Research

ST segment depression: the possible role of global repolarization dynamics

Bruce Hopenfeld

Angel Medical Systems, 1 Sheila Drive, Tinton Falls, New Jersey 07724, USA

author email corresponding author email

BioMedical Engineering OnLine 2007, 6:6doi:10.1186/1475-925X-6-6

Published:	9 February 2007

Abstract

Background

At least some clinical data suggests that, regardless of which major coronary artery is narrowed, the early ST segment body surface pattern is characterized by a minimum near precordial lead V5 and a broad area of left precordial negative potentials. Some clinical data also suggests that late ST segment potentials can localize an ischemic heart region.

Objective

A computer model of a heart/torso system was implemented to study the relationship between transmembrane potentials throughout the heart and clinically observed body surface potential patterns during the early and late ST segments in ischemic patients.

Methods

Transmembrane potentials were selected to produce body surface potentials that matched the clinical data.

Results

The early ST segment pattern was matched by assigning: (i) an epicardial transmembrane potential gradient that is consistent with the normal activation/repolarization sequence, according to which the left lateral epicardium activates relatively late; (ii) an endocardial transmembrane potential distribution with the lowest transmembrane potentials in the ischemic region; and (iii) overall lower transmembrane potentials to the endocardium compared to the epicardium. Late ST segment potentials, which localized the area of the ischemic region, were generated by reducing the epicardial transmembrane potential gradient and increasing the endocardial transmembrane potential gradient.

Conclusion

The non-localizing nature of early ST segment depression could be due to global epicardial and endocardial transmembrane potential gradients related to the activation/repolarization sequence, whereas the possibly localizing nature of late ST segment depression could be due to the relative removal of the epicardial gradient, and an increase of the transmembrane potential gradient across the endocardium.