Biomedical subjects
Publications and source records attributed to N Aihara.
Right ventricular morphologic and/or histologic abnormalities were present in 5 of 6 Japanese men with the Brugada syndrome. Results indicate that arrhythmogenic right ventricular cardiomyopathy may underlie the cardiac manifestations in the Brugada syndrome.
Diaphragmatic tumors, whether benign or malignant, may not generally reveal any symptoms in the early phase and may be found accidentally. During a pre-employment physical examination, a 20-year-old woman was found to have an abnormal shadow on the left diaphragm. An X-ray film, computed tomography and ultrasonography showed a giant mass on the left side, to the rear of the heart. She underwent surgery via a left thoraco-abdominal approach. The lesion was found to arise from the left diaphragm, and multiple disseminated lesions were scattered in the left thoracic cavity. Histological examination showed many large, oxyphilic rhabdoid cells between diffusely proliferating, spindle-shaped cells, and the tumor was subsequently diagnosed as a pleomorphic rhabdomyosarcoma of the diaphragm, of which the location and histological type were very rare. Despite adjuvant therapy, chest X-ray and CT revealed increasing tumor growth in the left cavity and she died one year after surgery.
The retrograde atrial potential at a successful ablation site is usually obscured by the wide and large ventricular potential during atrioventricular reentrant tachycardia or ventricular pacing, which makes it difficult to determine the appropriate ablation site for a concealed accessory pathway. A pacing maneuver named the "simultaneous pacing method" is proposed herein to differentiate the retrograde atrial potential from the ventricular potential for a successful ablation of the concealed accessory pathway. Catheter ablation was performed in 12 patients with a single left free-wall concealed accessory pathway. The atrial insertion site was determined by the simultaneous pacing method in six patients (group I) and by ventricular pacing in six patients (group II). In the simultaneous pacing method, electrograms recorded during ventricular pacing in the earliest retrograde atrial activation site are a fusion of the ventricular potential and the following retrograde atrial potential. When atrial and ventricular pacings are performed simultaneously (simultaneous pacing), the end portion of the electrograms recorded at the same site is solely the ventricular component, because atrial is activated earlier. The atrial potential can be confirmed during ventricular pacing in comparison with the electrograms during the "simultaneous pacing." Radiofrequency catheter ablation was successful in eliminating conduction through the accessory pathway in all 12 patients. The radiofrequency applications in group I were significantly fewer than those in group II (1.7 +/- 1.0 in group I, 5.3 +/- 3.2 in group II, P < 0.05). The total procedure time in group I was significantly shorter than in group II (57.8 +/- 15.7 vs 106.7 +/- 41.6 mins in group II, respectively, P < 0.05). The fluoroscopy time in group I was significantly shorter than in group II (54.0 +/- 7.9 vs 81.3 +/- 26.3 mins, respectively, P < 0.05). We were able to determine the atrial insertion site of accessory pathways by the simultaneous pacing method. The simultaneous pacing method was useful in eliminating concealed left free-wall accessory pathways.
We report a case of verapamil-sensitive idiopathic ventricular tachycardia in which a mid-diastolic potential (MDP) 45 msec preceding the Purkinje potential (P potential) was recorded. Pacing during the tachycardia caused concealed entrainment, and the stimulus-QRS interval was equal to the P potential-QRS interval. The interval between the last pacing stimulus and the next P potential (postpacing interval) was longer than the ventricular tachycardia cycle length, but the MDP was orthodromically activated. These findings suggest that the MDP was on the reentrant circuit and the P potential was not on the reentrant circuit, but a bystander.
INTRODUCTION: The role of increased dispersion of repolarization in the genesis of torsades de pointes in patients with long QT syndrome has been clarified, but its role in the genesis of idiopathic ventricular fibrillation (VF) is not yet known. To investigate the pathogenesis of VF, we recorded monophasic action potentials (MAPs) from two siblings (48- and 36-year-old males) with familial idiopathic VF. METHODS AND RESULTS: The elder brother (patient 1) showed a late r' wave in lead V1 and ST segment elevation in leads V1 through V3. The younger brother (patient 2) had late r' waves and ST segment elevation in leads II, III, and aVF, and the configurations were very similar to those of patient 1. MAPs were recorded from several sites in the right ventricular (RV) and left ventricular (LV) endocardium during constant right atrial pacing. The repolarization time (RT) was defined as the sum of the activation time (AT) and action potential duration (APD) at 90% repolarization. In patient 1, marked prolongation of the AT (140 msec) and the RT (380 msec) was recorded in the RV septum of the outflow tract, and the RT dispersion was markedly increased (125 msec). In contrast, patient 2 showed prolongation of the AT (80 msec) and RT (310 msec), and fractionated electrograms in the RV floor of the inflow tract. The RT dispersion was also increased (80 msec). VF and nonsustained polymorphic ventricular tachycardia were induced by double premature stimulation in patients 1 and 2, respectively. Chronic amiodarone therapy decreased the RT dispersion and suppressed the induction of ventricular tachyarrhythmias in patient 2, although late r' waves and slight ST segment elevation were unmasked in leads V1 and V2. CONCLUSION: Our data suggest that the increased dispersion of the RT, which was due mainly to a localized conduction delay in the RV, created an arrhythmogenic substrate in the two patients with familial idiopathic VF.
We present a patient with Brugada syndrome in whom 12-lead ECGs were recorded just before and after an episode of ventricular fibrillation (VF). A progressive elevation of both the RS-T segment and J waves just preceding and following the VF, and a close relationship between the amplitude of the RS-T segment and the preceding R-R intervals during atrial fibrillation, were documented. These findings support the hypothesis that RS-T elevation and a subsequent VF are related to a transient outward current-mediated spike-and-dome morphology of the epicardial action potential.
We describe herein the unusual case of a 68-year-old Japanese man who underwent laparotomy for an acute abdomen caused by diffuse peritonitis, which revealed perforation of the gallbladder without any stones. A cholecystectomy was subsequently carried out, and histological examination showed marked atherosclerosis of the gallbladder associated with acute inflammatory changes. It is most likely that circulatory disturbance of the gallbladder wall due to the atherosclerosis played an important role in the events leading to perforation. Acute acalculous cholecystitis is an uncommon condition which is extremely difficult to diagnose preoperatively. The clinicopathological features of this patient are of particular interest and importance in terms of pathogenesis as well as treatment.
In a patient with WPW syndrome and idiopathic dilated cardiomyopathy, intractable atrioventricular reentrant tachycardia (AVRT) was iatrogenically induced. QRS without preexcitation, caused by junctional escape beats after verapamil or unidirectional antegrade block of accessory pathway after catheter ablation, established frequent AVRT attack.
Early afterdepolarizations (EADs) have been linked to the mechanism of torsades de pointes in long QT syndrome. The purpose of this study was to investigate the role of EADs in Class IA induced torsades de pointes. We studied nine patients with Class IA induced torsades de pointes at the time this arrhythmia was present (acute period, n = 7) and after Class IA therapy was discontinued (chronic period, n = 6). ECGs and monophasic action potentials were recorded in both periods. In the chronic period, electrophysiological studies were performed before and after disopyramide infusion. In the acute period, QTc interval was markedly prolonged (655 +/- 32 ms1/2), and EAD-like activity was recorded in all patients. QTc interval returned to normal (428 +/- 45 ms1/2) and EAD-like activity disappeared after discontinuation of IA drug. Although, in the chronic period, disopyramide infusion prolonged QTc interval from 428 +/- 48 ms1/2 to 479 +/- 31 ms1/2 and induced EAD in three of six patients, the degree was not as marked as observed in the acute period. EADs may play an important role in the genesis of long QT and torsades de pointes. Disopyramide infusion in the chronic period could not reproduce marked repolarization abnormalities and torsades de pointes.
INTRODUCTION: Sympathetic stimulation plays an important role in the genesis of QT(U) prolongation and ventricular arrhythmias in congenital long QT syndrome (LQTS). Permanent pacemaker as well as beta blockers are reported to be effective in the management of this syndrome. The purpose of this study was to examine influence of epinephrine (alpha- and beta-adrenergic stimulation), propranolol (beta blocker), and atrial pacing on the spatial distribution of repolarization using body surface recovery time (RT) in congenital LQTS. METHODS AND RESULTS: Body surface mapping was recorded in 16 patients with congenital LQTS and 20 control patients before and after epinephrine infusion (0.1 microg/kg per min), oral propranolol (1 to 2 mg/kg per day), addition of epinephrine during oral propranolol, atrial pacing at a cycle length of 600 or 750 msec, and addition of epinephrine during atrial pacing. The RT, that is, the interval between the QRS onset and the maximum dV/dt point in the ST-T segment, was measured automatically by a computer from each of the 87 mapping leads, and the corrected RT (RTc) was calculated using Bazett's method. In patients with congenital LQTS, epinephrine markedly changed the T(U) wave morphology and spatial distribution of RT, especially the distribution of maximum RT of the left anterior chest and back. Epinephrine prolonged the maximum RTc and the minimum RTc in 87 leads and increased the RTc dispersion (difference between maximum and minimum RTc in each patient). Neither propranolol nor atrial pacing changed the T(U) wave morphology, spatial distribution of RT, or any RTc parameters at rest. Propranolol prevented the influences of epinephrine on the T(U) wave morphology, spatial distribution of RT, and RTc parameters, whereas atrial pacing did not. In control patients, marked changes of the T(U) wave morphology and RTc parameters were not recognized during the entire protocol. CONCLUSIONS: Our results indicate that epinephrine markedly changes the spatial distribution of repolarization and increases the dispersion of repolarization, which probably are linked to arrhythmogenesis in congenital LQTS. The data suggest that propranolol but not atrial pacing are effective to suppress repolarization abnormalities during sympathetic stimulation.
OBJECTIVE: To analyse heart rate variability in patients with atrial fibrillation after the Maze procedure, to investigate whether the procedure damages the cardiac autonomic fibres supplying the sinus node. DESIGN AND PATIENTS: Time and frequency domain analyses of RR variability were performed using 24 hour Holter monitoring one month after surgery in 12 patients with atrial fibrillation who underwent the Maze procedure (Maze group) and in seven patients who underwent cardiac surgery without the Maze procedure (control group). Mean RR intervals (mRR) and the standard deviation of successive RR intervals (SDRR) were determined by time domain analysis, and high frequency (HF), low frequency (LF), and total power (TP) spectral components of RR variability were calculated by frequency domain analysis. Holter monitoring was also performed at six and 12 months after cardiac surgery in the Maze group. RESULTS: Circadian variation (mean (SD)) in mRR (daytime to night time difference: 119 (60) v 302 (143) ms), SDRR (daytime: 8.4 (3.3) v 37.0 (12.0) ms), TP (daytime: 46.7 (16.0) v 171.8 (30.4) ms), HF (daytime: 19.6 (9.9) v 36.7 (7.1) ms2), and LF/HF (daytime: 0.31 (0.07) v 1.18 (0.46)) was decreased in the Maze group at one month compared with the control group (p < 0.01), but showed improvement at six and 12 months (p < 0.05). CONCLUSIONS: Surgery combined with the Maze procedure markedly suppressed the circadian variation of heart rate over a 24 hour period within one month after surgery, mainly because of damage to the innervation of the sinus node. However, at six and 12 months there was restoration of circadian variation, probably as the result of reinnervation of the sinus node.
Although the Maze procedure is highly successful in restoring sinus rhythm in patients with atrial fibrillation (AF), the electrophysiologic changes that occur after the Maze procedure and its mechanism of action are still unclear. The aims of the present study were to examine the electrophysiologic changes that occur in the arrhythmogenic substrate after the Maze procedure and to evaluate the mechanism by which it prevents lone and paroxysmal AF. The modified Maze procedure was performed in 6 patients (6 men, mean age 47 +/- 7 years) with lone and paroxysmal AF. Electrophysiologic studies were performed before and 35 +/- 8 days after the Maze procedure. Atrial mapping during sinus rhythm revealed that atrial activation propagated smoothly in a concentric circle from the sinus node to other regions in the right atrium and into the coronary sinus before the Maze procedure. Following the Maze procedure, atrial activation propagated selectively through routes produced by incisions or cryoablations in all 6 patients. In addition, double and triple potentials were recorded in regions where conduction blocks were created by the Maze procedure. Neither sinus node function nor AV conduction was changed following the Maze procedure. The Maze procedure did not affect the atrial effective refractory period or the zone of fragmented atrial activity, although the conduction delay zone was increased significantly (p < 0.05). AF was inducible in all 6 patients before the Maze procedure, whereas it was not inducible in any patients after the Maze procedure. The Maze procedure is effective in preventing AF without affecting sinus node function and AV conduction. Intra-atrial conduction block produced by incisions or cryoablations contributes to the prevention of AF.
OBJECTIVES: This study was performed to evaluate the frequency dependency of ventricular repolarization and the effect of epinephrine in patients with congenital long QT syndrome (LQTS). BACKGROUND: The efficacy of pacemakers in addition to antiadrenergic therapy in the treatment of congenital LQTS has been reported. METHODS: Monophasic action potentials were recorded from right and left ventricular endocardium during atrial pacing at heart rates from 70 to 140 beats/min at baseline and from 100 to 140 beats/min during epinephrine infusion (0.1 microgram/kg body weight per min) in 11 patients with congenital LQTS and 10 control patients. The response of monophasic action potential duration at 90% repolarization (MAPD90) and the dispersion of MAPD90 were examined. RESULTS: At baseline, both the MAPD90 and the dispersion of MAPD90 were significantly (p < 0.001) longer in the congenital LQTS group than the control group. The differences in these variables between the two groups significantly decreased (MAPD90: from 105 to 31 ms; dispersion of MAPD90: from 55 to 13 ms, p < 0.001) at heart rate was increased. Epinephrine prolonged the MAPD90 and increased the dispersion of MAPD90 significantly (p < 0.001) at all paced heart rates in the congenital LQTS group without frequency dependency but did not change in the control group. Thus, epinephrine increased the differences in these variables between the two groups. CONCLUSIONS: The repolarization abnormalities in congenital LQTS were attenuated by increasing the heart rate, which supported the efficacy of pacemaker therapy. However, during sympathetic stimulation, the effects of increased heart rate on these repolarization abnormalities were limited.
BACKGROUND: Electron-beam computed tomography (CT) may be useful for detecting myocardial fat infiltration and diagnosing arrhythmogenic right ventricular dysplasia (ARVD). There are several characteristic electron-beam CT findings of ARVD. However, the incidence, their relation to electrophysiological abnormalities, and the usefulness of electron-beam CT for evaluating left ventricular involvement are unknown. This study aimed to clarify these issues. METHODS AND RESULTS: Electron-beam CT was performed in 14 patients with ARVD (ARVD group), 16 age- and sex-matched patients with right ventricular enlargement and/or dysfunction without ARVD (RV enlargement group), and 13 control subjects (control group). The incidences of abnormal electron-beam CT findings in the three groups were examined. Furthermore, we examined the endocardial fat-infiltrated areas detected by electron-beam CT (CT-A) and electrophysiologically abnormal areas detected in the mapping electrophysiology study (EPS-A) and compared the relationship between them in the ARVD group. (1) The frequencies of abundant epicardial adipose tissue, low-attenuation trabeculations, scalloping of the right ventricular free wall, and intramyocardial fat deposits were 86%, 71%, 79%, and 50%, respectively, in the ARVD group, whereas these findings were not observed in the RV enlargement and control groups. (2) Three ARVD patients (21%) had adipose tissue involvement of the left ventricle. (3) The relationship between CT-A and EPS-A was as follows: CT-A > EPS-A, 71%; CT-A = EPS-A, 14%; and EPS-A only, 14%. CONCLUSIONS: Characteristic electron-beam CT findings are frequently observed only in patients with ARVD. Electron-beam CT is useful for evaluating for left ventricular involvement and can estimate EPS-A.
Reverse use dependence of action potential duration and effective refractory period by chronic oral sotalol was demonstrated by monophasic action potential recordings in the human ventricle. There were no changes of the QRS duration over the cycle length, indicating that sotalol had no sodium channel blocking effects.
In this study we examined the cerebellar response to mild traumatic brain injury by assessing microglial activation and Purkinje cell loss. Activated microglia were identified using the antibodies OX-42 and ED-1 as well as isolectin B4. The anti-Purkinje cell antibody PEP-19 was used to evaluate Purkinje cell loss after injury. The mechanism of cell injury was examined using a monoclonal antibody to the inducible 72-kDa heat shock protein. A monoclonal antibody to the N-terminal sequence of Fos was used as a marker for neuronal activation. There was progressive activation of microglia in the cerebellar vermis within a few days after forebrain injury. In coronal sections the processes of activated microglia were oriented in "stripes" perpendicular to the cortical surface. In sagittal sections the activated microglia were in irregularly shaped clusters or in a fan-like distribution that radiated from the Purkinje cell layer toward the cortical surface. There was a significant loss of Purkinje cells 7 days postinjury as compared to the control group. There was no evidence of induction of heat shock protein in the cerebellum. In addition, there was no evidence of induction of c-Fos protein in either the cerebellar cortex or inferior olivary nuclei within the first 3 h after injury. These studies demonstrate that a fluid percussive impact to the forebrain results in cerebellar damage. The close anatomical association between activated microglia and Purkinje cells suggests that Purkinje cell injury is the cause of the microglial activation. The mechanism of Purkinje cell death, however, remains unclear.
It is well known that an astrocytic response occurs after brain damage; however, the mechanisms initiating this acute astrocytic response remain unclear. In this study, we examined the immunolocalization of glial fibrillary acidic protein (GFAP) to investigate the astrocytic response within 72 h after injury. Further, we related these results to the distribution of extravasated plasma protein and the expression of stress protein. Adult male Wistar rats were subjected to a lateral fluid percussion brain injury. Animals were sacrificed at 1, 6, 24, and 72 h postinjury. Each brain section was immunostained for GFAP, extravasated albumin, and heat shock protein (HSP 72). Immunoreactive astrocytes, extravasated albumin, and HSP 72 positive cells were evaluated by light microscopy. Reactive astrocytes were defined by the presence of increased immunoreactivity to anti-GFAP. By 6 h, the presence of reactive astrocytes was restricted to the impact site and the hemorrhagic external capsule. At 24 h, reactive astrocytes were identified in the entire injured hemisphere. By 72 h, the immunoreactive astrocytes were more pronounced than at 24 h. At 1 h, extravasated albumin was found at the impact site, the hemorrhagic external capsule, the parasagittal cortex, hippocampus, thalamus, and midbrain. By 72 h, the immunostaining of albumin was more widely distributed. HSP 72 immunoreactive glia were detected only at the impact site and the hemorrhagic external capsule. In summary, the distribution of reactive astrocytes at 6 h was associated with HSP 72-positive glia rather than the extravasation of albumin. In contrast, the distribution of reactive astrocytes at 24 and 72 h paralleled that of extravasated albumin. These results suggest that the initial response of astrocytes is correlated to glial stress and/or injury and that humoral factors play a role in the subsequent responses.
Idiopathic ventricular tachycardia is widely believed to carry a favorable prognosis, although there have also been reports of sudden cardiac deaths. We present a case of sudden death in a patient with apparent idiopathic right ventricular tachycardia. This patient had long-standing and exercise-related symptoms, an essentially negative non-invasive cardiac evaluation, and spontaneous and inducible ventricular tachycardia of left bundle branch block and inferior axis morphology, that was treated with propranolol. After an uneventful 5-year course, the patient died suddenly. Postmortem examination revealed a severely dilated right ventricle and significant replacement of the right ventricular wall with adipose tissue. Interstitial fibrosis was also seen, but only to a very slight degree.