I just received this email today. I receive these fairly frequently:
Dear Dr. Smith:
I am an Emergency physician working in an outlying hospital in _________. We have an interventional hospital to which we refer cath lab patients. I had a 31 year old with typical chest pain and vomiting and the attached ECG. I was sure he was infarcting but couldn’t convince the interventionalist to take him (after emailing him the ECG).
I treated the patient aggressively with medical management and transfered him to the tertiary center. They did not take him to the cath lab emergently. When he went to the cath lab the next morning he had a 99% proximal LAD lesion and a massive troponin rise.
I found the experience a little frustrating and was wondering if there was any specific ECG criteria or feature that I could have used to convince the cardiologist to get out of his bed at midnight.
Thanks for your help on this.
Here is the ECG:
|There is minimal ST depression at the J-point in lead V3, and much more in V4-V6. In precordial leads, there should be some J-point elevation, especially in a young male (that is why the guidelines for STEMI require more than 2.5 mm for a male under age 40, although this is not very sensitive).|
There is a hyperacute T-wave in aVL, with reciprocal ST depression in II, III, aVF.
--This ECG is diagnostic of severe ischemia.
--Precordial T-waves are similar to de Winter's T-waves, but not quite as large.
--(de Winter's T-waves are hyperacute T-waves preceded by ST depression and diagnostic of LAD occlusion or subtotal occlusion).
My talk at SMACC-Chicago this year directly addresses this: the FALSE STEMI NonSTEMI Dichotomy. The lecture will be posted online some time this year.
This ECG clearly shows ischemia, but not STEMI. There is diffuse ischemic ST depression.
In this case, there is no reason for demand ischemia (type 2 MI). So this ischemia is due to thrombus causing subtotal occlusion, though not 100% occlusion (usually of LAD, but could be the Left Main). Thrombus propagates and can fully occlude at any moment.
Thrombus often lyses, then propagates, then lyses back and forth in a very dynamic process.
Both the American College of Cardiology/American Heart Association guidelines (ACC/AHA) (Circulation 130:2354-2394; Dec 23/30, 2014 p. 2367 or p. e368), and the European Society of Cardiology guidelines, recommend emergent angiogram and PCI for patients without STEMI who have:
1. Refractory ischemia
2. Hemodynamic instability
3. Pulmonary edema
4. Electrical instability
This may include patients without specific ECG findings or positive troponins, but only due to high clinical suspicion.
Here is the quote from the ACC/AHA:
4.4.4. Early Invasive and Ischemia-Guided Strategies:
4.4.1. An urgent/immediate invasive strategy (diagnosticangiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in patients (men and women¶) with NSTE-ACS who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures).42,44,138,338 (Level
of Evidence: A)
This patient has refractory ischemia. If you have managed his BP, given nitro, given aspirin and heparin and clopidogrel or ticagrelor, and beta blockers if not contraindicated (low stroke volume, bradycardia, AV block), and there is still ischemia, then the major societies recommend emergent angiogram.
Here is a quote from the European Society of Cardiology
“Optimal timing of PCI in Non ST Elevation-ACS has been studied extensively.” (see all studies outlined below)
•“Patients at very high risk”
• Refractory angina
• Severe heart failure
• Life-threatening ventricular arrhythmias
• Haemodynamic instability
•“Were not included in RCTs, in order not to withhold potentially life-saving treatment.”
•“Such patients may have evolving MI and should be taken to an immediate (less than 2 hours) invasive evaluation, regardless of ECG or biomarker findings.”
Finally, the ACC/AHA now recommends thrombolytics for some ACS with ST depression:
2013 STEMI guidelines approve lytics for ST depression with STE in aVR!!
Quote: "Fibrinolytictherapy should not be administered to patients with ST depression except when a true posterior (inferobasal) MI is suspected or when associated with ST elevation in lead aVR." 16,117–120 (Level of Evidence: B)
Circulation. 2013;127:529-555. this is on p. 537.
I'm attaching some critical slides from my talk.
You can send this to him/her.
This is my slide summarizing all trials of emergent vs. delayed PCI for NonSTEMI:
•ABOARD* trial (n=360), Montalescot, JAMA 302:947; 2009
–1 vs. 20 hours, no diff., LMWH mostly, No sophisticated ECG analysis
–Refractory symptoms excluded
•TIMACS,* Mehta, NEJM 360:2165; 2009, 3000 patients
–No diff except for patients with in-hospital GRACE score greater than 140 (Early is better)
–Early was not very early (14 vs. 50 hours)
–Excluded refractory ischemia (personal communication, Mehta. Even though the methods do not state it, Dr. Mehta wrote to me in an email: "I cannot imagine that anyone would have enrolled a patient with ongoing refractory ischemia")
•ISAR-COOL,* JAMA 290:1593, 2003; n = 410
–Better early (but 2.4 hours vs. 86 hours); included tirofiban and clopidogrel 600
–Death or Large MI: 11.6% vs. 5.9%;
–Before PCI: 3 death and 10 large MI in later group vs. 0 deaths and 1 small MI in early group; After PCI: 11 MI in both groups
•LIPSIA-NSTEMI, Thiele, Eur Ht. Journal 2011, n = 400
–1.1 vs 18.6 hours. Death or MI: 21% (delayed) vs. 16% (Immediate), p = 0.17, low statistical power to detect a difference
–Excluded refractory ischemia
•ELISA PCI, van’t Hof, Eur Ht J 24:1401; 2003. N= 220. Delayed always got GP IIb IIIa inhibitor (tirofiban). All received enoxaparin.
–6 vs. 50 hours. Patent vessel: 66% (late) vs. 82% (p = 0.05)
•Meta-analysis. Katritsis Eur Ht. J 32:32; 2011 (excludes LIPSIA-NSTEMI)
–In non-urgent cases, early PCI reduces recurrent ischemia and shortens length of stay
–Rapid/Urgent Cath for high risk, unstable, or refractory ischemia due to ACS.