ECG Blog #54 — Acute MI in a Cancer Patient?

The ECG in Figure 1 was obtained from a 60-year old man currently undergoing chemo- and radiation therapy for lung cancer. He presented to the ED (emergency department) with weakness and palpitations, but no chest pain.

• Should the cath lab be activated for acute STEMI?
• If so — what do you suspect the “culprit artery” is likely to be?
• Anything else likely to be going on given this clinical history?

Figure 1: ECG from a 60-year-old man with lung cancer. Is this ECG diagnostic of an acute STEMI?

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INTERPRETATION: The rhythm in Figure 1 is sinus tachycardia with one PVC (Premature Ventricular Contraction). The PR and QRS intervals are normal. The QT interval is difficult to assess given the tachycardia and lack of distinct end point of T wave inversion. The axis is normal at ~ +70 degrees. There is no chamber enlargement.

     

Regarding Q-R-S-T Changes ― there are no definite q waves; transition is normal (occurring between leads V2-to-V3). The most remarkable finding relates to ST-T wave changes:

• There is coved ST elevation in each of the inferior leads (II,III,aVF) ― and in lateral precordial (V4,V5,V6). In each of these leads, there appears to be T wave inversion following descent of the ST segment.
• There is scooped (reciprocal) ST depression in leads aVL and V2. Lead V3 shows transition between the reciprocal ST depression in lead V2 ― and the ST coving and T wave inversion that begins in lead V4.
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Initial IMPRESSION: The ECG in Figure 1 suggests acute STEMI (ST Elevation Myocardial Infarction). That said ― there are 3 elements about the history given and the ECG in Figure 1 that should be cause for contemplation:

1. There is no history of chest pain.
2. The patient has lung cancer with ongoing chemo- and radiation therapy.
3. The shape of the ST segment elevation is a bit “off” for acute STEMI ….

      Despite valid concern about possible acute infero-postero-lateral STEMI (either from a proximal right coronary vs dominant left circumflex occlusion) ― lack of defined “onset” of symptoms in the context of a patient with cancer should prompt additional data gathering prior to cath lab mobilization.

• Initial serum troponins were negative.
• The patient was taken to the cath lab. No acute lesion and no significant coronary disease was found.
• While in the cath lab ― additional lab values returned showing a markedly elevated serum calcium value = 17 mg/dL.
• Comparison ECGs were ultimately found. These were clearly abnormal. While a similar degree of ST elevation was not seen on prior tracings ― there was definite ST segment coving with T wave inversion present on one of the earlier tracings.

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CONCLUSION: All ST segment elevation is not necessarily the result of acute coronary occlusion. In addition to common other causes of ST elevation (ie, early repolarization variants; acute pericarditis) ― chronic ST elevation may result from either ventricular aneurysm or cardiomyopathy. This case serves to remind that Hypercalcemia is yet another potential STEMI-mimic.

• Textbooks describe QT interval shortening as the principal ECG manifestation of hypercalcemia. That said ― this is not an easy finding to detect because: i) Usually marked hypercalcemia (levels >12.0 mg/dL, if not much higher) are needed before the QT noticeably shortens; ii) it is often difficult clinically to distinguish between a QT interval that is within the “normal” range vs one that is shortened; and iii) ECG manifestations of hypercalcemia are superimposed on any baseline abnormalities that may be present.
• We mentioned above that the shape of ST segment elevation in this case was a bit “off” for acute STEMI. By that ― we mean that the coved ST segments seemingly peak a tad earlier than is usually seen. That said ― the overall QT interval in this case is not shortened, but if anything lengthened by preexisting T wave inversion that was seen to be present on prior comparison tracings.

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BOTTOM Line: Without the benefit of prior comparison tracings and the serum calcium value at the time the decision to emergently perform cardiac catheterization was made ― there is NO WAY (in our opinion) that one could rule out the possibility of acute STEMI.

• Much more than just coved ST elevation with symmetric T wave inversion ― there is also what appears to be indisputable reciprocal ST depression in both leads aVL and lead V2.
• Even knowing that the serum calcium value = 17 mg/dL ― we still feel that without availability of prior tracings for comparison ― that there is no way to rule out the possibility of concomitant hypercalcemia superimposed on acute STEMI.

"Take-Home" POINT: All that elevates ST segments is not necessarily acute STEMI. History is ever important. On rare occasions ― hypercalcemia not only shortens the QT interval, but may also elevate ST segments. ECG manifestations associated with electrolyte disturbance (be this due to abnormal potassium, magnesium or calcium values) are superimposed on any baseline ECG abnormalities that may be present.

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• ACKNOWLEDGMENT: My appreciation goes to Jiann Ruey Ong for allowing me to use this ECG and this clinical case.

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• See Section 11.0 on Electrolyte Disturbances (in ECG-2014-ePub) ― with the part on Hypercalcemia beginning in Section 11.1.

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