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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ECG Interpretation Review #53 (Peaked T - Hyperacute - DeWinter - Wellens - aVR)

The ECG in Figure 1 was obtained from a patient who walked into the ED (Emergency Department) with new-onset chest pain.

• Should the cath lab be activated for acute STEMI?
• If so – What do you suspect the “culprit artery” is likely to be?
• How many ECG signs support your impression?

Figure 1: ECG from a patient with chest pain. What are the findings of concern? (Reproduced from ECG-2014-ePub). 

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INTERPRETATION:  The ECG in Figure 1 is shows normal sinus rhythm. All intervals and the axis are normal. There is no chamber enlargement. There are however, a series of alarming findings that were recognized by the emergency team. Emergency cardiac catheterization was performed within 15 minutes after the patient walked into the ED ― with successful reperfusion of a 100% proximal LAD (Left Anterior Descending) coronary artery occlusion.

     Clues to the need for immediate catheterization and clues indicating localization of the “culprit artery” to the proximal LAD include the following:

• Hyperacute T waves in multiple leads. These are best seen in leads aVL, V2,V3,V4.
• DeWinter T wave complexes ― in which there is 1- to 3-mm of upsloping J-point ST depression in one or more precordial leads that continue into tall, positive symmetrical T waves (DeWinter – NEJM 359:2071, 2008). Although seen in Figure 1 to some extent in all precordial leads except for V1 ― the DeWinter T wave is best manifested in leads V3,V4.
• Loss of anterior R waves (with reduction in R wave amplitude between leads V1-to-V2).
• Marked inferior reciprocal ST depression.
• ST elevation in leads aVR and V1.
• Incomplete RBBB (rSr’ in lead V1; narrow terminal S waves in leads I and V6).

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DeWinter T Waves: A Sign of Proximal LAD Occlusion:

     Awareness of the relatively uncommon but highly characteristic DeWinter T wave sign is essential for not overlooking the approximate 2% of acute anterior infarction patients who present with this ECG manifestation (Ref 1). Rather than frank ST elevation that usually accompanies acute LAD occlusion ― there is instead the unique DeWinter complex with upsloping J-point ST depression blending into tall upright hyperacute T waves in a number of precordial leads (esp. leads V3,V4 in Figure 1). We emphasize the following key points about this syndrome.

• In patients presenting with new-onset chest pain ― there is extremely high specificity for the DeWinter T wave pattern and acute proximal LAD occlusion.
• Rather than evolution of tall, peaked (hyperacute) T waves into frank ST segment elevation ― the DeWinter T wave pattern was surprisingly static over the next few hours in the DeWinter series of patients.
• None of the patients in the DeWinter series who manifested this ST-T wave pattern had acute left main occlusion on catheterization.
• Despite prompt recognition and intervention ― a significant percentage of patients developed positive cardiac markers for acute infarction. One ECG sign that infarction may have already occurred is loss of anterior r wave amplitude (as is seen in Figure 1).

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TAKE-HOME POINT: Prompt recognition of the DeWinter T wave sign in patients with new-onset chest pain with immediate mobilization of the interventional cardiology team On-Call is essential for minimizing the extent of acute anterior infarction. 

• As is the case for Wellens’ Syndrome (See Section 10.54 of the pdf in the References below) ― precordial DeWinter T waves is another unique ECG sign with high correlation to acute anatomic coronary occlusion with mandate for immediate intervention.

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FINAL PEARLS:

     In addition to precordial DeWinter T waves and loss of anterior R wave amplitude between V1-to-V2 ― there are several additional ECG signs in Figure 1 suggestive/consistent with acute proximal LAD occlusion. These include:

• Significant ST segment elevation in leads aVR and V1.
• Incomplete RBBB (that is presumably new).
• Marked reciprocal inferior ST depression.
• Hyperacute T wave in lead aVL.

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ACKNOWLEDGMENT: My appreciation goes to Andrew Bowman for allowing me to use this ECG and this clinical case.

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NOTE: ― Relevant PDFs on ECG diagnosis of acute MI:

• http://tinyurl.com/DeWinter-NEJM ― Link to my dropbox for download of the original NEJM manuscript by Dewinter.
• Link to Section 10.0 from our ECG-2014-ePub.
• Figure 13.3-1 in Blog #126 shows another example of DeWinter T waves.
• Brief Summary of Wellens Syndrome —

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ECG Interpretation Review #52 (Wide Tacycardia - Toxins - Hyperkalemia - Ventricular Tachycardia - Sinoventricular Rhythm)

The ECG in Figure 1 was obtained from an acutely ill but alert (and hemodynamically stable) patient.

• Is the rhythm VT (Ventricular Tachycardia)?
• How certain are you of your diagnosis?
• If told that the patient was a 31-year old woman with abnormal renal function who presented in DKA (Diabetic KetoAcidosis) ― Could you come up with an explanation as to why the rhythm in Figure 1 might not be ventricular tachycardia?

Figure 1: WCT rhythm in a 31yo woman with renal disease and DKA. Is this VT? 

INTERPRETATION: The rhythm in Figure 1 is a regular WCT (Wide-Complex Tachycardia) at a rate of ~135/minute. No P waves are seen. The usual differential diagnosis for a monomorphic regular WCT of uncertain etiology is shown in Figure 2:

Figure 2: Common Causes of a Regular WCT when sinus P waves are not seen.

Our reason for listing VT as the first 8 entities in LIST #1 ― is that VT is by far the most common cause of a regular WCT of uncertain etiology – and – that VT should not be missed.

• Assessment of QRS morphology in Figure 1 reveals an exceedingly wide, amorphous QRS complex that does not at all resemble any form of bundle branch block.
• The QRS is entirely negative in lead V6 (deep QS complex) ― and it is entirely positive in lead aVR (monophasic R wave) ― both being features that under normal circumstances identify VT with near-100% specificity.
• There is extreme axis deviation (totally negative QRS in leads I and aVF) ― which also normally conveys near-100% specificity for a diagnosis of VT.

The above said – clinical circumstances in this case differ from the usual setting for VT, and are KEY to recognizing the correct diagnosis. The patient is a 31-year old woman with abnormal renal function and acute DKA. The reason for QRS widening is marked hyperkalemia! (serum K+=9.8 mEq/L at the time Figure 1 was obtained).

• ECG changes of hyperkalemia typically follow a progressive sequence (See ECG Blog #10). Initially ― there is generalized T wave peaking (serum K+ ~5.5-6.5 mEq/L).
• As serum K+ levels approach ~7-8 mEq/L range ― the QRS widens and P wave amplitude decreases.
• Eventually, P waves disappear. Interestingly, the sinus node is still able to transmit the electrical impulse to the ventricles even though no P wave is seen. This is known as a sinoventricular rhythm ― and could be an explanation for how the regular WCT in Figure 1 might reflect sinus rhythm despite the absence of P waves ... 
• Ultimately ― transmission of sinus impulses ceases, and a sinusoidal-widened pattern supervenes. Ventricular fibrillation or cardiac standstill invariably follow.

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BOTTOM LINE: Whether the rhythm in Figure 1 represents VT from marked electrolyte disturbance vs sinoventricular rhythm with QRS widening (and loss of P waves) from hyperkalemia is uncertain. We favor the latter ― because the treating clinician in this case recalled that onset of QRS widening was gradual following an initial ECG in which the QRS was narrow and T waves were peaked. IF the rhythm in Figure 1 had been VT ― we would have expected a much more abrupt onset of the regular WCT rhythm.

• Treatment with emergency K+-lowering treatment (calcium gluconate; glucose plus insulin; acute dialysis) resulted in resolution of QRS widening and return of electrically-evident sinus rhythm.

ADDENDUM: Perhaps List #1 in Figure 2 should be amended by addition of an Item #11 = “Something else” to include entities such as hyperkalemia and/or toxin effect (as might be seen with tricyclic overdose, in which marked QRS widening may be seen despite persistence of sinus mechanism).

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ACKNOWLEDGMENT: My appreciation goes to Dr. Harsha Nagarajarao (of Cardiology Boards) for allowing me to use this tracing.

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• See Section 11.0 on Electrolyte Disturbances (in ECG-2014-ePub) ― with the part on Hyperkalemia beginning in Section 11.3.

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ECG Interpretation Review #51 (Chamber Enlargement - LVH - Cardiomyopathy)

The ECG shown in Figure 1 was obtained from a 50-year-old man who presented to the office with dyspnea on exertion. No chest discomfort. He is a chronic smoker with a longterm history of alcohol consumption. The patient says he, “doesn’t see doctors”. He takes no medications. There is no obvious heart failure or wheezing on exam.

• Should the patient be admitted to the hospital because of his ECG?
• What clinical diagnosis do you strongly suspect?

Figure 1: ECG obtained from a 50yo smoker/drinker with dyspnea on exertion. What diagnosis is suggested by this ECG? NOTE - Enlarge by clicking on Figures - Right-Click to open in a separate window.

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INTERPRETATION:  The ECG shows sinus rhythm at a rate of about 85/minute. The PR and QRS intervals are normal; the QT is no more than borderline prolonged. The axis is normal (approximately +50 degrees). Beyond this point – a variety of interpretations are possible. We make the following points:

Point #1: There appears to be evidence of at least 3 chamber enlargement:

• RAA (Right Atrial Abnormality) – is diagnosed by the tall, peaked and pointed P wave in the inferior leads (that is >2.5 mm tall in lead II).
• LAA (Left Atrial Abnormality) – is suggested by the deep, negative component to the P wave in lead V1.
• Voltage for LVH (Left Ventricular Hypertrophy) – is diagnosed by the finding of deepest S wave in V1 or V2 + tallest R wave in V5 or V6 ≥35mm.
• True LV (left ventricular) chamber enlargement is strongly suggested (with ≥90% specificity) by the finding of voltage for LVH in an adult over 35 years of age when underlying heart disease is likely – IF there are ST-T wave changes consistent with “strain” (Figure 2). The difficult-to-describe ST-T wave abnormalities seen in leads V5,V6 of Figure 1 are clearly not normal findings in these lateral precordial leads. While they do not quite manifest a typical “Strain” pattern – they do qualify as a “strain equivalent” pattern that overwhelmingly favors a diagnosis of LVH in this patient.

Figure 2: Schematic depiction of LV "strain" and "strain equivalent" patterns. When either is present in addition to voltage for LVH - the specificity of the diagnosis is greatly increased.

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Point #2: The QRS complex and ST segments in Figure 1 are not normal:

• There is ST segment coving ("frowny" configuration) with some amount of ST elevation in leads V1,V2 (difficult to be sure where the J point begins in these 2 leads).
• The ST-T waves in leads V4,V5 are clearly abnormal (with appearance of at least some T wave inversion). There is abnormal ST-T flattening in other leads.
• In addition – the QRS complex looks abnormal in Figure 1 (with notching and slurring in several leads). That said – the QRS is really not widened, so no definite conduction defect is present.
• In the absence of a prior ECG – We can not rule out something acute going on (given the ST coving and elevation in leads V1,V2,V3). That said – Our "sense" is that the changes seen in Figure 1 are more likely to be longstanding and not acute.  Supporting this supposition is the lack of reciprocal changes.

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Point 3: The clinical diagnosis that we strongly suspect when we encounter an ECG such as seen in Figure 1 is of a cardiomyopathy (based on the history and ECG findings of abnormal though not necessarily prolonged QRS complex; multi-chamber enlargement; and clearly abnormal ST-T wave morphology).

• We would not necessarily admit this patient to the hospital on the sole basis of this ECG.  We would obviously feel better IF we could find an old ECG showing similar changes.  We'd use clinical judgement in the context of the clinical setting to guide our decision. 
• This patient would most likely be admitted to the hospital IF he presented in the middle of the night to an ED (Emergency Department).  IF he however presented to the office without any objective evidence of heart failure and without any chest discomfort – and his dyspnea was not new, not severe, and associated with a good office oxygen saturation – we would probably feel comfortable managing his presumed cardiomyopathy on an ambulatory basis.  One just has to be there to decide . . .

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• See ECG Blog #73  – for more on ECG diagnosis of LVH -
• See ECG Blog #75  – for more on Atrial Enlargement - 

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