in the era of molecular medicine, nuclear cardiology is uniquely primed to provide insight into underlying molecular and genomic aberrations of cardiovascular disease and foster the development of innovative therapeutic interventions in the future.
http://www.medhelp.org/posts/Heart-Disease/COREG-MEDICATION/show/496227
Journal of Nuclear Medicine Vol. 49 No. 3 399-413
A further understanding of CAD pathophysiology at the molecular and cellular levels will allow radionuclide imaging to evolve into a primary prevention tool by earlier detection of atherosclerosis as well as identification of vulnerable plaques and adaptations in myocardial metabolism.
Radionuclide tracers by their nature reflect physiologic processes at the cellular level. Nuclear imaging techniques are well suited for cardiac molecular imaging because of their relatively high intrinsic sensitivity and excellent depth penetration. Hence, in the era of molecular medicine, nuclear cardiology is uniquely primed to provide insight into underlying molecular and genomic aberrations of cardiovascular disease and foster the development of innovative therapeutic interventions in the future.
I have done some reading up of nuclear scans (thallium). Radioactive Thallium bonds to red corpuscles and travels around the body in the blood stream and will obviously end up in all areas. A nuclear perfusion scan (thallium) is not just about seeing blood supply through arteries, it reveals cell condition in the heart too, or anywhere in the body. All cells which are alive, will require oxygen to live. Even stunned or hibernating cells will require the oxygen and use it or they will simply shut down and die. As the cells absorb the oxygen, the Thallium is absorbed with it. The scan is not detailed enough to go into single cell detail, but areas will show up where oxygen is absorbed. Dark areas will be dead cells. Areas with a less intensity of colour will depict stunned/hibernating cells because they are not working with the rest of the heart, they are simply surviving in a rest state. These will absorb oxygen but not as much, hence being a lower intensity on the image. This is how they determine reversible ischaemia. When the scans are performed, there is one at rest and with stress levels. You would expect the heart to show a greater intensity of thallium in the stress scan due to the greater use of oxygen. Any areas of no change between the two images would suggest a blood flow restriction.
Some body cells (I haven't found out yet if heart cells are this type) can switch from using oxygen to fermenting sugars instead for energy, they turn anaerobic instead of aerobic. It has been shown that these cells are in a dangerous state whereby they can trigger into an out of control multiplication mode for survival. In other words, they multiply at a much higher rate than normal, turning cancerous. I would assume that dark areas on a nuclear scan are always dead cells, and not anaerobic activity or else heart cancer would be a very common thing.
So from what I can gather, to summarize....
Dull areas in first thallium scan refer to reversible ischaemia. Dark areas refer to dead cells.
When comparing first and second scans, areas with no change suggest ischaemia.
What I am confused about with this scanning technology is how accurate it is with regards to depth. Obviously heart muscle is not one cell thick, so what about underlying layers?
What about a septum wall? MVD is not going to be revealed (probably) ?
Some body cells (I haven't found out yet if heart cells are this type) can switch from using oxygen to fermenting sugars instead for energy, they turn anaerobic instead of aerobic. It has been shown that these cells are in a dangerous state whereby they can trigger into an out of control multiplication mode for survival. In other words, they multiply at a much higher rate than normal, turning cancerous. I would assume that dark areas on a nuclear scan are always dead cells, and not anaerobic activity or else heart cancer would be a very common thing.
So from what I can gather, to summarize....
Dull areas in first thallium scan refer to reversible ischaemia. Dark areas refer to dead cells.
When comparing first and second scans, areas with no change suggest ischaemia.
What I am confused about with this scanning technology is how accurate it is with regards to depth. Obviously heart muscle is not one cell thick, so what about underlying layers?
What about a septum wall? MVD is not going to be revealed (probably) ?
Thanks for the information.
Current technbology includes 3D depth perception and it seems the process is viewing a number of different images at different angles (slices) and then re-assembled for analysis...4D instrumentation includes blood flow.
There are currently several imaging methods that can be successfully used to study myocardial energy metabolism. PET, SPET and NMR can all be used to study certain areas of this topic. The methods provide a powerful way to increase the understanding of cardiac physiology and the mechanisms of disease. Due to the unique features and large number of existing tracers, PET appears to provide the most complete insight into myocardial energy metabolism in vivo. In the detection of myocardial viability, PET is regarded as the gold standard. The future role of these methods in clinical cardiology remains unclear and further studies are needed. Novel applications also depend on improved instrumentation and development of new tracers.
Imperial College Faculty of Medicine, London
Current technbology includes 3D depth perception and it seems the process is viewing a number of different images at different angles (slices) and then re-assembled for analysis...4D instrumentation includes blood flow.
There are currently several imaging methods that can be successfully used to study myocardial energy metabolism. PET, SPET and NMR can all be used to study certain areas of this topic. The methods provide a powerful way to increase the understanding of cardiac physiology and the mechanisms of disease. Due to the unique features and large number of existing tracers, PET appears to provide the most complete insight into myocardial energy metabolism in vivo. In the detection of myocardial viability, PET is regarded as the gold standard. The future role of these methods in clinical cardiology remains unclear and further studies are needed. Novel applications also depend on improved instrumentation and development of new tracers.
Imperial College Faculty of Medicine, London
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