Our objectives in this study were to determine the incidence of abnormal signal-averaged ECG (SAECG) and its relation to the extent and type of exercise in young healthy athletes, and to evaluate the association, if any, between the development of abnormal SAECGs and vigorous exercise. The presence of an abnormal SAECG was evaluated in 796 athletes (mean age 19 years), and its relation to findings on 12-lead electrocardiogram, echocardiogram, and the presence arrhythmias was studied using Holter monitoring. An SAECG was considered abnormal when any one of the three following criteria was met: filtered QRS duration of more than 114 msec, root-mean-square voltage in the terminal 40 msec of less than 20 μV, or a voltage of less than 40 μV for more than 38 msec. Abnormal SAECGs were present in 68 (8.5%) of the athletes and were associated with a smaller left ventricular mass. Athletes who performed anaerobic exercise tended to exhibit a high incidence of abnormal SAECGs, which was associated with a smaller left ventricular mass. No serious ventricular arrhythmias were observed on 24 h Holter monitoring or during the follow-up period of 20±10 months. There were no sudden cardiac deaths. Continuous anaerobic exercise may induce abnormal SAECGs through the development of delayed myocardial conduction or electrical inhomogeneity in cardiac tissue. The presence of an abnormal SAECG was unrelated to the development of arrhythmias in young athletes.

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Patients with sustained ventricular tachycardia (VT) in the post-infarction period, especially more than 48 h after acute myocardial infarction (AMI), have a high mortality. However, clinical characteristics of these patients are unknown, since previous studies have not clarified the relationship between sustained VT and acute myocardial damage. To clarify the prognostic factors in patients with sustained VT in the early post-infarction period, we retrospectively surveyed 961 consecutive patients with AMI. Eleyen patients (9 men and 2 women, aged 54 to 80 years) who had no previous myocardial infarction had at least one documented episode of sustained VT between 3 and 21 days after AMI. Late potentials were detected in 7 of 7 patients who underwent signal-averaged electrocardiography within 2 days after the first occurrence of VT. Entrainment was seen in 2 patients. The 5 patients who died in hospital had the following clinical characteristics: 1) cardiogenic shock, 2) extensive infarction, 3) a short interval from AMI to the onset of VT (mean±SD: 4±2 days), and 4) recurrent and refractory VT. In contrast, the 6 patients who survived had the following clinical characteristics: 1) no cardiogenic shock, 2) a relatively late occurrence of VT(mean±SD: 14±7 days), 3) few episodes of VT, and 4) no recurrence of VT during the follow-up period of 12 to 58 months. The occurrence of sustained VT within 3 weeks after AMI was influenced by the general condition of the patient, and the prognosis was mainly related to cardiac function.

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The effect of early reperfusion on the time course of signal-averaged ECG was examined in 90 patients with myocardial infarction. Abnormal signal-averaged ECG disappeared more frequently (p<0.05) and earlier in cases with early reperfusion than in those without. Serious arrhythmic events in the late phase (>7 days) occurred in patients with abnormal signal-averaged ECG, but not in cases with early reperfusion. These results indicate that dynamic changes in tissue structure and the physiological state of viable muscles after early reperfusion produce different time courses for signal-averaged ECG. The risk of arrhythmic events among patients with abnormal signal-averaged ECG seems to be lower in cases with early reperfusion than in those without.

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Several studies have demonstrated that myocardial infarction (MI) is likely to alter left ventricular diastolic function. However, it is unclear whether MI perse alters Doppler transmitral flow velocity patterns (TMF) clinically. To investigate how myocardial infarction alters TMF clinically, we assessed serial changes in TMF in 13 patients whose TMF patterns were recorded at a mean of 7 months before and after MI in relation to the size of MI. From TMF, early and atrial filling flow velcities (E and A (m/s), respectively), and the E/A ratio, were measured. From simultaneously recorded two-dimensional echocardiograms, left ventricular dimensions and wall motion score (WMS: sum of 17 segmental scores (dys/akinesis=3 to normal=0)) were determined. The patients were divided into two subsets based on the values for WMS in the convalescent stage; 8 patients had small MI (WMS&le;10) and 5 patients had large MI (WMS>10). In patients with small MI, although E and the E/A ratio decreased at day-1 compared with pre-MI values (pre-MI vs day-1, E; 0.54±0.12 vs 0.39±0.15, p<0.05, E/A ratio; 0.91±0.23 vs 0.68±0.14, p<0.05), these values increased to levels similar to those observed at pre-MI in the convalescent stage. There were no changes left ventricular dimensions between pre-MI and in the convalescent period. In patients with large MI, the changes in the TMF patterns varied among patients after MI. In 3 patients with WMS&le;25, E and the E/A ratio were decreased in the convalescent stage, compared with pre-MI values. In 2 patients with WMS>25, TMF patterns showed 'pseudonormalization'(E/A ratio>1.0) throughout the follow-up period, with a progressive increase in left ventricular dimension. Thus, MI per se does not always produce clear changes in the Doppler TMF pattern in clinical settings, and the size of the MI seems to be a determinant of the TMF pattern after MI.

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The purpose of this study was to examine the long-term course of conductivity in patients with second- or third-degree atrioventricular (AV) block after pacemaker implantation. Fifty-four patients (30 males and 24 females, mean age 59.5 years) had a 12-lead electrocardiogram (ECG) recorded prior to pacemaker implantation and again after a follow-up of more than 5 years (mean 108 months). The degree of AV block and the morphology of the QRS complex in the two ECGs were compared. Twenty-eight (85%) of the 33 patients with complete AV block and 15 (71%) of the 21 patients with second degree AV block before implantation showed complete AV block after the follow-up period. The progression of AV block was recognized only in patients with intra-His (BH) or infra-His (H-V) block. In 29 patients, escape QRS complexes were recorded in both ECGs. A change in the QRS complex was noted in 6 patients (21%), including 2 with new bundle branch block (BBB), 2 with wider BBB, 1 with new left axis deviation, and 1 with a change to another BBB. This change was particularly notable in the H-V block group (44%). In conclusion: (1) Most patients with complete AV block did not recover AV conductivity after the long-term follow-up. (2) Second-degree BH and H-V block tended to progress to complete AV block.

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The combined effects of pravastatin and probucol on high-density lipoprotein (HDL) apolipoprotein (apo) A-I kinetics in cholesterol (Ch)-fed rabbits were investigated. Japanese White rabbits were treated with 0.15% pravastatin and 0.5% Ch (group 1) or 0.15% pravastatin plus 1% probucol and 0.5% Ch (group 2) for 2 months. After treatment, the serum total cholesterol levels in groups 1 and 2 had significantly (p<0.01) increased (37.4±6.7 mg/dl vs 117.1±46.4 mg/dl, and 31.4±4.9 mg/dl vs 143.0±84.5 mg/dl, respectively). The serum HDL-cholesterol levels in both groups decreased (18.2±2.8 mg/dl vs 16.2±3.7 mg/dl, p<0.01 for group 1; 18.2±1.9 mg/dl vs 15.5±4.5 mg/dl, ns for group 2). Apo A-I kinetics were assessed by injecting ¹²⁵I-labeled HDL intravenously into both groups of rabbits, and taking blood samples periodically for 6 days. Kinetic parameters calculated from apo A-I specific radioactivity decay curves showed that the apo A-I fractional catabolic rates in rabbits fed pravastatin and Ch (group 1) were significantly less than those in rabbits fed pravastatin plus probucol and Ch (group 2)(0.546±0.017 /day vs 0.730±0.126 /day, p<0.05), while the synthetic rate of apo A-I was lower in group 2 than in group 1 (14.76±1.71 mg/kg per day vs 11.21±2.38 mg/kg per day, respectively, p<0.1). These data indicate that pravastatin and probucol have different effects on HDL-apo A-I kinetics in a diet which includes cholesterol.

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We report a 78-year-old woman with incomplete left atrial rupture following left atrial infarction associated with left ventricular myocardial infarction. An autopsy revealed a hemopericardium. A large hematoma was observed in the posterior wall of the left atrium and a few small tears were found on the same wall. Near its origin, the left circumflex artery was severely sclerotic and completely occluded by fresh thrombus. Histologic examination revealed that large intramural hematoma longitudinally dissected the inner third of the posterior wall of the left atrium, and transversely dissected through the necrotic tissue to the pericarcdial sac to result in rupture. Coagulation necrosis and intramyocardial hemorrhage were also observed throughout the entire left atrium and the postseptolateral wall of the left ventricle.

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5-Fluorouracil (5-FU) is widely used in the treatment of various solid tumors. However, 5-FU cardiotoxicity is being reported with increasing frequency. The main symptom of cardiotoxicity is chest pain at rest with ischemic electrocardiographic changes. Up until now, the underlying mechanism has been suspected to be coronary artery spasm. However, this chest pain associated with 5-FU has several characteristics that are incompatible with coronary artery spasm; eg, inefficacy of calcium-channel blocker and a slow increase in cardiac enzyme levels. We experienced a case of 5-FU-induced cardiotoxicity which showed clinical findings consistent with acute myocardial infarction. Based on the clinical findings, coronary angiography, and left ventricular angiography in a prolonged attack, we concluded that the cardiotoxicity in this case was not due to ischemia caused by coronary artery spasm.

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