Hot bathing has been associated with sudden death and so the present study investigated its effects on autonomic activity and hemodynamics in the elderly patient and the healthy young by analyzing heart rate variability (HRV). Subjects were 9 elderly men (mean age, 75 years) and 9 young men (mean age, 27 years), who were immersed up to shoulder level while in a sitting position for 10 min with the bath temperature at 40°C. Blood pressure (BP) and heart rate (HR) were monitored. BP in the young decreased during bathing (p<0.01), whereas in the elderly BP had a maximum value just at the start of immersion (p<0.05) with a slight decline at 4 min after the start of immersion. Although HR in the young increased (p<0.01), in the elderly there was an abrupt increase in HR just at the start of immersion (p<0.05), followed by a decrease in HR. With regard to HRV, the high-frequency (HF) component in the young men was suppressed during immersion (p<0.01), but was unaffected in the elderly. The LF (low frequency)/HF ratio in the elderly decreased at 4 min (p<0.05). In conclusion, hypotensive syncope may cause sudden death by drowning during hot bathing, and is a consequence of the decrease in sympathetic tone that develops approximately 4 min after immersion. (Jpn Circ J 2001; 65: 587 - 592)

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The present study investigated whether the circadian rhythm of sympathovagal activity is related to the severity of coronary spasm or multivessel coronary spasm. Heart rate variability was examined in 22 consecutive patients with vasospastic angina provoked by intracoronary injection of acetylcholine, who had either multivessel spasm (Group M, n=11) or single vessel spasm (Group S, n=11), in 20 subjects without coronary artery disease (Group C) and 20 patients with effort angina who had organic coronary artery stenosis (Group E). The frequency domain indices were analyzed, including low frequency (LF: 0.04-0.15 Hz) and high frequency (HF: 0.15-0.4 Hz), the latter being an index of efferent parasympathetic activity, and the ratio (L/H) as an index of sympathovagal balance. The circadian variation of the parameters was analyzed by its pattern and was quantified by the difference of the mean values between daytime and nighttime. Although the HF power increased during nighttime in Groups C and S, this increase was attenuated in Groups E and M. The circadian variation of the L/H ratio (ie, a drop during nighttime) was smaller in the S and M groups than in Groups C and E. Accordingly, in Group M, the circadian variation of both sympathetic and parasympathetic nervous activity was attenuated, but in Group S, the variation of sympathetic nervous activity, but not parasympathetic nervous activity, was decreased. These data suggest that relatively enhanced sympathetic nervous activity at night may be involved in the mechanism underlying multivessel coronary spasm. (Jpn Circ J 2001; 65: 593 - 598)

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A questionnaire was used to survey the experience of 8 Japanese institutions with percutaneous transluminal aortic valvuloplasty (PTAV) in children. Among 99 procedures reported in 88 patients, sufficient data for analysis was obtained from 76 procedures in 72 patients. In those 76 procedures the pressure gradient decreased significantly from 68±25 (20-140) to 33±22 (0-100) mmHg (p<0.01), whereas aortic regurgitation (AR) increased at least one grade in 26 cases (34%). None of the parameters analyzed in this study were predictors of an increase in AR. The reduction in pressure gradient was judged as good in 44 of the 76 procedures (58%). A larger ring diameter, larger balloon diameter and larger ratio balloon diameter/the normal predicted diameter of the aortic valve ring significantly contributed to an effective reduction of pressure gradient. Follow up data (mean interval, 4 years) was available for 26 of 39 clinically effective procedures. AR progressed at least 1 grade in 11 (42%), and the pressure gradient re-developed to more than 50 mmHg in 2 cases (8%). In Japan, PTAV has been accepted as a useful procedure for valvular aortic stenosis in children, but progressive AR or re-development of the pressure gradient is not uncommon even after clinically effective PTAV. (Jpn Circ J 2001; 65: 599 - 602)

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The renin-angiotensin system may play a pivotal role in reperfusion ventricular arrhythmias (RVA). The purpose of this study was to investigate the association between angiotensin-converting enzyme (ACE) gene polymorphism and RVA in patients with acute myocardial infarction (AMI) in a case - control study. Patients who had undergone successful coronary intervention for AMI were enrolled (n=127, male/female: 97/30, mean age, 62.6 years). The incidence of RVA was continuously monitored by ECG at a coronary care unit. The severity of ventricular arrhythmias was evaluated in terms of the Lown's grade and patients with a high risk of ventricular arrhythmias that may cause sudden cardiac death (Lown's grade ≥2) within 5 h of coronary intervention were defined as cases (n=59), and otherwise as controls (n=68). A receiver operating characteristic curve was used to determine the discriminatory ability of continuous variables and to produce dummy variables for use in a logistic regression analysis. Cases had a significantly higher body mass index, higher maximal levels of serum creatine kinase, and a shorter time preceding coronary intervention than controls. The severity of coronary atherosclerosis was similar between the 2 groups. The frequency distribution of ACE genotypes in cases differed from that in controls (II/ID/DD: 22.0%/52.6%/25.4% vs 44.1%/41.4%/14.7%, p<0.05, by the Mantel-Haenzel chi-square test). The ACE-D allele had additive and dominant effects with regard to the occurrence of significant ventricular arrhythmias after adjusting for other risk factors. The ACE-D allele may play a pivotal role in sudden cardiac death in patients with AMI. (Jpn Circ J 2001; 65: 603 - 609)

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Left ventricular (LV) contractility is constantly changing during atrial fibrillation (AF), which is dependent on the force - interval relationships. However, no information has been available on LV relaxation in patients with both AF and impaired LV systolic function. LV pressure was measured with a catheter-tipped micromanometer and the time constant of isovolumic LV pressure decline (τ_bf) was calculated with best exponential fitting from more than 10 consecutive beats. Patients with AF (5 with mitral valvular disease, 6 with idiopathic dilated cardiomyopathy, and 1 with no underlying disease) were subdivided into 2 groups: group A, with ejection fraction (EF) <0.5 (n=7); and group B, with EF ≥0.5 (n=5). Linear correlation coefficients (r) between τ and RR₂, RR₂/RR ₁, LV peak systolic pressure (peak LVP) were calculated. Although τ did not show a discrepancy between the 2 groups, τ_bf correlated better with RR₂/RR₁ only in the group A patients. The relation between τ and peak LVP showed a good correlation with a steep slope (R, Δτ/Δpeak LVP) only in the group A patients (accentuated afterload-dependence). R was significantly different between the 2 groups. Thus, a beat-to-beat analysis of τ may be a practical and feasible way for detecting LV relaxation abnormality in patients with AF. (Jpn Circ J 2001; 65: 610 - 616)

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The onset of acute myocardial infarction (AMI) shows characteristic circadian variations; that is, a definite morning peak related to biologic rhythms and a vague nighttime peak related to socioeconomic factors. The recent economic recession in Japan may change the circadian variation, especially the nighttime peak. This study evaluated the recent circadian variation of AMI in Osaka and specified the patient subgroups showing either a morning or nighttime peak predominantly. Of 1,609 consecutive patients with AMI registered from April 1998 to January 2000, 1,252 whose onset of AMI was definitely identified were studied. The day was divided into six 4-h periods with a morning peak between 08.01 h and 12.00 h, and nighttime peak between 20.01 h and 24.00 h. When subgroup analysis was performed, female patients aged 65 years or more showed a morning peak alone and male patients aged less than 65 years with an occupation and the habits of cigarette smoking and alcohol intake showed a nighttime peak alone. Thus, in Osaka nighttime socioeconomic factors may currently be more potent triggers of AMI than the morning surges in younger male workers who smoke and drink. (Jpn Circ J 2001; 65: 617 - 620)

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This study assessed the contribution of polymorphisms of angiotensin II (AngII) receptors and bradykinin B2 (BK-B2) receptor to hypertension and acute myocardial infarction (AMI) in a Japanese population: 150 subjects with essential hypertension, 150 subjects with AMI with/without hypertension, and 150 healthy, age- and sex-matched controls. Polymorphisms of the AngII type 1 receptor (1166 A/C) and type 2 receptor (3123 C/A), and the BK-B2 receptor (-58T/C, exon 1) were analyzed and significant differences of genotypes and allelic frequencies in the AngII type 2 receptor C/A and BK-B2 receptor -58T/C were found between the essential hypertension and control subjects. Further, a significantly higher incidence of the C allele of the BK-B2 receptor was seen in AMI subjects with hypertension compared with those without hypertension. Genetic variations in the AngII and BK-B2 receptors could prove to be significant pathophysiological mechanisms affecting essential hypertension and AMI, and genetic differences appear to be a new risk factor for these conditions. (Jpn Circ J 2001; 65: 621 - 626)

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Doppler echocardiographic indices of left ventricular (LV) diastolic function are widely used to evaluate the cardiac function of patients with cardiac disease. However, there have been few reports about the relationship between Doppler indices and exercise capacity and so 44 patients with myocardial infarction were investigated by cardiopulmonary exercise testing and 2-D and Doppler echocardiography. Diastolic performance was assessed using Doppler transmitral flow velocity and pulmonary venous flow velocity. The ratio of peak E wave velocity and peak A wave velocity (E/A) correlated with peak oxygen consumption (peak V_O2) (R=0.72), and there was a negative correlation between the deceleration time of E velocity (Dct) and peak V_O2 or anaerobic threshold (AT) (R=-0.65, -0.62, respectively). The ratio of peak S wave velocity and peak D wave velocity (S/D) negatively correlated with peak V_O2 (R=-0.58). Left ventricular ejection fraction did not correlate to exercise capacity. These results suggest that the Doppler echocardiographic indices of LV diastolic function correlate with exercise capacity in patients with mild cardiac dysfunction. (Jpn Circ J 2001; 65: 627 - 631)

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The present study evaluated a new technique that has the potential to improve the border detection of in-stent neointima using an echogenic contrast agent during intravascular ultrasound (IVUS). To confirm the reproducibility of IVUS imaging for measuring the cross-sectional in-stent neointima area, inter-and intra-observer variability and correlation were determined. Conventional IVUS (plain IVUS) and IVUS using a contrast agent (contrast IVUS) were performed in 24 subjects 6.5±1.5 months after undergoing a Palmaz - Schatz coronary stent implant. Conventional IVUS delineated completely the in-stent neointima in 6 subjects (25%). In the remaining 18 subjects (75%), delineation of the neointima was incomplete despite the use of various combinations of imaging conditions (eg, transmission, compress, post-process). With contrast IVUS, the boundary of the neointima, and therefore the neointima area, was clearly distinguishable, and this resulted in complete delineation of the neointima in all 24 subjects. With a contrast agent, inter-and intra-observer variability significantly decreased (0.94±0.69 mm² conventional IVUS vs 0.37±0.40 mm² contrast IVUS, p<0.001; 0.69±0.56 mm² conventional IVUS vs 0.07±0.10 mm² contrast IVUS, p<0.0001; respectively). Thus, contrast IVUS provides a reproducible method for the quantitative analysis of in-stent neointima with excellent inter- and intra-observer correlation. (Jpn Circ J 2001; 65: 632 - 636)

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Plasma brain natriuretic peptide (BNP) has diagnostic and prognostic value in heart failure. Cardiac dysfunction varies from systolic or diastolic dysfunction alone to the combination of both. In the present study, Doppler echocardiographic parameters, including the Doppler echocardiography-derived index (TEI index), were compared with plasma BNP levels in 74 patients with various heart diseases. Blood sampling was performed before an echocardiographic examination was conducted. The TEI index was defined as the summation of isovolumic contraction and relaxation time divided by ejection time. In patients with left ventricular (LV) systolic dysfunction (ejection fraction <50%), the TEI index and BNP were increased significantly compared with patients with normal LV systolic function (p<0.05). Patients with a TEI index ≥0.45 showed significantly increased BNP levels compared with patients with a TEI index <0.45, irrespective of LV systolic function (241.4 ±451.2 vs 65.9±81.8 pg/ml; p<0.05). The TEI index was significantly higher in patients with a BNP ≥73 pg/ml than in patients with BNP <73 pg/ml (0.57±0.24 vs 0.46±0.17; p<0.05). Other echocardiographic parameters did not correlate significantly with levels of plasma BNP. Of the echocardiographic parameters, a simple Doppler index (TEI index) that combines systolic and diastolic function can detect LV dysfunction in patients with high levels of plasma BNP in various heart diseases. (Jpn Circ J 2001; 65: 637 - 642)

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This study sought to clarify the relationship between magnesium (Mg) deficiency and coronary artery spasm provoked by pharmacologic agents in patients with a recent acute myocardial infarction (AMI). Twenty-three consecutive patients suffering from AMI were investigated with a Mg retention test (Mg: 0.1 mmol/kg for 4 h) in both the acute phase (within 1 week (3±2 days) of onset) and the subacute phase (3-4 weeks (24±6 days) of the onset). Early coronary arteriography was performed in all patients. Coronary stenosis in the infarct-related artery was less than 90% in all patients in the subacute phase. The spasm provocation test was performed in the subacute phase and coronary spasm was defined as transient subtotal or total occlusion in association with angina or electrocardiographic ST-segment deviation. Coronary artery spasm was provoked in only 13 of the 23 patients. Compared with the control subjects (12 patients without coronary artery disease or coronary spasm), the 24-h Mg retention was significantly higher in patients with AMI (acute phase: 78±27%, subacute phase: 66±32%, vs control: 48±12%, p<0.05). In the subacute phase, the 24-h Mg retention decreased in patients without coronary spasm (43±26%), but a high level of Mg retention was still observed in patients with coronary spasm (84±25%). There was no difference in the serum concentrations of Mg, calcium and phosphorus between the 2 groups on both phases. In conclusion, both Mg deficiency and provoked coronary artery spasm were noted in more than half of the Japanese patients with a recent AMI, suggesting a close association between Mg deficiency and AMI. (Jpn Circ J 2001; 65: 643 -648)

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Ventricular tachyarrhythmia (VT) is an independent risk factor for an increased overall mortality in patients with impaired left ventricular (LV) function, but there is not an established noninvasive tool to detect such patients. The present study aimed to clarify the most useful noninvasive approach for identification of patients with moderately or severely impaired LV function complicated by VT. Sixty-seven patients in New York Heart Association (NYHA) classes I-III with an LV ejection fraction (LVEF) less than 40% and an LV end-diastolic dimension (LVDD) of at least 55 mm on echocardiography were enrolled. Impaired LV function was caused by either ischemic (n=30) or nonischemic dilated cardiomyopathy (n=37). T-wave alternans (TWA), QT dispersion (QTD), and late potentials (LP) on signal-averaged electrocardiography were sequentially determined without using antiarrhythmic drugs. VT was defined as more than 6 consecutive ventricular ectopic beats. The mean NYHA class was 1.9±0.7, mean LVEF was 31±8%, and mean LVDD was 65±10 mm. A history of VT was present in 26 of the patients (39%). Univariate and multivariate logistic analysis showed that TWA and LP were closely related to VT, whereas NYHA ≥III, LVEF <30%, LVDD ≥70 mm, and QTD ≥90 ms were not. The combination of TWA and LP had the most significant value (p=0.0004, odds ratio=8.44) by univariate analysis, and only this combination had significant value in multivariate analysis (p=0.04). Therefore, the combination of TWA and LP could be a useful index for identifying those patients with impaired LV function who are at risk for VT. (Jpn Circ J 2001; 65: 649 - 653)

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Beta-blockade is widely reported to reduce the incidence of syncope in 75-80% of patients with congenital long QT syndrome (LQTS). However, despite full-dose β-blockade, 20-25% of patients continue to have syncopal episodes and remain at high risk for sudden cardiac death. In some patients refractory to β-blockade, the recurrence of arrhythmias is successfully prevented by left stellate ganglionectomy, and also by labetalol, a nonselective β-blockade with _α1-blocking action. These observations suggest that not only β-adrenoceptors, but also _α1-adrenoceptors, play an important pathogenic role, especially under sympathetic stimulation, in LQTS. The clinical effects of _α1-blockade in congenital LQTS were investigated in 8 patients with familial or sporadic LQTS. Two measurements of the QT interval were taken, from the QRS onset to the T wave offset (QT) and from the QRS onset to the peak of the T wave (QTp). Using the Bruce protocol, an exercise test was performed after administration of β-blockade alone and again after administration of _{α 1}-blockade. The following were compared: (1) Bazzet-corrected QT (QTc) and QTp (QTpc) intervals in the supine and standing position before exercise and in the early recovery phase after exercise; and (2) the slopes (reflecting the dynamic change in the QT interval during exercise) of the QT interval to heart rate were obtained from the linear regression during the exercise test. In the supine position before exercise, there was no change in the QTc before or after the addition of _α1-blockade (498±23 vs 486±23 ms [NS]). However, in the upright position before exercise and in the early recovery phase after exercise, QTc was significantly shortened from 523±21 to 483±22 ms (p<0.01), and from 521±30 to 490±39 ms (p<0.01), respectively, by _α1-blockade. The QTpc was unchanged in any situation. Consequently, QTc - QTpc was significantly shortened by _α1-blockade in the upright position before exercise and in the early recovery phase after exercise (131 ±36 to 105±37 ms (p<0.05), and 132±29 to 102±31 ms (p<0.01), respectively). The slopes of the QT interval - heart rate relation by linear regression became significantly steeper from -2.23±0.38 to -2.93±0.76 (p<0.01) with the addition of _α1-blockade. The findings suggest that the addition of _α1-blockade attenuated the exercise-induced prolongation of the QT interval and that the rate adaptation of the QT interval to heart rate during exercise was improved. This indicates that additional treatment with _α1-blockade may be beneficial to prevent cardiac events in LQTS patients in whom ventricular arrhythmia is resistant to β-blockade. (Jpn Circ J 2001; 65: 654 - 658)

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Cobra venom factor (CVF) transiently activates polymorphonuclear leukocytes (PMN) by complement activation, followed by rapid complement depletion and gradual reversal of PMN activation. Utilizing these sequential changes caused by CVF, the individual and combined effects of complement and PMNs on myocardial infarct size (IS) were investigated. Rats were treated with CVF, and/or anti-PMNs. Complement was depleted, but circulating PMNs were being activated at 4 h after CVF administration, and at 36 h after, complement was depleted, but PMNs were in a near basal condition. Under anesthesia, the rats had a 30-min coronary occlusion followed by 6 h of reperfusion. The IS was assessed by tetrazolium staining. CVF, as well as anti-PMNs, reduced myeloperoxidase (MPO) activity in the risk area and the reduced MPO resulted in a reduced IS, which was also the effect of anti-PMNs, but complement depletion by CVF, during which circulating PMNs were activated, failed to reduce the IS despite low MPO activity. These results suggest that complement and the condition of PMNs each play a role in determining the IS, and ischemic reperfusion injury might be produced even by relatively low myocardial MPO activity. (Jpn Circ J 2001; 65: 659 - 666)

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The fat pad at the junction of the inferior vena cava and inferior left atrium is the area of convergence of vagal projections into the atrioventricular node (AVN) region. The present study investigated whether radiofrequency (RF) ablation applied to the area around the coronary sinus (CS) ostium would impair vagal input to the AVN in the canine heart. Twenty-four dogs were anesthetized by sodium pentobarbital and RF energy was delivered at 20 W for 5-10 s. In the baseline state without vagal stimulation (10 Hz, 2 ms), the electrophysiological variables did not change significantly after RF ablation. Vagally induced changes in the sinus cycle length and effective refractory period of the right atrium and left ventricle did not differ after RF ablation. However, the effects of vagal stimulation on the AVN function were impaired after RF ablation to the CS area from the ostium to 10 mm within the ostium. After ablation was applied to the fast pathway area, the vagally induced changes in the AVN function decreased, but these changes were not affected after RF ablation in the slow pathway area. RF ablation in the vicinity of the CS would attenuate vagal input to the AVN. (Jpn Circ J 2001; 65: 667 - 672)

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N-methyl-1-deoxynojirimycin (NMDN), an α-glucosidase inhibitor, reduces myocardial infarct size by reducing the glycogenolytic rate through inhibition of the α-1,6-glucosidase of glycogen-debranching enzyme in the heart, in addition to possessing an antihyperglycemic action by blocking α-1,4-glucosidase in the intestine. Ischemic preconditioning (PC), which markedly reduces the size of the myocardial infarct, is known to reduce the activity of phosphorylase and reduce the glycogenolytic rate. Therefore, it was hypothesized that a combination of pharmacological inhibition of glycogenolysis by an α-1,6-glucosidase inhibitor, NMDN, and PC could markedly reduce myocardial infarct size more than NMDN or PC alone. Japanese white rabbits without collateral circulation were subjected to a 30-min coronary occlusion followed by 48-h reperfusion. The infarct sizes as a percentage of area at risk were significantly reduced by pre-ischemic treatment with either 100 mg/kg of NMDN or PC of 5 min ischemia and 5 min reperfusion alone (15.9±2.0%, n=8, and 10.3±1.2%, n=8, respectively) as compared with the control (43.9±2.2%, n=8). However, the combination of 100 mg/kg of NMDN and PC significantly reduced the infarct size (4.9±1.2, n=8) compared with NMDN or PC alone. Another 40 rabbits, also given 100 mg of NMDN, PC, NMDN + PC or saline before ischemia (n=10 in each group), were killed for biochemical analysis after 30 min of ischemia. NMDN and PC preserved the glycogen content and attenuated the lactate accumulation, respectively, as compared with the control. However, the combination of NMDN and PC preserved significantly more glycogen and significantly reduced lactate accumulation than either NMDN or PC alone. The combination of NMDN and PC markedly reduced the myocardial infarct size more than either process alone. The marked preservation of glycogen and marked attenuation of lactate accumulation by the combination of NMDN and PC suggest that the mechanism for this effect of NMDN + PC is related to the inhibition of glycogenolysis. (Jpn Circ J 2001; 65: 673 - 677)

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The present study investigated the effects of ischemic preconditioning (IPC) and nicorandil pretreatment on myocardial storage in a donor heart preservation model. Isolated rat hearts were separated into groups: group 1, non-preconditioned control group; group 2, 2.5 min of normothermic ischemia followed by 15 min of normothermic Langendorff perfusion (one IPC cycle); and group 3, 2 cycles of IPC. All hearts were subsequently stored in University of Wisconsin solution at 4°C for 2, 4 and 6 h, and the concentrations of high-energy phosphate metabolites were measured for each time point. Heart function parameters (aortic flow, coronary flow and cardiac output) were measured when the heart was reperfused following the 2, 4 or 6 h of preservation. The effects of nicorandil, an ATP-sensitive potassium channel opener, on heart function following preservation were also evaluated. Nicorandil was injected intravenously before heart harvesting. The results showed that the energy status was well preserved in the IPC groups. The 2-cycle IPC group showed better recovery of heart function following preservation. Pretreatment with nicorandil also improved functional recovery of the heart following preservation. The present study showed that IPC of the rat heart resulted in improved myocardial energy metabolism and functional recovery after hypothermic preservation, and that nicorandil has potential for pharmacological preconditioning in heart preservation for transplantation. (Jpn Circ J 2001; 65: 678 - 682)

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A 41-year-old woman was admitted with rapidly worsening dyspnea. Echocardiography disclosed interventricular septal flattening and a markedly decreased left ventricle, although left ventricular contraction remained normal. Computed tomography of the chest demonstrated slightly dilated main pulmonary arteries and fine reticulonodular densities in the lung. Examination of a transbronchial lung biopsy specimen revealed carcinomatous lymphangitis, and the patient died 7 days after admission. The clinical presentation of this patient was difficult to discriminate from that seen with pulmonary thromboembolism. (Jpn Circ J 2001; 65: 683 - 684)

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This report describes the clinical management of 2 patients with ventricular fibrillation (VF) who received inappropriate shocks from an implantable cardioverter defibrillator (ICD) due to T-wave oversensing. Cardiac sarcoidosis was confirmed as the underlying heart disease in 1 patient and idiopathic dilated cardiomyopathy in the other. Within 2 months after ICD implantation, both patients received several inappropriate shocks during sinus rhythm. Stored electrograms showed decreased R-wave amplitudes and increased T-wave amplitudes. The ICD sensed both R- and T-waves as ventricular activation, which met the rate criteria for VF treatment. Reprogramming the sensing threshold in association with administration of a drug to slow the heart rate decreased the incidence of the inappropriate shocks in both patients, but these palliative measures did not completely suppress the inappropriate shocks. To avoid T-wave oversensing, the repositioning or adding of a sensing lead is required. The potential risk of T-wave oversensing in ICD patients who have small R-wave amplitudes should be recognized. (Jpn Circ J 2001; 65: 685 - 687)

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A 13-year-old girl, who was suffering complications with bilateral pulmonary artery stenosis after intracardiac repair for tetralogy of Fallot, suffered life-threatening left pulmonary bleeding and edema following inadvertent unilateral stent implantation for a left pulmonary stenosis. Pulmonary edema and subsequent hypoxia persisted despite intensive medical treatment; however, contralateral stent deployment resolved her symptoms quickly. (Jpn Circ J 2001; 65: 688 - 690)

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This report describes a case of cardiomyopathy with a novel point mutation of mitochondrial DNA coding lysine tRNA in association with severe ultrastructural alterations of the mitochondria in the cardiomyocytes. Abnormalities of energy production and/or abnormal protein synthesis because of the mutation of mitochondrial DNA may have played an important role in the pathogenesis of this case, which showed severe cardiomyocyte degeneration and deterioration from hypertrophic cardiomyopathy to severe dilated cardiomyopathy. (Jpn Circ J 2001; 65: 691 - 694)

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