To Fluffy regarding test results

Did the nitro relieve your heart pain, if it did that is a somewhat reliable indication that the pain is associated due to ischemia (lack of blood flow to the heart.  Nitro will very quickly dilate the coronary arteries.

QUOTE:
WALL MOTION / VIABILITY.  THERE IS NORMAL CONTRACTILITY  ( THICKENING ) ON GATED STRESS
IMAGING.. GATED 3 D WALL MOTION DISPLAY ( MYOMETRIX ) DEMONSTRATES NO EVIDENCE OF
HYPOKINESIS OR DYSKINESIS.

There is no evidence shown for dyskinesis (impairment for voluntary motion) or hypokinesis (abnormal decrease in muscular movement).


IMPRESSION. THERE WAS A REVERSE PERFUSION DEFECT IN THE INFEROSEPTAL REGION AND THIS IS
ASSOCIATED WITH HYPOKINESIS OF THE SEPTUM AND INFERIOR SEPTUM NEAR THE CARDIAC APEX
AND MID CARDIAC SEGMENT.

There is some decrease in the wall movement of the septum (wall separating left and right side of the heart).   If there is some septum movement disorder that is not as significant as the heart wall.  Septum does not normally show much movement.  Both ventricles separated by septum contract at the same time so the septum won't normally have much movement.  The heart walls contract and squeezes blood valume against the septum to force the blood out of the chamber.

THIS AREA DOES NOT PERFUSE NORMALLY ON STRESS IMAGING. THE
SIGNIFICENCE OF A REVERSE OR PARADOXICAL PERFUSION DEFECT VARIES BUT THIS CONDITION MAY
OCCUR WITH A RECENT MI, PARTICUALLRY AFTER REVASCULARIZATION OR THROMBOLYTIC THERAPY.
CLINICAL CORRELATION IS ADVISED.OVERALL EJECTION FRACTION IS NORMAL. NO OTHER AREAS OF HYPOKINESIS SEEN.

There is not a firm conclusion of an MI (myoxcardia infarction) and other evidence is advised.  No other area shown for wall movement disorder.

[fluffypurrcat]

Thank you very much for explaining this to me, I kept asking and noone seemed to be able to give me an opinion. it is funny though, because one of the dr.s Cleveland Clinic when given my results, seemed to think I did indeed have an MI, although he thought most likely a small one. He allso thought I would get a catherization, etc, etc.

  I do have two questions, one is what does it mean though when it says it does not Perfuse normally under Stress imaging?
The last question is regarding the use of the Nitro, if I get a good effect from using the Nitro, then how do they determine if you have Ischemic disease? My dad had diagnosed Ischemic heart disease for a couple of years till he had an acute MI that killed him.
The fact that I have Raynaulds disease, Circulation problem, could that affect the blood flow to my heart?


        You have been so kind to explain all of this to me, it is very much appreciated. I have another test comming up, and I will have to wait for the results of that.

      Thank you again Kenkeith. Happier in the Redwoods,        Fluffypurrcat

[maggiemag]

I think also that nitro will help with chest pain due to esophageal spasm, not just coronary artery disease.  Sometimes things aren't as simple as they initially look.

[erijon]

The phrase "does not perfuse normally under stress" means that when you heart is at stress it does not distribute or "perfuse" the tracer into the heart muscle normally.  This means that ubder stress, this area of your heart is not getting enough blood as needed.  It does however at rest which is why they deem it reversible.

Kenkeith may correct me about this as he is more knowelgable than I, but it is my understanding that nitro will also have the same effect on pain from your esophogus as it does on heart pain as they both are affected by the same nerve bundle. I know that statement may just confuse the situation more but I thought I would throw it out there. My thoughts are that if all the indicators point to ischemia as the cause, changes on your EKG on your stress test, perfusion defects ect that's how the diaginosis is made.

Ken, am I off base?

Jon

[fizzixgal]

I could be all wet but from the references I've been able to bring up online, "reverse perfusion pattern" or defect usually means that the defect is seen at rest and at least partly normalizes under stress, the opposite of what is expected when the tissue is ischemic. "Does not perfuse normally under stress imaging" in this context could mean that the defect doesn't normalize completely, or maybe the area perfuses normally at rest but takes up more of the tracer under stress as compared with surrounding tissue, which would also be abnormal.

They do say "reverse or paradoxical" so it really doesn't sound to me like they are talking about a "reversible" defect (perfusion deficiency under stress that normalizes at rest).

[fluffypurrcat]

This is why I am so confused, there seems to be too much confusion about the word or term, Reverse Perfusion Defect or PARADOXICAL . SO the question is, well the way my dr. explained it to me, is that under Rest, I had more of the tracer or perfusion then at Stress, and that is was the Opposite of what you would expect to find. She said the pictures of my heart were : " lit up like a xmas tree: " ( meaning that my heart had absorbed more of the dye at rest than it should have. It should have absorbed more at stress when your heart needs more, so how do you explain that? I don't understand about the stunned myocardium either. How does the myocardium get stunned and how does it recover? I wonder if I could just take this test all over again, and if it would be the same, or if the heart recovers more the more time that passes after a MI incident? What do you all think? Please let me know.                                   fluflfypurrcat

[erijon]

You could be right, I get confused on the terminology at times, it all depends so much on so many factors.

Either way, hang in the fluffypurrcat. I understand your frustration about no real diagnosis. I remember when I was going through what you are, I was elated when I was told I needed immediate gallbladder surgery as I had stones stuck in the neck and bile duct. I shouold have been scared out of my mind but instead just having a final diagnosis was a great releif.

I hope all goes well for you,

Jon

[fizzixgal]

Sorry, no, I can't explain it. The part that is hardest to explain is why having less tracer uptake at stress than at rest is somehow unexpected or paradoxical, since from everything i have read and been told by cardiologists, that is an expected finding when the vessels supplying the area are stenosed. They cannot expand to meet the increased demand for blood supply under stress. But that would be a "reversible perfusion defect" as erijon was saying and not a "reverse" or "paradoxical" defect. I wish you could sit down and talk with your cardiologist about this as he is the only person in a position to explain your results to you.

I hope you will get more answers from your upcoming echo.

[kenkeith]

A reverse redistribution pattern during myocardial perfusion imaging is when stress images exhibit greater perfusion than rest. Radiopharmaceuticals may also yield a reverse perfusion pattern, but its significance is uncertain. It can test the hypothesis that reverse perfusion correlates with the presence and location of flow limiting coronary stenosis(es).

The reverse perfusion pattern is a poor predictor of flow limiting coronary disease, and does not correlate with stenosis location in those with significant lesions. Such patients should not undergo invasive investigation purely on the basis of this result.
Specifically, a reverse perfusion pattern in the infarct area is a frequent finding and is likely to be due to residual tissue viability.

"Tests have shown myocardial perfusion with tetrofosmin might appear considerably worse at rest than at stress in patients with MI and normal coronary arteries (NCA). Specifically, a reverse perfusion pattern in the infarct area is a frequent finding and is likely to be due to residual tissue viability. We postulate that in these patients the hyperemic response to exercise may mask resting underperfusion areas"

Reverse perfusion phenomenon does not predict coronary artery disease with high probability and may also be observed in myocardopathies. Where coronary artery disease does exist RP does not correlate well with the degree or location ofstenosis. Multiple mechanisms appear to be involved.

"Other physiologic variables which we have seen or postulated to explain RP include the combination of spasm and structural blockage; transmural compared with bendocardial infarct; perfusion status of contiguous and/or overlying and underlying segments; recanalization of atherosclerotic plaques in regions of previous infarct; incomplete infarction with intermingled viable and scarred myocardium; variability of the severity and duration of spasm; variability of the postischemic hyperemic response; variability of the exercise effort and physiologic response of the heart to that effort".

There has been a study  designed to assess the prognostic value of photon emission computed tomographic (thallium SPECT) perfusion imaging in patients evaluated for stable angina pectoris and to examine the relation, if any, between the presence and extent of myocardial defect and future fatal or nonfatal cardiovascular events (revascularization, secondary myocardial infarction). In patients with stable angina, normal thallium SPECT imaging indicates a low risk patient, and the extent of myocardial defect is an important prognostic predictive factor.

There are theories on the mechanism of reverse perfusion artefacts.  Increased marker tracing  washout from higher local blood flow at rest or inability of the myocardium to hold onto the tracing.

"Hibernating or stunned myocardium mixed with scarring, so that the involved tissues can receive the initial tracing cannot hold onto it effectively. In Pace's study, the idea of a stunned/hibernating myocardium (a result from previous coronary artery occlusions) supported by a lower MIBI uptake may explain the presence of RP associated with occluded but well collateralized coronary circulation, recruitment of collaterals at stress and Chronic Stable Coronary Artery Disease.

In some patient with severe stress induced ischemia (low uptake) this inhomogenity equilibrated within a few hours. In other patients with similar stress induced ischemia or much less severe ischemia, the equilibration takes much longer time, 12 hours or even 24 hours.

In about 40% of patients the stress - 4-hour redistribution protocol suffered from incomplete redistribution, which leads to false "rest or fixed" perfusion defects, ie. infarction and missed ischemia.

At some point, the physician might choose to look at parts of the imaging study that would help identify an artifact, such as the planar projections. If no artifact is present, other elements of the study can be assessed for corroborative evidence of true disease. Additional image findings such as an enlarged left ventricular myocardium, a change in left ventricular size from stress to rest, a prominent right ventricle, and the presence of tracer uptake in the lung can corroborate true disease.


One important element is the stress test result, which can help the reader determine whether the perfusion defect is due to significant disease. If the disease is believed to be real, the perfusion abnormality can be characterized by defect size; defect severity; defect location, including the likely culprit coronary vessel; and the presence or absence of a reversible pattern. If one or both parts of the study are electrocardiography gated, then left ventricular function can also be assessed and quantitated. These results can further illuminate the question of disease versus artifact.

Included: assessment of perfusion defects. Today, this often includes an opinion as to the vascular territory that is associated with the defect. Knowledge of the patient’s coronary anatomy from angiography can enhance the usefulness of the nuclear report.  

Conclusion:The reverse perfusion pattern is a poor predictor of flow limiting coronary disease, and does not correlate with stenosis location in those with significant lesions. Such patients should not undergo invasive investigation purely on the basis of this result.  THE SIGNIFICANCE OF A REVERSE OR PARADOXICAL PERFUSION DEFECT VARIES and the report requires professional interpretation and other clinical evidence and tests.  I didn't comment as it is part of the report and is inconclusive no finding.

Jon,  you are correct about relief with esophogeal (some) pain with nitro.  I haven't heard or read it relates to shared nerve bundle. That is interesting and certainly plausible!. You are much too generous with your compliment!  We all learn from each other. My comment regarding nitro for angina would be in the context with other heart-related signs and symptoms such an EKG, etc. as well as angina.

[fluffypurrcat]

While, this is a lot of information here. I wish I knew how to enterpret it all. I need a dictionary for some of these words. Basically I get the idea that there are so many factors, that without further tests, I won't know what this Reverse Perfusion means anyway. Basically I need more tests to determine what is going on.

Is it possible that I don't have blocked cornonary arteries, but that I have a blood flow problem, ( Ischemia) that some blood is not getting to some parts of my heart, and this MAY have caused either Spasms or a MI, or something similiar that caused the pain? Allso would this correlate with the repeat episodes that I have had in the last month and a half?
       Is a Echocardiogram going to be more prescise at determining what is going on with my heart chambers, wall, and other things that are not seen in the STress test?
What other possible things show up on the echo test? I wonder according to what you said above, and the fact the Dr. has not seen the pictures of my heart from the Perfusion Stress test, Would it help at this point if he saw the pictures that were taken, because I have a copy of the Pictures on disk? If I knew he didn't have them, I would have brought them. Would a repeat Stress test, ( on a treadmill ) be worthwhile at this time, or is it too late, or not worth it at this point? Allso you mentioned " Stunned myocardium" and the fact they dont pick up the tracer well, would this area show up as scar tissue on a Echo test, or some other evidence?
Where did you get all your information? I searched and searched, but kept comming up with the same studies and info that was nonconclusive and didn't use the same term,
Reverse Perfusion Defect. I appreicate your hard work and determnation to find this out for me. Even though it doesn't give me an exact answer, it is a whole lot more than I had before. I guess this is why my Cardio didnt like the report, thought it didn't answer enough questions, esp, not having the pictures to go along with it. One last question.
If you have some sort of conronary event or heart problem, is there a specific time frame that is best at showing up on different tests, or does it matter if it is one month ago, or two years ago, the results will be the same? Also, I am waiting for another episode, or angina, so I can test the Nitro, but havent' had one now for going on two weeks. They are actually getting farther apart, in the beginning after the intital Episode ( what I and my regular dr. have termed a MI  ) they have gone from being 3 or more episodes a week, to none in almost two weeks. Does that have any meaning at all?
There are still lots of questions, but this is one big one that at least now I have some understanding of, that there are too many variables and only the dr. can decide, and I guess he can only decide by history and more tests. Thank you once again kenkeith, and I am sure when I get my Echo test results, I will have more questions. You are a great source for so many here, and I am so glad you took the time to anwer my questions, and put some comfort in my mind.              fluffypurrcat

[kenkeith]

My post is a conglomeration of "cut and paste" of numerous sites and then reorganized and edited into a format that defines reverse perfusion, numerous hypotheses and postulations, what reverse perfusion does not indicate, other physiological variables which have been seen or postulated to explain RP that includes the combination of spasm and structural blockage, ischemia,  etc..

QUOTE REPORT:
THIS AREA DOES NOT PERFUSE NORMALLY ON STRESS IMAGING. THE
SIGNIFICENCE OF A REVERSE OR PARADOXICAL PERFUSION DEFECT VARIES BUT THIS CONDITION MAY
OCCUR WITH A RECENT MI, PARTICUALLRY AFTER REVASCULARIZATION OR THROMBOLYTIC THERAPY.
CLINICAL CORRELATION IS ADVISED.OVERALL EJECTION FRACTION IS NORMAL. NO OTHER AREAS OF HYPOKINESIS SEEN.

The report points out there are paradoxical (contradictions but possibly true) perfusion defect that varies...I provided information that supports that contention and does not establish evidence of a recent MI....but it cannot be ruled out as there appears to be hypokinesis in the septum area.  (I have seen my echo, and it appears to me there is very little if any septum wall movement normally).   If there were an MI in all likelyhood your EF would not be normal and that is paradoxical also as there is some evidence of hypkinesis.  You require further testing...

What will show up on an echo is impaired heart wall movement impairment displayed in real time on the monitor.  My first "tech" for an echo was an MD, and he explained the procedure, the observations (I saw my valve regurgitation), there appeared to be some heart wall impairment at the distal part of the heart (very little movement there normally).  You should ask to watch the monitor during your echo.

If heart cells are stunned, it may not be seen shortly after revascularization or possibly medication as stunned cells are revitalized when the blood supply is sufficient to the area in question.  If heart cells are hibernating, that condition is different from stunned cells, hibernating are cells deprived of oxygen over a period of time and the cells self-protect by shutting down, but not necrotic.  If the oxygen deprived cells receive a sufficient oxygen supply the cells could be revitalized.  I can't put a time response to the cells except the stunned cells appear to need oxygen quickly (my be due to the fact the oxygen supply had been quickly reduced or stopped).  The slowly deprived (hibernating) cells from oxygen have a different physiological effect and response.  

I think I answered all your questions, if not, let me know.:)

You don't have chest pain (angina) when exercising?