Question about MIBI scan

I just a mibi done. I'm in my early 40's, get only the minority of chest pain which sometimes I wonder if it's GI related. It's fleeting and usually very specific to what I would say is my PMI area. I also have mildly elevated chol and have normal BP. I used to smoke but quit 15 years ago. There is cardiac history in my family but only in the 70's.

My Mibi shows an "area of concern." My doctor sent me at my request because I wanted a stress test before I start exercising again since it's been a few years.

My main question is, how accurate are these? I really don't want to have a cath which I assume is the next step.

Here's a follow up to my message. Sorry for the delay, I was at work.
I have read all the comments so far and very much appreciate them.

Here are the main highlights:

Exercise to 12 minutes, bruce 4 to 12.9 METS. HR from 62 to 169 at peak. BP from 120/100 to 170/106 at peak. 2.5 mm flat ST depression in 2,3,avf starting 7 minutes and lasting 1 minute into recovery. 1.5 mm flat ST depression in v5 and v6 starting at 10 minutes lasting 1 minute into recovery. Everything was normal with the perfusion except a "small" reversible inferoseptal defect EF was 60%

I would like to point out that I am usually not hypertensive but must have been nervous. I have had my wife who's an RN check since then.
I am more in the range of 110/80.

To try and describe my "chest pain" better, it is in fact more like an occasional sensation of something wrong. Such as a grain of sand on the left either below or lateral to the nipple. It is very slight and pain is probably not even the word to describe it. I only feel it at rest but not if I do any heavy manual house work or occasional exercise or during every day activity. I have a history of heart burn and sometimes it seems GI related but at other times not. On a second note however, there was one time about 3 or 4 years ago where I was running on my treadmill and felt a momentary tear like substernal sensation which lasted for a few seconds. It caused me to stop running out of surprise but never occurred after that with a run again. I was relatively athletic at that time.

Back to the MIBI. I had no chest pain during the exercise but did feel quite winded during the last 25% of it. I am out of shape at present and am about 40 pounds overweight. What was difficult about the exam was just getting enough air for the run. The test mentions my heart rate to be 169 at max but I observed it into the high 180's during the test.

This is kind of a wild question, but from a respiratory standpoint I had reached my max, can this somehow effect the ST changes?

I'm also curious, do the ST changes shown correlate with the inferoseptal defect on scan?

Overall, does my cardiac picture look bad? Is this something you would find on an otherwise healthy 43 year old, the ones who just never had the test done in the first place?

If it is suggested do you think I should follow up with a cath or just toss it up as being a false positive and check again in 10 years?

I have not been able to either speak to my doctor directly because he's away but do have a cardiologist appointment set for next week.

I appreciate any replies.

And this is for coronary flow obstruction only, which is a late manifestation of atherosclerosis. MIBI scans cannot detect non-intrusive atherosclerosis which is often the cause of an acute coronary syndrome. I would encourage you to find out more specifically what "area of concern" really means by asking your doctor for more information, or send your report to me and I'll give you my 2 cents worth.

you are correct, and unfortunately it is often the next step regardless of the outcome of the nuclear scan.

As to risk of the procedure, seek them out. You might be suprised. MIBI scans require an intravenous dose of radioactive dye. There is no safe dose of radiation, no matter how low the exposure.

A heart cath carries even more risk for complications. I remember quite well a patient of mine, 45 years of age, with chest discomfort, underwent the course of evaluation you are pursuing now. I met her while serving as the attending resident on the stroke rehab unit. She is now in a nursing home and cannot converse with her children. Her heart, however, was just fine.

A very high sensitivity, when negative, rules out disease. The disease a
MIBI nuclear perfusion scan rules out is myocardial ischemia from any cause.

yes, but again, we both are assuming the myocardial ischemia is from atherosclerosis.

we must agree to disagree here, as we have many times before about the definition of atherosclerosis.

Yes, you are correct about specificity. It has everything to do with ischemia but not necessarily occlusive atherosclerosis. A very specific test, when positive, rules in disease. For a MIBI nuclear perfusion scan the test is for myocardial ischemia. Most often myocardial ischemia is caused by flow limiting atherosclerosis and not, say, trauma.

No, I mean non-intrusive, assuming that there is no plaque vulnerability upstream of ischemic myocardium. Non-intrusive atherosclerosis will not result in occlusion unless vulnerable plaque triggers thromboembolic episodes. For silent non-intrusive atherosclerosis, a MIBI nuclear scan will be negative; MIBI scans cannot detect (silent) non-intrusive atherosclerosis.

Non-intrusive is found with positive remodeling of the artery; an atheroma is present, can be vulnerable, but does not intrude into the arterial lumen. Non-intrusive positive remodeling continues for quite some time in non-diabetics.
http://tinyurl.com/xs30

The carotid IMT of 75 patients with multiple complex coronary plaques was significantly larger than that of 50 patients with solitary plaques (p <
0.0003). CONCLUSIONS: In acute coronary syndrome, multiple complex coronary plaques are associated with positive carotid remodeling, suggesting that plaque vulnerability may be a systemic phenomenon.
http://tinyurl.com/xs40

RESULTS: Soft plaque was observed more frequently in acute than in stable coronary syndrome (59% vs 31%), whereas hard plaque was more common in stable coronary syndrome (69% vs 41%) (P = 0.03). The EEM CSA (15.11 +/-
2.89 mm(2) vs 13.25 +/-3.10 mm(2), P = 0.019) and plaque CSA (10.83 +/-2.62 mm(2) vs 9.30 +/-2.84 mm(2), P = 0.035) were significantly greater at target lesions in patients with acute rather than stable coronary syndrome, while lumen CSA and percent area stenosis were similar in both groups. RI was significantly higher (1.08 +/-0.16 vs 0.95 +/-0.14, P = 0.002) and positive remodeling was more frequent in acute coronary syndrome (53% vs
23%, P = 0.019), whereas negative remodeling was more common in stable coronary syndrome (58% vs 24%, P = 0.007).

ahem... http://tinyurl.com/xs40

RESULTS: Soft plaque was observed more frequently in acute than in stable coronary syndrome (59% vs 31%), whereas hard plaque was more common in stable coronary syndrome (69% vs 41%) (P = 0.03).

The mechanism of occlusion in acute coronary syndrome results from thromboembolism, not from the actual atherosclerosis. Thrombosis, although associated with atherosclerosis, is a triggered event of platelet aggregation. Occlusion can occur without thrombosis, albeit much slower, but can occur exclusively from atheroma growth without thrombosis and with an intact fibrous cap. In other words, someone can have a non-occlusive vulnerable atheroma giving rise to acute coronary syndrome. In fact, non- occlusive atheromas, or vulnerable plaques, are the primary cause of ACS.

Often is the key word. Not always, but often.

In this study, 15% of the time.
http://tinyurl.com/xred

The study population consisted of 334 patients. Their mean age was 56 +/-10 years, and 80% were men. Of the patients, 30% were asymptomatic, 29% had angina, and only 6% had recent acute myocardial infarction or unstable angina. Fifty-one patients (fifteen percent) were subsequently referred for coronary angiography.

I would consider 15% "often" considering the risk of coronary angiography and its kissing cousin, angioplasty. http://tinyurl.com/xrwg

"let's warm up the cath lab".
http://tinyurl.com/xrxy

...and quite tragic.

For those interested here were my cardiologist recommendations:

Do a stress echo to see if it correlates with the mibi although the general feeling is that the original test is non specific and likely falsely positive based on my symptomatology. Also to start statins, weight loss, exercise ect. Watch salt intake. He didn't seem to concerned.

http://tinyurl.com/xw5e

CONCLUSION: Of 270 consecutive patients, 41 (15%) referred to coronary angiography due to reversible MIBI uptake defects showed coronary artery stenoses < 50%. Twenty-six (10%) of these presented angiographically normal coronary arteries. The significantly higher proportion of left ventricular hypertrophy and LAFB in patients with reversible MIBI uptake defects without significant CAD suggest microvascular disease, angiographically underestimated CAD, and conduction abnormalities as underlying mechanisms.

In other words, you might consider an echocardiogram to identify your left ventricular size. However, ecocardiograms are risk free and give a tremendous amount of information about left ventricular size and is very well validated. You should also be screened for diabetes.

It is not a wild question. Hyperventilation can effect ST segment. Before all exercise treadmill test I supervise, I expect the technician to perform supine, standing, and standing hyperventilation ECGs to ensure there is no
ST changes from these positions and with hyperventilation.

First of all, do not panic. Do not make a hasty decision. Learn about your options first.

sometimes, but echocardiography is your best option since it will throw the questionable MIBI scan into a whole new light. If you do not have LVH, then you must also consider the absence of a standing hyperventilation ecg as being an important missing part of the scan. I suspect however, that the poor protocol of the study will be downplayed by those involved with it.

It is my opinion that you can engage in mild exercise for the time being, but it is also important to know what medications you are currently taking.
Please include all supplements and over the counter as needed medications.

Hyperventilation can induce coronary vasospasm. Coronary vasospasm is not always due from atherosclerosis, and is often the achilles' heel of coronary angiography.
http://tinyurl.com/xy75

We are discussing the 'scan' and not just the 'images'. The 'scan' includes the images and the ecg interpretation together. A finding on one can influence the interpretation of the other. Because of this, it would be interesting to have the ecg strips and the perfusion images read independently by different doctors, and see if indeed the two still correlate.

OK, I'm leaving my terra firma, but I would like you to clarify this for me in the perspective of Starling's law. LVEF is a reflection of contractility of the heart, and not the size of the myocardium. LVH is a reflection of the myocardial size, and not of contractility.

No we are not, and I should have stated "and with us at SMC" instead. Thank you for clarifying this; it is quite important.

I disagree. It may help identify a false positive for macrovascular atherosclerosis on his scan.

If he did not have a pre exercise hyperventialtion ecg, then there is a quality concern about the technical accuracy of the scan itself.

2,3 aVf are isolated for the inferior wall, but I am not certain what leads would become involved with the septum.