Wireless LAN security management with location detection capability in hospitals.

OBJECTIVES: In medical institutions, unauthorized access points and terminals obstruct the stable operation of a large-scale wireless local area network (LAN) system. By establishing a real-time monitoring method to detect such unauthorized wireless devices, we can improve the efficiency of security management. METHODS: We detected unauthorized wireless devices by using a centralized wireless LAN system and a location detection system at 370 access points at the University of Tokyo Hospital. By storing the detected radio signal strength and location information in a database, we evaluated the risk level from the detection history. We also evaluated the location detection performance in our hospital ward using Wi-Fi tags. RESULTS: The presence of electric waves outside the hospital and those emitted from portable game machines with wireless communication capability was confirmed from the detection result. The location detection performance showed an error margin of approximately 4 m in detection accuracy and approximately 5% in false detection. Therefore, it was effective to consider the radio signal strength as both an index of likelihood at the detection location and an index for the level of risk. CONCLUSIONS: We determined the location of wireless devices with high accuracy by filtering the detection results on the basis of radio signal strength and detection history. Results of this study showed that it would be effective to use the developed location database containing radio signal strength and detection history for security management of wireless LAN systems and more general-purpose location detection applications.

A randomized comparison of the straight linear approach with electrogram mapping focal approach in selective slow pathway ablation.

The aim of this study was to evaluate the efficacy and safety of the anatomic linear approach in selective AVN slow pathway ablation, in comparison to the widely used electrogram mapping focal approach. It remains undetermined whether or not anatomic linear ablation has a greater potential for eliminating slow pathway conduction than does focal ablation. Fifty consecutive patients (21 men, 29 women, age 56 +/- 14 years) with common type AVNRT were randomly assigned to the linear approach (25 patients) or local electrogram mapping approach (25 patients). A linear lesion was created between the tricuspid annulus, at the midlevel of the coronary sinus (CS) ostium, and the anterior aspect of the CS infundibulum. In 22 (88%) patients in the linear group, the AVNRT was successfully eliminated by 1.5 +/- 0.8 linear RF applications without any complications. All 25 patients in the focal group satisfied the endpoint criteria after 3.8 +/- 2.4 focal RF deliveries. The success rate did not significantly differ between the two groups. Out of the 22 patients with a successful outcome in the linear group, 17 (77%) attained complete abolition of the slow pathway conduction, whereas this was observed in only eight (32%) patients in the focal group (P < 0.005). The session time was significantly shorter in the linear group. Recurrence of the tachycardia was not documented in any patient during a mean follow-up of 18 +/- 8 months except one with residual slow pathway conduction in the focal ablation group. In conclusion, the anatomic linear approach can be performed safely and possesses a greater potential for slow pathway interruption compared to the electrogram mapping focal approach.

Three-year follow-up of patients with right bundle branch block and ST segment elevation in the right precordial leads: Japanese Registry of Brugada Syndrome. Idiopathic Ventricular Fibrillation Investigators.

OBJECTIVES: We sought to determine the prevalence of right bundle branch block (RBBB) and ST segment elevation in the working Japanese population, as well as the event rate during a three-year prospective follow-up period. BACKGROUND: A poor prognosis of RBBB and ST segment elevation has been reported in Europe and South America, even in asymptomatic patients; however, a large population of asymptomatic patients with sporadic RBBB and ST segment elevation has not been studied. METHODS: Ten thousand 12-lead electrocardiograms (ECGs) were obtained during annual check-ups of working adults in the Tokyo area. This three-year prospective follow-up study consisted of 105 patients, including 20 with ventricular fibrillation, 18 with syncope and 67 who were asymptomatic. They were registered from 46 institutions in Japan. RESULTS: The prevalence of ECG abnormalities in working adults was 0.16%. A coved-type ST segment elevation was related to a history of cardiac events, and 18% of registered patients had PR prolongation and 9.5% had left-axis deviation. The cumulative cardiac event-free rate was 67.6% in the symptomatic group and 93.4% in the asymptomatic group (p = 0.0004) after three years. CONCLUSIONS: The recurrence rate of cardiac events in symptomatic patients was similar to that reported previously, but it was very low in sporadic asymptomatic patients. The ECG findings may help us to select patients for further examination and more accurate evaluation of their prognoses.

Quantitative analysis of termination of vagally induced canine atrial fibrillation by mutual information.

Atrial fibrillation (AF) is often described as a disorganized phenomenon, but many features that qualitatively suggest an underlying order have recently been reported. The present study aimed to disclose this underlying order of AF in a quantitative manner, using a new method of mutual information (MI), which is a measure for gauging the general correlation between 2 time series. Frequency analysis and the MI method were used to analyze 5 epicardial potentials on both atria during AF induced by vagal stimulation (Vs) in 15 dogs. Unipolar electrodes were placed on the right atrial appendage (Rap), the high right atrium (HRA), and the left atrial appendage (Lap). The other 2 electrodes were placed equidistantly between HRA and Rap (RA1-RA2). The power spectrum of AF had a discrete peak around 17Hz during Vs. After Vs was stopped, the discrete peak shifted from 17Hz to 7 Hz on all epicardial leads. Taking RA2 as a reference, MI was calculated between RA2 and each of the other electrodes. The MI values (0.066+/-0.005) were greater than 0.047 (the critical value for correlated data) even during Vs. The MI values increased significantly from the highly active process of AF during Vs to the less active one (0.126+/-0.006) before termination of AF. In addition, the MI values increased more at the electrodes close to RA2 (RA1 and Rap) than at those far from it (HRA and Lap). These findings suggest that multiple wavelets, which are not random, progressively organize into a few major waves toward the termination of AF; therefore, AF is not a random phenomenon in this model.

Risk factors for thromboembolism in patients with paroxysmal atrial fibrillation.

There is some controversy concerning which clinical characteristics predict thromboembolism and whether treatment with class I antiarrhythmic drugs reduces thromboembolim in patients with paroxysmal atrial fibrillation (AF). This retrospective, multicenter study was undertaken to determine risk factor or factors for thromboembolism in patients with paroxysmal AF. Seven hundred forty patients with paroxysmal AF (mean age 56 years) without prior thromboembolic events were followed retrospectively. Cerebral thromboembolism, including transient ischemic attack and embolism of peripheral arteries, were selected as primary end points. Independent risk factors were determined with multivariate analysis, and event-free survival curves were estimated. During 3.4-year follow-up period, primary end points occurred in 55 patients (2.2% per year). Patients with thromboembolism had a higher prevalence of underlying heart disease (p <0.01), less frequent treatment with antiarrhythmic drugs (p <0.01), and received diuretics more often (p <0.01) compared with patients without thromboembolism. Age (>/=65 years, RR 3.33, p = 0.0001) and gender (male, RR = 2, p = 0.0291) emerged as predictors of thromboembolism by multivariate analysis with Cox's proportional hazard model. Treatment with antiarrhythmic drugs (RR = 0.57, p = 0.0578) and aspirin (RR = 0.52, p = 0.1094) showed trends toward reducing thromboembolic risks. It is suggested that elderly men (>/=65 years) with paroxysmal AF are at risk for thromboembolism, but the risk tended to be reduced by treatment with antiarrhythmic drugs and aspirin.

Pharmacokinetics of landiolol hydrochloride, a new ultra-short-acting beta-blocker, in patients with cardiac arrhythmias.

OBJECTIVES: To elucidate pharmacokinetics and pharmacodynamics of landiolol hydrochloride, newer developed ultra-short-acting beta-blocker, in patients with various cardiac tachyarrhythmias. BACKGROUND: The short duration of action and titratability of landiolol hydrochloride make it ideal for use in patients with a clinical need for beta-blockers. METHODS: In a total of 31 examinations we infused the drug in 19 patients (mean age, 55 +/- 14 years). After the persistence of the tachyarrhythmias was confirmed, continuous infusion was started at rates of 0.005, 0.01, 0.02, 0.04, and 0.08 mg/kg/min for 5 minutes (for paroxysmal atrial fibrillation, paroxysmal supraventricular tachycardia, and ventricular tachycardia) or 15 minutes (for ventricular premature complex). We analyzed the pharmacokinetics of 16 examinations. A one-compartment model provided a close fit for each blood concentration-time curve. RESULTS: The maximum blood concentrations obtained clearly showed the dose dependency and revealed very short half-lives (range, 2.3 to 4.0 minutes). Area under the blood concentration-time curves also increased, showing dose dependency. In paroxysmal atrial fibrillation, landiolol hydrochloride reduced the heart rate from 111 +/- 20 to 90 +/- 10/min. Sinus rhythm was restored, without any adverse effects, in three of five patients with paroxysmal supraventricular tachycardia and one patient with ventricular tachycardia. There was no significant change in peripheral blood pressure. CONCLUSIONS: Landiolol hydrochloride has a shorter elimination half-life than any other beta-blocker, and it can be administered safely to patients with various tachyarrhythmias.

Analysis of posterior mitral annular activation during entrainment and catheter ablation of mitral isthmus ventricular tachycardia using a coronary sinus catheter.

A detailed analysis of the ventricular activation along the posterior aspect of the mitral annulus was made using a multipolar catheter positioned in the coronary sinus in a patient with mitral isthmus ventricular tachycardia (VT) associated with a remote inferior myocardial infarction and prior cryosurgical ablation for the elimination of a different preexisting VT. A change in the timing and sequence of the ventricular activation along the isthmus could be observed during induction of the VT and entrainment pacing. A radiofrequency (RF) current application directed at the posterolateral region of the isthmus successfully eliminated this tachycardia. During the RF delivery, complete conduction block was confirmed by a sudden change in the activation sequence during sinus rhythm.

Identification of the slow conduction zone in idiopathic left ventricular tachycardia.

The mechanism of verapamil sensitive idiopathic left ventricular tachycardia (ILVT) is considered to be reentry. However, the nature of the reentry circuit, including the location of the slow conduction zone, is unclear. We sought the local electrical activity that would reflect slow conduction by precise mapping around the tachycardia exit (TE) in nine patients with ILVT (mean age, 28 +/- 10 years) undergoing radiofrequency catheter ablation (RFCA). The TE was defined as the earliest discrete spiky potential (SP) recorded during the tachycardia, or as a complete configuration-matched pacemap 12-lead electrocardiogram (ECG). In all patients, the TE was located at the mid or inferior distal portion of the septum. The SP at the TE preceded the surface QRS by 20 +/- 9 ms. The pacemap score at the TE was 11.4 +/- 0.6 points. In three patients, fractionated potentials (FP) were recorded during the tachycardia. The onset of the FP preceded the surface QRS by 47 +/- 8 ms and was earlier than the SP at the TE (P < 0.01). The sites where an FP was detectable were restricted to a small area, and were at a distance of 14 +/- 4 mm from the TE. The direction of the FP site from the TE was more basal in two patients and inferior in one. Pacemap ECGs at the sites with an FP showed poor matching (9 +/- 1 points), presumably because of predominant capture of the local ventricular muscle rather than an electrically isolated reentry circuit. Successful RFCA was achieved at the site of the FP in all three patients in which one was recorded, and at the TE in the other six patients. The FP, which has been shown to reflect the slow conduction of the ventricular tachycardia circuit in structural heart disease, was also detected in ILVT in the present study, and it is likely to reflect electrical excitation of the distal rim of the slow conduction zone.

Temporal and spatial dispersion of repolarization during premature impulse propagation in human intact ventricular muscle: comparison between single vs double premature stimulation.

AIMS: This study was performed to determine whether or not the kinetics of action potential duration restitution during double premature stimuli (S3) differ from that during single premature stimuli (S2) in the human intact right ventricle. METHODS AND RESULTS: A monophasic action potential (MAP) was simultaneously recorded from the right ventricular apex (RVA) and outflow tract (RVOT) during programmed ventricular pacing in 11 patients with symptomatic bradyarrhythmias (five males, six females, mean age 58 years). In the five most recent patients, the RV pressure and its dp/dt were also obtained during the protocol. A substantial difference in the restitution of the MAP duration (MAPD) between S2 and S3 was observed at short diastolic intervals (< l00 ms), that is, the restitution curve of S2 showed an early biphasic pattern (upward hump), while such a phenomenon was not seen during the restitution of S3. All the quantitative parameters of MAPD restitution representing its kinetics were significantly greater in S3 than S2. Maximum attainable dispersion of repolarization between the two MAPs was significantly greater during S3 than S2 (76 +/- 17 vs 59 +/- 17 ms, P<0.05) and was mainly caused by the difference in the MAPD difference, thus by the difference in the restitution kinetics of S2 and S3. The dp/dt of the RV pressure was significantly greater during S3 than S2 for all diastolic intervals tested. CONCLUSION: It was concluded that similar to previously reported canine experimental studies, the APD restitution of S3 is substantially different from that of S2 in the human intact ventricle (endocardium).

Local slow potential preceding the surface QRS complex detected at the subvalvular mitral annulus in patients with a left-sided concealed accessory pathway. Incidence, electrophysiological characteristics and the possible mechanism, with demonstration of anterograde concealed conduction through the pathway.

AIM: We sought to evaluate the incidence and electrophysiological features of the local slow potential preceding the surface QRS complex (pre-QRS potential) which was detected more frequently at successful sites of catheter ablation of left parietal concealed accessory pathways, than at unsuccessful sites. METHODS AND RESULTS: Thirty eight consecutive patients with a single left sided concealed accessory pathway underwent radiofrequency catheter ablation exclusively from the subvalvular mitral annulus. The local bipolar electrograms during sinus rhythm from the target sites were carefully analysed and the incidence of pre-QRS potentials was compared between successful and unsuccessful ablation sites. All ablation sessions attained a successful outcome with a total of 84 radiofrequency current applications (38 at successful sites, 46 at unsuccessful sites). The incidence of pre-QRS potentials (preceding by 10 ms or more) was 12/38 at successful sites (32%) and 1/46 at unsuccessful sites (2%) (P<0.001). The QV interval, defined as the interval between the upstroke of the QRS complex and the ventricular electrogram, including the pre-QRS potential, was -5.6+/-9.1 ms at successful sites, while it was 1.2+/-6.1 ms at unsuccessful sites (P<0.001). The pre-QRS potential disappeared during atrioventricular reciprocating tachycardia and right ventricular pacing, and was eliminated by successful ablation. CONCLUSIONS: Detection of the pre-QRS potential was clinically relevant and could be distinguished from artifact. This potential may be caused by anterograde concealed conduction through the accessory pathways.

Incidence and clinical significance of junctional rhythm remaining after termination of radiofrequency current delivery in patients with atrioventricular nodal reentrant tachycardia.

The aim of this study was to elucidate the electrophysiologic characteristics and clinical significance of the accelerated junctional rhythm (JR) that remains after termination of radiofrequency (RF) current delivery during catheter ablation (CA) for atrioventricular nodal reentrant tachycardia (AVNRT). Fifty consecutive patients with AVNRT (21M, 29F, age 48 years) underwent RF-CA targeting the slow pathway. JR occurred at 124 out of a total of 236 ablation sites (53%) during the RF delivery. With 15 RF deliveries (6.4%, n=10), JR remained after termination of the RF delivery (Post-JR). The mean cycle length of the Post-JR immediately after termination of the RF delivery was 639+/-124 ms and its duration was widely distributed from 3 s to more than 1 h. The Post-JR exhibited a spontaneous rate deceleration and overdrive suppression by rapid atrial pacing. The JR during the RF delivery followed by Post-JR had a greater time span in which the JR appeared, compared with that without Post-JR. The Post-JR had less sensitivity(18 vs 96%), but greater specificity (97 vs 59%) and a positive predictive value (60 vs 39%) in predicting successful ablation compared with JR seen only during the RF delivery. It is concluded that the presence of Post-JR might be a reflection of the intense effect of RF energy on the nodal or peri-nodal tissue.

[Historical perspectives on the mechanism of atrial fibrillation].

A number of experimental studies have been proposed to show that reentry is an important electrophysiological mechanism related to the development of atrial fibrillation. The beginning of the computer era enabled us to analyze the atrial activation during atrial fibrillation. The results of these studies were fascinating and allow for the development of theories and speculations on the mechanism of atrial fibrillation. Sophisticated computer techniques also allowed Moe to simulate atrial electrical activity during atrial fibrillation, and their team formulated so-called multiple wavelet theory which was subsequently supported by experimental evidence. Spiral wave for ventricular fibrillation was also proposed for the atrial activation mechanism during atrial fibrillation in the experimental model. The evidence available at the moment warrants the statement that atrial fibrillation is caused by multiple wavelet reentry. These studies will allow a better understanding of the relative importance of wavelength and structural inhomogeneities in the genesis of atrial fibrillation.

[Possible contribution of alpha-adrenergic abnormalities to cerebral ischemia in the patients with sinus bradycardia. Analysis by pharmacologic autonomic nervous test].

BACKGROUND: Syncope of patients with bradyarrhythmia is perceived as severe sign of low cardiac output caused by bradycardia and as a major criteria for pacemaker implantation (PMI). However, it has been reported that PMI can not always prevent syncope; it has been suggested that not bradycardia but an abnormality of the autonomic nervous system plays a part in syncope. PURPOSE: To investigate the relation between autonomic nervous dysfunction and syncope in cases of sinus bradycardia (SB). SUBJECTS: Thirty-nine patients with SB were divided into two groups according to the presence (group S, n = 16, 46.9 +/- 20.0 years) or absence (group N, n = 23, 40.4 +/- 17.6 years) of syncope or presyncope. METHODS: Corrected sinus node recovery time (CSNRT) was measured by electrophysiologic study. Pharmacologic autonomic nervous tests were performed as follows in a quiet room. Increased HR by application of 0.04 mg/kg atropine (para-tone), and by 0.004 microgram/kg/min isoproterenol divided by 0.004 (beta-sens) were evaluated, beta-tone was obtained by subtracting HR after application of propranolol (0.2 mg/kg) from that of atropine. Basal beta-sympathetic activity was evaluated by beta-sec that was obtained by beta-tone/beta-sens. Increased SBP by application of 0.4 microgram/kg/min phenylephrine divided by 0.4 (alpha-sens) was evaluated. alpha-tone was obtained by subtracting minimum SBP after 0.2 mg/kg phentolamine from SBP after application of propranolol. Basal alpha-sympathetic activity was evaluated by alpha-sec, that was obtained by alpha-tone/alpha-sens. RESULT: There were no significant differences in basal clinical characteristics (age, sex, cardiac function) between the groups. The parameters of the functions of parasympathetic and beta-sympathetic receptors (para-tone, beta-sens, beta-tone, beta-sec) showed no significant differences between the groups, alpha-sens was attenuated (P < 0.01) and alpha-sec was augmented (P < 0.0001) significantly in group S. CONCLUSION: It was suggested that syncope or presyncope in SB patients could be attributed to failure of vasoconstriction mediated by alpha-sympathetic receptor but to severity of sinus node dysfunction.

Uncommon atrial flutter originating in the left atrioventricular groove: emergence after successful catheter ablation for a left concealed accessory pathway.

This report describes a 49-year-old male with concealed Wolff-Parkinson-White syndrome in whom a true uncommon atrial flutter suddenly emerged 2 weeks after successful catheter ablation of a left-sided accessory pathway. The earliest atrial activation during the atrial flutter was recorded at the posterolateral mitral annulus 2 cm proximal to the previous successful ablation site for the accessory pathway. Two applications of radiofrequency (RF) current directed at the supravalvular mitral annulus could not terminate the atrial flutter. A subsequent delivery of RF current directed at the subvalvular annulus, where a local fragmented potential preceded the earliest atrial activation, eliminated the atrial flutter.

[QT dispersion in premature beats produced by extrastimuli from the right atrium and right ventricle].

The difference between the maximum and minimum QT interval measured from a 12-lead electrocardiogram was defined as an index of spatial inhomogeneous repolarization of the ventricular myocardium. The causal relationship between QT dispersion and incidence of ventricular arrhythmias has been pointed out in various heart diseases, but until now it was discussed mainly related to sinus rhythm. QT dispersion in extrasystole may be more important in the development of arrhythmias. We examined 5 cases (mean age 34 +/- 12 years) with a history of paroxysmal supraventricular tachycardia, who underwent electrophysiologic study. Both atrial and ventricular premature stimuli were given at a basic cycle length of 600 msec respectively. The QT interval and the ventricular activation time (VAT) (period from premature test stimulus to the summit of QRS) of the premature beats were measured in a simultaneously recorded 12-lead electrocardiogram. QT dispersion (the difference between the longest QT interval and the shortest QT interval) and VAT dispersion (the difference between the longest VAT and the shortest VAT) were measured. In atrial premature beats, there were no significant changes in the QT dispersion or VAT dispersion when the coupling interval of the premature beats was shortened. In the ventricular premature beats, however, both the QT dispersion and the VAT dispersion tended to increase with the shortening of the coupling interval. We concluded that only a short coupled ventricular premature beat induces greater QT and VAT dispersion. A ventricular couplet with short coupling interval may contribute to the development of ventricular tachyarrhythmias.

[Autonomic nervous function of the patients with neurally mediated syncope].

Although diagnosis of neurally mediated syncope (NMS) using head-up tilt (HUT) test has been established, the exact mechanism of NMS has not yet been elucidated. We evaluated beta and alpha-adrenergic function in NMS patients by pharmacological autonomic function test. The alpha-adrenergic sensitivity of NMS patients was significantly lower than that of control subjects. The patients who need low dose isoproterenol for provocation of syncope showed higher beta-adrenergic sensitivity than patients who developed syncope without isoproterenol. Thus, pharmacological autonomic function test was useful for evaluation of NMS patients.

Detection of a local slow potential preceding the surface QRS complex during non-preexcited impulse propagation--a phenomenon reflecting anterograde concealed conduction through the accessory pathway?

A case of Wolff-Parkinson-White (WPW) syndrome with several interesting electrophysiologic findings is presented. Although manifest preexcitation had not been documented in clinical routine check-ups for the 2 years before the ablation session, an intermittent preexcitation emerged after an initial unsuccessful radiofrequency current delivery directed at the subvalvular mitral annulus 1 cm distal from the subsequent successful ablation site. During intermittent manifestation of preexcitation, the following observations were made: (1) during manifest preexcitation, a possible Kent potential was recorded at the successful ablation site; (2) during non-preexcited impulse propagation, a local slow potential preceding the QRS complex (pre-QRS potential) was clearly observed at the same site; (3) the pre-QRS potential disappeared during orthodromic atrioventricular reciprocating tachycardia, spontaneous atrial premature contraction and after the subsequent successful ablation; and (4) when the pre-QRS potential was obvious, a small change in QRS morphology of the body-surface ECG was appreciable, compared with that during beats of negative pre-QRS potential. A comparable preceding component was also detected in a signal-averaged ECG. It is considered that the pre-QRS potential might be related to the anterograde concealed conduction through the accessory pathway.

Abnormality of alpha-adrenergic vascular response in patients with neurally mediated syncope.

Although diagnosis of neurally mediated syncope (NMS) using the head-up tilt (HUT) test has been established, the precise etiologic mechanism of NMS is still obscure. Previously, we reported the contribution of impaired alpha-adrenergic vascular response to syncope in patients with various arrhythmias. This study evaluates alpha-adrenergic vascular response in 21 NMS patients with syncope and a positive HUT test (80 degrees, 30 minutes, and low-dose isoproterenol, NMS group, mean age 31 +/- 14 years) and 21 control subjects (C group, 33 +/- 14 years) who had no evidence of syncope and no structural heart disease. After 30 minutes in a recumbent position, pharmacologic total autonomic blockade was attained using atropine and propranolol. Thereafter, increased systolic blood pressure with 0.4 microg/kg/min phenylephrine (designated as deltaBPphenyl) and decreased systolic blood pressure with 0.5 microg/kg/30 seconds of phentolamine (designated as deltaBPphent) were measured as indexes of alpha-adrenergic vascular sensitivity and activity, respectively. DeltaBPphenyl in the NMS group (70.0 +/- 37) was significantly less than that in C group (107 +/- 38, p <0.005). DeltaBPphent was significantly greater in the NMS group than in the C group (33.5 +/- 10 vs 21.0 +/- 14, p <0.005). Thus, decreased alpha-adrenergic vascular sensitivity and elevated alpha-adrenergic vascular tone were observed in patients with NMS. Although it is not known whether the mechanism causing NMS can be attributed to this abnormal alpha-adrenergic vascular response, the abnormality could at least contribute to augmenting the symptoms of NMS.