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Background: Scarce data are available regarding the electrocardiographic (ECG) and echocardiographic changes in athletes of Asian origin., Design: We investigate the ECG and echocardiographic patterns in Japanese (J) compared with African-Caribbean (AC) and Caucasian (C) athletes., Methods: A total of 282 professional soccer players (68 J, 96 AC and 118 C) matched for age, gender, sport and level of achievement was examined., Results: ECGs were without alterations in 62% of J (versus 69% of C, p = non significant and 44% of AC, p < 0.001). The most common alterations in J were sinus bradycardia (69%), incomplete right bundle branch block (RBBB; 43%), early repolarization (18%), isolated increase in R/S-wave (10%), Q-waves (9%). Remarkably, no J athlete showed deeply T-wave inversion, in contrast to 6% of AC (p < 0.05). Occasionally, J showed J-point upward/domed ST-elevation with inverted/biphasic T-wave (6% versus 16.5% in AC, p < 0.01). J demonstrated larger left ventricular (LV) cavity compared with AC and C players (55.2 ± 3.3 versus 52.2 ± 3.8 and 53.9 ± 3.7 mm, respectively, p < 0.01), with an important subset ( > 4%) presenting a markedly enlarged cavity (>60 mm), in the presence of normal systolic/diastolic function and no segmental abnormalities. Therefore, J showed a more eccentric remodelling compared with AC and C (relative wall thickness: 0.31 ± 0.05, 0.38 ± 0.06 and 0.36 ± 0.06, respectively, p < 0.01)., Conclusion: J players show the most eccentric LV remodelling compared with C and AC players. In association, certain training-related ECG patterns, i.e. sinus bradycardia and isolated increase in R/S-wave voltage, are present in a larger proportion of J players than previously described in C players. Conversely, no J athlete showed deeply T-wave inversion, as commonly found in AC and occasionally in C.

The relationship between the location and size of an infarction and QT dispersion was investigated in 84 Japanese patients with chronic myocardial infarction (54 with anteroseptal infarction and 30 with inferior infarction). The control group consisted of 23 subjects without ischemic heart disease (13 normal subjects and 10 hypertensive patients). Corrected QT dispersion (maximum corrected QT interval minus minimum corrected QT interval: QTc dispersion), was significantly larger in the anterior infarction group than in the control group (69.9+/-21.5 msec vs 53.0+/-17.6 msec), while the inferior infarction group showed no significant difference from control subjects. QTc dispersion was significantly greater in the patients with large anterior infarcts than in those with small anterior infarcts (80.5+/-20.5 msec vs 61.9+/-18.8 msec). In patients with chronic myocardial infarction, QT dispersion is influenced by the infarct location and size. Accordingly, interpretation of QT dispersion data should take these factors into consideration.

Objectives: We sought to determine the prevalence of right bundle branch block (RBBB) and ST segment elevation in the working Japanese population, as well as the event rate during a three-year prospective follow-up period., Background: A poor prognosis of RBBB and ST segment elevation has been reported in Europe and South America, even in asymptomatic patients; however, a large population of asymptomatic patients with sporadic RBBB and ST segment elevation has not been studied., Methods: Ten thousand 12-lead electrocardiograms (ECGs) were obtained during annual check-ups of working adults in the Tokyo area. This three-year prospective follow-up study consisted of 105 patients, including 20 with ventricular fibrillation, 18 with syncope and 67 who were asymptomatic. They were registered from 46 institutions in Japan., Results: The prevalence of ECG abnormalities in working adults was 0.16%. A coved-type ST segment elevation was related to a history of cardiac events, and 18% of registered patients had PR prolongation and 9.5% had left-axis deviation. The cumulative cardiac event-free rate was 67.6% in the symptomatic group and 93.4% in the asymptomatic group (p = 0.0004) after three years., Conclusions: The recurrence rate of cardiac events in symptomatic patients was similar to that reported previously, but it was very low in sporadic asymptomatic patients. The ECG findings may help us to select patients for further examination and more accurate evaluation of their prognoses.

To detect the minute electric potential inside the QRS complex, a new frequency domain method was designed using short-time First Fourier Transforms (SFFT) and high-frequency sampling (oversampling). SFFT improved the frequency resolution by oversampling that was applied to this analysis. The electric potential data of 15,000 points received weighted, running average processing and was subtracted from the original waveform to reduce the low-frequency component. The data in a segment of 160 ms, including QRS, was processed by frequency analysis with the SFFT computation routine. The ECG of healthy individuals was analyzed by this method and its usefulness evaluated. The processing waves of the X-axis, Y-axis, and Z-axis of a representative normal subject were formed into 3 groups of peak electric potential. SFFT enabled the detection of the structure inside the QRS complex without signal averaging, and is considered capable of evaluating the process of excitement inside the QRS complex in the various heart diseases.

Unlabelled: QT dispersion (QTd: maximum QT interval-minimum QT interval) is associated with severe cardiac arrhythmia and with abnormal ventricular repolarization. We investigated the influence of exercise on QTd in patients with ischemic heart disease. On standard 12-lead electrocardiograms, QTd was measured before and after treadmill exercise in 7 normal subjects, 17 patients with effort angina pectoris (and > or = 75% stenosis on coronary arteriography), and 33 patients with old myocardial infarction. Bazett's formula was used to obtain the corrected QTd (QTcd). The pre-exercise resting QTcd was 45.9 +/- 10.6, 44.3 +/- 15.2, and 74.8 +/- 28.1 msec in the respective groups, being significantly greater in the infarct group (p < 0.05). The QTcd at 5 min after exercise was respectively 49.3 +/- 9.0, 58.8 +/- 19.9, and 75.4 +/- 30.9 msec (p = 0.0347, infarct vs. controls). The difference in QTcd was significant for the angina group before and after physical exercise (p = 0.0003). There was a significant increase of QTcd after exercise in the angina group whether or not the patients were receiving beta-blockers. The infarct patients without beta-blocker therapy showed an increase of QTcd after exercise, while those receiving beta-blockers showed a decrease. The post-exercise difference between these subgroups was significant (p = 0.0351)., Conclusions: QTcd was significantly increased by exercise in the angina group, possibly reflecting impaired repolarization due to ischemia. Inhibition of the increase in QTd by beta-blockers suggested a possible preventive effect on severe arrhythmias due to nonhomogeneous ventricular repolarization.

The relationship between ischemic ST depression and oxygen uptake kinetics was examined during cardiopulmonary exercise test using the ramp protocol in 22 patients (17 males and 5 females, mean age 61.4 +/- 8.1 years) with ischemic ST change (horizontal or down sloping ST depression over 1 mm) during a previous multi-stage exercise test (Bruce method). Patients were classified into three groups according to coronary angiographic findings: absence of significant stenosis group (control, n = 7), single-vessel disease group (n = 7) and multivessel disease (MVD) group (n = 8). Peak exercise time, peak heart rate, peak systolic blood pressure, anaerobic threshold, peak oxygen uptake (peak Vo2), exercise time, heart rate, systolic blood pressure, and oxygen uptake at appearance of ischemic ST change were measured. The ratio of oxygen uptake increase at appearance of ischemic ST change was calculated. Peak Vo2 was lower in the MVD group than in the control group (20.9 +/- 6.2 vs 27.3 +/- 3.3 ml/min/kg, p < 0.05), and exercise time from the beginning of ramp exercise to the appearance of ischemic ST depression was shorter in the MVD group than in the control group (5.2 +/- 2.1 vs 8.2 +/- 1.9 ml/min/kg, p < 0.05). The ratio of oxygen uptake increase was smaller in the MVD group than in the control group (0.7 +/- 0.3 vs 1.2 +/- 0.2, p < 0.01). These results could be caused by impaired increase of cardiac output due to myocardial ischemia occurring during exercise. In the clinical setting, these phenomena could be used as a parameter for differentiating ischemic from non-ischemic ST depression or evaluating the sensitivity of ischemic heart disease.

Changes of the surface ECG and monophasic action potential induced by isoproterenol injection were investigated under normo- and hypercalcemic conditions in dogs. (1) Biphasic time course of T wave changes, initially inverted and subsequently uprightly tall, was observed after intravenous injection of isoproterenol in doses of more than 2 microgram. (2) Initial prolongation and subsequent shortening of the phase 2 of action potential were observed on the ventricular surface in accordance with the biphasic time course of the T wave changes on the surface ECG after isoproterenol injection. (3) Giant T wave inversion associated with QT prolongation was obtained by isoproterenol injection under hypercalcemia. (4) Marked prolongation of total duration as well as phase 2 of action potential was observed in accordance with the giant negative T wave on the surface ECG. Although the mechanism of this experimental model of giant negative T wave is not clear, this model could have important suggestions on the unknown mechanism of giant negative T wave observed in various clinical status.

In 30 patients with nocturnal angina, the night-time ECGs were continuously recorded, and the time and duration of attack, cyclic character of attacks, the relation of chest pain to ischemic ECG changes and arrhythmias during attack were compared between 18 cases with ST elevation and 12 cases with ST depression during attack. In cases with ST elevation, 1) attacks occurred between 2:00 and 8:00 a.m., being most frequent between 4:00 and 5:00 a.m. 2) the duration of attack measured from the duration of ischemic ECG changes was less than 5 min in 88% of the attacks, 3) the attack often recurred with intervals less than 30 min and ECG changes were often unaccompanied bt chest pain, 4) the attack was complicated with various kinds of arrhythmias. These features were in marked contrast to the cases with ST depression, in which attacks were evenly distributed over the night-time, of longer duration, sporadic in occurrence and far less complicated with arrhythmias. These data suggest that the difference of mechanisms causing attacks between both groups.

False-positive exercise test responses are frequently observed in women. To differentiate a false-positive from a true-positive test response, the effect of postures for recording a postexercise electrocardiogram to the recovery process of ST depression was investigated in 26 women with nonischemic ST depression and in 14 patients with typical angina pectoris. Exercise tests were performed twice, and the postexercise electrocardiogram was recorded while standing during the first test and in the supine position during the second test. In the false-positive test, maximal ST depression occurred immediately after exercise and showed a rapid recovery process in the early recovery phase. However, ST depression persisted without complete recovery, or increased in the late recovery phase as long as subjects were kept standing. In contrast, ST depression returned to the control level when subjects changed to the supine position after exercising. This discrepant pattern in the recovery process of ST depression by changing postures was not observed in the true-positive test results. Changing postures for recording postexercise electrocardiograms could be helpful in differentiating a false-positive response from a true ischemic response.

1) Body surface mapping was performed in 15 patients with ischemic heart disease and 5 control subjects before and after isoproterenol infusion. In ischemic heart disease, ST map developed negative areas in the left anterior chest wall extending from mid line to left axillar line after isoproterenol. This distribution on ST depression was different from that of left ventricular hypertrophy or complete left bundle branch block which spared mid anterior chest. The point of maximal ST depression corresponded to one of the conventional chest lead in 6 of 15 cases. In other 9 cases, the point of maximal ST depression was mostly located superiorly to V3-V5. epsilon ST depression correlated well with the maximal ST depression (r = 0.90) but not very well with ST depression at V5 (r = 0.70). On 201 T1 stress scan, a reversible large perfusion defect was detected in 2 out of 5 patients with marked ST depression. These findings suggested that isoproterenol induced ST map changes are useful in diagnosis of myocardial ischemia. 2) Body surface map was obtained in 16 cases with chronic pulmonary disease. The location of the maximum R and initial R was relatively inferior to that of normal controls. Relatively deep S waves were frequently observed. Pulmonary function tests correlated with the maximum R voltage but not with the deepest S. Cases with relatively high pulmonary conus voltage were proved to have right ventricular hypertrophy on 201 T1 myocardial scintigraphy or on echocardiography.

The incidence and forms of ventricular premature complexes (VPCs) in apparently healthy subjects were studied to determine long-term reproducibility of day to day variation on Holter electrocardiogram. The study included 152 men and 68 women ranging in age from 20 to 78 years who were having routine check-ups that revealed no cardiovascular abnormalities. In addition to routine measurements, Holter electrocardiography was recorded during daily life, and the total number of VPCs occurring during 24 hours was visually calculated on replayed electrocardiographic tracings. Forms of VPCs and incidence of VPCs in 10-year age groups of the subjects were also recorded. No VPCs were observed in 56% of the subjects; 93% showed less than 50 VPCs and the other 7% of the 220 subjects had greater than or equal to 50 VPCs. Forty-one of the 220 subjects returned for routine follow-up 1 year later. Repeated Holter electrocardiograms at this time showed high reproducibility of less than 50 VPCs. A small number of multiform VPCs were reproducible but paired VPCs were not. Physiologic definition of VPCs in healthy subjects appears to be clinically significant.

Eighteen paroxysms were documented on Holter electrocardiogram both at the onset and the termination of paroxysmal atrial fibrillation in 14 apparently healthy subjects. There were large inter- and intraindividual variations and no definite trend was observed in the time and duration of paroxysms. Heart rate at the onset of paroxysms was consistently higher than that at sinus rhythm immediately before atrial fibrillation started. There were 2 patterns in the sequence of heart rate during paroxysms. One was an almost constant heart rate during paroxysms, and the other was a trend toward a decrease in heart rate from the onset to the termination of paroxysms. The duration of paroxysms was within 2 hours in the former group and more than 2 hours in the latter group. There was a reverse correlation between heart rate at the termination of paroxysms and their duration.

Left ventricular scanning by echocardiography and ultrasono-cardiotomography was performed to search the possible muscular abnormality in 9 cases with giant T wave inversion without documented cause. The deeply inverted T wave was more than 1.2 mV (average was 1.63 mV) in the left precordial leads. All the cases had electrocardiographic left ventricular hypertrophy of obscure origin and ischemic episode was absent. Conventional echo beam direction to measure the short axis of the left ventricle disclosed almost normal thickness and movement of both interventricular septum (IVS) and the posterior wasll (PW), so that the report of these cases is frequently within normal limits. However, ultrasono-cardiotomography (sector B scan) disclosed the fairly localized hypertrophy near the left ventricular apex, and conventional echocardiography also revealed the same area of either IVS or PW or both below the insertion of the papillary muscles, when the scanning towards the apex was performed (asymmetrical apical hypertrophy: AAH). Control study of 9 cases with IHSS showed asymmetrical septal hypertrophy (ASH) with almost equally hypertrophied IVS from base to apex. All cases had inverted T waves, but these were of lesser degree. Three cases had relatively deep T wave compatible with those of AAH, and these cases also had the apical hypertrophy of considerable degree (unusual type of IHSS, i.e., intermediate type between AAH and ASH). The close relationship between the depth of the inverted T waves and the Apex/Mid wall thickness ratios suggests that the altered recovery process of the hypertrophied apical musculature is responsible for the giant T wave inversion of heretofore unsolved origin. Until the connective link of AAH to the other forms of hypertrophic cardiomyopathy is disclosed, the cases with such a T wave and the apical hypertrophy may be designated as asymmetrical apical hypertrophy (AAH).

The sequence of localized changes in ventricular repolarization time during and after temporary coronary artery occlusion was studied in 10 open chest dogs. Immediately after the onset of coronary occlusion functional refractory periods (FRPs) prolonged slightly in the ischemic area, then shortened with continued occlusion. Within the first minute following release of occlusion, FRPs underwent a further brief decrease in duration. By varying the period of occlusion from 1 1/2 to 6 1/2 min, evidence was obtained that the post-release shortening of RFPs was temporally related to release of the clamp and not to the onset of occlusion. Ventricular fibrillation occurred in 2 dogs, in each instance soon after release of the coronary artery occlusion. The possible relationship of these experimental FRP changes to waveform abnormalities and arrhythmias in ischemic heart disease is discussed.