The trusted source for
healthcare information and
Has There Been Anterior Infarction?
By Ken Grauer, MD, Professor Emeritus in Family Medicine, College of Medicine, University of Florida. Dr. Grauer is the sole proprietor of KG-EKG Press, and publisher of an ECG pocket brain book.
Scenario: The ECG above was obtained in the office from an older woman with hypertension and atypical chest discomfort. Has there been anterior infarction, or is this a "pseudo-infarct" pattern?
Interpretation: The ECG shows normal sinus rhythm at 75/minute. The PR, QRS, and QT intervals are normal. There is marked LAD (left axis deviation). Criteria for LAHB (left anterior hemiblock) are met, given that the QRS complex in lead II is predominantly negative (which puts the axis at approximately -40 degrees). Criteria for LVH (left ventricular hypertrophy) are met in lead aVL, with QRS amplitude in this lead clearly exceeding the required 12 mm. The interesting aspect about R wave progression is that there is "loss of R wave" between leads V2-to-V3. Transition is delayed, and does not occur until between leads V5-to-V6. S waves persist through to leads V5,V6. ST-T waves show nonspecific flattening, but no acute changes. This probably reflects a "strain equivalent" in lead aVL given the very tall R wave in this lead.
Several conditions may account for "loss" of R wave in the anterior leads. The two most common are anterior infarction and lead placement errors. Two less common causes are "competing conditions" of LVH and LAHB. Occasionally when there are very tall R waves in lateral precordial leads these forces may overcome the forces of normal R wave progression. Although voltage criteria for LVH are easily met in lead aVL, lateral precordial lead amplitude is small.
A much more likely cause of the poor R wave progression seen here is LAHB. Anatomically, the posterior hemifascicle lies slightly behind the left anterior hemifascicle. Consequently, block in the anterior hemifascicle may result in predominance of posterior precordial forces, leading to "loss of R wave" in anterior precordial leads. That said, it is impossible to tell from this single tracing if there has been prior anterior infarction, or if all changes are due to LAHB.