Biomedical subjects

Atsushi Iwasa

Publications and source records attributed to Atsushi Iwasa.

17 recordsLinked to original sources

PubMed2006

Cardiac-directed expression of adenylyl cyclase VI facilitates atrioventricular nodal conduction.

OBJECTIVES: The purpose of this study was to test the hypothesis that cardiac-directed expression of adenylyl cyclase VI (AC(VI)) facilitates atrioventricular (AV) nodal conduction. BACKGROUND: Cardiac-directed expression of AC(VI), unlike other strategies to increase cyclic adenosine monophosphate generation, reduces mortality in murine cardiomyopathy. Recent reports suggest that AC(VI) expression may also protect against lethal bradycardia. METHODS: We performed immunofluorescence staining for AC(VI) in the AV node of transgenic mice. We then performed electrophysiologic studies (EPSs) using a 1.7-F octapolar catheter at the AV junction in 11 transgenic AC(VI) mice and 14 control mice. RESULTS: Immunofluorescence staining revealed increased AC(VI) expression in the AV node of transgenic mice versus controls. During EPS, AV intervals approximated PR intervals (R2 = 0.99) and related linearly to atrial-to-His intervals (R2 = 0.98; both p < 0.0001). Thus, we studied AV intervals to avoid electrocardiogram pacing artifacts and inconsistent inscription of His bundle electrograms. At baseline, AC(VI) mice had shorter AV intervals (47 +/- 9 ms) than controls (57 +/- 11 ms; p = 0.02), despite similar sinus rates. In pacing, AV intervals were shorter in AC(VI) mice than controls for a wide cycle-length range (p < 0.01). The AC(VI) mice also had shorter AV Wenckebach cycle lengths (AC(VI): 114 +/- 12 ms; control: 131 +/- 28 ms; p = 0.05) and ventriculo-atrial effective refractory periods (AC(VI): 97 +/- 21 ms; control: 127 +/- 15 ms; p = 0.05). We observed no differences between groups in sinus node function, and ventricular arrhythmias were not inducible. CONCLUSIONS: Cardiac-directed expression of AC(VI) facilitates AV nodal conduction without altering sinus node function. These results suggest the need to define a role for AC(VI) gene transfer in treating diseases of AV conduction.

Adenylyl Cyclases↗

PubMed2006

Effects of amiodarone on electrical and structural remodeling induced in a canine rapid pacing-induced persistent atrial fibrillation model.

Structural in addition to electrical remodeling may be induced by persistent atrial fibrillation per se and make atrial fibrillation refractory to antiarrhythmic drug therapy. Matrix metalloproteinases (MMPs) contribute to structural remodeling in the interstitial space. Amiodarone is effective in treating persistent atrial fibrillation compared with other antiarrhythmic drugs. In mongrel dogs, right atrial pacing at 540 beats/min (bpm) was performed along with ventricular pacing at 100 bpm for 6 weeks after atrioventricular node ablation. Right atrial pacing at 400 bpm was continued for 4 weeks with (n=5) or without (n=5) oral amiodarone (30 mg/kg/day). In sham dogs, only ventricular pacing was done with (n=4) or without (n=6) amiodarone. In atrial pacing without amiodarone group, electrical remodeling characterized by monophasic action potential duration shortening, loss of action potential duration-rate adaptation and depressed conduction velocity and structural remodeling characterized by slightly but significantly increased interstitial fibrosis and enhanced MMP-2 activity compared with sham group were observed, and sustained atrial fibrillation was easily induced. In atrial pacing with amiodarone group, both electrical and structural remodeling were reversed and sustained atrial fibrillation was not induced. In sham group with amiodarone, action potential duration prolongation and depressed conduction velocity compared with sham without amiodarone were observed, but either increased fibrosis or enhanced MMP-2 activity was not observed. Not only electrical but structural remodeling were induced in a canine persistent atrial fibrillation model. Amiodarone reversed both of them, which may be related to its high efficacy in preventing recurrence of persistent atrial fibrillation.

Action Potentials↗

PubMed2006

Accumulation of risk factors increases risk of thromboembolic events in patients with nonvalvular atrial fibrillation.

BACKGROUND: Accumulation of risk factors could increase thromboembolic event rates in patients with nonvalvular atrial fibrillation (NVAF). To validate this hypothesis, a post hoc analysis was performed to determine the relationship of risk levels and thromboembolic events in patients with NVAF from our previous prospective study. METHODS AND RESULTS: Risk levels were quantified using the CHADS2 index in 509 patients with NVAF (66.3+/-10.3 years old). One point each was given for patients with advanced age (>or=75 years), hypertension, congestive heart failure, and diabetes mellitus, and 2 points, to those with prior ischemic stroke or transient ischemic attack. Patients with a CHADS2 score of 0 were classified as low risk, 1 to 2 a moderate risk and 3 or more were high risk. Because hypertrophic cardiomyopathy had emerged as an independent risk factor for thromboembolism, the original CHADS2 score was modified by adding 1 point to patients with hypertrophic cardiomyopathy. Warfarin was given to 263 patients (mean international normalized ratio (INR) at enrollment, 1.86), antiplatelets (aspirin or ticlopidine) to 163 patients and no antithrombotic therapy to 83. During a mean follow-up period of 2 years, 31 thromboembolic events occurred. As the risk level (modified CHADS2 score) increased, the event rate increased for both the patient groups receiving warfarin (p=0.035) and those not receiving warfarin (p=0.048). When a thromboembolic event occurred in patients who had been treated with warfarin, the mean INR level was 1.41. Twelve (75%) of 16 patients complicated with thromboembolism during warfarin treatment had INR levels below the optimal levels (1.6-2.6) for Japanese patients. CONCLUSION: Accumulation of risk factors could increase risk of thromboembolic events in patients with NVAF. Adherence to the guidelines for anticoagulation therapy is recommended.

Aged↗

PubMed2005

D-dimer level influences thromboembolic events in patients with atrial fibrillation.

BACKGROUND: Elevated coagulative molecular markers could reflect the prothrombotic state in the cardiovascular system of patients with non-valvular atrial fibrillation (NVAF). A prospective, cooperative study was conducted to determine whether levels of coagulative markers alone or in combination with clinical risk factors could predict subsequent thromboembolic events in patients with NVAF. METHODS: Coagulative markers of prothrombin fragment 1+2, D-dimer, platelet factor 4, and beta-thromboglobulin were determined at the enrollment in the prospective study. RESULTS: Of 509 patients with NVAF (mean age, 66.6 +/- 10.3 years), 263 patients were treated with warfarin (mean international normalized ratio, 1.86), and 163 patients, with antiplatelet drugs. During an average follow-up period of 2.0 years, 31 thromboembolic events occurred. Event-free survival was significantly better in patients with D-dimer level < 150 ng/ml than in those with D-dimer level>or==150 ng/ml. Other coagulative markers, however, did not predict thromboembolic events. Age (>or==75 years), cardiomyopathies, and prior stroke or transient ischemic attack were independent, clinical risk factors for thromboembolism. Thromboembolic risk in patients without the clinical risk factors was quite low (0.7%/year) when D-dimer was < 150 ng/ml, but not low (3.8%/year) when D-dimer was >or==150 ng/ml. It was >5%/year in patients with the risk factors regardless of D-dimer levels. This was also true when analyses were confined to patients treated with warfarin. CONCLUSIONS: D-dimer level in combination with clinical risk factors could effectively predict subsequent thromboembolic events in patients with NVAF even when treated with warfarin.

Aged↗

PubMed2005

"V-H-A Pattern" as a criterion for the differential diagnosis of atypical AV nodal reentrant tachycardia from AV reciprocating tachycardia.

BACKGROUND: During ventricular extrastimulation, His bundle potential (H) following ventricular (V) and followed by atrial potentials (A), i.e., V-H-A, is observed in the His bundle electrogram when ventriculo-atrial (VA) conduction occurs via the normal conduction system. We examined the diagnostic value of V-H-A for atypical form of atrioventricular nodal reentrant tachycardia (AVNRT), which showed the earliest atrial activation site at the posterior paraseptal region during the tachycardia. METHODS: We prospectively examined the response of VA conduction to ventricular extrastimulation during basic drive pacing performed during sinus rhythm in 16 patients with atypical AVNRT masquerading atrioventricular reciprocating tachycardia (AVRT) utilizing a posterior paraseptal accessory pathway and 21 with AVRT utilizing a posterior paraseptal accessory pathway. Long RP' tachycardia with RP'/RR > 0.5 was excluded. The incidences of V-H-A and dual AV nodal physiology (DP) were compared between atypical AVNRT and AVRT. RESULTS: V-H-A was demonstrated in all the 16 patients (100%) in atypical AVNRT and in only 1 of the 21 (5%) in AVRT (P < 0.001). DP was demonstrated in 10 patients (63%) in atypical AVNRT and in 4 (19%) in AVRT (P < 0.05). The sensitivity of V-H-A for atypical AVNRT was higher than that of DP (P < 0.05). Positive and negative predictive values were 94% and 100%, respectively, for V-H-A and 71% and 74%, respectively, for DP. CONCLUSIONS: The appearance of V-H-A during ventricular extrastimulation is a simple criterion for differentiating atypical AVNRT masquerading AVRT from AVRT utilizing a posterior paraseptal accessory pathway.

Adolescent↗

PubMed2005

Abnormal heart rate turbulence predicts the initiation of ventricular arrhythmias.

BACKGROUND: Abnormal heart rate turbulence (HRT) reflects autonomic derangements predicting all-cause mortality, yet has not been shown to predict ventricular arrhythmias in at-risk patients. We hypothesized that HRT at programmed ventricular stimulation (PVS) would predict arrhythmia initiation in patients with left ventricular dysfunction. METHODS: We studied 27 patients with coronary disease, left ventricular ejection fraction (LVEF) 26.7 +/- 9.1%, and plasma B-type natriuretic peptide (BNP) 461 +/- 561 pg/mL. Prior to arrhythmia induction at PVS, we measured sinus cycles after spontaneous or paced premature ventricular contractions (PVCs) for turbulence onset (TO; % cycle length change following PVC) and slope (TS; greatest slope of return to baseline cycle). T-wave alternans (TWA) was also measured during atrial pacing. RESULTS: At PVS, abnormal TO (> or =0%) predicted inducible ventricular tachycardia (VT; n = 10 patients; P < 0.05). TO was greater in inducible than in noninducible patients (2.3 +/- 3.1% vs -0.02 +/- 2.8%, P < 0.05) and correlated with LVEF (P < 0.05) but not with BNP. TS did not differ between groups. Conversely, ambulatory HRT differed significantly from HRT at PVS (TO -0.55 +/- 1.08% vs 0.85 +/- 3.02%, P < 0.05; TS 2.63 +/- 2.09 ms/RR vs 8.70 +/- 6.56 ms/RR, P < 0.01), and did not predict inducible VT but trended (P = 0.05) to predict sustained VT on 739 +/- 179 days follow-up. TWA predicted inducible (P < 0.05) and spontaneous (P = 0.0001) VT but did not co-migrate with HRT. CONCLUSIONS: Abnormal HRT measured at PVS predicted the induction of sustained ventricular arrhythmias in patients with ischemic cardiomyopathy. However, HRT at PVS did not correlate with ambulatory HRT, nor with TWA, both of which predicted spontaneous ventricular arrhythmias. Thus, HRT may reflect the influence of autonomic milieu on arrhythmic susceptibility and is likely complementary to traditional arrhythmic indices.

Aged↗

PubMed2004

Efficacy of a microwave antenna for ablation of the tricuspid valve--inferior vena cava isthmus in dogs as a treatment for type 1 atrial flutter.

INTRODUCTION: Radiofrequency catheter ablation of the tricuspid valve-inferior vena cava (TV-IVC) isthmus for treatment of atrial flutter (AFL), may in some cases require a large number of energy applications and a long procedure and fluoroscopy time. AIMS OF STUDY: Therefore, we studied the safety and efficacy of a 4 cm long microwave antenna mounted on a steerable 9Fr catheter for linear ablation of the TV-IVC isthmus. METHODS: In 6 anesthetized dogs, multi-electrode catheters were positioned in the coronary sinus (decapolar), at the His bundle (quadripolar) and around the TV annulus (decapolar) for pacing and recording atrial activation sequences before and after ablation. The microwave antenna was then positioned across the TV-IVC isthmus from the TV annulus (identified by equal A and V potentials) to the inferior vena cava with slight traction on the catheter to ensure adequate endocardial contact. Microwave energy was then applied at a fixed power for 120 seconds during each ablation attempt. Ablation was repeated until bi-directional isthmus block was demonstrated during pacing from the coronary sinus ostium and low lateral right atrium, respectively. RESULTS: Linear microwave ablation of the TV-IVC isthmus was completed in all ten dogs using a total of 2.6 +/- 1.17 energy applications per dog. Power was applied in a range of 45-50 watts. There were no acute procedural complications. Bi-directional TV-IVC isthmus block was achieved in all ten dogs, as demonstrated by a strictly descending activation wavefront in the ipsilateral atrial wall, during pacing from the CSO and LLRA respectively. In addition, after ablation conduction time to the LLRA during pacing from the CSO increased from 52 +/- 16.62 before to 87 +/- 12.74 msec (p <.05), and to the CSO during pacing from the LLRA from 51 +/- 12.43 before to 79.50 +/- 9.85 msec (p <.05). Gross and histological examination of the TV-IVC isthmus after ablation revealed continuous transmural lesions, ranging from 3-5 mm in width, spanning the entire TV-IVC isthmus in all ten dogs. CONCLUSIONS: (1) Microwave ablation of the TV-IVC isthmus was safe and effective in this study. (2) Ablation of the entire width and thickness of the TV-IVC isthmus can be rapidly achieved using a long microwave antenna in a fixed trans-isthmus position.

Animals↗

PubMed2004

Effects of anticoagulation intensity on hemostatic markers in patients with non-valvular atrial fibrillation.

BACKGROUND: Elevation of hemostatic markers may account for the increased risk of ischemic stroke in patients with non-valvular atrial fibrillation (NVAF). The aim of this study was to determine the effects of anticoagulation intensity on hemostatic markers in patients with NVAF. METHODS AND RESULTS: In 509 patients with NVAF, comprising 263 patients treated with warfarin and 246 patients without warfarin, the hemostatic markers of prothrombin fragment F1.2 (F1.2), fibrin D-dimer, platelet factor 4 (PF4), and beta-thromboglobulin were determined and compared with those in 111 patients with sinus rhythm. F1.2 was inversely related with anticoagulation intensity and D-dimer increased with age. All hemostatic markers, except F1.2, were greater in patients with NVAF than in patients with sinus rhythm. F1.2 and D-dimer were significantly lower in patients with international normalized ratio (INR) > or =1.5 than in NVAF patients without warfarin and were not different between NVAF patients with INR of 1.5-1.9 and with INR > or =2.0. CONCLUSIONS: Low intensity of anticoagulation (INR 1.5-1.9) suppresses the elevated concentration of F1.2 and D-dimer in patients with NVAF, and might be favorable in Japanese patients with NVAF in view of the balance between prevention of thromboembolism and the adverse effect by warfarin (ie, bleeding).

Adult↗

PubMed2004

Attitudes of Japanese cardiologists toward anticoagulation for nonvalvular atrial fibrillation and reasons for its underuse.

BACKGROUND: Although warfarin reduces embolic events in patients with nonvalvular atrial fibrillation (NVAF), it is used less frequently in Japan and so the aim of the present study was to determine the attitudes of Japanese cardiologists toward antithrombotic therapy for NVAF patients. METHODS AND RESULTS: Subjects were NVAF patients enrolled in a prospective study in 1999. Clinical characteristics, type of NVAF and antithrombotic therapy, risk factors for embolism, and contraindications to warfarin were analyzed. Risk factors included advanced age (>75 years), hypertension, diabetes mellitus, congestive heart failure, and prior embolic events. Contraindications to warfarin included bleeding tendency, malignant tumors and others. Among 509 patients (66.6+/-10.3 years old), 359 had at least one risk factor for embolism and of these 359 patients, 200 (55.7%) received warfarin (ie, modest adherence to the guideline for antithrombotic therapy). There were 159 patients who had at least one risk factor but did not receive warfarin; 70.4% of these received antiplatelet drugs. Contraindications were found in only 22.6% and paroxysmal nature of NVAF seemed a possible reason for non-use of warfarin in 47.2% of 159 patients. CONCLUSIONS: In Japan warfarin is not used extensively for treatment of NVAF patients having risk factors and the reasons for not using antithrombotic therapy seemed inappropriate in most of patients.

Anticoagulants↗

PubMed2003

Mechanism of ST elevation and ventricular arrhythmias in an experimental Brugada syndrome model.

BACKGROUND: Although phase 2 reentry is said to be responsible for initiation of ventricular tachycardia (VT) in Brugada syndrome, information about the activation sequence during VT is limited. METHODS AND RESULTS: We developed an experimental Brugada syndrome model using a canine isolated right ventricular preparation cross-circulated with arterial blood of a supporter dog and examined the VT mechanism. Two plaque electrodes (35x30 mm) containing 96 bipolar electrodes were attached to the endocardium and epicardium. Saddleback and coved types of ST elevation in transmural ECG were induced by pilsicainide, a pure sodium channel blocker, and pinacidil, a KATP channel opener. Eighteen polymorphic VT episodes were recorded in 9 of the 12 preparations associated with ST elevation. Fourteen episodes spontaneously developed in 5 preparations after an extrasystole during basic drive pacing. Analysis of local recovery times revealed increased dispersion especially in epicardium, and the extrasystole originated from a site with a short recovery time, suggesting that phase 2 reentry was its mechanism. The other 4 VTs in 4 preparations were induced by premature stimulation. Analysis of the activation sequences during VT revealed reentry between epicardium and endocardium or reentry around an arc of a functional block confined to epicardium or endocardium with bystander activation of the other. CONCLUSIONS: Electrical heterogeneity in the recovery phase was induced in this experimental Brugada syndrome model, which can be a substrate for the development of phase 2 reentry and the subsequent reentry around an arc of the functional block, resulting in sustained VT.

Animals↗

PubMed2003

Impaired longitudinal conduction in crista terminalis is necessary for sustenance of experimental atrial flutter.

Sustained atrial flutter (AFL) can be induced by creating a lesion between the vena cava in dogs. In previous studies on this model, the crista terminalis (CT) was often injured, and thus, role of CT in sustained reentry was not well understood. We hypothesized that impaired longitudinal conduction in CT is necessary for sustained AFL. In 16 anesthetized, open-chest dogs, linear radiofrequency ablation of the intercaval region was performed without interrupting CT. Intra-atrial conduction times (IAT) along CT were measured using a plaque electrode (25x35 mm) containing 30 bipolar electrodes before and after additional ablation of CT (group A, n=10) or the pectinate muscle (PM) region (group B, n=6). In group A, IAT along CT was 27 +/- 5 ms at baseline and was increased to 43 +/- 3 ms after ablation of CT (P<0.001). In group B, IAT along CT was 28 +/- 4 ms at baseline and 27 +/- 3 ms after ablation of PM (P=NS). Sustained AFL lasting >20 minutes was induced in 10/10 dogs in group A only after additional ablation of CT, and in 0/6 dogs in group B (P<0.001). The cycle lengths of AFL after ablation of the intercaval region and additional ablation of CT were 119 +/- 14 and 140 +/- 14 ms, respectively (P<0.01). There was a significant positive correlation between the cycle length of AFL and IAT along CT (r2=0.63, P<0.001). These results indicate that longitudinal conduction property in CT and not in PM strongly affects sustenance of AFL in this model.

Analysis of Variance↗

PubMed2003

Identification of pulmonary vein potentials by differential site atrial pacing in patients with paroxysmal atrial fibrillation: enhanced detection by pulmonary vein pacing.

INTRODUCTION: Pulmonary vein (PV) isolation may cure paroxysmal atrial fibrillation (PAF); however, identification of PV potentials may be difficult in sinus rhythm. Studies have suggested that atrial pacing may improve the identification of PV potentials. METHODS AND RESULTS: In 25 consecutive patients who underwent PV isolation for PAF, the results of pacing from the distal PV, distal and proximal coronary sinus, and high right atrium compared to sinus rhythm were analyzed to determine the most effective pacing site for identification of PV potentials. The percentage of confirmed PV potentials and the longest interval between atrial and PV potentials in each PV were compared during differential site pacing and sinus rhythm. PV potentials were confirmed in 63 (82%) of 77 PVs that could be mapped during the complete pacing protocol and during sinus rhythm. Distal PV pacing identified significantly more PV potentials (left upper pulmonary vein [LUPV] 100%, left lower pulmonary vein [LLPV] 84%, right upper pulmonary vein [RUPV] 80%, right lower pulmonary vein [RLPV] 53%) compared to other pacing sites and sinus rhythm. Among atrial pacing sites, those ipsilateral to the PV being mapped were the most effective for identifying PV potentials. The intervals between atrial and PV potentials were significantly longer during distal PV pacing than pacing at other sites (LUPV 81.6 +/- 26.2 ms, LLPV 61.4 +/- 26.1 ms, RUPV 59.7 +/- 33.2 ms, RLPV 39.7 +/- 26.7 ms). CONCLUSION: (1) Distal PV pacing was most effective for identifying PV potentials. (2) The interval between atrial and PV potentials was longest during distal PV pacing.

Atrial Fibrillation↗

PubMed2003

Effect of allopurinol pretreatment on free radical generation after primary coronary angioplasty for acute myocardial infarction.

Allopurinol, an inhibitor of xanthine oxidase, was shown to improve the regional ventricular function after coronary artery occlusion and reperfusion in animal models. The effects of oral administration of allopurinol on a transient increase in free radical generation after primary percutaneous transluminal coronary angioplasty (PTCA) in patients with acute myocardial infarction (AMI) and on their clinical outcomes were examined. Thirty-eight AMI patients undergoing primary PTCA were randomly assigned to control (group 1, n = 20) and allopurinol treatment groups (group 2, n = 18). Allopurinol (400 mg) was administered orally just after the admission (approximately 60 min before reperfusion). Free radical production was assessed by successive measurement of urinary excretion of 8-epi-prostaglandin F(2alpha) (PGF(2alpha)) after PTCA. Urinary 8-epi-PGF(2alpha) excretion was increased by twofold at 60-90 min after PTCA compared with the baseline value in group 1. This increase was completely inhibited in group 2. Plasma allopurinol concentration was 1,146 +/- 55 ng/ml in group 2 when reperfusion was achieved. Slow flow in the recanalized coronary artery after PTCA occurred less frequently in group 2 than in group 1. Cardiac index determined just after reperfusion and left ventricular ejection fraction at 6 months after PTCA were both significantly greater in group 2 than in group 1 although pulmonary capillary wedge pressure was similar in the two groups. In conclusion, allopurinol pretreatment is effective in inhibiting generation of oxygen-derived radicals during reperfusion therapy and the recovery of left ventricular function in humans.

Administration, Oral↗

PubMed2003

Bioavailable testosterone with age and erectile dysfunction.

PURPOSE: Symptoms of partial androgen deficiency of the aging male (PADAM), such as sexual dysfunction and depression, are receiving increased attention. Currently bioavailable testosterone (BT) is considered the most reliable marker for establishing the presence of hypogonadism. We clarified the relationship between BT and other hormones with respect to patient age and PADAM symptoms. MATERIALS AND METHODS: A total of 130 patients who visited our special clinics for sexual function were included in this study. Endocrinological profiles were evaluated as appropriate, and sexual dysfunction and depression as symptoms of PADAM were assessed by a self-reported questionnaire. The relationship between age and several measures of testosterone, between BT and other hormonal measures, and between BT and PADAM symptoms were analyzed. RESULTS: Although serum total testosterone did not decrease with age, sex hormone binding globulin increased significantly. BT and free testosterone decreased significantly, and total and free testosterone correlated significantly with BT. The International Index of Erectile Function-5 score for erectile function increased significantly with increases in BT. However, the relationship between the depression score and BT was not significant. CONCLUSIONS: We consider that BT is a useful marker for diagnosing and treating patients with PADAM because BT correlates significantly with age and International Index of Erectile Function-5 scores. We emphasize that measuring serum testosterone is necessary in aging males.

Adult↗

PubMed2002

The clinical studies of sildenafil for the ageing male.

Erectile dysfunction (ED) represents an important quality-of-life issue for many ageing men. Low serum testosterone level and other factors may be involved. Sildenafil is effective and well tolerated in patients with ED of various aetiologies, showing an efficacy of about 75%. However, few efficacy and adverse effect studies have focused specially on ageing men. In 150 patients below 65 years and 44 patients over 65 years, sildenafil was used to treat ED. Efficacy in the younger group (89.1%) was greater than in the older group (65.7%; p < 0.01). Mean serum luteinizing hormone (LH) and follicle-stimulating hormone concentrations (11.0 and 18.9 mIU/mL, respectively) in the older group were higher than in younger group (5.2 and 8.7 mIU/mL, respectively; p < 0.01). Serum testosterone and prolactin (PRL) were similar between groups. Older patients showed higher prevalence of diabetes mellitus, hypertension, and benign prostatic hyperplasia. Only diabetes appeared to decrease efficacy of sildenafil in older patients (p=0.019). A high prevalence of diabetes might be one of the many causes of lower efficacy rate of sildenafil in older men, although efficacy in patients even without diabetes in older men was relatively low. Sildenafil can be used safely and it is still effective for ageing male, because nearly two-thirds of our older subjects had a good response to the drug and no adverse effect was specific to older patients.

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed2002

Atrial activation sequence during junctional tachycardia induced by thermal stimulation of Koch's triangle in canine blood-perfused atrioventricular node preparation.

Junctional tachycardia is observed during radiofrequency ablation of the slow pathway. The authors investigated the atrial activation sequence during junctional tachycardia induced with thermal stimulation in canine blood-perfused atrioventricular node (AVN) preparation. The canine heart was isolated (n = 7) and cross-circulated with heparinized arterial blood of the support dog. The activation sequence in the region of Koch's triangle (15 x 21 mm) was determined byrecording 48 unipolar electrograms. Atrial sites anterior to the coronary sinus ostium (site AN), close to the His-potential recording site (site N) and superior to site N (site F), were subjected to a continuous temperature rise from 38 degrees C to 50 degrees C with a heating probe. The temperature of the tissue adjacent to the heating site was monitored simultaneously. Junctional tachycardia at a rate of 92+/-12 beats/min with the His potential preceding the atrial one in the His-bundle electrogram was induced during thermal stimulation at site AN (temperature 42.1 degrees C+/-0.9 degrees C) in all seven preparations, whereas junctional tachycardia was induced during stimulation at site N in one and at site F in none. In each case, the temperature rose only at the site of stimulation. The earliest activation site during junctional tachycardia induced by site AN stimulation was at the His-potential recording site in five preparations and the middle of Koch's triangle in the other two. After creating an obstacle between sites AN and N, atrial tachycardia at a rate of 85+/-11 beats/min was induced during site AN stimulation. The earliest activation site during this tachycardia was site AN. Thus, junctional tachycardia induced by thermal stimulation was suggested to originate from the AN thermal stimulation site. The impulse from the stimulation site appeared to conduct via the posterior input to the compact AVN and junctional tachycardia was generated. When the posterior input was interrupted, atrial tachycardia was generated.

Animals↗

PubMed2002

Left ventricular outflow tract tachycardia originating from the right coronary cusp: identification of location of origin by endocardial noncontact activation mapping from the right ventricular outflow tract.

Idiopathic left ventricular outflow tract (LVOT) tachycardia has been shown to originate from a supravalvular site in some patients. Considerable attention recently has focused on identifying this variant of LVOT tachycardia on 12-lead ECG. We report the case of 15-year-old boy in whom a noncontact three-dimensional mapping electrode deployed in the right ventricular outflow tract (RVOT) assisted in identifying a supravalvular LVOT tachycardia. Observation of two early breakthrough sites in the RVOT and right ventricular septum suggested a right aortic cusp origin of the tachycardia. Pace mapping in the right aortic cusp identified a successful ablation site.

Adolescent↗