Why did this patient have ventricular fibrillation?

A previously healthy 50-something collapsed while exercising.  He underwent CPR and defibrillation and was brought to the ED.

Here is his initial ED ECG:

What do you think?

Analysis
1. Sinus tachycardia due to post arrest state.
2. I see no evidence of STEMI or even of subtle coronary occlusion.  I see no evidence of ischemia.
3. In some leads, there appears to be a very long QT, but it lead II across the bottom is used, it becomes apparent that the P-wave is mimicking the T-wave in some leads.  QT is normal.
4. There is no evidence of structural heart disease or congenital ion channel disease.
5. There are non-diagnostic Q-waves in inferior leads.  These could represent old inferior MI, which provides the substrate (scar) for ventricular fibrillation.



The patient went for emergent angiography.  Here are the findings:

LAD with obstruction, TIMI-1 flow, opened and stented.  Other diffuse non-obstructive disease.




The peak troponin I was only 0.85 ng/mL.

The next day formal echocardiogram was totally normal (no old MI).




In November 2016, this study was published in Resuscitation:

Millin MG et al.  Patients without ST elevation after return of spontaneous circulation may benefit from emergent percutaneous intervention: A systematic review and meta-analysis.  Resuscitation 2016, Vol.108, p.54-60.

The authors looked at many studies of patients with out-of-hospital cardiac arrest (OHCA) in which angiogram findings were correlated with ECG findings.  They found that 1/3 of patients who did not have STEMI on the ECG had culprit lesions that "required intervention."  They caution that this does NOT mean that all patients with cardiac arrest without ST elevation need emergent cath lab activation.  They caution that it is not clear which of these patients do need the cath lab or how to identify which will have culprits that need intervention.  Further study is needed.

However, here is a subgroup of OHCA that definitely should go:

Previously healthy patients who have ventricular fibrillation without a clear cause.  This includes, but is not limited to, patients with ECG findings such as:

1) Old MI with scar (Q-waves diagnostic of old MI)

2) Brugada syndrome

3) Hypertrophic cardiomyopathy.

4) Evidence of arrhythmogenic RV dysplasia

5) Evidence of chronic cardiomyopathy (along with echo evidence of very poor LV function).  Most of these patients are not previously healthy.

6) Other?

If no definite etiology can be found, the ventricular fibrillation was likely due to coronary ischemia (from acute coronary syndrome, with plaque rupture and thrombus) that is not evident on the ECG.

Common coronary findings in patients with ACS that results in OHCA:

1. Fixed tight lesion(s) which, during exercise, resulted in ischemia (not ACS, intervention not always needed, at least not emergently)

2. Thrombosis which was occlusive or nearly occlusive, but is no longer so because of some spontaneous thrombus lysis (requires intervention).   

3. Culprit lesion which showered downstream platelet-fibrin aggregates, resulting in small vessel ischemia.  These culprits are dangerous because the thrombus can propagate again and occlude the artery (requires intervention).

4. Thrombus with persistently limited flow, as in this case, even thought the ECG that does not show evidence of ischemia (requires intervention).

5. Other?

Learning point:

ST Elevation, and especially ST elevation criteria, are not sensitive for ACS and not even very sensitive for coronary occlusion.  ST depression may also not be present.  A high pretest probability, such as unexplained ventricular fibrillation, is ample reason to activate the cath lab.