Weird STEMI case

[leviathan]

I took care of a 62 y/o female who had an initial syncopal episode followed 1 hour later by substernal CP that radiated to the left arm, at which point she decided to seek medical aid. She had no cardiac hx, no DM, but was a smoker with HTN. Is there a good explanation for the lag in development of ischemic symptoms? Was the syncope possibly not due to the MI, but a sign of an impending MI?

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[Apollyon]

My last year of residency, on a Sunday afternoon, had a lady that was diabetic that had a syncopal episode only - no chest pain, no SOB. One of the interventional cards attendings happened to be in-house, so he came down with the fellow (although I don't recall why I called cards, because she had RSR on her EKG). The story was good enough, so they took her to the cath lab, finding a 100% circumflex. While she was in the cath lab, her troponin T came back at 73 - not 0.73, but the whole thing. They squirted her in the lab, and she made a full recovery.

What can I theorize in your case? There could have been some ventricular irritability, leading to some nonsustained VT, giving her the syncope. The lesion might not have been occluding enough at that point to cause ischemia, but getting to "critical mass" one hour later to give the classical chest pain.

 

[leviathan]

What can I theorize in your case? There could have been some ventricular irritability, leading to some nonsustained VT, giving her the syncope. The lesion might not have been occluding enough at that point to cause ischemia, but getting to "critical mass" one hour later to give the classical chest pain.

So your theory is that there was a lesion followed by a slowly growing thrombus that:
1) caused an initial syncopal episode due to minor ischemia + ventricular irritability and
2) eventually grew large enough to cause a full-blown infarct + classic ischemic symptoms

That would definitely explain the progression of her case. Have you / anyone else seen a case where someone has atypical signs of an MI progressing into "typical" signs?

 

[SoCuteMD]

So your theory is that there was a lesion followed by a slowly growing thrombus that:
1) caused an initial syncopal episode due to minor ischemia + ventricular irritability and
2) eventually grew large enough to cause a full-blown infarct + classic ischemic symptoms

That would definitely explain the progression of her case. Have you / anyone else seen a case where someone has atypical signs of an MI progressing into "typical" signs?

probably not a "slow growing thrombus" but an unstable thrombosis - they change size very quickly

Yes - definitely. Not that unusual

 

[southerndoc]

So your theory is that there was a lesion followed by a slowly growing thrombus that:
1) caused an initial syncopal episode due to minor ischemia + ventricular irritability and
2) eventually grew large enough to cause a full-blown infarct + classic ischemic symptoms

That would definitely explain the progression of her case. Have you / anyone else seen a case where someone has atypical signs of an MI progressing into "typical" signs?

I agree. The syncopal event was likely due to an arrhythmia. The patient probably developed a thrombus to cause the arrhythmia, and then as the area of ischemia grew it created chest pain. The initial area of ischemia could have been supplied with a watershed area or collaterals, which didn't supply 100% of its demand. As the myocardium continued to work, the demand could have significantly outpaced supply and that led to the chest pain developing and further ischemia. Alternatively, the patient could have developed a thrombus that broke free only to happen again.

My memory escapes me, but I recall reading something in one of my cardiac physiology texts that it took something near 30 minutes of cardiac ischemia before pain occurred. Adenosine seems to be the stimulator of cardiac-related pain, and one could theorize that large amounts of adenosine antagonists (e.g., caffeine) might suppress this.

Remember, a small but not insignificant number of MI's are silent. I've seen one case of syncope that had a STEMI with no chest pain. Was taken to the lab to find a total occlusion of his LAD. I'm still surprised that guy walked out of the hospital.

 

[NKMU]

Not exactly the same, but we had a cool STEMI case recently.

70's male in an express room with complaint of finger pain and swelling, not unlike his gout pain. He was signed out to my colleague with the instructions to tap the affected joint to r/o septic arthritis, then send home with gout treatment. When the resident aspirated the joint, the patient had presumed vasovagal symptoms of nausea and weakness. The resident when back to check on him a little while later, and he complained off chest pain and said, "by the way, i have a few stents..." EKG had big anterior ST elevations, and he went to the cath lab. Near 100% LAD as I recall.

First case we've had of a level 4 finger pain that went for emergent cath.

 

[SoCuteMD]

I guess in my (very limited, I openly admit) experience I rarely think in terms of "Is this a typical presentation or an atypical presentation of an MI?" I more think in terms of chief complaints and systems potentially involved. For chest pain - MI makes the list. For abdominal pain - MI makes the list in patients with MI risk factors or who are older. For syncopal episode, MI is on there in the same group (risk factors/older).