Wednesday, July 29, 2015

ECG BLOG #115 (Early Repolarization — Peaked T Waves — Anterior STEMI — DeWinter)


The 12-lead ECG shown in Figure-1 was obtained from a 50-year old man with chest discomfort.
  • How would you interpret this ECG?
  • Are the findings seen suggestive of Early Repolarization — or something else?
  • Clinically — What would you do?
Figure-1: 12-lead ECG obtained from a 50-year old man with chest discomfort. NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
ANSWERS: Assessment of the ECG shown in Figure-1 in view of the limited history provided (ie, a middle-aged man with chest discomfort) — is indeed a challenging task. Practically speaking — a definitive answer to the question of whether the ECG picture in Figure-1 represents a normal repolarization variant vs early anterior STEMI (ST Elevation Myocardial Infarction) is not forthcoming from interpretation of this single tracing.
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Our Interpretation of Figure-1: The rhythm is sinus — with slight variability in rate (sinus arrhythmia). All intervals and the mean QRS axis are normal. Although QRS amplitudes are somewhat difficult to discern in some of the chest leads (due to overlap of complexes) — there does not appear to be ECG evidence for chamber enlargement (the R wave amplitude in V5 = 21mm + the 9mm S wave in V2 fall shy of the required 35mm threshold for LVH).
  • Superficial Assessment of Q-R-S-T Changes: There are no Q waves. Transition occurs normally between V3-to-V4. There is no more than minimal ST elevation in leads I and V2. All T waves are upright (except in aVR) — and there appears to be no obvious ST depression. The shape of the upsloping segment of T waves in leads V2-thru-V6 is concave up (ie, “smiley”-configuration).
  • More Discriminating Assessment of Q-R-S-T Changes: The patient is a 50-year old man with chest discomfort. This fact alone calls for far greater scrutiny in assessing Q-R-S-T changes than would be the case if the patient was asymptomatic. Although Q waves are absent and transition occurs normally between V3-to-V4 (since the R wave in V4 appears slightly taller than the S wave is deep) — r wave amplitude is decidedly reduced in V1,V2,V3. In this context — the T waves seen in leads V2,V3 appear to be disproportionately tall and peaked, with a rounder (fatter) T wave peak in V2 than should-be-expected given the relatively low amplitude rS complex in this lead. Closer scrutiny of the limb leads reveals that they are not completely “normal” as was initially suggested by superficial assessment. Instead, the ST segments in leads III and aVF appear flattened (despite the presence of upright T waves in these leads) — and the subtle-but-real 0.5mm J-point ST elevation in lead I might in fact be relevant.
BOTTOM LINE: All of these findings are extremely subtle. They may mean nothing. But in a 50-year old man with new chest discomfort — they could also be harbingers of an important acute event about to evolve …
  • KEY POINTS: It is OK not to be certain about the clinical significance of a single ECG. This happens often. Awareness that early on, an acute STEMI (especially when anterior in location) — may be difficult to recognize is essential. More discriminating ECG assessment is needed in such cases. Reduced anterior r wave amplitude with taller-than-expected anterior T waves (especially if peaked T waves look broader than-they-should-be) should prompt more careful assessment of limb leads for subtle abnormalities. The finding of a longer-than-expected (albeit not necessarily prolonged) QT interval would add support to the possibility of an acute event. But even if meticulous ECG assessment does not suggest clear abnormalities — a patient with potentially worrisome symptoms of new cardiac onset should not be sent home until the provider can attain a comfort level that nothing acute is evolving.
  • WHAT To DO: In addition to obtaining a more complete history and performing a careful physical exam — 3 interventions may be extremely helpful: i) Looking to see if prior ECGs are available for comparison (transmission from a distance being expedited if necessary by smart phone messaging); ii) Repeating the ECG as needed (since an acute evolving event may produce significant ECG changes in a surprisingly short period of time); and iii) Performing ECHO at the bedside (normal LV function in a patient with chest pain is reassuring — whereas localized wall motion abnormality suggests an acute event).
WHAT Happened: The ECG in Figure-2 was obtained just 8 minutes after the Figure-1 ECG. Is the diagnosis now more clear?
Figure-2: Follow-up ECG obtained 8 minutes after the ECG shown in Figure-1.
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Interpretation of Figure-2: We doubt anyone would have predicted how emphatically the original ECG from Figure-1 has changed in as short a time period as 8 minutes!
  • Sinus rhythm persists in Figure-2. There is now dramatic (>5mm) ST elevation in leads V2,V3 — with a lesser (but still very significant) degree of ST elevation in leads I,aVL and V4,5,6. Increased T wave amplitude and peaking is evident in leads V2-thru-V6, with hyperacute ST-T waves in virtually all of the leads with ST elevation. Small-but-real q waves now appear to be present at least in leads I, aVL and V6. In addition — there is now marked reciprocal ST depression in leads III and aVF. The combination of findings are strongly suggestive of acute LAD (Left Anterior Descending coronary artery) occlusion.
Comparing the ECG picture of the original tracing (Figure-1) with the follow-up ECG obtained just 8 minutes later (Figure-2) — We note the following:
  • There are now small-but-real new lateral q waves. In addition — the rSR’ complex seen in leads V2,V3 (just before onset of the marked J-point ST elevation in these leads) — probably serves as a “Q-wave equivalent” given slight-but-real loss of r wave from V1-to-V2 and obvious large ongoing acute anterior infarction.
  • The subtle ST elevation in lead I and ST flattening in leads III,aVF from Figure-1 were indeed real findings that came before the obvious evolution of ST-T wave changes that are seen in these same leads in Figure-2.
  • Finally — Figure-2 adds support that the chest lead T wave peaking with disproportionately tall T waves (and fatter-than-expected T wave peak) in leads V1,V2 of Figure-1 was indeed a subtle harbinger of the dramatic ST-T wave changes that followed just 8 minutes later …
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P.S. — While one may debate the pros and cons of routine high-sensitivity troponin assessment for all comers with chest discomfort — dependence on a first early troponin assay (with the term “early” referring to the time of the blood draw with respect to the time of symptom onset) — regardless of what the troponin result turns out to be (positive or negative) is unlikely to: i) Completely rule out the possibility of an early acute event (since early on, there may be false negatives … ); or ii) Be the deciding factor for determining whether or not the interventionist should perform immediate cardiac catheterization. Our bias is therefore that other factors (ie, clinical history and exam; initial and serial ECGs; stat Echo) are more important than the initial troponin value for determining whether a patient like the one in this case has an acute coronary occlusion likely to benefit from acute reperfusion therapy.
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ACKNOWLEDGMENT: My thanks to Haris Skrbo (of Capjlina in Bosnia & Herzegovina) for allowing me to reproduce this tracing and clinical case.
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