Search

Nine patients of sick sinus syndrome with atrial programmable pacemaker (3 males and 6 females, aged from 53 to 72 years) were studied to assess the effect of heart rate on the body surface potential distribution. Body surface maps (87 lead points) and M-mode echocardiograms were recorded at 20-beat increments of heart rate from 60 to 140 beats/min during atrial pacing. The potential changes of R and S voltages were evaluated quantitatively and were correlated with the changes of echocardiographically measured left ventricular dimension. As the heart rate increased, left ventricular dimension in end-diastole (LVDd) decreased gradually (Table 1), and a significant decrease was observed when the heart rate increased from 80 to 100 beats/min and from 100 to 120 beats/min, respectively, (p less than 0.05). With a decrease in LVDd, the distance between the left ventricular posterior wall and the anterior chest wall decreased and the left ventricular wall increased in its thickness. These changes, however, were not statistically significant. With an increase in the heart rate, R voltages decreased gradually in the left lateral chest and the sum of R voltages (sigma R) of six lead points in the left lateral chest including leads V5-6 decreased significantly when the heart rate increased from 60 to 100 beats/min and from 80 to 120 beats/min, respectively (p less than 0.02) (Table 2). On the other hand, R voltages remained unchanged in the left anterior chest during atrial pacing, then the sum of R voltages of six lead points in the left anterior chest including leads V2-4 and the sum of R voltages of 87 lead points did not show any significant changes (Table 2). An increase in the absolute value of S voltages was observed in the left anterior chest and the sum of S voltages of six lead points in the left anterior chest including leads V2-4 increased when the heart rate increased from 60 to 100 beats/min and from 80 to 120 beats/min, respectively (p less than 0.1) (Table 3) A decrease of R voltages in the left lateral chest was consistent with the reduction in LVDd (p less than 0.005). It is concluded that the changes in body surface QRS amplitudes during atrial pacing are related to those in the left ventricular dimension and that R voltages in the left lateral chest are fairly sensitive to see the changes in LVDd in cases with no abnormal wall motion of the left ventricle.(ABSTRACT TRUNCATED AT 400 WORDS)

Body surface mapping (map) was used to evaluate various cardiac diseases quantitatively. For 30 cases with old anterior myocardial infarction (AMI), map parameters were compared with infarct size assessed by left ventriculography and 201Tl myocardial scintigraphy (LV% asynergy and 201Tl% defect, respectively). Parameters used in the present study were nSubtraction 40 (sigma Subtr. 40), which were obtained by the summation of voltages less than the lower limit of normal range (mean--2SD) at 40 msec from the QRS onset and nSubtraction 10-60 (sigma Subtr. 10-60), which was obtained by the integral of voltages below the normal range, calculated each 10 msec to 60 msec, as well as the number of lead points with Q waves of 30, 40 msec duration (nQ30, nQ40), and the summation of R voltages over the entire body surface (sigma R). In 19 cases with aortic regurgitation (AR), R and S voltages in each lead were compared with left ventricular diastolic dimension (LVDd) obtained by echocardiography. In 43 healthy persons and two patients with RV pacing, the ventricular activation time was measured in each lead (VAT map). In AMI, nSubtr. 40 correlated best with LV% asynergy (r = 0.70, p less than 0.001). EF and 201Tl% defect were related to nSubtr. 10-60 (r = 0.83, p less than 0.001 and r = 0.85, p less than 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

This study was performed to evaluate the usefulness of the body surface isochrone map (VAT map) for identifying the ventricular activation sequence, and it was correlated with the isopotential map. Subjects consisted of 42 normal healthy adults, 18 patients with artificial ventricular pacemakers, and 100 patients with ventricular premature beats (VPB). The sites of pacemaker implantations were the right ventricular endocardial apex (nine cases), right ventricular epicardial apex (five cases), right ventricular inflow tract (one case), left ventricular epicardial apex (one case), and posterior base of the left ventricle via the coronary sinus (two cases). An isopotential map was recorded by the mapper HPM-6500 (Chunichi-Denshi Co.) on the basis of an 87 unipolar lead ECG, and a VAT isochrone map was drawn by a minicomputer. The normal VAT map was classified by type according to alignment of isochrone lines, and their frequency was 57.1% for type A, 16.7% for type B, and 26.2% for type C. In the VAT map of ventricular pacing, the body surface area of initial isochrone lines represented well the sites of pacemaker stimuli. In the VAT map of VPB, the sites of origin of VPB agreed well with those as determined by the previous study using an isopotential map. The density of the isochrone lines suggested the mode of conduction via the specialized conduction system or ventricular muscle. The VAT map is a very useful diagnostic method to predict the ventricular activation sequence more directly in a single sheet of the map.