A 78-year-old man presented with coronary heart disease during anterior/’anteroseptal’ ischemia (minimal J-point deviations in Vl–V3 and 5T depressions in V5–V6) and bradycardia (43bpm) of supraventricular origin (frontal plane mean P-vector [axis] not calculable due to P-wave configurations). There was P-wave prolongation (P duration >100ms), most clearly seen in lead I (P duration 160ms), where P was bifid: the right atrial (RA) and left atrial (LA) components had peaks separated by more than 40ms—a highly specific sign of left atrial enlargement—the RA component is typically rounded (‘dome’), and the LA component is typically sharp (‘spike’). Elsewhere, widened P waves were biphasic (RA positive and LA negative). Excessive P duration indicated late LA activation, which is most often due to delay/block in Bachmann’s muscular interatrial bundle (BB). Biphasic P waves, especially in II, III, and aVF, occur because of advanced/complete interatrial block (IAB), which forces RA activation to reach the LA through an alternate route rather than proceeding from right to left via the BB. After the RA is activated (positive P component in II, III, and aVF) net atrial conduction deviates in an inferior to superior direction (negative P component in II, III, and aVF). IAB is reflected in the P-terminal force (Ptf) in lead V1, where the terminal negativity (LA component is negative) lasts more than 40ms.mm (the product of its depth and duration)—a highly specific sign of LA enlargement. Unusually for advanced IAB, leads V2–V6 also showed comparable biphasic P waves. (The usual morphology of the far more common incomplete IAB is seen in all leads except V1 to resemble this patient’s P in lead 1, since interatrial conduction is only delayed [incompletely blocked] between the atria, and its pathway [via the BB or other pathways] is presumably normal). There was first degree AV block (prolonged P-R), which, along with the bradycardia, is not known to be related to IAB. Absent septal Q-waves (leads I, aVL, and V6), especially with QS in V1, were consistent with an anteroseptal infarct of unknown duration.
American Heart Hospital Journal 2009;7(1):63–4