It seems with your question that, pt came due to chest pain, not due to arrythmia.

Serial ECGs and Blood test with specific Cardiac enzyme , High Sensitive Tropinin

also done serially. If they are normal that means the possibilty of this chest pain may be non specfic. In every case if the history of chest pain very suggestive of ischemic Chest pain, then these paties are admitted to do serial ECGs and troponine as IN patients.

If troponine is positive that means pt has an event called NONSTEMI.

STMI is diagnosed with typical ECG changes and is not necessary for to wait for any blood test, and these patents are directly taken to Cath LAB for Primary angioplasty.

If the facility of Primary angioplasty not awailable in a facility near by then Thrombolytic therapy is given.

Those Patients who were discharged are low risk and are called to do stress TEST, which can be Stress ECG, Stress MIBI, Pharmocological MIBI, or stress ECHO.

and some time Cardiac CT with calcium score.

Since this group is low risk, it is extermly unlikely, they may die while waiting for the test.

Arrythmia is altogether is a different condition. This broadly can be devided into Tachy Arrythmia where heart rate goes high, or Bradiarrythmia where heart rate goes low.

Detial fo different Tachy and brady arrythmia is niot the issue to discuss here.

There is a very minimal role of MIBI in arrythmia as it is usally to see if there is any ischemia to myocardiam or not.

If your concern is arrhythmia in the early time fram after patient leaves ER, consider cardiac monitoring. A 30 day cardiac event monitor will automatically detect and transmit arrhythmias.

Hi both,

Thank you for your replies.

The patients were mainly sportsmen who came with tachy arrhythmia. But no blood tests, scans etc. done. Purely 5 rounds of ECG. But the ED MO d/w Consultant just discharge  them after 1 hr observation citing tachy NOS. No holter monitor issued. Only 1 was referred for MIBI f/u. 2 returned dead by ambulance in interval of 1 hr each and 2 never returned at all. If MIBI is not the gold standard for tachy arrhythmia, what is/are?

There is standard guidelines for investigating suspected Tachyarrhythmia as well in sportsman subjects.

1. They all should have ECHOCARDIOGRAM, to rule out Hypertrophic cardiomyopathy

2. All should have Holter preferably 48 hours, even this will not be able exclude tachyarrhythmia.as it is difficult to predict the onset of tachyarrhythmia.

3. If there is any suspicion of Brugada, need Ajmalin test or EP study.

4. Also need Stress ECG to precipitate any arrhythmia during controlled environment of stress ECG.

5. some when there is strong evidence in favour of possibility of tachyarrhythmia may require loop recorder for 6-12 months period

In my experience a 24 or even 48 hour Holter is often unhelpful in documenting AF. I almost always use a 30 day event recorder and with the newest technology the recorder will automatically send abnormal rhythm strips and patient activations to your office. They should always have a transthoracic echo with or w/o stress if suspicion of ischemia.

I knew a patient who had 24 hr Holter monitoring. And was very careful not to exert himself during that time because of the monitor. Predictably, the monitoring showed nothing, and he died a week later of a cardiac arrest. Moral of story, not only do monitoring, but instruct patient that they should go about their business as usual so that any abnormality they might usually have is detected.

First, to rule out acute coronary syndrome causing arrhythmia, an ECG with Troponin T level are enough. MIBI scan at ED settings are for early baseline mapping of area of reduced myocardial perfusion. It's usually followed by 2nd MIBI to assess myocardial recovery. This has shown to have prognostication in small study.

If you are talking about arrhythmia per se, baseline ECG and then 24hr Holter monitoring are usually enough. An EPS study can be performed if high clinical suspicious but negative Holter. An Echocardiography can also be useful to look for Hypertrophied Obstructive Cardiomyopathy. To my opinion, the rationale for post-attack MIBI is to look for previous myocardial ischemia causing arrhythmia.

99mTc-sestaMIBI [MIBI] is a perfusion agent, arrythmia can also be caused by a number of causes that bear little relation with myocardial perfusion. So however MIBI [or for that matter: tetrofosmin] is actually used in any clinical protocol, it can never be used as a gold standard to rule out arrythmia irrespective of cause.

In the physiology of the myocardial uptake of MIBI no hidden suggestion can be found that it is suited for arrythmia detection.

A normal stress MIBI scan has only been shown to be associated with a good long term prognosis when used in patients who were suspected of having ischaemic heart disease. No such statements can be made for the use in patients with symptomatic arrythmia, without

To my knowledge, when arrythmia in isolation is suspected a completely different diagnostic strategy is adhered to.

So I think the question needs to be modified a little:

Could MIBI be the only gold standard to rule out ischemia induced arrythmia?

I think not, because in case of cardiac imaging, anything that can be done using 99mTc-sestaMIBI can also be done using 99mTc-tetrofosmin. Only a small adjustment of cut-off values suffices for any switch-over.

 MIBI is not at all the gold standard to rull out arrythmia. MIBI is only one of the diagnostic methods to rull out coronary heart disease. Deadly arrythmia is not allways caused by coronary heart disease, especially in young sportsmen where MIBI study would probably be normal and the patients could still have a deadly arrythmia.