Human parvovirus B19 infection showing follicular purpuric papules with a baboon syndrome-like distribution.
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Humans↗
Biomedical subjects
A Iwasa
Publications and source records attributed to A Iwasa.
Effects of verapamil and lidocaine on two components of the re-entry circuit of verapamil-senstitive idiopathic left ventricular tachycardia.
OBJECTIVES: We characterized pharmacologically the slow conduction zone of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) with regard to the late diastolic potential (LDP). BACKGROUND: We showed that the slow conduction zone of ILVT could be divided into two components by LDP; that is, the distal component with a tachycardia-dependent conduction delay property and the proximal one without it. METHODS: Electrophysiologic studies were performed in eight consecutive patients. The LDP was recorded during left ventricular (LV) mapping during ILVT. Entrainment was performed from the right ventricular outflow tract while recording LDP. The effects of lidocaine (1 mg/kg body weight) and verapamil (0.5 or 1.0 mg) were examined during entrainment. RESULTS: The LDPs preceding the Purkinje potential (PP) were serially recorded from the upper third to the middle of the LV septum along the narrow longitudinal line. The ventricular tachycardia (VT) cycle length increased after lidocaine (p < 0.05), and further after verapamil (p < 0.05). The increments in the VT cycle length after administration of the drugs strongly correlated with those in LDP-PP (r > 0.9 for both drugs). The interval from the ventricular potential to LDP was unchanged after administration of the drugs. In one patient, verapamil terminated VT by local conduction block between LDP and PP. The LDP-PP measured during entrainment increased after lidocaine, and further after verapamil, whereas the interval from the stimulus to LDP remained unchanged. CONCLUSIONS: The component distal to LDP is mainly calcium channel-dependent and partly depressed sodium channel-dependent. The proximal component is considered to be sodium channel-dependent (normal).
Adolescent↗
NO is involved in MCh-induced accentuated antagonism via type II PDE in the canine blood-perfused SA node.
The possible role of type II (cGMP-stimulated cAMP hydrolysis) phosphodiesterase (PDE) in the accentuated antagonism of muscarinic effects on heart rate during beta-stimulation via endogenous nitric oxide (NO) was evaluated. The canine isolated sinoatrial node preparation was cross circulated with arterial blood of a support dog. The sinoatrial rate of the preparation was 96 +/- 5 beats/min (n = 16) at control. Methacholine (MCh; 0.01-1 microg) injected into the right coronary artery in a bolus fashion caused dose-dependent decreases in sinoatrial rate. Under an intra-arterial infusion of isoproterenol (1 microM), resulting in approximately 50% increase in sinoatrial rate, MCh-induced decreases were markedly augmented from -18 +/- 3% to -44 +/- 4% at 0.3 mg of MCh. When N(G)-nitro-L-arginine methyl ester (100 microM) or N(G)-monomethyl-L-arginine (100 microM) were continuously infused, the augmented MCh-induced decreases in sinoatrial rate were significantly suppressed (-29 +/- 3% or -25 +/- 3%, respectively, P < 0.01). Pretreatment with either 3-isobutyl-1-methylxanthine (IBMX; 20 microM), a non-selective PDE inhibitor, or amrinone (20 microM), a selective type III (cGMP inhibited cAMP hydrolysis) PDE inhibitor, doubled the isoproterenol-induced increase in the sinoatrial rate. However, the augmented MCh-induced decreases in sinoatrial rate were significantly depressed by IBMX (from -23 +/- 5% to -14 +/- 1%, P < 0.01) but not by amrinone (to -20 +/- 3%). These results suggest that MCh-induced accentuated antagonism in the sinoatrial node pacemaker activity can be modulated by endogenous NO via an activation of the type II cyclic GMP-stimulated cAMP PDE.
Acetylcholine↗
Immunocytochemical localization of beta-citryl-L-glutamate in primary neuronal cells and in the differentiation of P19 mouse embryonal carcinoma cells into neuronal cells.
The immunocytochemical localization of beta-citryl-L-glutamate (beta-CG) in primary neuronal cells and in the differentiation of P19 cells was examined. 1: Cells with the morphological features of neurons in the primary culture were specifically stained with the anti-beta-CG antibody both in neurites and in the cell body. 2: The neuronal cells differentiated from P19 cells were distinctly stained with the anti-beta-CG antibody both in neurites and in the cell body, while the non-neuronal cells were not. 3: The concentration of beta-CG was low in the P19 cells, but increased significantly with the differentiation of P19 cells into neurons. It was shown that beta-CG was localized exclusively in neurons. These findings suggest that beta-CG plays functional roles in the differentiation and growth of neuron.
Animals↗
Electrogram characteristics indicative of a recurrent conduction site after ablation of the inferior vena cava-tricuspid annulus isthmus: a study in the canine blood-perfused atrioventricular preparation.
Analysis of the electrograms recorded along the ablation line can identify a recurrent conduction site after ablation of the isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA) for atrial flutter. The present study examined the relationship between the activation sequence and electrogram characteristics using a model of recurrent conduction in the isthmus. The canine heart was isolated (n=8) and cross-circulated with the arterial blood of a support dog. A plaque electrode was placed at the isthmus, and 42 bipolar electrograms (filtered and unfiltered) were recorded during pacing at 120beats/min from the lateral right atrium before and after creating a narrow gap by 2 discontinuous incisions from the TA to the IVC. All bipolar electrodes, with the cathode in the TA side and the anode in the IVC side, were placed perpendicular to the TA. Before creating the incisions, the wavefront (WF) from the pacing impulse traveled uniformly in the isthmus and almost in parallel to the TA, and the filtered electrogram at each site showed a single potential. After creating the incisions, the WF propagated through the gap and spread radially to the area distal to the incisions. In close proximity to the incision lines opposite to the pacing site, the WF advanced from the gap towards the TA and IVC perpendicularly to the TA. Filtered electrograms on the incision lines showed double or split potentials, whereas those on the gap showed a single or fractionated potential. In unfiltered electrograms recorded from the TA to the IVC in close proximity to the incision lines opposite the pacing site, reversal of electrogram polarity was noted at the gap. A single or fractionated potential between double potentials indicates a gap between lines of conduction block. Electrogram polarity reversal along the ablation line indicates the presence of 2 opposing WF arising from the gap.
Animals↗
Purification and characterization of factor VII inhibitor found in a patient with life threatening bleeding.
We recently observed a patient with acquired inhibitor-induced F.VII deficiency whose plasma level of F.VII was < 1.0%. However, the biochemical nature of the inhibitor has not yet been clarified. In the present study, we purified the F.VII inhibitor from the patient's plasma by using activated F.VII (F.VIIa)-conjugated gel and characterized the inhibitor. The results showed that the inhibitor comprised two kinds of antibodies: one was eluted with EDTA (antibody 1) and the other with glycine-HCl buffer (pH 2.3) (antibody 2) from the F.VIIa affinity gel. SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting analysis of these inhibitors demonstrated that both antibodies had features of immunoglobulin G1 (IgG1) with kappa and lambda-light chains. Antibody 1 bound to the immobilized F.VIIa with a high affinity in the presence of calcium ion, while antibody 2 bound to the F.VIIa very weakly and the binding was independent of calcium ion. Immunoblotting analysis demonstrated that antibody 1 bound to the light chain of F.VIIa after reduction with 2-mercaptoethanol, while it did not react with either the gamma-carboxyglutamic acid (Gla)-domainless light chain of F.VIIa or the heavy chain with the protease domain. Antibody 1 markedly inhibited the activity of tissue factor-F.VIIa complex. Based on these observations, it is suggested that F.VIIa autoantibody (antibody 1) recognizes the calcium-dependent conformation within or near the Gla domain and inhibits F.VIIa activity by interacting with the light chain.
Antibodies↗
Significance of late diastolic potential preceding Purkinje potential in verapamil-sensitive idiopathic left ventricular tachycardia.
BACKGROUND: Verapamil-sensitive idiopathic left ventricular tachycardia (VT) is due to reentry with an excitable gap. A late diastolic potential (LDP) is recorded during endocardial mapping of this VT, but its relation to the reentry circuit and significance in radiofrequency (RF) ablation remain to be elucidated. METHODS AND RESULTS: Sixteen consecutive patients with this specific VT were studied (12 men and 4 women; mean age, 32 years). In all patients, sustained VT was induced and during left ventricular endocardial mapping, LDP preceding Purkinje potential (PP) was recorded at the basal (11 patients), middle (3 patients), or apical septum (2 patients). The area with LDP recording was confined to a small region (0.5 to 1.0 cm2) in each patient and was included in the area where PP was recorded (2 to 3 cm2). The relative activation times of LDP, PP, and local ventricular potential (V) at the LDP recording site to the onset of QRS complex were -50.4+/-18.9, -15.2+/-9.6, and 3.0+/-13.3 ms, respectively. The earliest ventricular activation site during VT was identified at the posteroapical septum and was more apical in the septum than the region with LDP in every patient. In 9 patients, VT entrainment was done by pacing from the right ventricular outflow tract while recording LDP. During entrainment, LDP was orthodromically captured, and as the pacing rate was increased, the LDP-to-PP interval was prolonged, whereas stimulus-to-LDP and PP-to-V interval were constant. In 3 patients, the pressure applied to the catheter tip at the LDP region resulted in conduction block between LDP and PP and in VT termination. RF energy application at the LDP recording site successfully eliminated VT. CONCLUSIONS: LDP was suggested to represent the excitation at the entrance to the specialized area with a conduction delay in response to the increase in the rate within the critical slow conduction zone participating in the reentry circuit of this VT. LDP can be a useful marker for successful RF ablation for this VT.
Action Potentials↗
Prolonged nocturnal penile tumescence caused by epinastine.
PURPOSE: We report a case of prolonged nocturnal penile tumescence (NPT) caused by the antiallergic agent epinastine. METHODS/RESULTS: We measured NPT using Rigiscan-Plus (DacoMed, Minneapolis, MN, USA) with or without the patient having taken epinastine. CONCLUSIONS: Considering its pharmacological effects on cyclic nucleotides, epinastine may have an effect on erectile function.
Dibenzazepines↗
Atrial ectopy originating from the posteroinferior atrium during radiofrequency catheter ablation of atrioventricular nodal reentrant tachycardia.
Atrial ectopy sometimes appears during RF ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia (AVNRT). However, its origin, characteristics, and significance are still unclear. To examine these issues, we analyzed 67 consecutive patients with AVNRT (60 with slow-fast AVNRT and 7 with fast-slow AVNRT), which was successfully eliminated by RF ablation to the sites with a slow potential in 63 patients and with the earliest activations of retrograde slow pathway conduction in 4 patients. During successful RF ablation, junctional ectopy with the activation sequence showing H-A-V at the His-bundle region appeared in 52 patients (group A) and atrial ectopy with negative P waves in the inferior leads preceding the QRS and the activation sequence showing A-H-V at the His-bundle region appeared in 15 patients (group B). Atrial ectopy was associated with (10 patients) or without junctional ectopy (5 patients). Before RF ablation, retrograde slow pathway conduction induced during ventricular burst and/or extrastimulus pacing was more frequently demonstrated in group B than in group A (9/15 [60%] vs 1/52 [2%], P < 0.001). Successful ablation site in group A was distributed between the His-bundle region and coronary sinus ostium, while that in group B was confined mostly to the site anterior to the coronary sinus ostium. In group B, atrial ectopy also appeared in 21% of the unsuccessful RF ablations. In conclusion, atrial ectopy is relatively common during slow pathway ablation and observed in 8% of RF applications overall and 22% of RF applications that successfully eliminated inducible AVNRT. Atrial ectopy appears to be closely related to successful slow pathway ablation among patients with manifest retrograde slow pathway function.
Adult↗
Effects of pilsicainide and propafenone on vagally induced atrial fibrillation: role of suppressant effect in conductivity.
The effects of pilsicainide on vagally induced atrial fibrillation and on electrophysiological parameters were compared with those of propafenone in alpha-chloralose-anesthetized dogs. Conduction velocity, effective refractory period, wavelength, averaged atrial fibrillation cycle length and activation sequence in the right atrial free wall were determined before and after drug administration. Pilsicainide (2 mg/kg/5 min and 3 mg/kg/h)(n=10) or propafenone (2 mg/kg/15 min and 4 mg/kg/h)(n=10) was intravenously infused during stable atrial fibrillation sustaining > 30 min. Pilsicainide terminated atrial fibrillation in nine dogs, while propafenone did so in three (p < 0.01). After the drug, conduction velocity was suppressed more in the pilsicainide than in the propafenone group(p < 0.01). There was no difference in effective refractory period after drug between the two groups. Mean wavelength was prolonged from 46.0 to 70.4 mm in the pilsicainide group and from 45.0 to 110.8 mm in the propafenone (p < 0.01 vs. pilsicainide). Activation mapping during atrial fibrillation showed Type II or III atrial fibrillation as previously defined [Konings, K.T.S., Kirchhof, C.J.H.J., Smeets, J.R.L.M., Wellens, H.J.J., Penn, O.C., Allessie, M.A., 1994. High-density mapping of electrically induced atrial fibrillation in humans. Circulation. Vol. 89, pp. 511-521.] before the drug, and changed to Type I before atrial fibrillation termination. Thus, pilsicainide was more effective to terminate vagally induced atrial fibrillation than was propafenone despite a greater effect of propafenone than of pilsicainide on wavelength. In this canine atrial fibrillation model, the suppression of conduction velocity may play an important role in changing the activation pattern of atrial fibrillation and thus, terminating atrial fibrillation.
Animals↗
Slow potential-guided radiofrequency catheter ablation in atrioventricular nodal reentrant tachycardia: characteristics of the potential associated with successful ablation.
To examine the characteristics of Haïssaguerre's slow potential (SP) specific to effective catheter ablation of the slow pathway in AV nodal reentrant tachycardia, the properties of SP and its recording site were analyzed in 52 patients who underwent successful SP-guided ablation. The properties of SP included the ratio of the amplitude of SP to that of atrial potential (A)(SP/A), the SP duration, the interval between His-bundle potential (HP) and SP (HP-SP), the interval between A and SP (A-SP), the interval between SP and ventricular potential (V) (SP-V), and the ratio of A-SP to the interval between A and the V (A-SP/A-V). The SP recording site was determined by the ratio of the amplitude of A to that of V (A/V) and by the relative position of the ablation catheter on X ray (right anterior oblique projection), expressed as the ratio of the distance between the coronary sinus ostium and SP site to that between the coronary sinus ostium and HP recording site (relative SP position). Twenty-eight slow pathways were ablated with a single energy application, while the other 24 required applications > or = 2. In all successful applications, SP/A, SP duration, HP-SP, A-SP, SP-V, A-SP/A-V, A/V, and relative SP position were 51% +/- 25%, 28 +/- 5 ms, -11 +/- 9 ms, 57 +/- 25 ms, 68 +/- 13 ms, 46% +/- 9%, 15% +/- 13%, and 51% +/- 13%, respectively. A significant correlation was observed between the relative SP position and A-SP, and between the relative SP position and A-SP/A-V (r = 0.60 and 0.37, respectively), while it was not between the relative SP position and HP-SP, nor between the relative SP position and SP-V. When the characteristics of SP were comparatively analyzed between the effective and ineffective applications in 24 patients in whom applications > or = 2 were required, there was no difference observed in HP-SP, A-SP, SP-V, A-SP/A-V, and A/V. However, SP/A, SP duration, and the relative SP position in the effective applications were all greater than those in the ineffective ones (56% +/- 20% vs 35% +/- 18%, P < 0.001; 29 +/- 4 vs 26 +/- 5 ms, P < 0.01; and 52% +/- 15% vs 33% +/- 11%, P < 0.001, respectively). These results indicate that SP with an amplitude over a half of A amplitude and recorded at the mid-septum of the tricuspid annulus can be a marker for successful slow pathway ablation. Although the local atrial electrogram appears late as the SP recording site shifts to the lower position, the timing of SP relative to HP and V remained unchanged, suggesting that SP is independent of the local atrial activation.
Action Potentials↗
Influence of chronic nitric oxide inhibition of coronary blood flow regulation: a study of the role of endogenous adenosine in anesthetized, open-chested dogs.
The effect of chronic inhibition of endothelium-derived nitric oxide (NO) synthesis on the regulation of coronary blood flow (CBF) is yet to be elucidated. A chronic canine model of inhibited NO synthesis was created and the role of adenosine in the regulation of coronary blood flow in this model was examined. Dogs were fed a diet supplemented with 40 mg/kg per day N(G)-nitro-L-arginine methyl ester (L-NAME group, n=8) or a regular diet without L-NAME supplementation (control group, n=8) for 4 weeks. The experiments were performed in an anesthetized, open-chest state and the results were compared in the L-NAME and control groups. Chronic L-NAME treatment significantly increased arterial pressure. Neither basal CBF in the left anterior descending artery nor heart rate differed between the L-NAME and control groups. In the L-NAME group, the response of CBF to intracoronary acetylcholine and adenosine was blunted, but that to glyceryl trinitrate was not. In addition, myocardial reactive hyperemia following 20 sec coronary occlusion was blunted in the L-NAME group. During atrial pacing at a rate 60 beats/min faster than the sinus rate, CBF increased to a similar degree in the L-NAME and control groups, and systolic wall thickening (SWT) changed similarly in both groups. Intracoronary 8-phenyltheophylline (8-PT), an adenosine receptor blocker, decreased basal CBF in the L-NAME group but not in the control group. In the L-NAME group, pacing-induced increase in CBF was abolished and SWT deteriorated after 8-PT administration. Basal myocardial adenosine release was significantly increased in the L-NAME group compared with the control group. It is concluded that in anesthetized, open-chest dogs with chronic inhibition of NO synthesis, adenosine may play a compensatory role in the regulation of coronary blood flow, as concomitant blockade of adenosine causes deterioration of coronary circulation and cardiac function.
Acetylcholine↗
The upper turnover site in the reentry circuit of common atrial flutter.
The upper turnover site of the reentry circuit of common atrial flutter was examined with the uses of atrial activation mapping and extrastimulus techniques during atrial flutter. The findings suggest that it is anterior to the orifice of the superior vena cava, i.e., between the superior vena cava and tricuspid annulus.
Adult↗
Characteristics of slow conduction zone demonstrated during entrainment of idiopathic ventricular tachycardia of left ventricular origin.
Idiopathic ventricular tachycardia (VT) with the right bundle branch block pattern and left-axis deviation has been shown to be due to reentry, but the property of the slow conduction zone within the reentry circuit is little understood. In 7 patients (mean VT cycle length [CL]: 361 +/- 49 ms), rapid pacing from the right ventricular outflow tract was performed during VT while recording electrograms at the early activation site in the left ventricle and at the right ventricular apex; also, conduction times from the pacing site to these recording sits (St-A and St-B intervals, respectively) were measured. Both constant fusion (except for the last paced beat) and progressive fusion were seen in all patients, indicating VT entrainment. The left ventricular site was captured orthodromically with an St-A of 394 +/- 57 ms at the pacing CL of 351 +/- 47 ms during entrainment, while the right ventricular apex was captured directly with an St-B interval of 63 +/- 19 ms. The St-A interval was gradually prolonged with the shortening of the pacing CL, whereas the St-B interval remained unchanged. VT was interrupted in all patients at the pacing CL of 279 +/- 39 ms. The effects of intravenous lidocaine (1 mg/kg) and verapamil (1 mg) were examined in 5 and 7 patients, respectively. Neither drug terminated VT but the VT-CL was increased to 369 +/- 57 ms after lidocaine (p <0.05) and to 413 +/- 69 ms after verapamil (p <0.05) (p <0.05 vs after lidocaine). The St-A interval was significantly increased after lidocaine (p <0.05) and after verapamil (p <0.05), while the St-B interval remained unchanged. A significant correlation between changes in St-A interval and VT-CL after verapamil was noted (p <0.001). In conclusion, the slow conduction zone of this VT shows tachycardia-dependent conduction delay, and the mechanism of this slow conduction involves mainly calcium channel-dependent conduction and partly depressed sodium channel-dependent conduction.
Adolescent↗
[Management of atrioventricular tachycardia via left accessory pathway].
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Catheter Ablation↗
Clinical experience with the ACS RX Lifestream coronary dilatation catheter: a new low profile perfusion balloon catheter.
BACKGROUND: Although the use of the perfusion balloon catheter (PBC) has been widely accepted, there are some indicational limitations in percutaneous transluminal coronary angioplasty (PTCA). A new low profile perfusion balloon catheter, the ACS RX Lifestream Coronary Dilatation Catheter, was developed by Advanced Cardiovascular Systems, Inc. in which material and structures were improved to reduce previous limitations. PURPOSE AND STUDY DESIGN: In order to evaluate the ACS RX Lifestream Catheter's performance not only in PTCA but also in stent implantation, we used the catheter in 45 consecutive patients (male = 35, mean age 66 years) with combined use of 6F guiding catheter. Exclusions included total occlusions, long diffuse and acute MI lesions. There were 4 with Left Main Trunk Disease (LMTD), 15 with single vessel disease, 26 with multi-vessel disease, 20 with prior MI, 4 with prior CABG, and 10 with unstable angina. In bare stent procedures, a Johnson & Johnson metal stent was mounted on an ACS RX Lifestream Catheter previously used for predilation. Stent delivery and post-dilatation were performed using the same balloon. RESULTS: Forty-nine lesions in 45 cases (de novo lesion-31) including 7 of Type A, 15 of Type B1, 19 of Type B2, and 8 of Type C lesions were successfully dilated without any complications. Primary guiding catheter use was 6F in 40, 7F in 2 and 8F in 3 cases. The perfusion balloon was used alone in 30 cases and combined with stent placement in 15 cases. In 40 cases of 6F use, the ACS RX Lifestream Catheter could not cross the lesion in 3 cases at first attempt, of which 2 cases were successfully dilated with the balloon after predilatation with standard low-profile balloon catheters. Two cases with 7F use were bail-out cases after PTCA for long diffuse lesions. In one case of 8F guide use, flow patterns of ACS RX Lifestream Catheters and ACS RX Flowtrack Coronary Dilatation Catheters were examined with a flow-wire in the same lesion for comparison. All 15 stent cases performed using bare technique (10 with 6F, 2 with 7F and 3 with 8F guiding catheters) including 7 primary and 8 secondary use, were successful. Percent diameter stenosis pre-dilatation was 81% and 12.8% post-procedure. CONCLUSION: ACS RX Lifestream Catheter is a useful device in both PTCA and bare stent procedures. Consequently, it is possible to expand its indications to more difficult types of lesions.
Aged↗
High levels of expression of neuropeptide Y mRNA in human phaeochromocytomas.
1. Neuropeptide Y (NPY) gene expression in human phaeochromocytomas was investigated by measuring the levels of NPY mRNA and NPY-immunoreactivity (NPY-IR) in human phaeochromocytoma tissues in comparison with those in normal human adrenal tissues. 2. The amounts of NPY mRNA and NPY-IR in human phaeochromocytomas were 18 and 93 times higher, respectively, than those in normal adrenal glands. In contrast, beta-actin gene expression was similar in human phaeochromocytomas to that in normal adrenal glands. 3. The amount of NPY mRNA relative to total cellular RNA was 6-fold higher in phaeochromocytoma tissues than in normal human adrenal medulla, suggesting increased NPY gene expression in the tumour cells. 4. Induction of differentiation of PC12 rat phaeochromocytoma cells by compounds, such as dexamethasone and nerve growth factor, resulted in a marked increase in the NPY mRNA level. 5. These findings suggest that NPY gene expression is increased in well-differentiated human phaeochromocytoma cells. Its high level of expression could be responsible for the marked overproduction of NPY by this tumour.
Actins↗
An unusual foreign body in the urinary bladder.
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Adult↗