Myocarditis is thought to be commonly caused by various viruses, and accumulating evidence links viral myocarditis with the eventual development of dilated cardiomyopathy. Recently, the importance of hepatitis C virus infection was noted in patients with dilated and hypertrophic cardiomyopathy. Cytokines are being increasingly recognized as an important factor in the pathogenesis and pathophysiology of myocarditis and cardiomyopathy. Elevated levels of circulating cytokines have been reported in patients with heart failure, and various cytokines have been shown to depress myocardial contractility in vitro and in vivo. A number of reports have shown that cytokines generated by activated immune cells cause an increase in nitric oxide (NO) via induction of NO synthase. Increased generation of NO may induce negative inotropism and myocardial damage. This review discusses the etiology and pathogenesis of myocarditis and cardiomyopathy from this point of view. (Jpn Circ J 1997; 61: 275 - 291)

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We analyzed signal-averaged electrocardiograms (ECG) obtained in 50 patients with recent myocardial infarction (RMI: 25 anterior and 25 inferior) and 20 normal subjects to determine the relationship between the initial portion of the signal-averaged QRS complex and cardiac function and infarct size. We examined (1) the root mean square voltage (RMS_10-40, μV), (2) the integration (A_10-40, μV·msec) at 10-msec intervals over the first 40 msec of the signal-averaged QRS complex, and (3) the intervals (T) of the magnitude of the signal-averaged ECG achieved at 10-μV intervals over the first 40 μV (T_10-40, msec). The mean RMS_10-40 (p<0.01) and A_10-40 (A₁₀, p<0.05; A_20-40, p<0.01) were significantly lower and the T_10-40 (p<0.01) was significantly longer in RMI patients than in normal subjects. The RMS_10-40 (p<0.01) and A_10-40 (p<0.05) were significantly lower and the T_10-40 (T_10,20, p <0.01; T_30,40, p<0.05) was significantly longer in patients with anterior RMI patients than in patients with inferior RMI. The A₃₀ Was correlated with the ejection fraction and total creatine kinase (CK) release in all patients (r=0.73, and -0.78, respectively, p<0.001). These results suggest that the A₃₀ may be an important predictor of ventricular dysfunction and infarct size in patients with RMI. (Jpn Circ J 1997; 61: 292 - 298)

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To determine whether specific psychological characteristics are associated with angina pectoris in clinically stable patients 1 to 6 months after recovery from an acute coronary event, a battery of tests was administered to 92 Japanese and 646 North American participants (22% females) in the Multicenter Study of Myocardial lschemia. Of these 738 patients, 541 had originally suffered acute myocardial infarction, 188 had unstable angina, and 9 were admitted for other acute ischemic events. At the time of enrollment, an average of 2.7 months after the index event, 205 patients reported having had anginal symptoms during the preceeding month. Compared to those who did not report angina, these patients scored higher on a modified Autonomic Perception Questionnaire (p=0.04) and lower on the Internal Health Locus of Control Scale (p=0.004). These differences were generalized across the Japanese and North American cohorts. These results indicate that in these patients, angina pectoris was associated with an increased awareness of a wide range of physical symptoms and a decreased sense of personal control over one's own health and prognosis. (Jpn Circ J 1997; 61: 299 - 307)

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Recent clinical trials have demonstrated that the administration of angiotensin-converting enzyme (ACE) inhibitors to patients with myocardial infarction reduces the incidence of recurrent myocardial infarction. It has also been reported that an elevated level of plasminogen activator inhibitor (PAI) appears to constitute a marker of the risk of recurrent coronary thrombosis. To determine whether the ACE inhibitor captopril reduces plasma PAI inhibitor activity, we measured changes in plasma PAI activity (IU/ml), tissue plasminogen activator (t-PA) antigen (ng/ml), and serum ACE activity (IU/L) in 14 survivors of myocardial infarction receiving captopril therapy (37.5 mg daily) and compared them with the values in 15 placebo-treated patients chosen at random. Blood sampling was performed at 07.00 h. In the captopril-treated group, serum ACE activity decreased significantly, from 14.0±0.8 to 11.5±1.2 IU/L 24 h after captopril therapy (p<0.01), and those of PAI activity and t-PA antigen also decreased significantly - from 11.9±2.8 to 5.5±2.2 IU/ml (p<0.02) and from 9.9±1.0 to 7.5±0.9 ng/ml (p<0.05), respectively 48 h after captopril therapy. However, the levels of ACE activity, PAI activity, and t-PA antigen remained unchanged during the study period in the placebo group. Thus, our data indicate that the administration of captopril to patients with acute myocardial infarction may result in a reduced frequency of recurrent coronary thrombosis by increasing fibrinolytic capacity. (Jpn Circ J 1997; 61: 308 - 314)

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Serum creatine kinase (CK) isoforms were examined to detect the progression of left ventricular (LV) enlargement with reduced motion, resembling dilated cardiomyopathy (DCM), in hypertrophic cardiomyopathy (HCM). Changes in LV indices were determined annually by echocardiography in 51 patients until serum measurements (first follow-up period, 6.5±2.2 years). Serum creatine isoforms (CKMM1, CKMM2 and CKMM3) were measured with high-voltage electrophoresis in 35 of these patients from 1991 to 1992, and the data for these latter patients are reported here. Serum total CK, CKMB, lactate dehydrogenase and its isoenzyme LDH1 were also measured. The changes in LV indices were further monitored until January, 1995 (second follow-up). During the 2 follow-up periods, the patients in the on-going group showed a reduction in the LV ejection fraction (LVEF) to <55% with LV end-diastolic dimension (LVDd) <55 mm, and those in the DCM-like group showed a reduction in LVEF to <55% and an increase in LVDd to ≥55 mm. During the first follow-up period, LVEF and LVDd remained at ≥55% and <55 mm, respectively, in 26 patients (nonprogressive-disease group), while 3 patients entered the on-going group and 6 entered the DCM-like group. The CKMM3/CKMM1 ratios in the on-going and DCM-like groups were significantly higher than those in the control and nonprogressive-disease groups. The CKMM3/CKMM1 ratio was significantly correlated with the annual rate of change for the LV end-systolic dimension (LVDS), LVDd, and LVEF, with the closest correlation observed for the annual change in LVDs. Moreover, 5 patients in the nonprogressive-disease group with elevation of the CKMM3/CKMM1 ratio to >+2SD above the mean for the controls had an elevated annual change in LVDs Within ±1SD of the mean in the DCM-like group. These results indicate that the ratio of CKMM3 to CKMM1 can be used to predict the progression of LV enlargement in HCM. (Jpn Circ J 1997; 61: 315 -322)

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The effects of adenosine triphosphate (ATP) on ventriculoatrial (VA) conduction were examined before and after accessory pathway (AP) ablation, with emphasis on assessment of the complication of dual atrioventricular (AV) node pathway. By evaluating the differences in the response to ATP of APs and other pathways, we assessed the usefulness and problems of this method. Of 59 patients who underwent AP ablation, 31 showed pre-excitation and 28 had concealed APs. A dual AV node pathway was found in 9 patients (15.3%) before ablation. After ablation, a dual AV node pathway was newly found in 9 patients. Thus, the total number of patients with a dual AV node pathway was 18 (30.5%). VA conduction over APs was not blocked in 26 of 29 patients, but the remaining 3 APs were blocked transiently by ATP. ATP caused VA block over the AV node in 15 of 16 patients and a dual AV node pathway in all 11 patients. In contrast, VA conduction over the retrograde fast pathway was blocked in 9 of 14 patients with AV node re-entrant tachycardia. ATP has little effect on APs, so observation of the response to ATP provides a more reliable and useful means of evaluating successful ablation. With this method, however, it is important to consider the possibility of the presence of ATP-sensitive APs and ATP-resistant retrograde fast pathways. The influence of ablation-induced injury has not been fully clarified. It is therefore essential to take into account various data, including the comparison between data obtained before and after ablation. (Jpn Circ J 1997; 61: 323 - 330)

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In order to estimate the number of deaths from ischemic heart disease (IHD) in a Japanese city, we re-evaluated heart disease deaths among residents aged 25-74 years by examining their clinical records. During the 2-year period from 1987 to 1988, 271 deaths among this population were attributed to heart disease. The recorded underlying cause of death was IHD in 96 cases, heart failure in 123 cases, and other heart disease in 52 cases. Re-evaluation of the cause of death yielded 57 cases of acute myocardial infarction (AMI), 85 cases of sudden death, 37 cases of heart disease other than IHD, and 63 cases of non-heart disease. In the remaining cases, there was insufficient information for evaluation. According to some autopsy studies, about 50% of sudden deaths are due to IHD. Thus, 50% of the number of sudden death cases may be added to the total number of IHD deaths. Accordingly, the total number of IHD deaths may have been 100, ie, 57 cases of AMI plus 43 cases of sudden death. The difference between the number of IHD deaths after re-evaluation and the number for which IHD was recorded as the underlying cause was small, with the former only 4% higher than the latter. The number of false-positives was equal to the number of false-negatives, and hence the number of IHD deaths recorded in this area seems to be close to the actual figure. We speculate that more accurate death certification will result in a decrease in the total number of deaths attributable to heart disease, as in 23% of deaths attributed to heart disease the underlying cause of death was not in fact heart disease. (Jpn Circ J 1997; 61: 331 - 338)

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To assess whether left ventricular (LV) diastolic function is a determinant of exercise capacity in patients who have suffered a previous myocardial infarction (MI), we investigated the relationship between maximum exercise duration and resting LV diastolic function in 65 MI patients. Each patient underwent both a symptom-limited exercise test and LV biplane angiography with simultaneous high-fidelity pressure measurements. LV relaxation was assessed by the time constants (T_1/e and T_1/2) of isovolumic pressure decay, and LV diastolic distensibility was assessed by the LV end-diastolic volume (V) index-pressure (P) ratio. The time constants of relaxation did not correlate with maximum exercise capacity (r= -0.19 for T_1/e, NS; r= V0.17 for T_1/2, NS). LV diastolic distensibility also did not correlate with exercise capacity (r= -0.08, NS). These results suggest that the resting LV diastolic dysfunction is unlikely to be the principal cause of exercise intolerance in MI patients without congestive heart failure. (Jpn Circ J 1997; 61: 339 - 343)

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Ischemic preconditioning (PC) induced by 1 cycle of 5-min coronary occlusion and 5-min reperfusion limits infarct size (IS) after 30-min sustained ischemia in rabbits. The shortest ischemic period that induces the PC effect in rabbits is 3 min. To establish the maximum ischemic period to induce a beneficial PC effect, we examined the effect of PC periods of 10 and 15 min on IS after sustained ischemia. The IS in control rabbit hearts after 30 min of sustained occlusion of the left anterolateral coronary. artery and 48-h reperfusion was compared with that of hearts treated as follows before being subjected to PC: 5-min occlusion and 5-min reperfusion; 10-min occlusion and 5-min reperfusion; or 15-min occlusion and 5-min reperfusion. In addition, the IS after 15-min or 45-min occlusion and 48-h reperfusion was measured. There was no significant difference in blood pressure, heart rate, or area at risk (AAR) among the rabbits in 5 groups. The IS measured histologically was 40±4% of AAR in the control, 10±3% after 5-min PC, and 12±2% after 10-min PC. However, in the 15-min PC group, the IS was 77±4% of AAR, which was significantly larger than that of the controls, but similar to that of hearts subjected to 45-min ischemia and reperfusion (67 ±3%). As 15 min of preconditioning ischemia alone caused small infarcts (18±1% of AAR), the infarcts caused by sustained ischemia per se in the 15-min PC group was estimated to be 72±5% of AAR, which was still significantly higher than in the control groups. We conclude that the maximum period of preconditioning ischemia that induces cardioprotection in rabbits is 10 min. When the ischemic period is longer than this, the IS after sustained ischemia is increased rather than restricted. However, the infarcted size in the 15-min PC group was not higher than that in the group subjected to 45-min continuous ischemia. This may be a major limitation for any clinical application of PC. (Jpn Circ J 1997; 61: 344 - 352)

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The first manifestation of dilated cardiomyopathy is usually dyspnea as a result of left heart failure, In this report we describe an unusual patient with third-degree atrioventricular (AV) block unaccompanied by left ventricular dysfunction. Severe left ventricular dysfunction occurred 5 years after the implantation of a permanent pacemaker. We conclude that AV block should not be overlooked as an initial clinical manifestation of dilated cardiomyopathy. (Jpn Circ J 1997; 61: 353 - 357)

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Traumatic tricuspid regurgitation (TR) and congenital pericardial defects are rare conditions, there being fewer than 200 recorded cases of each. Here we describe the interesting case of a patient with traumatic TR due to rupture of chordae tendineae in association with a congenital pericardial defect. We suggest that the association of traumatic TR and congenital pericardial defect has a high probability of occurrence. We hypothesize that traumatic rupture of valvular structures occurs readily in patients with congenital pericardial defects. (Jpn Circ J 1997; 61: 358 - 360)

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We describe a patient who was treated with amiodarone for ventricular arrhythmia based on arrhythmogenic right ventricular dysplasia and who subsequently developed severe amiodarone-induced thyrotoxicosis. Discontinuation of amiodarone resulted in sustained ventricular tachycardia, which was successfully treated with a DC electrical shock, and subsequently atrial fibrillation, leading to brain embolism due to occlusion of the left middle cerebral artery. Combination treatment with amiodarone and prednisolone was effective both in reducing the serum concentration of thyroid hormones and in improving the patient's general condition. As the use of amiodarone becomes more widespread, treatment with prednisolone for this kind of thyrotoxicosis, which is resistant to conventional treatment, will be required increasingly frequently because iodine overload of the thyroid gland persists for some time after discontinuation of amiodarone treatment. (Jpn Circ J 1997; 61: 361 - 366)

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