An 80 - something with h/o hypertension and hyperlipidemia complained of chest pain off and on all day, then recurring acutely. He called 911.
Prehospital ECG
The computer called it ***STEMI*** and the medics activated the cath lab.
Smith: The computer was correct. STE in leads I and aVL which is not only diagnostic of OMI, but has 1 mm in 2 consecutive leads (STEMI criteria), with a deep Q-wave in aVL. There is also STE in V2 with a deep QS-wave. There is STE in V1 and STD in V5, V6, suggesting an LAD occlusion proximal to the septal perforator with septal injury and reciprocal STD in lateral leads. Most importantly in confirming OMI, there are hyperacute T-waves in I and aVL and V2-V4.
The QS-wave in V2 does not appear to be "old MI with persistent STE" (LV aneurysm) because there is a large T-wave: the T/QRS ratio = 4/7 = 57% (greater than 36% in any one of leads V1-V4 is indicative of acute -- vs. old -- MI).
The ECG is diagnostic of acute proximal LAD occlusion or first diagonal occlusion.
Case progression
Initially the patient rated the pain as 6/10 for severity, but pain was down to 1/10 after prehospital aspirin and NTG, after which he arrived and had this ED ECG recorded:
Angiogram: Conclusions/Summary
"Indication: Chest pain with dynamic EKG changes concerning for ACS"
--CAD with moderate stenosis of ostial left main.
--CAD with long segment of serial stenosis of proximal to mid LAD.
--Successful PCI of proximal to mid LAD with placement of 3.5 x 38 and 3.5 x
LAD: Large caliber vessel.
There is a long segment of serial 50-80% stenosis noted in the mid portion of the vessel. The LAD is severely tortuous and there is large caliber diagonal after an acute bend in the mid vessel. The distal and apical segments are without significant stenosis.
Lesion on Mid LAD was stented in a complicated procedure.
Echo
Estimated LV ejection fraction-lower limits of normal; 54%.
Regional wall motion abnormality-septum, hypokinesis.
Left ventricular hypertrophy, concentric-mild.
This is the interesting note, and the reason this was flagged as a false positive activation:
"This is an 8X-year-old gentleman with past medical history significant for hypertension and hyperlipidemia who presents as a prehospital Cath Lab activation for anterior ST elevation myocardial infarction. Subsequent prehospital EKG showed dynamic changes with improvement in ST elevation following aspirin and nitroglycerin. Inferior ST depression and sub-millimeter ST elevation in the high lateral leads associated with small Q waves persisted.
"His EKG on arrival did not demonstrate ST elevation. Due to his persistent chest pain and high risk EKG features he was taken emergently to the cardiac catheterization lab where he was found to have moderate left main disease and 90% proximal LAD status post PCI.
"Ultimately this is not a true STEMI, but rather ACS/high risk NSTEMI based on angiographic features which did not show an acute thrombotic lesion, but rather what appears to be more long-standing disease. He remained hemodynamically stable during the case. He was chest pain-free at its conclusion.
Diagnosis: NSTEMI
But this was indeed a STEMI (+) OMI!!
A STEMI that resolves is still a STEMI. It is not NSTEMI. It called a transient STEMI.
In many cases, the thrombus can lyse spontaneously and not show on the angiogram.
In my view, a transient STEMI still needs emergent cath lab activation. Not everyone agrees.
See this post:
Timing of revascularization in patients with transient STEMI: a randomized clinical trial
In this trial, 142 patients with transient STEMI were randomized to emergent vs. next day angiogram with PCI. MRI measure infarct size was the same in both. All patients received aspirin, a P2Y12 inhibitor, and an anticoagulant.
However, and this is a big however, 4 patients in the delayed group had recurrent ischemia and needed to go emergently to the cath lab.
Thus, as I have frequently promoted, if cath is delayed for patients with transient STEMI, one must have continuous 12-lead ST segment monitoring.
Some other interesting cases of Transient STEMI:
excellent blog, Steve. i reviewed the 2012 case as well. the point is that a STEMI is a STEMI is a Stemi whether it resolves spontaneously or not.
ReplyDeletethank you, again.
Thanks for the Blog Doctor Smith!
ReplyDeleteCan I tell that the fragmented QRS in V2 is another positive point favoring STEMI,can't I?
that is supportive, yes.
Delete