A 30-something with history of 2 pack per day smoking complained of sudden left arm and chest pain while working construction. It was very distressing for him. He presented by private transportation, stating that his pain was decreasing.
At triage, he had this ECG recorded:
No significant abnormalities were seen in triage, and the patient had to wait 2 hours. By the time he was roomed, his pain was gone.
A second ECG was recorded, pain free:
His first troponin I, drawn 4 hours after arrival, was 1.6 ng/mL.
Analysis:
--There is subtle ST Elevation in inferior leads II, III, aVF, with reciprocal ST depression in aVL. This is diagnostic of inferior injury. The fact that it resolved with resolution of chest pain simply verifies this.
--There is also a decrease in the size of the lateral precordial T-waves.
--Notice that the ST elevation on the first ECG does NOT meet STEMI criteria. There is not 1 mm of STE in any lead.
--But that ECG is diagnostic of injury.
The patient was started on heparin.
Shortly thereafter, he had a run of ventricular tachycardia. Therefore he was taken urgently to the cath lab. [Patients with ACS who have persistent refractory pain, hemodynamic or electrical instability, or pulmonary edema, should go emergently to the cath lab]
The angiogram was clean!!
An MRI was diagnostic of myocarditis.
--There were no wall motion abnormalities (although they are frequently seen in myocarditis)
--No evidence of microvascular obstruction
--Delayed enhancement sequences obtained at 10 mins after gadolinium administration reveal multiple (at least 3) foci of delayed enhancement, measuring about 2 centimeters in the
Troponin I profile:
Time after arrival Troponin I
4 1.613
6.5 5.887
13.5 10.969
15.5 11.347
19 9.001
21.5 7.521
25 6.175
Learning Points:
1. Learn to recognize subtle injury. This could have been an early STEMI. The patient's reperfusion time would have been delayed.
2. It is particularly easy to miss these when you are shown an ECG completely out of clinical context, as often happens with triage ECGs.
3. Injury NOT due to ischemia also is high risk: in this case, the risk of ventricular dysrhythmias.
4. Myocarditis and STEMI are often indistinguishable. They may have injury on ECG, wall motion abnormalities, and elevated troponins. ACS may also have a negative angiogram if there is autolysis of thrombus! MRI makes the diagnosis.
Here is another interesting related case:
At triage, he had this ECG recorded:
 |
| The computer read that there is incomplete right bundle branch block. QRS duration 102 ms. What do you think? |
No significant abnormalities were seen in triage, and the patient had to wait 2 hours. By the time he was roomed, his pain was gone.
A second ECG was recorded, pain free:
 |
| If you didn't see anything wrong with the first one, maybe you can see it now by comparison with this one. |
His first troponin I, drawn 4 hours after arrival, was 1.6 ng/mL.
Analysis:
--There is subtle ST Elevation in inferior leads II, III, aVF, with reciprocal ST depression in aVL. This is diagnostic of inferior injury. The fact that it resolved with resolution of chest pain simply verifies this.
--There is also a decrease in the size of the lateral precordial T-waves.
--Notice that the ST elevation on the first ECG does NOT meet STEMI criteria. There is not 1 mm of STE in any lead.
--But that ECG is diagnostic of injury.
The patient was started on heparin.
Shortly thereafter, he had a run of ventricular tachycardia. Therefore he was taken urgently to the cath lab. [Patients with ACS who have persistent refractory pain, hemodynamic or electrical instability, or pulmonary edema, should go emergently to the cath lab]
The angiogram was clean!!
An MRI was diagnostic of myocarditis.
--There were no wall motion abnormalities (although they are frequently seen in myocarditis)
--No evidence of microvascular obstruction
--Delayed enhancement sequences obtained at 10 mins after gadolinium administration reveal multiple (at least 3) foci of delayed enhancement, measuring about 2 centimeters in the
inferior septum, and approximately the same size in the inferior wall.
--There is subendocardial sparing demonstrated (this pretty much establishes myocarditis, as ischemia would preferentially affect the subendocardium.
--There is subendocardial sparing demonstrated (this pretty much establishes myocarditis, as ischemia would preferentially affect the subendocardium.
Troponin I profile:
Time after arrival Troponin I
4 1.613
6.5 5.887
13.5 10.969
15.5 11.347
19 9.001
21.5 7.521
25 6.175
Learning Points:
1. Learn to recognize subtle injury. This could have been an early STEMI. The patient's reperfusion time would have been delayed.
2. It is particularly easy to miss these when you are shown an ECG completely out of clinical context, as often happens with triage ECGs.
3. Injury NOT due to ischemia also is high risk: in this case, the risk of ventricular dysrhythmias.
4. Myocarditis and STEMI are often indistinguishable. They may have injury on ECG, wall motion abnormalities, and elevated troponins. ACS may also have a negative angiogram if there is autolysis of thrombus! MRI makes the diagnosis.
Here is another interesting related case:
Wonderful case and my thanks to Dr Smith for bringing this rather under diagnosed but a commonly encountered scenario in Emergency Cardiology ! Since,in this case, everything was done an ideal copy-book style like Quick Angio,Cardiac MRI etc..........many Hospitals dont have these facilitie but they do have such cases in abundance. I request Dr Smith to enlighten us with some clinical steps ,so that such cases can be dealt with some rationale.Also, is some reference article can be sighted ,it will be very good.
ReplyDeleteThere is one classic article referenced at the link above.
DeleteWow, nice case!
ReplyDeleteAnd whats the cause of miocarditis?
Any specific agent was identified?
That was not determined in this case.
DeleteAlways find these cases to be interesting as these are otherwise diagnostic of coronary occlusion. Other than myo(peri)carditis and maybe vasospasm (prinzmetals or other) is there any other disease process that you can think of that would give this ECG and a clean angiogram? A dissection would still be seen on angiogram and I can't think of anything else that would potentially lead astray.
ReplyDeleteThanks for posting!
-Dan
Any cause of coronary occlusion. 1% of thrombotic occlusions have competely normal coronary arteries. Thrombus generated in an artery with no visible atherosclerosis on angiogram, then thrombus autolysis. In such a case, the MRI would look different.
DeleteHow can you explain very fast ECG dynamic? It is not tipical thing for miocarditis. And why you ruled out a coronary spasm? How many diagnostic point of miocarditis youll seen in this case?
ReplyDeleteIt is a very good question. My outstanding radiologist is 98% certain that this is myocarditis, and the fact that the endocardium is spared is excellent evidence. I think we may have an inaccurate notion that myocarditis is not dynamic. I used to believe that troponin would be fairly steady state in myocarditis, but it is not. And there is not reason that the ECG does not have to be dynamic.
DeleteOk. So, in your opinion - ethyology of myocarditis in this case?
Deletecould only be a guess: viral
DeleteAm i the only one that cant see STE in lead II as stated? R wave progression in v2 is poor and small TWI's
ReplyDeleteIn the first EKG there is definitely ST elevation. In the second, it is gone or almost gone.
DeleteThank you very much Dr Smith. Years ago as a junior resident I had a 42yo male carpenter who developed mild chest pain after shifting some heavy boxes, and the pain settled after rest in the ER. He thought it was just a muscle strain and the NUM wanted to get him out. There were only some very subtle changes on the ECG, and it took the consultant to diagnose him with an NSTEMI. Being a cautious resident I had ordered a troponin, which the registrar was annoyed about, as they wanted to get him out, but it came back positive to confirm the STEMI diagnosis. I wasn't able to keep the ECG, so it was great to be able to see this example and read your analysis. Many thanks! (Dr Rowena Christiansen, Melbourne, Australia)
ReplyDeleteThank you Aurora! — :)
Delete