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Using high-fidelity micromanometers and flow velocity sensors at right heart catheterization, we compared pulmonary hemodynamics and wave reflections in age-matched normal adults and those with atrial septal defects, separated into three subgroups based on levels of mean pulmonary artery pressure: low (<17 mmHg), intermediate (17-26 mmHg), high (>26 mmHg). We made baseline measurements in all groups and after intravenous sodium nitroprusside in the subgroups. All of the subgroups had higher than normal baseline pulmonary flows and corresponding power that did not differ among the subgroups. The pulmonary vascular resistance, input resistance, and characteristic impedance in the subgroups did not differ from normal. Aside from the elevated flow and power, the hemodynamics in the low subgroup did not differ from normal. The intermediate subgroup had significantly higher than normal right ventricular and pulmonary artery pressures, wave reflections, and shorter wave reflection time, which all reverted to normal after nitroprusside. The high subgroup had similar changes as the intermediate subgroup. Unlike that subgroup, however, the pressures, wave reflections, and reflection return time did not revert to normal after nitroprusside. Hence, elevated wave reflections, but not resistance or characteristic impedance, are the hallmark of pulmonary hypertension in adults with atrial septal defects. Our results demonstrate that detailed measurements of hemodynamics and assessment of responsiveness to vasodilators provide important information about the pulmonary circulation in atrial septal defect. Coupled with studies after defect closure, those results may be a better foundation than current ones for clinical decisions.

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Compared to age-matched normotensive adults, those with essential hypertension have been shown to have distinct arterial hemodynamic abnormalities consisting of increased peripheral resistance, pulse wave velocity, and wave reflection magnitude as well as decreased wave reflection time and aortic compliance. These abnormalities are further exacerbated by beta-adrenergic blockade. To see if there are similar hemodynamic abnormalities that antedate the onset of fixed hypertension, we compared age-matched normotensives with prehypertensives selected from patients undergoing diagnostic cardiac catheterization. Ascending aortic pressure and flow were measured with a micromanometer and flow velocity sensor in the baseline state and after beta-adrenergic blockade. In the baseline state the prehypertensive compared to the normotensive group had elevated blood pressure, resistance, left ventricular end-diastolic pressure (LVEDP), and wave reflections. Beta-adrenergic blockade increased resistance, LVEDP, and wave reflections in both groups. Some of these findings are the same as those we previously reported in young persons with established, essential hypertension. The differences in LVEDP and wave reflections, both in the baseline state and after beta-blockade, were still present in subgroups with no differences in blood pressure. Hence, the elevated wave reflections in prehypertensives do not appear to be directly related to the level of blood pressure. These results support the notion that the elevated blood pressure in hypertension may represent a later manifestation of an already abnormal vascular system rather than the vascular abnormalities resulting from hypertension. Consequently, even before blood pressure becomes elevated, early diagnosis and treatment of the vascular abnormalities in prehypertensives may be warranted.

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BACKGROUND: Previous studies have shown that the highest dominant frequency (DF) is located in the left atrium (LA) during atrial fibrillation (AF) in pacing-induced AF. However, there have been few studies on the mechanisms of the increased DF of AF during acute atrial dilatation. The purpose of this study was to investigate the mechanisms of the increased maximal DF (max DF) in pacing-induced AF during acute atrial dilatation. METHODS: In eight Langendorff-perfused canine hearts (26 +/- 2 kg), noncontact balloon catheters were placed into the right atrium (RA) and LA, respectively. AF was induced by extrastimulation pre- and postdilatation in the atrium (0 and 15 cm H(2)O, respectively). Fast Fourier transformation analysis was performed to analyze the max DF and harmonic index (HI) from the bi-atrial unipolar virtual electrograms during AF. The fibrillation cycle lengths were obtained from different atrial sites. The number of wavefronts was analyzed during AF. The frequency of regional splitting was defined as the number of wavefront splits per second in different atrial regions during AF. The percentage of the low-voltage zones (<0.5 mV) was defined as the ratio of the area of the low-voltage zones to the total atrial surface area. RESULTS: The DF was measured during AF. The shortest fibrillation cycle length was located in the LA posterior wall and became shorter during acute atrial dilatation. The max DF was located in the LA posterior wall and increased during acute atrial dilatation (7.1 +/- 0.8 vs 8.8 +/- 2.1, P = 0.02). The max DF of the LA correlated with the wavefront number (r = 0.797, P < 0.001 predilatation; r = 0.860, P < 0.001 postdilatation). The splitting of wavefronts facilitated the formation of new wavefronts. During acute atrial dilatation, the frequency of regional splitting was closely correlated with the percentage of the low-voltage zones (r = 0.876, P < 0.001). Furthermore, the LA posterior wall had a higher percentage of the low-voltage zones than the other sites. CONCLUSION: In acute atrial dilatation, the percentage of the low-voltage zones increased, especially in the LA posterior wall, which correlated with the regional splitting of the AF wavefronts. The increase in the splitting facilitated the formation of new wavefronts and resulted in a higher max DF during acute atrial dilatation.

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OBJECTIVES: This study was aimed at evaluating the efficacy of non-contact mapping and ablation of non-incisional atypical right atrial (RA) flutters. BACKGROUND: The majority of atypical RA flutters were reported in patients after surgical incision of the RA. METHODS: The study group consisted of 15 patients (61 +/- 13 years, 8 males) with atypical atrial flutter (AFL). The RA activation during AFL was delineated using a non-contact mapping system (EnSite 3000 with Precision Software, Endocardial Solutions, St. Paul, Minnesota). The narrowest part of each reentrant circuit was targeted using radiofrequency energy. RESULTS: In all 15 patients, non-contact mapping showed AFLs confined to the RA with RA activation time accounting for 100% of the cycle length (210 +/- 19 ms). During single-loop re-entry in seven patients, the activation wave front circulated around the central obstacle (CO) in the anterolateral wall with conduction through the channel between the CO and the crista terminalis (CT). During figure-of-eight re-entry in eight patients, simultaneous upper and lower loop re-entry through the conduction gap in the CT was found in four patients, and simultaneous upper loop and free-wall single-loop re-entry was observed in four patients. Radiofrequency ablation of the free-wall channel and/or CT gap was effective in eliminating these AFLs in 13 patients. During a follow-up of 16.8 +/- 3.8 months, two patients had recurrence of left AFL, and one had recurrence of atrial fibrillation. CONCLUSIONS: Atypical RA flutters could arise from single-loop or double-loop figure-of-eight re-entry. Radiofrequency ablation of the free-wall channel and/or the CT gap was effective in eliminating these arrhythmias.

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Transplanted renal artery stenosis (TRAS) is one of the major causes of poor blood pressure control, progressive renal dysfunction and finally renal graft failure in uremic patients receiving renal allograft transplantation. Percutaneous transluminal balloon angioplasty (PTA) with stenting is an effective treatment for TRAS but has rarely had validation for the ostial lesions of TRAS. We reported 2 patients developing drug-refractory hypertension along with impaired renal function who received PTA plus stent deployment therapy for severe ostial stenosis of graft renal artery. Both of the patients had improved allograft function gradually, and satisfactory blood pressure control after 3 months follow-up. In conjugation with balloon angioplasty, stenting could provide a safe and effective revascularization strategy in conjunction with balloon angioplasty for ostial lesions of TRAS.

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INTRODUCTION: The aim of this study was to delineate activation patterns around the crista terminalis (CT) using high-resolution noncontact mapping. METHODS AND RESULTS: Twenty-six patients with typical atrial flutter (20 counterclockwise and 6 clockwise) were enrolled in the study. A noncontact mapping system was used to map atrial flutter. There were three activation patterns around the line(s) of block. Type I (n = 6) showed activation around a single complete line of block located in the CT. Type II (n = 17) showed activation around a single incomplete line of block with a conduction gap in the CT. Type III (n = 3) showed activation around double lines of block, one located in the CT and the other located in the sinus venosa region. Simultaneous activation around the tricuspid annulus and through the CT gap could result in double loop reentry (n = 12). After successful ablation of the cavotricuspid isthmus (CTI) in 24 patients, upper loop reentry was still induced in 12 patients with double loop reentry. Subsequent ablation of the CT gap was performed successfully in these 12 patients, and no arrhythmia was inducible thereafter. During the follow-up period of 8.4 +/- 4.1 months, there was no recurrence of atrial flutter in any patient. CONCLUSION: During typical atrial flutter, the CT might be an incomplete barrier. Simultaneous conduction through the CTI and CT gap could result in double loop reentry. Radiofrequency ablation of the CTI and CT gap was effective in eliminating this arrhythmia.

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Electrochemical reactions between blood and metal electrodes have been studied since 1928. Little is known about the actual current density induced during the reaction. In this study, an in situ continuous monitoring method was developed to detect the progress of thrombosis on an oxidized 316L stainless steel coil was deployed inside the artery. Three stages of current density were observed on a 316L wire passivated with polycrystalline oxide film. In contrast, no significant current density was detected for a wire passivated with amorphous oxide film. Results showed that this in situ electrochemical monitoring method is sensitive to the passivated film on the stainless steel coil and could provide efficient and reliable information on the control of thrombosis on cardiovascular devices.

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INTRODUCTION: The incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction during AV nodal reentrant tachycardia has not been well reported. Among previous studies, controversy also existed about the site of the 2:1 AV block during AV nodal reentrant tachycardia. METHODS AND RESULTS: In patients with 2:1 AV block during AV nodal reentrant tachycardia, the incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction and change of electrophysiologic properties during spontaneous transition were analyzed. Among the 20 patients with 2:1 AV block during AV nodal reentrant tachycardia, a His-bundle potential was absent in blocked beats during 2:1 AV block in 8 patients, and the maximal amplitude of the His-bundle potential in the blocked beats was the same as that in the conducted beats in 4 patients and was significantly smaller than that in the conducted beats in 8 patients (0.49 +/- 0.25 mV vs 0.16 +/- 0.07 mV, P = 0.007). Spontaneous transition of 2:1 AV block to 1:1 AV conduction occurred in 15 (75%) of 20 patients with 2:1 AV block during AV nodal reentrant tachycardia. Spontaneous transition of 2:1 AV block to 1:1 AV conduction was associated with transient right and/or left bundle branch block. The 1:1 AV conduction with transient bundle branch block was associated with significant His-ventricular (HV) interval prolongation (66 +/- 19 ms) compared with 2:1 AV block (44 +/- 6 ms, P < 0.01) and 1:1 AV conduction without bundle branch block (43 +/- 6 ms, P < 0.01). CONCLUSION: The 2:1 AV block during AV nodal reentrant tachycardia is functional; the level of block is demonstrated to be within or below the His bundle in a majority of patients with 2:1 AV block during AV nodal reentrant tachycardia, and a minority are possibly high in the junction between the AV node and His bundle.

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Some patients with atrial fibrillation (AF) treated by antiarrhythmic drugs (AAD) can develop typical atrial flutter, but the mechanism is not clear. This study included 21 patients with AF. Group I (n = 7) had typical atrial flutter due to amiodarone therapy. Group II (n = 7) did not develop atrial flutter after amiodarone treatment. Group III (n = 7) did not receive AAD treatment. A 7 Fr, 20-pole electrode catheter was placed along the CT identified by fluoroscopy and intracardiac echocardiography. After restoration of the sinus rhythm, decremental pacing near the CT was performed until 2 to 1 atrial capture. Complete transverse conduction block was defined as the appearance of double potentials with opposite activation sequence along the CT. Focal transverse conduction delay was defined as the appearance of double potentials at > or = 2 recording sites. Focal transverse conduction delay was observed during pacing at the cycle length of 693 +/- 110 ms in group I, 360 +/- 97 ms in group II and 343 +/- 109 ms in group III (P = 0.001). Complete transverse conduction block was observed during pacing at the cycle length of 391 +/- 118 ms in group I and 231 +/- 23 ms in group II (P = 0.001), but not in group III. In conclusion, focal transverse conduction delay in the CT was common in patients with AF. A predisposition to the line of the conduction block in the CT might contribute to the conversion of AF to typical atrial flutter due to amiodarone therapy.

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The extraction of event-related oscillatory neuromagnetic activities from single-trial measurement is challenging due to the non-phase-locked nature and variability from trial to trial. The present study presents a method based on independent component analysis (ICA) and the use of a template-based correlation approach to extract Rolandic beta rhythm from magnetoencephalographic (MEG) measurements of right finger lifting. A single trial recording was decomposed into a set of coupled temporal independent components and corresponding spatial maps using ICA and the reactive beta frequency band for each trial identified using a two-spectrum comparison between the postmovement interval and a reference period. Task-related components survived dual criteria of high correlation with both the temporal and the spatial templates with an acceptance rate of about 80%. Phase and amplitude information for noise-free MEG beta activities were preserved not only for optimal calculation of beta rebound (event-related synchronization) but also for profound penetration into subtle dynamics across trials. Given the high signal-to-noise ratio (SNR) of this method, various methods of source estimation were used on reconstructed single-trial data and the source loci coherently anchored in the vicinity of the primary motor area. This method promises the possibility of a window into the intricate brain dynamics of motor control mechanisms and the cortical pathophysiology of movement disorder on a trial-by-trial basis.

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INTRODUCTION: High recurrence rate is still a major problem associated with ablation of paroxysmal atrial fibrillation (AF). Most of the recurrences occur within 6 months after ablation. The characteristics of very late recurrent AF (>12 months after ablation) have not been reported. METHODS AND RESULTS: Two hundred seven patients with drug-refractory AF underwent successful focal ablation or isolation of AF foci. After the first ablation procedure, Holter monitoring and event recorders were used to evaluate symptomatic recurrent AF. A second ablation procedure was recommended if the antiarrhythmic drugs could not control recurrent AF. During long-term follow-up (mean 30 +/- 11 months, up to 51 months), 70 patients had recurrent AF, including 13 patients (6%) with very late (>12 months) recurrent AF (group 1) and 57 patients (28%) with late (within 12 months after ablation) recurrent AF (group 2). Group 1 patients had a significantly lower incidence of multiple (> or = 2) AF foci (23% vs 63%, P = 0.02) than group 2 patients. In addition, the incidence of antiarrhythmic drugs use (38% vs 84%, P = 0.001) to maintain sinus rhythm after the first episode of recurrent AF was significantly lower in group 1 than group 2 patients, and the incidence of a second intervention procedure (8% vs 35%, P = 0.051) tended to be lower in group 1 than group 2 patients. CONCLUSION: The incidence of very late recurrent AF after ablation of paroxysmal AF is very low, and the clinical outcome of patients with very late recurrent AF is benign.

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BACKGROUND: Most of the ectopic beats initiating paroxysmal atrial fibrillation (PAF) originate from the pulmonary vein (PV). However, only limited data are available on PAF originating from the non-PV areas. METHODS AND RESULTS: Two hundred forty patients with a total of 358 ectopic foci initiating PAF were included. Sixty-eight (28%) patients had AF initiated by ectopic beats (73 foci, 20%) from the non-PV areas, including the left atrial posterior free wall (28, 38.3%), superior vena cava (27, 37.0%), crista terminalis (10, 3.7%), ligament of Marshall (6, 8.2%), coronary sinus ostium (1, 1.4%), and interatrial septum (1, 1.4%). Catheter ablation eliminated AF with acute success rates of 63%, 96%, 100%, 50%, 100%, and 0% in left atrial posterior free wall, superior vena cava, crista terminalis, ligament of Marshall, coronary sinus ostium, and interatrial septum, respectively. During a follow-up period of 22+/-11 months, 43 patients (63.2%) were free of antiarrhythmic drugs without AF recurrence. CONCLUSIONS: Ectopic beats initiating PAF can originate from the non-PV areas, and catheter ablation of the non-PV ectopy has a moderate efficacy in treatment of PAF.

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BACKGROUND: The aim of this study was to test the electrophysiological effects of continuous enhanced vagal tone on dual atrioventricular (AV) nodal and accessory pathways. METHODS AND RESULTS: This study included 10 patients with typical, slow-fast AV nodal reentrant tachycardia (AVNRT) and 10 patients with AV reciprocating tachycardia. Electrophysiological data were measured before and during continuous vagal enhancement by using phenylephrine infusion (0.6 to 1.5 microg/kg per min). For patients with AVNRT, during phenylephrine infusion, 1:1 conduction times over the anterograde fast and slow and retrograde fast pathways were prolonged (453+/-64 to 662+/-120 ms, P<0.001; 379+/-53 to 443+/-95 ms, P<0.05; 405+/-112 to 442+/-118 ms, P<0.05). The effective refractory period and functional refractory period of the anterograde fast pathway were prolonged with phenylephrine (394+/-73 to 544+/-128 ms, P<0.001; 454+/-60 to 596+/-118 ms, P<0.001). In contrast, the effective refractory period and functional refractory period of the anterograde slow and retrograde fast were not significantly changed. No significant change was observed in the conduction or refractoriness of the accessory pathways in patients with AV reciprocating tachycardia nor in atrial or ventricular refractoriness. CONCLUSIONS: Enhanced vagal tone produces disparate effects on the refractoriness of the slow and fast AV nodal conduction pathways, with the anterograde fast pathway being the most sensitive. These changes are conducive to induction of AVNRT with a premature atrial complex and may explain in part the relatively common occurrence of AVNRT during sleep or other periods of presumed increased parasympathetic tone.

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Recent evidence suggests that myocardial ischemia may occur in patients with neurally mediated syncope and normal coronary angiograms. This study was conducted to evaluate if coronary microvascular function is impaired in such patients. Coronary hemodynamic studies and head-up tilt table tests (HUTs) were performed on 30 consecutive patients with normal coronary angiograms and recurrent syncope. Another ten subjects with atypical chest pain and no evidence of myocardial ischemia or syncope served as a control. Great cardiac vein flow (GCVF) and coronary sinus flow (CSF) were measured by the thermodilution method at baseline and after dipyridamole infusion (0.56 mg/kg i.v. for 4 minutes). Coronary flow reserve (CFR), derived from CSF and GCVF, was significantly lower in the 15 patients with positive HUT than in the other 15 patients with negative HUT (1.75 +/- 0.48 vs 2.64 +/- 0.8, P < 0.01 and 2.29 +/- 0.45 vs 3.07 +/- 0.63, P < 0.01, respectively). Ischemic-like ECG was noted during treadmill exercise test in 40% of the former and in 7% of the latter group (P = 0.01). There was no significant difference in CFR between patients with negative HUT and control subjects. Coronary microvascular function was impaired in syncopal patients with positive HUT and relatively preserved in those with negative HUT, suggesting the possible linkage between coronary microvascular dysfunction and the development of neurally mediated syncope.

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BACKGROUND: Our understanding of genes that predispose to essential hypertension is poor. METHODS: A genome-wide scan for linkage at approximately 10 cM resolution was done on 1425 sibpairs of Chinese and Japanese origins that were concordant for hypertension (N = 661), low-normal blood pressure (BP) (N = 184), or discordant for BP (N = 580). RESULTS: There was no significant evidence of linkage to a single locus in the genome. There was suggestive evidence of linkage to chromosome 10p, with a LOD score of 2.5. CONCLUSIONS: We can exclude the possibility that a single gene accounts for at least 15% of the variance in hypertension in this population.

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BACKGROUND: Diabetes mellitus (DM) is one of the major risk factors of coronary artery disease (CAD). Both short- and long-term prognoses of plain old balloon angioplasty (POBA) are poorer in CAD patients with DM than in those without. Recent evidence indicates that coronary stenting significantly improves clinical results of POBA in CAD patients. However, the benefit of coronary stenting remains controversial in DM patients. The purpose of this study was to evaluate the acute and late clinical outcomes of coronary stenting as compared with POBA in diabetic patients with CAD in the real setting of our daily practice. METHODS: Between June 1997 and September 1998, more than 400 consecutive CAD patients receiving POBA with or without coronary stenting were evaluated. The patients were those who had definite clinical diagnosis of DM and received coronary intervention for the first time on their de novo, native lesion(s). Patients were divided into 2 groups according to POBA alone or balloon dilatation followed by coronary stenting. The immediate angiographic results and clinical outcomes, including major adverse cardiovascular events (MACE) as well as recurrent angina within 24 hours after the procedure (acute) and more than 6 months (late) after the procedure were evaluated in the both groups of patients. RESULTS: A total of 124 DM patients, aged 68 +/- 8 years with 85% male and 60% multivessel disease, were studied. There was no difference in baseline demographic data between those patients receiving POBA alone (POBA, n = 79) and in combination with coronary stenting (stent, n = 45). The minimal luminal diameter of the target lesion immediately after balloon dilatation was smaller in the stent group than in POBA group (1.36 +/- 0.67 vs. 1.96 +/- 1.31 mm, p < 0.001). However, the final luminal gain was much larger (1.60 +/- 0.64 vs. 0.80 +/- 0.88 mm, p < 0.001) and the acute event-free survival rate was higher (97.7% vs. 82.9%, p = 0.019) in stent group than in POBA group. While the percutaneous revascularization rate tended to be less in patients with stent than with POBA (31.8% vs. 49.3%, p = 0.08), the total late MACE rate was similar between both groups (50% vs. 64.7%, p = NS). However, the late event-free survival rates were significantly higher in stenting patients than in those with POBA (34.9% vs. 16.4%, p = 0.037). CONCLUSIONS: Diabetic patients with significant CAD were clinically found to be old and largely with multivessel disease for coronary intervention. The immediate angiographic results were better if treated with stenting than with POBA alone. Though the rate of late MACE was similarly high in both groups, coronary stenting rendered a better acute event-free survival rate and especially late event-free survival rate, suggesting its benefit for percutaneous coronary revascularization in diabetic patients.

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INTRODUCTION: Atrial dilatation may play an important role in the occurrence of atrial fibrillation (AF) in clinical situations. However, the electrophysiologic characteristics of dilated atria are still unclear. METHODS AND RESULTS: In 18 isolated Langendorff-perfused canine hearts (14.6 +/- 2.2 kg), we measured atrial effective refractory periods (ERPs) at four different sites, conduction velocity and percentage of slow conduction on the right atrium (using a high-density electrode plaque), and assessed the inducibility of AF at the baseline (0 cm H(2)O) and high (15 cm H(2)O) atrial pressure. The atrial ERPs did not change significantly, but the dispersion of ERP increased significantly (40 +/- 18 vs 25 +/- 9 vs ms, p = 0.01) during high atrial pressure. The percentage of slow conduction (< 25 cm/s) over the mapping area, and the inducibility of AF increased during high atrial pressure (23.7 +/- 10.2 % vs 32.1 +/- 12.5 %, p = 0.02). The AF inducibility significantly correlated with the ERP dispersion (R = 0.75, p < 0.001) and maximal percentage of slow conduction (R = 0.88, p < 0.001). Furthermore, ERPs were significantly shorter in the induced AF group than those without induced AF (68 +/- 17 vs 84 +/- 16 ms, P < 0.05). CONCLUSIONS: The increased inhomogenity in atrial electrophysiological properties during atrial dilatation contributed to the inducibility of AF.

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Angiotensin-converting enzyme (ACE) inhibition has been shown to improve clinical myocardial ischemia in patients with syndrome X (angina pectoris, positive treadmill exercise test, normal coronary angiograms, and no evidence of coronary spasm). This study was conducted to investigate the effects of long-term ACE inhibitors on endothelial nitric oxide (NO) metabolism and coronary microvascular function in patients with syndrome X. After a 2-week washout period, 20 patients with syndrome X were randomized to receive either enalapril, an ACE inhibitor, 5 mg twice daily (n = 10) or placebo (n = 10) in a double-blind design for 8 weeks. Another 6 age- and gender-matched subjects with negative treadmill exercise tests were also studied as controls. Compared with control subjects, patients with syndrome X had significantly reduced coronary flow reserve, reduced plasma levels of nitrate and nitrite (NOx), and a reduced plasma L-arginine to asymmetric dimethylarginine (ADMA) ratio (an index of systemic NO metabolism), as well as reduced endothelial function. These patients also had increased plasma levels of ADMA, which is an endogenous inhibitor of NO synthase and of von Willebrand factor, a marker of endothelial injury. Baseline characteristics including exercise performance and coronary flow reserve were similar between enalapril and placebo groups. After an 8-week treatment period, exercise duration (p = 0.001) and coronary flow reserve (p = 0.001) significantly improved with enalapril but not with placebo. Enalapril treatment, but not placebo, reduced plasma von Willebrand factor (p = 0.03) and ADMA levels (p = 0.01) and increased NOx levels (p = 0.01) and the ratio of L-arginine to ADMA (p <0.01). In patients with syndrome X, the plasma NOx level was positively and ADMA level inversely correlated with coronary flow reserve before and after the treatment. In conclusion, long-term ACE inhibitor treatment with enalapril improved coronary microvascular function as well as myocardial ischemia in patients with syndrome X. This may be related to the improvement of endothelial NO bioavailability with the reduction of plasma ADMA levels.

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The aim of the study was to define the factors that may predict the outcomes of radiofrequency ablation from the right ventricular outflow tract (RVOT) in patients with idiopathic VT with a QRS morphology of LBBB. Endocardial mapping and RF ablation from the RVOT were performed in 35 patients (14 men, mean age 41 +/- 14 years), and VT was successfully ablated in 30 patients. There was no significant difference with regard to clinical characteristics and electrophysiological findings between patients with successful and failed ablation. The VTs with successful ablation showed an rS (n = 16) or QS (n = 14) pattern in lead V1, and all five VTs with failed ablation showed an rS pattern in lead V1. Although the absence of an R wave in lead V1 did not differ between patients with successful and failed ablation (P = 0.13), the absence of an R wave in lead V1 predicted VT successfully ablated from the RVOT (positive predictive value 100%; negative predictive value 24%). The VTs with successful ablation had a median precordial transitional zone at lead V4 (range V3-V6), whereas all five VTs with failed ablation had precordial transition zones at lead V3 (P = 0.004). Furthermore, a presence of an R wave in lead V1 associated with a precordial transition zone at lead V3 predicted VT not successfully ablated from the RVOT (positive predictive value 100%; negative predictive value 100%). In conclusion, some VTs with LBBB and inferior or normal axis cannot be ablated from the RVOT. The presence of an R wave in lead V1 associated with a precordial transition zone at lead V3 suggest that some VTs may not arise from the RVOT.

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BACKGROUND: Complete bi-directional isthmus block is the endpoint of typical atrial flutter ablation. The purpose of this study was to investigate the feasibility of the local double potential (DP) interval and the change in transisthmus conduction time for predicting complete isthmus block after ablation of the cavotricuspid isthmus. METHODS: The study population consisted of 32 patients with typical atrial flutter after a procedure of radiofrequency (RF) ablation of the cavotricuspid isthmus (16 had incomplete block and 16 had complete block). The transisthmus conduction time was determined during pacing from the proximal coronary sinus and low lateral right atrium before and after RF ablation. The DP interval close to the ablation line was evaluated after final RF energy application. RESULTS: In the counterclockwise direction, transisthmus conduction time had an increase of 37 +/- 25.4% and 127.3 +/- 35.5% (P < 0.001), and the DP interval was 63.3 +/- 8.7 ms and 120 +/- 17.4 ms (P < 0.001) after achievement of incomplete and complete block, respectively. The sensitivity, specificity, positive and negative predictive values of an increase in the transisthmus conduction time > or =50% were 100%, 81%, 84% and 100%, respectively; those of DP interval > or =100 ms were 100%. In the clockwise direction, transisthmus conduction time had an increase of 38.8 +/- 28.6% and 135.7 +/- 63.6% (P < 0.001), and the DP interval was 63.6 +/- 13.8 ms and 127.7 +/- 27.1 ms (P < 0.001) after achievement of incomplete and complete block, respectively. The sensitivity, specificity, positive and negative predictive values of an increase in the transisthmus conduction time > or =50% were 100%, 67%, 83% and 100%, respectively; those of the DP interval > or =100 ms were 100%. CONCLUSIONS: The transisthmus conduction time > or =50% increase or DP interval > or =100 ms was feasible to predict complete bi-directional isthmus block.

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