Perspectives on Body Surface Mapping
in Acute Ischemic Syndromes

Helena Hänninen^ab, Jukka Nenonen^b, Markku Mäkijärvi^ab,
Toivo Katila^b, Lauri Toivonen^ab

^aDivision of Cardiology and BioMag Laboratory, Helsinki University Central Hospital, Helsinki, ^bLaboratory of Biomedical Engineering, Helsinki University of Technology, Espoo, Finland

Correspondence: H Hänninen, Helsinki University Central Hospital, Division of Cardiology, Cardiovascular Laboratory, P.O. Box 340, FIN-00029 HUCH, Finland. E-mail: helena.hanninen@hus.fi, phone +358 40 591 2261, fax +358 9 4717 4574

1.    Introduction

The diagnostic power of the 12-lead electrocardiogram (ECG) in acute ischemia and myocardial infarction (MI) may not be optimal since the coverage of the standard precordial leads over the thorax is limited. Body surface potential mapping (BSPM), defined as the temporal sequence of potential distributions observed on the thorax throughout one or more electrical cardiac cycles, is an extension of conventional ECG aimed at refining the noninvasive characterization and use of cardiac-generated potentials. The improved characterization is accomplished by increased spatial sampling of body surface ECG, recorded as tens or even hundreds of unipolar ECGs either simultaneously or individually with subsequent time alignment [Lux, 1989; Flowers and Horan, 1995]. Recent studies imply that in acute coronary syndromes BSPM may improve the detection of ischemia-induced electrocardiographic changes.

2.    Transient Subendocardial Ischemia

In BSPM studies transient subendocardial ischemia has mainly been studied in a controlled manner in form of exercise-induced ischemia. As in 12-lead ECG, the ischemic exercise-induced ST depression does not localize the anatomic site of coronary artery obstruction in BSPM [Kubota et al., 1985; Nakajima et al., 1988; Montague et al., 1990; Hänninen et al., 2001a]. The optimal recording sites to detect ischemia-induced ST depression, irrespective of the culprit coronary artery, have been identified over the left side, region relatively well covered by the standard precordial leads [Hänninen et al., 2001a]. Some evidence exists that T-wave changes in BSPM may be useful in localizing the ischemic myocardial region [Ishikawa et al., 1988; Nakajima et al., 1988; Kubota et al., 1985 and 1989; Hänninen et al., 2001b and 2003].

3.    Acute Coronary Occlusion

3.1. Acute Myocardial Infarction

BSPM has markedly improved the detection of right ventricular or posterior infarction associated with inferior left ventricular wall infarction compared to right precordial leads V₂R or V₄R (42% vs. 58%) or posterior chest leads V7 or V9 (2% vs. 27%) [Menown et al., 2000a]. In BSPM, resolution of the infarction-induced ST deviations has been proven more accurate than the corresponding ST deviations in 12-lead ECG in the evaluation of reperfusion after thrombolysis treatment [Menown et al., 2000b]. In addition, BSPM has demonstrated superior sensitivity to 12-lead ECG (88% vs. 38%) while maintaining good specificity (75% vs. 81%) in detection of acute myocardial infarcts [Menown et al., 2001].

In patients with non-Q-wave MI minor potential losses by serial analysis of the QRS complex have been identified in BSPM, while corresponding changes were undetectable in 12-lead ECG [Medvegy et al., 2000]. BSPM has also been applied to identify the optimal recording sites to detect ischemia-induced ST deviations in patients representing with acute MI. Of these six optimal leads, identified by use of discriminant index analysis, five were outside the standard precordial leads V₁-V₆ of 12-lead ECG [Kornreich et al., 1993]. These findings thus imply that improved detection of ischemic changes can be achieved by BSPM.

3.2. Percutaneous Coronary Intervention (PCI)

In contrast to the acute infarction studies, some evidence exists that 18-lead ECG (12-lead ECG plus right precordial leads V_3R-V_5R plus posterior leads V₇-V₉) may be more valuable in monitoring acute transmural ischemia during PCI than the six optimal leads identified by Kornreich and coworkers [1991 and 1993] [Wung and Drew, 1999]. This could be due to the difference in the definition of the baseline between the MI and PCI studies: in the former no baseline ECG was available, while in the latter the baseline ECG served as a reference point for measuring ST deviation between periods of acute ischemia and no ischemia in the same individual [Wung and Drew, 1999].

Unlike in exercise-induced subendocardial ischemia, in patients undergoing PCI the distributions of body surface ST-segment deviations have differed markedly in patients with anatomically different ischemia regions [Shenasa et al., 1993; Lux et al., 1995; MacLeod et al., 1995; Horáček et al., 2001; Horáček and Wagner, 2002]. ST-segment mapping in BSPM thus shows a strong ischemia localization capacity, feature potentially advantageous in the noninvasive identification of the culprit coronary lesion. The better ischemia-localization capability in transmural than in exercise-induced subendocardial ischemia could be due to the more local nature of the former, whereas in latter the nature of ischemia may be more global, possibly caused by elevated left ventricle end-diastolic pressure [Kubota et al., 1985].

4.    Remote Myocardial Infarctions

In a BSPM study including patients with recent or old MI, the diagnosis of both acute non-Q-wave and Q-wave MIs has been improved by appropriate selection of optimal ECG leads and PQRST features [Kornreich et al., 1991]. In accordance, in patients having both acute and remote MIs, changes in QRS body surface maps have all differed markedly in patients with anatomically different MI regions, thus demonstrating MI localization capability [Montague et al., 1986; Montague and Witkowski, 1989; Horan et al., 1990]. Since serial analysis of the QRS complex has allowed detection of minor potential losses in acute non-Q-wave MIs, not detectable by 12-lead ECG [Medvegy et al., 2000], it is reasonable to expect this approach may well be useful not only in detecting but also localizing remote MIs.

5.    Conclusion

Body surface potential mapping currently serves as an excellent research tool for studying the electrophysiological manifestations of acute coronary syndrome to the body surface. The improved characterization of these phenomena may well aid in noninvasive localization and estimation of the size of the infarcted myocardial region. Further studies are, however, needed to evaluate the real value of BSPM in the diagnostic assessment of acute coronary syndromes.

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