Body surface potential mapping of ST segment changes in acute myocardial infarction. Implications for ECG enrollment criteria for thrombolytic therapy.
BACKGROUND
Several large, randomized clinical trials have shown that early thrombolytic therapy substantially reduces early mortality after acute myocardial infarction (MI). In most trials, eligibility criteria include typical chest pain and diagnostic ST segment elevation in two or more contiguous leads of the standard 12-lead ECG. Unfortunately, large areas of the thoracic surface are left unexplored by the standard electrode positions. As a consequence, acute MI patients with ST elevation in regions not interrogated by the conventional electrodes may not receive reperfusion therapy and its attendant benefits.


RESULTS
The present study compares 120-lead body surface potential map (BSPM) data from 131 patients with acute MI and 159 normal control subjects (N). The MI population was stratified according to the location of ventricular wall motion abnormalities evidenced by radionuclide imaging into 76 patients with anterior MI (AMI), 32 patients with inferior MI (IMI), and 23 patients with posterior MI (PMI). BSPM were recorded within 24 hours of admission. Group mean BSPM of the ST segment were obtained for N, AMI, IMI, and PMI by sampling the time-normalized ST-T waveform at 18 equal intervals and averaging the voltages at each electrode site over the first five of these 18 ST-T time instants. Corresponding discriminant maps were also computed for each pairwise comparison (AMI versus N, IMI versus N, and PMI versus N) by subtracting the normal group mean voltages from each MI group mean voltages and by further dividing each resulting difference by the composite standard deviation calculated from the pooled groups. Discriminant analysis for each bigroup classification was also performed using as measurements the ST magnitudes in 120 electrode sites from each individual. Finally, the number of patients in each MI group with ST changes outside the 95% normal range was calculated for each electrode position. The following results were obtained: 1) In each MI group, ST depression departs more significantly from normal values than ST elevation. 2) The most significant ST changes (both ST elevation and ST depression) are observed in IMI, the least significant in AMI. 3) For each pairwise comparison, measurements from two lead sites are entered into the stepwise discriminant procedure: the first measurement is ST depression, the second ST elevation. Classification rates are 82% for AMI, 93% for PMI, and 100% for IMI at a specificity level of 95%. 4) From the six leads selected for optimal classification of the three MI groups, five are outside the area sampled by the conventional precordial electrodes. 5) The use of site-dependent thresholds for ST measurements based on 95% normal range yields the best compromise between sensitivity and specificity. A fixed threshold of 1 mm for ST elevation or ST depression produces increased sensitivity in AMI at the cost of marked loss in specificity and reduces sensitivity in both IMI and PMI with no benefit in specificity.


CONCLUSIONS
Analysis of BSPM identifies areas on the torso where the most significant ST changes most frequently occur in acute MI. Two leads from areas with the most abnormal ST changes achieve optimal classification in each MI class. Of these six leads, five are outside the standard precordial lead positions. ST depression is the most potent discriminator for each MI group and contains information independent from ST elevation. Quantitative analysis of ST magnitude at each electrode site allows determination of best thresholds for ECG criteria. Appropriate selection of ECG leads may help remove inconsistencies in current ECG selection criteria and improve comparability of treatment results.
Kornreich
F
F
Unit for Cardiovascular Research and Engineering, Free University Brussels, Belgium.
Montague
T J
TJ
Rautaharju
P M
PM
D000328:Adult; D016002:Discriminant Analysis; D004562:Electrocardiography / Q000379:methods*; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D012016:Reference Values; D012189:Retrospective Studies
D005343:Fibrinolytic Agents