This young male had ventricular fibrillation during a triathlon. He was resuscitated with chest compressions and defibrillation and 1 mg of epinephrine. On his bib it stated that he had a congenital heart disorder. He arrived in the emergency department hemodynamically stable. His initial ECG is shown here.
There is profound LVH with anterolateral ST elevation and reciprocal ST depression in II, III, aVF, and ST depression in V5 and V6 that could all be secondary to LVH or could represent ischemia superimposed on the repolarization abnormalities of LVH: note that wherever there is ST depression, it is associated with a very high voltage R-wave. The ST elevation in V1-V3 is typical of LVH (high voltage S-waves), but the ST elevation in aVL is concordant to (in the same direction as) the high voltage and thus very suggestive of injury pattern.
ACS would be highly unusual in a young athlete, and given the information on his race bib, one must first suspect that the abnormal ST elevation is due to demand ischemia, not ACS.
A bedside echo performed by the emergency physician showed no wall motion abnormality and confirmed LVH. A repeat ECG after a few minutes of cool down is shown.
A bedside echo performed by the emergency physician showed no wall motion abnormality and confirmed LVH. A repeat ECG after a few minutes of cool down is shown.
| Now there is much less ST segment deviation, less elevation and less depression. |
The troponin returned positive, and the maximum troponin was 3.8 ng/ml. The next day, and angiogram showed normal coronary arteries. An echocardiogram confirmed aortic stenosis with a large pressure gradient. The stress of the triathlon cause demand ischemia and ventricular fibrillation. He awoke and did well.
Thus, this patient had increased ST elevation (current of injury) superimposed on the ST elevation of LVH and simulating STEMI.
Would be interested in his EF as well as when he plans to replace his aortic valve. Does he alsohave cardiomyopathy?
ReplyDeleteEF is normal. Treatment plan is uncertain now.
ReplyDelete"...The troponin returned positive, and the maximum troponin was 3.8 ng/ml...it is not due to ACS..."
ReplyDeletecan you pls explain this??
A positive troponin only tells us that there is myocardial cell death. It does not tell us why. Myocarditis causes a positive troponin. In this case, the cell death is due to ischemia, but not all ischemia is due to ACS. In fact, I have data on consecutive MIs showing that only 25-30% of MI (cell death due to ischemia) is due to ACS. The remainder were due to stress on the heart from hypertension, tachycardia, sepsis, pulmonary embolism, etc.
ReplyDeletecan you please comment on QRS and ST of aVL in ECG1 ?
ReplyDeleteBoth the QRS and ST have an axis, or vector, of + 90 degrees, or directly upward, so that there is minimal ST elevation in aVL ( 0.5mm). This superior ST axis is reflected in the inferior ST depression. It is concordance to the superiority oriented QRS axis, and is therefore concordat, which in LVH suggests injury ( in contrast to subendocardial ischemia. Whether it is a bit of injury or an insignificant finding is u certain.
ReplyDeleteGood question!
Steve Smith
maybe resuscitation has caused the rise of troponin
ReplyDeleteYes, but that is ischemia incurred during arrest and resuscitation. So it is still due to ischemia. There are many reasons to have ischemia, and most are supply/demand issues (as in this case) and not ACS.
DeleteThanks, Steve Smith
Hi Steve,
ReplyDeleteCan you comment on the "normalization" of the T-waves in multiple leads here on the 2nd ECG in the acute phase? Clearly this wasn't "pseudonormalization",(the opposite, if anything) as the ST-Segment deviation improved and ultimately the patient clearly did not have ACS.
Sam, sorry for the delay! There was ischemia superimposed on the LVH on the first ECG, but it was (as you are aware) not due to ACS. When the patient stabilized and the heart rate came down, the ischemia resolved and you can see this in the resolution of the ST deviation and the T-wave inversion.
DeleteSteve