ECG Blog #386 — OMI or Something Else?

The ECG in Figure-1 was obtained from a previously healthy middle-aged man — who while performing his regular exercise routine, developed "slight" chest discomfort and "palpitations". These symptoms persisted for over an hour, which led the patient to contact EMS. Surprisingly — he was hemodynamically stable with minimal discomfort at the time his initial ECG in Figure-1 was recorded.

QUESTIONS:

• How would YOU interpret the rhythm in Figure-1?
• How certain are you of your diagnosis?
• Could the patient have WPW?
• What would you do?

Figure-1: The initial ECG in today's case.

MY Thoughts:

Surprisingly — Today's patient was hemodynamically stable in association with the rhythm shown in Figure-1. By definition — this means that there was at least a moment in time to contemplate the etiology of the rhythm before having to begin treatment. 

By the Ps, Qs, 3R Approach (as reviewed in ECG Blog #185):

• The QRS complex is obviously wide.
• I do not see P waves.
• The rhythm is Regular — at a Rate of ~230/minute.
• 
  
• Impression: The rhythm in Figure-1 is a regular WCT ( = Wide-Complex Tachycardia) at ~230/minute, without clear sign of atrial activity. As I've often emphasized on this ECG Blog (See ECG Blog #220 and ECG Blog #361 — among many others) — Statistical odds in a middle-aged man with new symptoms, that a regular WCT without P waves will turn out to be VT — are at least 80-90%, even before we look at QRS morphology. As a result — Assume VT until proven otherwise!

We can easily increase the certainty of our diagnosis for today's rhythm that is shown in Figure-1 — by attention to QRS morphology:

• There is extreme axis deviation (ie, an all negative QRS not only in lead I — but also in each of the inferior leads)!
• The QRS is all positive in lead aVR (which implies the impulse is coming from below — and is therefore not supraventricular).
• The QRS is all negative in lead V6 (similarly implies an impulse coming from below).
• There is no biphasic complex in any chest lead (ie, the QRS is all positive in V1,V2 — and all negative in V3,4,5,6 — so no chest lead has any kind of RS complex).
• QRS morphology for ECG #1 does not resemble any known form of conduction defect. Instead — the QRS is amorphous.
• 
  
• BOTTOM LINE: I would estimate the odds that the regular WCT in Figure-1 is VT as >98-99%!

PEARL #1: Any one of the 5 bullets shown above would increase the odds that today's regular WCT is VT to >95%. Assuming today's patient is not hyperkalemic — taken together, the above 5 bullets regarding QRS morphology for today's regular WCT make it hard to imagine this rhythm is anything other than VT.

PEARL #2: An important confounder to be aware of as a non-VT cause of a regular WCT rhythm — is WPW. That said — QRS morphology in Figure-1 essentially rules out WPW.

• Activation of the ventricles over an AP (Accessory Pathway) — should generally proceed from the base of the heart toward the apex. This should result in at least some positivity of QRS complexes as one moves toward the lateral chest leads. The finding of all negative QRS complexes in leads V3-thru-V6 therefore strongly suggests that the arrhythmia-associated impulse is not traveling over an AP (Steurer et al — Clin. Cardiol 17:306-308, 1994).
• Although the sensitivity of this criterion for ruling out WPW is poor (ie, most VTs do not have all negative QRS complexes in 3 or more of the most lateral chest leads) — when you do see an all negative QRS in leads V4,V5 and V6 — this essentially rules out a WPW-related tachyarrhythmia.

The CASE Continues:

The rhythm in ECG #1 was interpreted as VT and treated accordingly. In view of the patient being hemodynamically stable — a dose of IV Amiodarone was tried, but without success. 

• Given the rapid rate of the tachycardia and the amorphous shape of the QRS — the decision was made to sedate the patient and cardiovert. This resulted in the tracing shown in Figure-2.

QUESTIONS:

• How would YOU interpret the ECG in Figure-2?
• Is prompt cath indicated for a presumed acute MI?

Figure-2: How would you interpret this 12-lead tracing obtained immediately after synchronized cardioversion?

MY Thoughts on ECG #2:

The "good news" — is that synchronized cardioversion successfully resulted in sinus rhythm! That said — there are significant ST-T wave abnormalities. I see the following in ECG #2:

• Upright P waves in lead II, with a constant and normal PR interval that therefore confirms conversion to sinus rhythm — here at a rate of ~85/minute.
• The QRS is fragmented (notched) in several leads (ie, leads III, aVL, V3) — but is not prolonged.
• Given the heart rate — the QTc is at least borderline prolonged.
• The frontal plane axis is normal (about +60 degrees).
• There is no chamber enlargement.
• There is deep, symmetric T wave inversion in leads V3-thru-V6 (most marked in V3,V4). Nonspecific ST-T wave flattening is seen in the limb leads.
• 
  
• IMPRESSION: The rhythm is now sinus. There are marked ST-T wave abnormalities. The question arises as to whether these changes in ECG #2 represent acute infarction as the cause of VT? (with need for prompt cath with PCI?).

PEARL #3: It's important to be aware of a "memory" effect. This phenomenon may sometimes be seen following an episode of a sustained tachycardia — in which marked ST-T wave abnormalities not due to infarction may be seen for a period of hours, or even days!

• Despite the marked ST-T wave abnormalities in ECG #2 — I would suspect that these are not the result of acute infarction because: i) There is no ST elevation in this post-cardioversion tracing; ii) There is no reciprocal ST depression; and, iii) The shape of the ST-T wave changes is fairly similar in leads V3-thru-V6 — with no more than nonspecific ST-T wave flattening in the other 8 leads (ie, This post-conversion ECG just doesn't "look" like an acute infarction). That said — I was not 100% certain about this interpretation.

The CASE Continues:

• An initial hs-Troponin-I assay was positive, with a value = 94 ng/L (normal is <34 ng/L for a man of this patient's age). That said, immediately after sinus rhythm was restored — the patient's symptoms resolved! He remained pain-free.
• On questioning after restoration of sinus rhythm — the patient denied any preceding angina symptoms before this hospitalization.
• 
  
• Bedside Echo was done (4-Chamber view shown in Figure-3).

Figure-3: Bedside Echo 4-Chamber View (See text).

QUESTION:

• Does the bedside Echo in Figure-3 help to explain the abnormal ST-T wave findings in ECG #2?

ANSWER: The bedside Echo view in Figure-3 shows dramatic apical hypertrophy — with no more than a slit-like apical internal ventricular lumen. Despite this finding, overall ventricular function is preserved (Estimated EF = 54% — with no wall motion abnormality).

• KEY Point: Rather than acute coronary occlusion — this bedside Echo suggests that the primary problem can most likely be attributed to severe apical cardiomyopathy!
• This is consistent with the patient's history — in that the patient had no prior history of anginal symptoms — and the slight chest discomfort he experienced in association with his VT promptly resolved as soon as sinus rhythm was restored.
• 
  
• PEARL #4: Taking another LOOK at QRS morphology during VT (ie, in Figure-1) — the monophasic positive QRS in right-sided lead V1 and the all negative QRS complex in chest leads V3-thru-V6 — suggest a left-ventricular apical origin for his VT, which is completely consistent with the severe apical hypertrophy seen on Echo.

The CASE Continues: Additional Testing ...

Additional testing was done. Along the way — the decision was made to cancel the initial call for cardiac catheterization, and instead to obtain a less invasive CT coronary angiogram. 

Selected results of additional testing are noted below.

• A follow-up ECG done the next day ( = ECG #3 in Figure-4).
• Troponins were repeated — reaching a peak elevation of >31,000 ng/L!
• 
  
• CT coronary angiogram — No obstructive coronary disease.
• Cardiac MRI —  consistent with severe apical hypertrophy (See Figure-5). No sign of ARVC. EF ~60%. 

Figure-4: Comparison between the post-conversion 12-lead ECG — and the ECG repeated the next day.

Figure-5: Selected CT scan slice (IVS = InterVentricular Septum; LV Wall; slit-like LV cavity).

Figure-6: Selected Cardiac MRI view.

DISCUSSION:

There are many important aspects of this case.

• The patient presented in a regular WCT rhythm without P waves, at the rapid rate of ~230/minute (Figure-1). QRS morphology suggested with virtual certainty that the rhythm was VT. Since the patient was hemodynamically stable — brief trial with Amiodarone is reasonable and was attempted, but when this did not convert the rhythm — synchronized cardioversion was applied.
• 
  
• Synchronized shock successfully converted the rhythm to sinus — but there was marked ST depression on the 12-lead (Figure-2). Although essential to rule out OMI (ie, an acute coronary occlusion) as the cause of VT — the astute clinician in charge of the case cancelled the initial call to activate the cath lab because: i) The post-conversion 12-lead in Figure-2 lacked ST elevation and other ECG indicators of acute infarction; ii) The patient's symptoms immediately resolved once he was converted to sinus rhythm; iii) This previously healthy middle-aged adult had no history of angina nor other reason to suspect underlying coronary disease; and, iv) Bedside Echo suggested marked apical hypertrophy and no wall motion abnormality (Figure-3).

Subsequent testing supported the presumption of apical cardiomyopathy as the cause of this patient's sustained VT.

• CT coronary angiogram showed no obstructive coronary disease. 
• As seen in Figure-5 — this CT scan slice supports the bedside Echo finding of marked apical hypertrophy, resulting in minimal chamber volume for ventricular filling
• The selected Cardiac MRI view shown in Figure-6 — shows similar findings of marked apical thickening with good contractility, but no more than a slit-like LV cavity opening for LV filling.

Additional Teaching Points:

• Type-2 MI (Myocardial Infarction) — is defined by an increase in troponin with evidence of ischemia that is not due acute coronary disease, but which instead results from a mismatch in oxygen supply and demand (Smilowitz et al — Coron Artery Dis 29(1):46-52, 2018). Today's case is illustrative because it shows how high troponin may rise despite the absence of acute coronary occlusion! (ie, Severe subendocardial ischemia from sustained VT in a patient severe apical cardiomyopathy resulted in a peak troponin >31,000 ng/L in today's case).
• 
  
• Bedside Echo proved invaluable for providing a rapid explanation for the patient's sustained VT that obviated the need for prompt cath.
• 
  
• Post-VT ST-T wave abnormalities do not necessarily indicate acute coronary occlusion, even when troponin is markedly elevated. Comparison in Figure-4 of the immediate post-cardioversion tracing ( = ECG #2) — with the repeat 12-lead ECG done the following day ( = ECG #3) shows persistence of ST-T wave abnormalities (if anything, with slight increased T wave inversion seen in the inferior leads of ECG #3). Whether these ST-T wave changes are the result of "memory" following an episode of sustained VT — or — whether they are longstanding in this patient with apical cardiomyopathy (and/or some combination of both conditions) — is uncertain. But immediate resolution of chest pain once VT was converted — and — the normal CT coronary angiogram — essentially ruled out acute coronary disease as the cause.
• 
  
• P.S.: Despite marked apical hypertrophy — QRS voltage was not in the least increased in either ECG #2 or ECG #3. The ECG is an imperfect tool for detection of LVH. Echo is far superior for this purpose. 

CASE Conclusion:

• Today's patient was deemed high-risk. As a result — an ICD (Implantable Cardioverter-Defibrillator) was placed, and he was discharged on a ß-blocker.

 

==========================================

Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and this tracing.

==========================================

================================== 

Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Systematic Ps, Qs, 3R Approach to Rhythm Interpretation.
• 
  
• ECG Blog #361 and ECG Blog #220 — Review in detail the clinical approach to a regular WCT (Wide-Complex Tachycardia).
• 
  
• ECG Blog #337 — The importance of the new OMI (vs the old STEMI) Paradigm (and My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog). 

============================================

ADDENDUM (7/15/2023):

The original 3 ECGs in today's case were recorded using the Cabrera lead format. This ECG recording format is favored in Norway, Sweden, Germany — and in a number of other countries. 

• Given the ever expanding use of the internet — virtually all clinicians everywhere are likely to encounter this format at the very least, from time to time. As a result — I show in Figure-7, the initial ECG in today's case as it was originally recorded using the Cabrera format (Please see my Editorial Note near the top of the page in ECG Blog #365 for review of the basics of the Cabrera recording system). 
• 
  
• For comparison — I've reproduced in Figure-8 the post-conversion tracing shown in today's case (which I initially showed in Figure-2) — in which I've simulated the standard recording format used in the U.S. and most other countries (ie, I inverted lead aVR — and moved the location of various limb leads).

Figure-7: The post-conversion tracing in today's case — as it was originally recorded using the Cabrera format. (Given ever expanding use of the internet — it's good to become familiar with this recording format, that in many ways is more logical than the standard format we are used to — as discussed in ECG Blog #365). 

Figure-8: For comparison purposes — I've reproduced the post-conversion tracing in today's case that was shown in Figure-2.