Chest pain and Bradycardia

An elderly male complained of chest pain.  He had no previous cardiac history and was only on aspirin, a statin, and a proton pump inhibitor. He was hypotensive but in no distress and well perfused.  Here is the prehospital ECG:

The heart rate is 38.  There are no p-waves and the baseline appears to fibrillate.  Thus, there is new atrial fibrillation with a slow response.  The ventricular rate is regular.  The QRS is narrow.  There is inferior ST elevation and ST depression in V1-V4.  Diagnosis: Atrial Fibrillation with complete (3rd degree) AV block and inferoposterior STEMI.

The medics activated the cath lab.

In the 1980's, it was believed that the right precordial ST depression that frequently accompanies inferior STEMI was due to "anterior subendocardial ischemia."  Then numerous angiographic studies refuted this and showed that it is almost always due to posterior STEMI.   [There are exceptions to this and in most cases the patient has reason for demand ischemia - hypotension and/or tachycardia - AND the ST depression is diffuse, including the precordium].

Atrial fibrillation in STEMI: Atrial fibrillation is uncommonly an acute and immediate result of STEMI, but is a common pre-existing condition in elderly patients with STEMI.  When new onset, it is usually accompanied by a rapid ventricular response because the patient is not already on AV nodal blockers.

When initiated in acute STEMI, atrial fibrillation may be due to sympathetic output, atrial stretch due to LV or RV dysfunction, or atrial infarction.  It occurs much more often in large infarcts or anterior infarcts, especially during the hospital course in those who develop CHF, ventricular dysrhythmias, advanced AV block, or pericarditis.   It may also occur in inferior STEMI because the RCA supplies the sinoatrial nodal artery.

Had this patient had atrial fibrillation with rapid ventricular response, cardioversion would have been indicated (hypotension and very recent onset).  Obviously, in the setting of heart block, cardioversion will have no benefit.


On arrival, here is the ED ECG:

No significant change.

Heart block in inferior STEMI is due to ischemia of the AV node.  In anterior MI, heart block is much more dangerous, as it is due to ischemia of the Bundle of HIS and Purkinje fibers.  Thus, in inferior MI, there is usually a high (junctional or HIS) escape which is narrow.  In anterior STEMI, if there is block, the escape is usually low and is slower and a wide complex (ventricular, or perhaps involves escape of the left or right bundle, which will result is RBBB or LBBB pattern, respectively). 

There was consideration for pacing for this heart block with hypotension, but the patient was not in shock (in spite of hypotension) and the best management for him is to get to the cath lab.

As this may be a nodal escape, and the AV node is responsive to atropine, atropine was given with a temporary increase in heart rate to 50.

A right sided ECG was performed.  Inferior STEMI is often associated with right ventricular MI, especially when the patient is hypotensive.  This is usually accompanied by ST elevation in V1.  However, such ST elevation can be attenuated or cancelled by the (reciprocal) ST depression of posterior STEMI.  So it is not unreasonable to record a right sided ECG.  If (+), the patient is more likely to respond well to fluids without pulmonary edema.

V1-V6 are really V1R (V1 right) to V6R (V6 right), where V1R = V2 and V2R = V1.  As you can see, the R=wave amplitude is low on the right side.  There is no ST elevation.  0.5 mm of STE is the standard criterion for right ventricular MI.  There is none here. 

While waiting for the cath team, posterior leads V7-V9 were recorded.  V7 is at the posterior axillary line, V9 at the paraspinal border, and V8 between them, all at the level of the tip of the scapula:

These are a mirror image of V1-V3, EXCEPT they are lower voltage, as the impulse must travel through an air-filled chest.  There is greater than 1 mm of ST in all 3 leads.  The standard "criterion" for posterior MI, with about 80% sensitivity andd specificity, is 0.5 mm (presumably in 2 consecutive leads, but this important study by Wung et al in 2001 is vague on that). So this easily meets criteria for posterior STEMI.

In the cath lab, a temporary transvenous pacer was quickly placed.  Then the artery was opened with some difficulty and a large thrombus burden was suctioned out. 

Here is the post cath ECG:

There is now sinus rhythm (restored with restoration of perfusion) and there is persistent ST elevation (and precordial depression).

When microvascular reperfusion is incomplete, there may be persistent ST elevation after PCI.  This is more likely to result in long term persistent ST elevation and even diastolic dyskinesis of the inferior and posterior walls ("aneurysm").

A couple days later, the patient was tachycardic and had this ECG recorded:

There is sinus tachycardia and now there is much more ST elevation and depression.  ST elevation and depression can be exaggerated by tachycardia, and this is the probably mechanism here.  Because I don't know the exact clinical situation at this moment, I am not certain.

The patient did well and was sent home.   His last troponin I was 152 ng/ml.   His EF was 40% with a hypokinetic inferior wall.  Posterior wall was not commented on.