Taking Cardiac Imaging to New Dimensions: Body Surface Mapping

November 1, 2006

When your patient presents with chest pain and other symptoms of an acute coronary syndrome (ACS), yet a standard 12-lead ECG shows no evidence of ST-segment elevation myocardial infarction (STEMI), you may face a diagnostic dilemma. The patient could have a non-STEMI ACS for which conservative treatment will suffice--or he could have a STEMI in an electrocardiographically "silent" area and need acute reperfusion therapy.

When your patient presents with chest pain and other symptoms of an acute coronary syndrome (ACS), yet a standard 12-lead ECG shows no evidence of ST-segment elevation myocardial infarction (STEMI), you may face a diagnostic dilemma. The patient could have a non-STEMI ACS for which conservative treatment will suffice--or he could have a STEMI in an electrocardiographically "silent" area and need acute reperfusion therapy.

Typically, to know which scenario was the correct one, you would have to wait either until results of cardiac serum marker measurements were available to "rule in" MI or until progressive changes on the ECG demonstrated significant ST-segment-T-wave abnormalities consistent with a STEMI. By that time, the patient might have failed to receive needed treatment in a timely manner--because of a shortcoming of the standard 12-lead ECG.

A new ECG technique--body surface mapping (BSM)--may be able to resolve such dilemmas. It can also provide a valuable enhancement of the standard ECG evaluation in other settings. BSM uses numerous ECG leads to provide a more complete imaging of the heart and potentially greater sensitivity for the detection of STEMIs.1-3 Rather than replacing the 12-lead ECG, the BSM ECG is an extension of the traditional ECG; it can further define ACS-related injury.

HOW BSM WORKS, WHAT IT SHOWS

BSM uses 80 different leads--64 anterior and 16 posterior (Figure 1)--to produce a single electrical recording of cardiac activity. Clinical information obtained via BSM is displayed in 3 basic formats:

•A standard 12-lead ECG (Figure 2).

•An 80-lead ECG (Figure 3).

•Color contour, or body maps (Figure 4).

The first 2 formats are interpreted in a fashion similar to standard ECGs. A color contour map, a markedly different way of imaging the heart, depicts the anterior and posterior thorax. These maps can be presented as "flat" maps (Figure 5) or as torso maps (see Figure 4). The 2-dimensional flat map is a basic projection of the anterior and posterior thorax. The torso map, a 3-dimensional representation, is an anatomically oriented depiction of the thorax. Color coding (Figure 6) is used to depict the magnitude and deflection of the ECG signal (either the QRS complex or the ST segment). The significance of the various colors used is as follows:

•Green represents the isoelectric position of the ST segment.

•Red represents a net positive deflection of the ST segment.

•Blue represents a net negative deflection of the ST segment.

A BSM ECG includes 4 separate maps, each analogous to a different component of the standard ECG (see Figure 4):

•A QRS isointegral map, which images the QRS complex.

•An STT isointegral map, which images the ST-segment and T-wave complex.

•An ST0 isopotential map, which images the ST segment at the J point.

•An ST60 isopotential map, which images the ST segment 60 milliseconds after the J point.

APPLICATIONS OF BSM

BSM can be used in patients with ACS to detect "unanticipated" STEMIs (unanticipated based on a 12-lead ECG), to further define the extent of ACS injury, to select appropriate therapies, and to observe the response to these treatments. BSM should not necessarily be the initial ECG study performed in a patient with chest pain and suspected ACS. Instead, perform a standard evaluation, including a 12-lead ECG.

Detection of STEMI in electrocardiographically silent areas. If the 12-lead ECG demonstrates a nondiagnostic pattern (ie, shows no evidence of a STEMI), you are then faced with the question, "Is this patient experiencing a non-STEMI ACS--or a STEMI that is occurring in an electrocardiographically silent area (the inferior, lateral, or posterior wall of the left ventricle or the right ventricular region)?" If the answer to this question is a possible STEMI in a "silent" area, then a BSM ECG is a reasonable next step in the evaluation.

For example, one ECG presentation--anatomically oriented ST-segment depression--can represent a non-ST-segment elevation acute MI. It is theorized that a subset of patients who present in this manner are, in fact, experiencing a STEMI that is not apparent on the initial 12-lead ECG.

Menown and colleagues4 used BSM to further evaluate patients with suspected ACS and isolated ST-segment depression on a standard ECG. The investigators noted that many patients in this population with serum marker-confirmed acute MIs demonstrated ST-segment elevation on body map regions not imaged by the standard 12-lead ECG, including the inferior, lateral, posterior, and right ventricular regions.4

An illustrative case in which BSM is used to detect a STEMI in an electrocardiographically silent area with another 12-lead-ECG presentation appears in the Box on pages 1454-1455.

Further evaluation of STEMI already detected. In this application of BSM, the 12-lead ECG has demonstrated a STEMI and the evaluation is largely complete. However, you can opt to perform a BSM ECG to more thoroughly evaluate the STEMI--that is, to determine whether additional anatomic areas are involved.

In a multicenter trial, Ornato and colleagues2 compared 12-lead ECGs and BSM ECGs in the evaluation of patients with chest pain and acute MI. They found that the BSM ECG was more sensitive than the 12-lead ECG for the detection of additional STEMIs; specificities of the 2 types of ECG were similar.

In another group of patients with STEMIs (those with diagnosed inferior-wall STEMIs), Menown and colleagues1 investigated the ability of BSM to detect both posterior and right ventricular wall MI. The investigators compared the BSM ECG with a 16-lead ECG that used V2R, V4R, V7, and V9 in addition to the 12 standard leads. ST-segment elevation over the right ventricle and posterior wall was detected in significantly more patients with the BSM ECG than with the additional-lead ECG. The investigators concluded that BSM more directly visualized the right ventricle and the posterior wall of the left ventricle and increased the rate of diagnosis of STEMIs in these poorly imaged regions of the heart.1

Possible uses in guiding management. Certainly, the detection of ST-segment elevation on a BSM ECG in an anatomic area that is not imaged on a 12-lead ECG can influence management decisions. For example, a finding of right precordial ST-segment depression on a 12-lead ECG in a patient with chest pain and suspected ACS does not represent a scenario that mandates acute reperfusion therapy. However, this ST-segment depression may, in fact, represent a STEMI of the posterior wall of the left ventricle; if this is the case, the patient may be a candidate for fibrinolysis or percutaneous coronary intervention.

Clearly, BSM provides more complete imaging of the heart in patients with ACS. What remains to be seen is the impact of this information on additional therapeutic interventions and risk prognostication. *

References:

REFERENCES:

1.

Menown IBA, Allen J, Anderson JM, Adgey AA. Early diagnosis of right ventricular or posterior infarction associated with inferior wall left ventricular acute myocardial infarction.

Am J Cardiol

. 2000;85: 934-938.

2.

Ornato JP, Menown IBA, Riddell JW, et al. 80-Lead body map detects acute ST-segment elevation myocardial infarction missed by standard 12-lead electrocardiography.

J Am Col Cardiol

. 2002;39:332A.

3.

McClelland AJJ, Owens CG, Menown IBA, et al. Comparison of the 80-lead body surface map to physician and to 12-lead electrocardiogram in detection of acute myocardial infarction.

Am J Cardiol

. 2003;92:252-257.

4.

Menown IBA, Allen J, Anderson JM, Adgey AA. ST-segment depression only on initial 12-lead ECG: early diagnosis of acute myocardial infarction.

Eur Heart J

. 2001;22:218-227.