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N Aihara

Publications and source records attributed to N Aihara.

At least 37 records · Page 2Linked to original sources
PubMed2001

[A case of polyneuropathy associated with increased levels of vascular endotherial growth factor (VEGF) insera].

A 54-year-old woman began to notice numbness and motor weakness in the lower extremities in July 1999. These symptoms rapidly progressed and she could not walk any more. When she admitted to our hospital, she showed peripherally dominant, moderate motor weakness, drop foot and loss of superficial and deep sensation in the lower extremities, but only slight weakness in the hands. Cranial nerves were intact. Deep tendon reflexes were all absent. Nerve conduction velocities were reduced and cerebrospinal fluid protein was elevated. VEGF was greatly increased in serum (1,850 pg/ml), which has been found to be increased exclusively in patients with Crow-Fukase syndrome. Many characteristic manifestations of the syndrome except polyneuropathy are well explained to be resulted from the abnormal production of VEGF. She did not, however, exhibit any constellation of Crow-Fukase syndrome such as edema, skin change, organomegaly, bone lesions or M-proteinemia. Steroid therapy improved her symptoms and lessened the levels of serum VEGF and cerebrospinal fluid protein. This case indicated that overproduction of VEGF could induce polyneuropathy rather than the other symptoms of Crow-Fukase syndrome, and that a polyneuropathy associated with increased VEGF might exist.

Endothelial Growth Factors↗
PubMed2000

Mode of onset of ventricular fibrillation in patients with Brugada syndrome detected by implantable cardioverter defibrillator therapy.

OBJECTIVES: We sought to demonstrate the mode of spontaneous onset of ventricular fibrillation (VF) in patients with Brugada syndrome. BACKGROUND: The electrophysiologic mechanisms of VF in Brugada syndrome have not been fully investigated. METHODS: Nineteen patients (all male, mean age 47 +/- 12 years) with Brugada syndrome were treated with an implantable cardioverter defibrillator (ICD). The implanted devices were capable of storing electrograms during an arrhythmic event. We investigated the mode of spontaneous onset of VF according to the electrocardiographic features during the episode of VF, which were obtained from stored electrograms of ICDs and/or electrocardiographic (ECG) monitoring. RESULTS: During a follow-up of 34.7 +/- 19.4 months (range 14 to 81 months), 46 episodes of spontaneous VF attacks were documented in 7/19 (37%) patients. The event-free period between ICD implantation and the first spontaneous occurrence of VF was 14.6 +/- 12.1 months (range 3.7 to 27.4 months). We investigated 33/46 episodes of VF, for which electrocardiographic features (10 to 20 s before and during VF) were obtained from ICDs and/or ECG monitoring in five patients. A total of 22/33 episodes of VF were preceded by premature ventricular contractions (PVCs), which were almost identical to the initiating PVCs of VF. Furthermore, in three patients who had multiple VF episodes, VF attacks were always initiated by the same respective PVC. The coupling interval of the initiating PVCs of VF was 388 +/- 28 ms. CONCLUSIONS: Spontaneous episodes of VF in patients with Brugada syndrome were triggered by specific PVCs. These findings may provide important insights into the pathophysiological mechanisms causing VF in Brugada syndrome.

Bundle-Branch Block↗
PubMed2000

Effect of sodium channel blockers on ST segment, QRS duration, and corrected QT interval in patients with Brugada syndrome.

INTRODUCTION: Brugada syndrome is characterized by an ST segment elevation in leads V1-V3 and a high incidence of ventricular fibrillation (VF). A mutation in a cardiac Na+ channel gene, SCN5A, has been linked to Brugada syndrome, and sodium channel blockers have been shown to be effective in unmasking the syndrome when concealed. The aim of this study was to examine the effects of Na+ channel blockers on ST segment elevation, QRS, corrected QT (QTc) interval, and ventricular arrhythmias in patients with Brugada syndrome. METHODS AND RESULTS: We examined the effects of three different Na+ channel blockers (flecainide, disopyramide, and mexiletine) on the amplitude of the ST segment 20 msec after the end of QRS (ST20), QRS duration, QTc interval measured from 12-lead ECG, and ventricular arrhythmias in 12 Brugada and 10 control patients. Maximum ST20 observed in the V2 or V3 leads under baseline conditions was greater in the Brugada patients than in control patients, whereas QRS duration and maximum QTc interval were no different between the two groups. Flecainide and disopyramide, but not mexiletine, significantly increased maximum ST20 and QRS duration in both groups, although these effects were much more pronounced in the Brugada patients. The increases in ST20 and QRS duration with flecainide were significantly larger than those with disopyramide. An increase of 0.15 mV in ST20 with flecainide separated the two groups without overlap. Ventricular premature complexes developed only with flecainide in Brugada patients (3/12) displaying a marked ST elevation but not widening of QRS. CONCLUSION: Our findings suggest that Na+ channel blockers amplify existing I(Na) and possibly other ion channel defects, with a potency inversely proportional to the rate of dissociation of the drug from the Na+ channel, thus causing a prominent elevation of the ST segment and, in some cases, prolongation of QRS duration in patients with Brugada syndrome.

Adult↗
PubMed2000

Clinical characteristics of patients with spontaneous or inducible ventricular fibrillation without apparent heart disease presenting with J wave and ST segment elevation in inferior leads.

INTRODUCTION: The clinical characteristics of three patients with spontaneous or inducible ventricular fibrillation (VF) without apparent heart disease, who presented with J wave and ST segment elevation in inferior leads, are described. METHODS AND RESULTS: All patients were male and experienced syncope. Their symptoms occurred at night or early in the morning. Holter ECG revealed infrequent premature ventricular complexes. Injection with disopyramide 2 mg/kg augmented ST segment elevation. CONCLUSION: These characteristics were very similar to those of patients with Brugada syndrome. These three patients with these specific features might have a variant of Brugada syndrome.

Adult↗
PubMed2000

Recovery time dispersion measured from 87-lead body surface potential mapping as a predictor of sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy.

INTRODUCTION: The clinical usefulness of QT dispersion in 12-lead ECG has been controversial in identifying subjects at risk for sustained ventricular tachycardia (VT) in patients with idiopathic dilated cardiomyopathy (DCM). We hypothesized that increasing the spatial resolution of the ECG improves the accuracy of risk stratification. The purpose of this study was to test the ability of recovery time dispersion measured from 87-lead body surface potential mapping (BSPM) to identify patients at risk for sustained VT in idiopathic DCM. METHODS AND RESULTS: We obtained 87-lead BSPM and 12-lead ECG in 33 patients with idiopathic DCM (15 patients with a history of sustained VT [VT(+) group] and 18 patients without a history of sustained VT [VT(-) group]) and in 20 normal control subjects. We measured the corrected QT dispersion and corrected recovery time dispersion from 12-lead ECG (QTc-12 dispersion and RTc-12 dispersion, respectively) and 87-lead BSPM (QTc-87 dispersion and RTc-87 dispersion, respectively). Signal-averaged ECG also was recorded in 25 patients. Neither the QTc-12 nor QTc-87 dispersion discriminated between the VT(+) and VT(-) groups patients. The VT(+) group patients had a larger but insignificant RTc-12 dispersion than the VT(-) group patients. In contrast, the RTc-87 dispersion was significantly larger in the VT(+) group patients than in the VT(-) group patients (236 +/- 39 msec vs 184 +/- 28 msec, P < 0.001). Receiver operating curve analysis indicated that the RTc-87 dispersion was as good as late potentials in predicting susceptibility to sustained VT; its sensitivity, specificity, and negative predictive value were 73%, 76%, and 76%, respectively (cutoff value 200 msec). RTc-87 dispersion >200 msec combined with positive late potentials provide high sensitivity (92%) and high negative predictive value (88%) for sustained VT. CONCLUSION: The RTc-87 dispersion is a useful tool to identify subjects at risk for sustained VT in patients with idiopathic DCM.

Body Surface Potential Mapping↗
PubMed2000

Body surface distribution and response to drugs of ST segment elevation in Brugada syndrome: clinical implication of eighty-seven-lead body surface potential mapping and its application to twelve-lead electrocardiograms.

INTRODUCTION: Body surface distribution and magnitude of ST segment elevation and their reflection in 12-lead ECGs have not been clarified in Brugada syndrome. METHODS AND RESULTS: Eighty-seven-lead body surface potential mapping and 12-lead ECGs were recorded simultaneously in 25 patients with Brugada syndrome and 40 control patients. The amplitude of the ST segment 20 msec after the end of QRS (ST20) was measured from all 87 leads, and an ST isopotential map was constructed. The maximum ST elevation (maxST20) was distributed in an area of the right ventricular outflow tract in all Brugada patients, and it was larger than that in control patients (0.37 +/- 0.13 vs 0.12 +/- 0.04 mV; P < 0.0005). The maximum was observed on the level of the parasternal fourth intercostal space, on which the V1 and V2 leads of the standard 12-lead ECG were located, in 18 of the 25 Brugada patients in whom typical coved- or saddleback-type ST elevation was seen in leads V1 and V2. The maximum was located on the second intercostal space in the remaining seven Brugada patients in whom only a mild saddleback-type ST elevation was seen in leads V1 and V2 of the 12-lead ECG. Typical ST segment elevation was recognized in leads V1 and V2, which were recorded on the second or third intercostal space. ST elevation in Brugada patients was dramatically normalized by isoproterenol, a beta-adrenergic agonist (maxST20 = 0.17 +/- 0.08 mV; P < 0.0005 vs control conditions), and accentuated by disopyramide, an Na+ channel blocker (maxST20 = 0.50 +/- 0.15 mV; P < 0.0005 vs control conditions), without any change in the location of the maxST20. CONCLUSION: Our data indicate that recordings of leads V1-V3 of the 12-lead ECG on the parasternal second or third intercostal space would be helpful in diagnosing suspected patients with Brugada syndrome. The data suggest that Na+ channel blockers are capable of accentuating ST elevation in leads V1-V3.

Action Potentials↗
PubMed2000

Pineal region metastasis appearing as hypointensity on T2-weighted magnetic resonance imaging--case report.

A 48-year-old female presented with headache and limitation of upward gaze. She had a history of total gastrectomy for gastric adenocarcinoma 2 years previously. Computed tomography with contrast medium and T1-weighted magnetic resonance (MR) imaging with gadolinium showed ring-like enhancement of a solitary mass in the pineal region with obstructive hydrocephalus. T2-weighted MR imaging showed the tumor as hypointense. This MR imaging finding complicated the preoperative diagnosis, but malignancy was suspected from the medical history. The tumor was subtotally resected via the occipital transtentorial approach with a rigid endoscope. Histological examination of the surgical specimen revealed adenocarcinoma cells with extensive coagulation necrosis, which might have contributed to the hypointensity on T2-weighted MR imaging. Correct diagnosis of metastatic adenocarcinoma based only on MR imaging may be difficult in such cases, but metastatic adenocarcinoma of the pineal region must be considered in the differential diagnosis of pineal tumors.

Adenocarcinoma↗
PubMed1999

Argyrophilic dark neurons distribute with a different pattern in the brain after over hours treadmill running and swimming in the rat.

Argyrophil III staining is a useful method for the detection of dark neurons (DNs) that would reflect an early cytopathic feature. We examined the appearance of DNs following the stressful exercises (0.5-3 h swimming in a pool of 25-45 cm depth; 1-2 h running on a treadmill at the speed of 600-1200 cm/min) in the rat. After the swimming, DNs were detected in the hippocampus (CA1-2 pyramidal cell layer, oriens layer), somatosensory cortex, entorhinal cortex, hypothalamus, habenular nucleus, amygdaloid nucleus, striatum, accumbens and sometimes in lateral septal nucleus. After the running, DNs appeared in the visual cortex, deepest layer of area 17 and 18a, motor cortex, red nucleus, somatosensory cortex, entorhinal cortex, and hippocampus (dentate gyrus). Thus, the DNs appeared mainly in the limbic structure after the swimming, and in the limbic structure, motor-related regions and visual cortex after the running. Further, the number of the DNs and the extent of area where they distributed were dependent on the strength and the duration of the exercises. In hematoxylin-eosin (H-E) staining, we often detected pycnotic cells (dark stained soma) in CA1 hippocampus where argyrophil positive cells were most abundant. The picnotic cells were not so common in other areas. Data suggest that DNs are induced by stressful exercises. They might reflect an early cell injury following stress and overexcitation.

Animals↗
PubMed1999

Deterioration of ocular motor dysfunction after transvenous embolization of dural arteriovenous fistula involving the cavernous sinus.

We treated 9 patients with the dural arteriovenous fistula involving the cavernous sinus by transvenous embolization. Two patients experienced deterioration of oculo-motor dysfunction after transvenous embolization. We can speculate about two different kind of causes by which patients symptoms deteriorated according to the result of intrasinus pressure recorded during the embolization [1]: high intrasinus pressure caused by the obliteration of the drainage pathway resulted in cranial nerve palsy in one case [2]; implanted coils directly compressed the cranial nerve in another case. Fortunately our cases recovered, but some kind of preventative measures may be needed in similar cases.

Arteriovenous Fistula↗
PubMed1999

Exercise-induced ST elevation in patients with arrhythmogenic right ventricular dysplasia.

To test the hypothesis that local or diffuse wall motion abnormalities in the right ventricle in patients with arrhythmogenic right ventricular dysplasia (ARVD) may induce the ST-segment elevation in response to exercise, we examined exercise electrocardiograms in patients with ARVD. In 17 patients with ARVD, who demonstrated right ventricular wall motion abnormalities without organic coronary lesions, we conducted a treadmill exercise test. Significant exercise-induced ST-segment elevation (ESTE) was defined as a 0.1 mV or more ST-segment elevation at J point. ESTE was observed in 11 patients (65%). It manifested most frequently in right-sided precordial leads. Severe right ventricular asynergy was seen in all but one (91%) among 11 with ESTE, whereas it was seen only in two (33%) among six without ESTE (P<.05). The maximal magnitude of ESTE inversely correlated with right ventricular ejection fraction (r = -0.58, P<.05). ESTE was seen in two thirds of ARVD patients, helping us noninvasively diagnose ARVD. The fact that ventricular wall motion abnormalities could cause ESTE in the absence of organic coronary lesions suggested the critical role of mechanical factors in the genesis of ESTE.

Adolescent↗
PubMed1999

The circadian pattern of the development of ventricular fibrillation in patients with Brugada syndrome.

AIMS: Brugada syndrome is considered to be a distinctive subgroup of idiopathic ventricular fibrillation. Identification of the circadian pattern of ventricular fibrillation would contribute to the elucidation of its underlying pathophysiology, but this pattern remains unknown in patients with Brugada syndrome. METHODS: and Results A total of 12 consecutive Brugada syndrome patients (46+/-14 years, all male) who underwent implantation of an implantable cardioverter defibrillator were studied. The distribution of the time of ventricular fibrillation detection was examined and classified into four 6-hour time periods of the day. The mean follow-up period following implantation was 777+/-535 days. In six out of the 12 patients, ventricular fibrillation occurred during follow-up. The data logs revealed that ventricular fibrillation was detected 30 times (range, 3-9). Ventricular fibrillation was observed more frequently at night ( 1800 h to 0600 h) than in the day (0600 h to 1800 h) (93.3% [28/30] vs 6.7%[2/30], P<0.001), and during sleep than while awake (86.7% [26/30] vs 13.3%[4/30], P<0.001). Ventricular fibrillation occurred most frequently between midnight and 0600 h in patients with ventricular fibrillation episodes during sleep (76.9% [20/26] vs 23.1%[6/26], P<0.01). CONCLUSION: These results suggest that increased nocturnal vagal activity and withdrawal sympathetic activity may play an important role in the arrhythmogenesis of the Brugada syndrome.

Adult↗
PubMed1999

Paraganglioma in the frontal skull base--case report.

A 56-year-old female presented with a paraganglioma in the left anterior cranial fossa who manifesting as persistent headache. Computed tomography and magnetic resonance imaging showed a solid, enhanced tumor with a cystic component located medially. The tumor was attached to the left frontal base and the sphenoid ridge. Angiography demonstrated a hypervascular tumor fed mainly by the left middle meningeal artery at the left sphenoid ridge. The preoperative diagnosis was meningioma of the left frontal base. The tumor was totally resected via a left frontotemporal craniotomy. Histological examination revealed the characteristic cellular arrangement of paraganglioma generally designated as the "Zellbaren pattern" on light microscopy. Only 10 patients with supratentorial paraganglioma have been reported, seven located in the parasellar area. The origin of the present tumor may have been the paraganglionic cells which strayed along the middle meningeal artery at differentiation.

Cerebral Angiography↗
PubMed1998

Preparation of Anisotropic Gold Particles Using a Gemini Surfactant Template.

Anisotropic gold particles were prepared in a gemini cationic surfactant solution by reduction of HAuCl4 with UV irradiation. With increasing concentrations of both HAuCl4 and the surfactant, fibrous gold particles were obtained and their length increased. These results suggest that the gemini surfactant which provides threadlike micelles operates as a soft template for anisotropic gold particles. Copyright 1998 Academic Press.

Journal Article↗
PubMed1998

Diagnostic value of plasma levels of brain natriuretic peptide in arrhythmogenic right ventricular dysplasia.

BACKGROUND: Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by local or diffuse wall motion abnormalities in the right ventricle (RV), associated with recurrent ventricular tachycardia (VT) of RV origin. Brain natriuretic peptide (BNP) was first isolated from a porcine brain extract. In humans, BNP is expressed predominantly in the ventricles of failing hearts, and its expression has been observed primarily in myocytes in the interstitial fibrous area in dilated cardiomyopathy. We hypothesized that BNP is increasingly secreted from the residual myocytes within the atrophic tissue in patients with ARVD. METHODS AND RESULTS: Plasma BNP levels were measured in 17 patients with ARVD, 12 patients with idiopathic RV outflow tract tachycardia (RVOT), and 120 control subjects. We performed cardiac catheterization, RV endomyocardial biopsy, electron- beam CT, and biventricular endomyocardial mapping in the ARVD patients. There was a significant increase in plasma BNP levels in the ARVD patients compared with the RVOT patients and control subjects (61.4+/-59.6 pg/mL versus 8.3+/-5. 5 pg/mL and 9.3+/-5.8 pg/mL; P<0.0001, respectively). The plasma BNP levels had no correlation with any of the hemodynamic data, but they had a significant correlation with the RV ejection fraction (r=-0. 588, P=0.025) and with the fractionated-area scores (r=0.705, P=0. 005). Light microscopic immunohistochemistry showed strong BNP immunoreactivity in residual myocytes with fibrofatty replacement. CONCLUSIONS: These results suggest that plasma BNP levels were not increased in RVOT patients but were increased in ARVD patients, and that the increased BNP levels indicate the severity of both the RV dysfunction and the arrhythmogenic substrate.

Adolescent↗
PubMed1998

Clinical and electrophysiologic features of idiopathic left ventricular aneurysm with sustained ventricular tachycardia.

We examined 10 patients with idiopathic left ventricular (LV) aneurysm with sustained ventricular tachycardia (VT) (Id-An group), and compared them with those in 16 age- and sex-matched patients who had postinfarction aneurysm and VT (MI-An group) to clarify detailed clinical and electrophysiologic characteristics of idiopathic LV aneurysm. The clinical and laboratory data and results of electrocardiography, electrophysiologic, and morphologic examinations in the two groups were compared. In the Id-An group, the LV aneurysms were located more often at the posterior and/or inferior wall, while in the MI-An group, they were more often located at the anterior and/or apical wall (P<0.001). The LV end-diastolic volume index was significantly smaller and the LV ejection fraction was significantly higher in the Id-An group (P<0.001). The size of the aneurysm and the area with abnormal electrograms in the Id-An group were significantly smaller than those in the MI-An group (P<0.005 and P<0.001, respectively). The inducibility of VT was high in both groups, and ventricular pacing during VT showed entrainment phenomenon in most of the patients. Thus, in both groups, the abnormal electrograms were closely associated with the wall motion abnormality, and reentry was suggested as the mechanism of VT. In the Id-An group, since the lesions were anatomically and electrophysiologically confined to the posterior and/or inferior wall, the global LV function was more well preserved compared with the MI-An group.

Cardiac Catheterization↗
PubMed1998

Localization of optimal ablation site of idiopathic ventricular tachycardia from right and left ventricular outflow tract by body surface ECG.

BACKGROUND: Idiopathic ventricular tachycardia (VT) is known to arise from the right ventricular (RV) and left ventricular outflow tracts (LVOT). However, reliable noninvasive methods to localize the optimum ablation site for VT have not been reported. METHODS AND RESULTS: Body surface maps (BSM) and 12-lead ECGs were investigated in 35 VTs from the RVOT and 5 VTs from the LVOT in which the origin was confirmed during the ablation procedure. The RVOT was classified into 8 subdivisions with the use of a 3-dimensional anatomic relation: anterior (A) posterior (P), right (R) left (L), and superior (S) inferior (I). On the BSM, the following 3 indexes differentiated each location of the origin, with a diagnostic accuracy of 88% (A-P), 92% (R-L), and 77% (S-I): (1) the location of the minimum at the early-to-mid QRS (right, A; left, P), (2) the isopotential distribution in the left shoulder area after 30 ms of QRS (positive, R; negative, L), and (3) the downward moving time of the minimum at the early-to-mid QRS (>/=50 ms, S; <50 ms, I). On the 12-lead ECG, (1) the QRS duration (>140 ms, A; </=140 ms, P) and the R-wave pattern in leads II and III (RR' or Rr', A, R, P), (2) the QS wave amplitude in aVR and aVL (aVR>/=aVL, R; aVR /=1 in lead V3 was an index suggesting the LVOT origin. CONCLUSIONS: The origin or the optimum ablation site of idiopathic VT from RVOT and LVOT can be localized with the use of indexes obtained with a BSM or 12-lead ECG.

Adolescent↗
PubMed1998

Improvement of repolarization abnormalities by a K+ channel opener in the LQT1 form of congenital long-QT syndrome.

BACKGROUND: This study used monophasic action potential (MAP) to examine the effect of nicorandil, a K+ channel opener, on repolarization abnormalities induced by epinephrine in the LQT1 form of congenital long-QT syndrome in which the KvLQT1 mutation underlies the defect in the channel responsible for the slowly activating component of the delayed rectifier potassium current. METHODS AND RESULTS: MAPs were recorded simultaneously from two or three sites on the right ventricular and left ventricular endocardium in 6 patients with a congenital form of LQT1 syndrome with KvLQT1 defect (17 sites) and 8 control patients (24 sites). In LQT1 patients, epinephrine infusion prolonged the QT interval and 90% MAP duration (MAPD90) and increased the dispersion of MAPD90. Epinephrine also induced early after depolarizations (EADs) as well as ventricular premature complexes (VPCs) in 2 of the 6 patients. Nicorandil during epinephrine infusion abbreviated the QT interval and MAPD90, decreased the dispersion of MAPD90, and abolished the EADs as well as the VPCs in 1 patient. Addition of propranolol completely reversed the effect of epinephrine in prolonging the QT interval and MAPD90 and increasing the dispersion and eliminated the EADs and VPCs in another patient. In control patients, the effect of epinephrine and that of additional nicorandil and propranolol on repolarization parameters were much less than in the LQT1 patients. CONCLUSIONS: Our results suggest that nicorandil, a K+ channel opener, improves repolarization abnormalities in the LQT1 form of congenital long-QT syndrome with KvLQT1 defect.

Adolescent↗