Kai Tsuiki

Isointegral analysis of body surface maps for the assessment of location and size of myocardial infarction

To estimate the location and size of myocardial infarction (MI), an isointegral mapping technique was adopted from among various body surface electrocardiographic mapping techniques. QRS isointegral and departure maps were made in 35 patients with MI. These patients were separated into 3 groups, based on the location of MI: anterior, inferior, and anterior plus inferior. The severity and location of MI were estimated by thallium-201 myocardial perfusion imaging and the degree of scintigraphic defect was represented by a defect score. The extent of MI was expected to be reflected on the QRS isointegral maps as a distribution of negative QRS complex time-integral values. However, the extent and the location of MI were hardly detectable by the original maps. A departure mapping technique was then devised to observe the distribution of departure index on the body surface. Particular attention was given to the area where the departure index was less than -2, and this area was expected to reflect the location and size of specific abnormality of isointegral map due to MI. There were strong correlations between departure area and defect score in the anterior and inferior MI cases (r = 0.88 and r = 0.79, respectively). However, patients with anterior MI plus inferior MI showed no such correlation. Q-wave mapping was compared with QRS isointegral mapping, and QRS isointegral mapping was found to be more accurate in the estimation of the location and size of MI than Q wave mapping. Thus, QRS isointegral mapping, especially departure mapping, is more useful and convenient for detecting the location and size of MI than methods such as isopotential and Q wave mapping.

Dilatation of the left ventricular cavity on dipyridamole thallium-201 imaging: A new marker of triple-vessel disease

To investigate the significance and mechanism of dilatation of the left ventricular cavity on dipyridamole thallium-201 imaging, we performed both dipyridamole thallium-201 imaging and dipyridamole radionuclide angiography on 83 patients with known angiograms. The dipyridamole/delayed ratio of the left ventricular dimension from the thallium-201 image was defined as the left ventricular dilatation ratio (LVDR). An LVDR greater than the mean + two standard deviations in patients without coronary artery disease was defined as abnormal. Twenty-two of 83 patients showed an abnormal LVDR, and 18 of the 22 patients (82%) had triple-vessel disease. By defect and washout analysis, the sensitivity and specificity for correctly identifying the patients as having triple-vessel disease was 72% and 76%, respectively, whereas LVDR had a sensitivity of 72% and a specificity of 93%. When LVDR was used in combination with the defect and washout criteria, sensitivity increased to 84% without a loss of specificity. In those 22 patients with abnormal LVDRs, end-diastolic volume measured by radionuclide angiography did not change after dipyridamole infusion. Dilatation of the left ventricular cavity on dipyridamole thallium-201 imaging reflected relative subendocardial hypoperfusion induced by dipyridamole rather than actual chamber enlargement. The LVDR was moderately sensitive and highly specific for triple-vessel disease and provided complementary information to dipyridamole thallium-201 imaging.

Functional recovery of hibernating myocardium after coronary bypass surgery: does it coincide with improvement in perfusion?

To determine the relationship between functional recovery and improvement in perfusion after coronary artery bypass graft surgery (CABG), 49 patients were studied. Radionuclide angiography was performed before, 1 month after, and 6 to 12 months after CABG to evaluate regional wall motion. Exercise thallium-201 myocardial perfusion imaging was done before and 1 month after CABG to assess regional perfusion. Preoperative asynergy was observed in 108 segments, and 74 of them showed an improvement in wall motion 1 month after CABG (segment A). Sixty-six of these segments (89%) were associated with an improvement in perfusion. Eight segments that had not improved 1 month after CABG demonstrated a delayed recovery of wall motion 6 to 12 months after CABG (segment B). However, seven of eight segments (88%) already showed an improvement in perfusion 1 month after CABG. A total of 82 segments exhibited functional recovery after CABG and were considered hibernating segments. In the preoperative study segment B more frequently had areas of akinesis or dyskinesis than segment A (75% vs 34%, p less than 0.05). The mean percent thallium-201 uptake in segment B was lower than that in segment A (74% +/- 9% vs 83% +/- 8%, p less than 0.05). Functional recovery of hibernating myocardium usually coincided with an improvement in perfusion. However, delayed functional recovery after reperfusion was observed in some instances. Severe asynergy and severe thallium-201 defects were more frequently observed in these segments with delayed recovery. Hibernating myocardium might remain stunned during those recovery periods.

Body surface distributions of ST segment changes after exercise in effort angina pectoris without myocardial infarction.

To investigate the sites of exercise-induced ST segment changes on the body surface in effort angina pectoris without myocardial infarction, we performed 87-lead ECG mapping in 61 patients before and 1.5 and 5 minutes after treadmill exercise. ST segment depression most often occurred in the left anterior chest leads and ST segment elevation developed mainly in the right upper chest leads. There was a good correlation between the number of lead points that showed ST segment depression (nSTd) and the number of those that showed ST segment elevation (nSTe) 1.5 minutes after exercise (r = 0.92). From 1.5 to 5 minutes after exercise, changes in nSTd for individual patients correlated well with changes in nSTe (r = 0.89). It was suggested that the ST segment elevation observed in this study directly reflected the subendocardial ischemia of the left ventricle. In patients with one-vessel disease (n = 32), there was wide overlap in the sites of ST segment changes among patients with left anterior descending artery disease (n = 19), those with left circumflex artery disease (n = 6), and those with right coronary artery disease (n = 7). These findings should lead to a better understanding of exercise-induced ST segment changes for the diagnosis of coronary artery disease.

Segmental wall motion abnormalities in dilated cardiomyopathy: Hemodynamic characteristics and comparison with thallium-201 myocardial scintigraphy

This study assessed the hemodynamic characteristics of segmental wall motion abnormality of the left ventricle in patients with dilated cardiomyopathy (DCM) and its relation to the thallium-201 (TI-201) myocardial scintigraphy (MPI). Left ventriculograms and MPI in 23 patients were analyzed by the use of quantitative indexes of regional wall motion and TI-201 uptake based on a mean and a standard deviation of 13 normal subjects. Relative normokinesis in our definition was more frequently seen in the inferior wall than in the anterior wall (p less than 0.01). In contrast, severe asynergy was more often seen in the anterior wall than in the inferior wall (p less than 0.01). There were 11 patients who had relative normokinesis and asynergy together. By means of the index of wall motion, the DCM patients were divided into two groups, one with segmental wall motion abnormality (SWMA) and another with diffuse wall motion abnormality (DWMA). The DWMA group had higher left ventricular end-diastolic pressures (p less than 0.05) and the tendency of large left ventricular end-diastolic volumes than the SWMA group. There was a rough correlation (r = 0.58) between the quantitative indexes of TI-201 uptake and wall motion at the same region of the left ventricle. Thus, the nonuniformity of the left ventricular wall motion was recognized in the patients with DCM and more increased preload was shown in the patients with DWMA than in the group with SWMA. Further, the regional asynergy may be related to the localized fibrosis within the left ventricle in DCM, considering the result that the worse TI-201 uptake was roughly accompanied by the more severe asynergy.

Detection of diseased coronary artery by exercise ST-T maps in patients with effort angina pectoris, single-vessel disease, and normal ST-T wave on electrocardiogram at rest

To examine the clinical significance of ST-T isopotential maps, 87-lead body surface mapping was performed after treadmill exercise in 21 patients with effort angina pectoris, single-vessel disease, and normal ST-T waves on the resting electrocardiogram. Single-vessel disease was found in the left anterior descending artery (LAD) (nine patients), in the right coronary artery (RCA) (seven patients), and in the left circumflex artery (LCx) (five patients). At 40 msec after the J point, the isopotential maps showed the site of the minimum to be in the left anterior chest in all patients. According to the changes in the position of the minimum from the ST segment to the T wave, postexercise maps were classified into four types. Type A maps (n = 8) were characterized by the persistence of the minimum in the left anterior chest until its negativity decreased and until it became less negative than another minimum that subsequently appeared in a different position. Type B maps (n = 6) were characterized by the gradual movement of the minimum toward the lower thoracic surface. Type C maps (n = 5) were characterized by the gradual movement of the minimum to the left upper direction and then to the back. Type D maps (n = 2) did not show any of the characteristics of A, B, or C. All patients with type A, type B, or type C maps had single-vessel disease of LAD, RCA, or LCx, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of left ventricular volume on right ventricular end-systolic pressure-volume relation. Resetting of regional preload in right ventricular free wall.

Effect of left ventricular (LV) volume on right ventricular (RV) end-systolic pressure-volume relation (ESPVR) was investigated, and the mechanism was examined from a standpoint of the alteration of RV free wall mean fiber length. Twelve cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were controlled independently were used, and RV-ESPVR was determined at three different LV volume levels. At small (10.2 ± 0.6 ml), middle (IS J ± 1.0 ml), and large (20.5 ± 1.4 ml) LV volume, the slope of the RV-ESPVR was 2.63 ± 0.13, 2.74 ± 0.13, and 2.89 ± 0.12 mm Hg/ml, respectively, and each value was significantly different from the others (p <0.01). The volume intercept (V0) of the relation (RV-V0) was significantly decreased with the increment of LV volume (RV-V0 in small, middle, and large LV volume; 3.92 ± 0.68, 3.39 ± 0.67, and 2.87 ± 0.71 ml, respectively; p <0.01). In nine hearts, RV free wall lengths in latitudinal and meridional direction were measured at three LV volume levels when RV volume was held constant (16.1 ± 1.1 ml). RV latitudinal end-diastolic length was significantly augmented with increasing LV volume (latitudinal length in small, middle, and large LV volume; 9.68 ± 0.55, 9.81 ± 0.56, and 9.92 ± 0.55 mm, respectively). RV meridional end-diastolic length also increased significantly with increasing LV volume. We concluded that RV-ESPVR showed upward-leftward shift with increasing LV volume and that this shift could be, at least in part, explained by the alteration of end-diastolic length in RV free wall that occurred with constant RV volume (resetting of regional preload), probably due to the deformation of RV becoming more crescent.

Body surface mapping of high-frequency components in the terminal portion during QRS complex for the prediction of ventricular tachycardia in patients with previous myocardial infarction.

To study the clinical significance of terminal QRS high-frequency components for the prediction of ventricular tachycardia, an 87-lead body surface signal-averaged mapping was performed in 21 healthy subjects (control) and in 41 patients with previous myocardial infarction (anterior, 20; inferior, 21). Mapping data were analyzed and averaged (129.7 +/- 26.5 beats) for 160 seconds, and the signal-averaged beat was filtered with a bidirectional bandwidth (80-250 Hz) digital filter. J-point was determined from the 87-lead RMS voltage of nonfiltered QRS. For each lead, we calculated the sum of the absolute value of filtered QRS from 20 msec ahead of the J-point to the J-point (A-20). The body surface distribution of A-20 was expressed as A-20 map. The maxima in A-20 maps were mainly located on the upper sternal region in healthy subjects, on the left anterior chest in patients with previous anterior myocardial infarction, and on the central anterior chest in patients with previous inferior myocardial infarction. In the patients in both the group with anterior myocardial infarction and the group with inferior myocardial infarction, the value of maximum was significantly greater than in the subjects in the control group (0.181 +/- 0.086 and 0.138 +/- 0.048, respectively, vs. 0.075 +/- 0.031 mV.msec; p less than 0.01). In patients with myocardial infarction (n = 41), the value of maximum was significantly greater with ventricular tachycardia (n = 11) than without ventricular tachycardia (n = 30) (0.240 +/- 0.076 vs. 0.130 +/- 0.043 mV.msec; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Non-invasive detection of coronary artery disease by body surface electrocardiographic mapping after dipyridamole infusion†

Electrocardiographic changes after dipyridamole infusion (0.568 mg/kg/4 min) were studied in 41 patients with coronary artery disease and compared with those after submaximal treadmill exercise by use of the body surface mapping technique. Patients were divided into three groups; 19 patients without myocardial infarction (non-MI group), 14 with anterior infarction (ANT-MI) and eight with inferior infarction (INF-MI). Eighty-seven unipolar electrocardiograms (ECGs) distributed over the entire thoracic surface were simultaneously recorded. After dipyridamole, ischemic ST-segment depression (0.05 mV or more) was observed in 84% of the non-MI group, 29% of the ANT-MI group, 63% of the INF-MI group and 61% of the total population. Exercise-induced ST depression was observed in 84% of the non-MI group, 43% of the ANT-MI group, 38% of the INF-MI group and 61% of the total. For individual patients, there were no obvious differences between the body surface distribution of ST depression in both tests. The increase in pressure rate product after dipyridamole was significantly less than that during the treadmill exercise. The data suggest that the dipyridamole-induced myocardial ischemia is caused by the inhomogenous distribution of myocardial blood flow. We conclude that the dipyridamole ECG test is as useful as the exercise ECG test for the assessment of coronary artery disease.

Improved diagnostic performance on the severity of left ventricular hypertrophy with body surface mapping.

To improve the diagnostic usefulness of electrocardiography (ECG) in determining the severity of left ventricular hypertrophy (LVH) with body surface mapping, 87 unipolar ECGs were recorded from 57 patients with left ventricular (LV) concentric hypertrophy and 30 with LV dilatation. Body surface ECG features due to LVH were evaluated by increase of QRS voltage and delayed local activation. We measured for each lead R voltage, net area of QRS (AQRS), ventricular activation time (VAT), and departure index (DI) of AQRS and VAT (DI = mean/SD). From these measurements, seven parameters were calculated for each patient: Rmax, the maximal R wave voltage; AQRSmax, the maximal AQRS; AQRS-Dmax, the maximal AQRS DI; AQRS-Darea, the area size where DIs of AQRS are more than 2; VATmax, the maximal VAT; VAT-Dmax, the maximal VAT DI; and VAT-Darea, the area size where DIs of VAT are more than 2. Among these parameters, the most effective for diagnosis of LVH were selected by stepwise multiple regression analysis. In the concentric hypertrophy group, the combination of VAT-Darea and Rmax was determined to be the best for estimating wall thickness. The regression equation determined from them correlated well to wall thickness (r = 0.73). In the LV dilatation hypertrophy group, only AQRSmax was selected for estimating LV dilatation. A good correlation between AQRSmax and LV internal dimension was observed (r = 0.73). With the body surface distribution of VAT prolongation, septal hypertrophy was separated from the other LVH. These were superior to the conventional method of 12-lead ECGs. ECG diagnosis of LVH severity improved by incorporating a mapping study. Also, prolongation of VAT and increase in QRS voltage were shown to be important when determining the severity of LVH.