Kozue Ikeda

Significance of discordant ST alternans in ventricular fibrillation.

With the use of epicardial mapping, we investigated the electrical alternans of the ST segment during acute myocardial ischemia and studied the difference in ST alternans between dogs with resultant ventricular fibrillation and those without it. During the 7-minute occlusion of the left anterior descending coronary artery below its first diagonal branch, 60 epicardial unipolar electrograms were recorded simultaneously at 1-minute intervals by a computerized mapping system. ST alternans was found in the eight dogs we observed. The amplitude of ST alternans (difference in the ST segment elevation of two consecutive electrograms) was greater in dogs with ventricular fibrillation (n = 4) than in those without it (n = 4) (3.92 +/- 1.24 versus 0.58 +/- 0.49 mV, p less than 0.05). Three of the four dogs with ventricular fibrillation demonstrated discordant ST alternans (i.e., adjacent leads were out of phase). Results from the present study indicate that an increased amplitude and discordance of ST alternans during acute myocardial ischemia are related to ventricular fibrillation and act as indicators of time and spatial unevenness of ventricular repolarization.

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.

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)

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.

Detection of posterior myocardial infarction by body surface mapping: a comparative study with 12 lead ECG and VCG.

To examine the diagnostic ability of body surface mapping in posterior myocardial infarction (PMI), mapping was performed in 11 patients with PMI proven by left ventriculography and T1-201 myocardial perfusion imaging (PMI group) and in 44 normal subjects (N group). Map data was analysed by the following methods: (1) potential departure maps at 10, 20, 30, 40 and 50 msec after the onset of QRS; each map indicates the area of decreased potential out of the normal range at the time. (2) AQRS departure map which indicates the area of decreased time-integral value of QRS out of the normal range. True positive (TP) in the PMI group and false positive (FP) in the N group were calculated for each method, and were compared with those of various criteria for PMI with standard 12-lead electrocardiogram (ECG) and Frank lead vectorcardiogram (VCG). The potential departure maps and the AQRS departure map had high TP (10/11 and 8/11) and low FP (0/44 and 0/44). The diagnostic ability of mapping is considered to be higher than that of ECG and VCG. Mapping, especially the departure map technique, is a sensitive and specific method to detect posterior infarction.

Relation between recovery sequence estimated from body surface potentials and T wave shape in patients with negative T waves and normal subjects.

BackgroundAdvances in analytical methods of the epicardial electrical potentials allowed us to demonstrate spatial distributions of local recovery. Because local recovery will be reflected in events on body surface ECG mapping, abnormalities in recovery sequence that may be responsible for the origin of negative T waves can be detected from body surface potentials. Methods and ResultsEighty-seven unipolar ECGs were recorded simultaneously from the entire thorax in patients having negative T waves on left anterior precordial leads and in normal subjects. These included 40 patients with anterior myocardial infarction (MI), 21 patients with left ventricular hypertrophy (LVH), and 44 male volunteers. We measured T., time, defined as the instant of maximal first derivative of the T wave as the index of local recovery (Wyatts method). Parameters related to T wave potentials were positive T wave amplitude, negative T wave amplitude, and T integral. Significant correlations were observed between the TMAX time and each of the T wave potentials. The T wave potentials were dependent on TMAX times. In the anterior MI, the late Tma times were located on the upper left anterior chest and early T.a. times on the lower right lateral chest. In the LVH, the area showing a delayed recovery was displaced in a left downward direction compared with anterior MI. ConclusionsBody surface TMAX time distributions clearly separate two negative T wave groups, i.e., anterior MI and LVH. Appearance of the negative T waves correlates well with the presence of the area with delayed TMAX time on the spatial distribution.