A 60-something male with a history of an LAD stent presented with intermittent episodes of left-sided chest pain for the past few weeks. It is associated with right arm symptoms. He received sublingual NTG, but I'm not sure if it was before or after the ECG, and for how long he had had CP.
He had this ED ECG recorded:
This ECG is diagnostic of occlusion, usually occlusion MI (OMI) with reperfusion. There is inferior ST Elevation with inverted T-waves (reperfusion T-waves), and reciprocal ST depression in aVL with a reciprocally upright T-wave.
Another ECG was recorded at a moment when the patient was clearly chest pain free:
40 minutes later
The patient was started on a heparin drip and aspirin was given.
Serial Troponins were as follows:
The patient did NOT have an acute MI, which would require at least one troponin above the 99th percentile.
The inpatient team stopped the heparin and wrote that they thought this was "Prinzmetal's angina." But the majority of what seems to be "spasm" is really thrombus that propagates and lyses.
Then the patient had a run of symptomatic monomorphic ventricular tachycardia overnight.
The next day, they did a stress test:
So stress echo was normal but the patient had symptoms and the stress ECG showed ischemic ST elevation.
So an angiogram was done:
Learning points:
1. Certain ECG findings are very specific for ischemia. The first ECG is diagnostic, and confirmed when it resolves with resolution of pain.
2. Spasm is much less likely than ACS.
3. Unstable angina still exists. It is uncertain if this would have been detected by high sensitivity troponins.
He had this ED ECG recorded:
 |
| What do you think? |
This ECG is diagnostic of occlusion, usually occlusion MI (OMI) with reperfusion. There is inferior ST Elevation with inverted T-waves (reperfusion T-waves), and reciprocal ST depression in aVL with a reciprocally upright T-wave.
Another ECG was recorded at a moment when the patient was clearly chest pain free:
40 minutes later
 |
| Reperfusion T-waves are deeper STE has resolved. |
The patient was started on a heparin drip and aspirin was given.
Serial Troponins were as follows:
The inpatient team stopped the heparin and wrote that they thought this was "Prinzmetal's angina." But the majority of what seems to be "spasm" is really thrombus that propagates and lyses.
Then the patient had a run of symptomatic monomorphic ventricular tachycardia overnight.
The next day, they did a stress test:
The patient exercised for 6:22 minutes on the standard Bruce protocol and achieved a peak heart rate of 139 bpm representing 89% of age predicted maximum heart rate and an estimated work load of 7.4 METs. Test was terminated because of fatigue. Patient did report chest pain.
Normal stress echocardiogram with a moderate degree of certainty.
1. No echocardiographic evidence of ischemia at the cardiac workload
achieved.
2. Left ventricular function normal at rest, improved with stress.
3. Equivocal ECG response with adequate heart rate (the inferior leads with stress).
4. The patient did report angina with stress.
5. Exercise capacity was fair (95% predicted METS for age and gender).
Stress ECG had 1 mm ST Elevation:
There is no echocardiographic evidence of ischemia, but the EKG changes and ischemic symptoms are abnormal. Microvascular dysfunction could be considered.
Stress ECG had 1 mm ST Elevation:
There is no echocardiographic evidence of ischemia, but the EKG changes and ischemic symptoms are abnormal. Microvascular dysfunction could be considered.
So an angiogram was done:
ACS - Unstable Angina .
Patent stent in LAD
Culprit is 90% stenosis in the mid RCA .
Stented
Learning points:
1. Certain ECG findings are very specific for ischemia. The first ECG is diagnostic, and confirmed when it resolves with resolution of pain.
2. Spasm is much less likely than ACS.
3. Unstable angina still exists. It is uncertain if this would have been detected by high sensitivity troponins.
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