Comparison of endothelial vasodilator function, inflammatory markers, and N-terminal pro-brain natriuretic peptide in patients with or without chronotropic incompetence to exercise test.

OBJECTIVE: To investigate the role of endothelial function, inflammatory markers, and N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with impaired chronotropic response during exercise test. METHODS: 86 subjects were enrolled. Treadmill exercise test was conducted according to the modified Bruce protocols. Brachial ultrasound was used to measure endothelium dependent flow mediated vasodilatation (FMD). Chronotropic incompetence was defined as either failure to achieve 85% of the age predicted maximum heart rate or a low chronotropic index (< 0.8). RESULTS: Of the 86 patients, 20 (23%) exhibited chronotropic incompetence. The patients were divided into three groups according to chronotropic index: group 1, < 0.8 (n = 20); group 2, 0.8-1.0 (n = 26); and group 3, > 1.0 (n = 40). Patients with impaired chronotropic response had significantly lower FMD than those with higher chronotropic response (mean (SD) 2.8 (1.9)% v 5.0 (2.8)% v 5.3 (2.5)%, p = 0.002, for groups 1, 2, and 3, respectively). Serum concentrations of high-sensitivity C reactive protein (hsCRP), monocyte chemoattractant protein-1 (MCP-1), and NT-proBNP were significantly higher in group 1 than in groups 2 and 3 (hsCRP: 19 (12) v 9 (6) v 9 (6) mg/l, p < 0.05; MCP-1: 140 (51) v 133 (60) v 108 (46) pg/ml, p = 0.046; NT-proBNP: 4760 (1980) v 3710 (850) v 3910 (1060) mg/l, p = 0.019, respectively). In addition, chronotropic index was significantly related to FMD (r = 0.380, p = 0.001) and inversely related to hsCRP (r = -0.267, p = 0.013). By multivariate analysis, impaired chronotropic response was significantly related to endothelial dysfunction (p = 0.012). CONCLUSION: Patients with impaired chronotropic response to graded exercise had endothelial dysfunction, enhanced systemic inflammation, and higher NT-proBNP concentrations. These findings may partly explain the mechanism of chronotropic incompetence as a predictor of cardiovascular risk and increased mortality.

Antihypertensive action and blockade of alpha1-adrenoceptors by DL-017, a quinazoline derivative.

3-[[4-(2-Methoxyphenyl)piperazin-1-yl]methyl]-5-(methylthio)-2,3-dihydroimidazo[1,2-c]quinazoline (DL-017), a quinazoline derivative, exhibits alpha 1 -adrenoceptor antagonistic and type I antiarrhythmic effects on mammalian cardiac tissues. In the current study, the effects of DL-017 on the hemodynamic profile in anesthetized, spontaneously hypertensive rats were evaluated. Intravenous administration of DL-017 induced dose-dependent reductions of heart rate and blood pressure, which persisted over 2 h. DL-017 exerted a maximal antihypertensive effect at 0.1 mg/kg, which was similar to that of 0.1 mg/kg of prazosin. DL-017 was able to block the pressor response to phenylephrine but not to angiotensin II. Regional cerebral blood flow of the right parietal cortex decreased by 14 +/- 4% 10 min after bolus injection and then rapidly returned to control levels while the arterial pressure was still low. These results indicate that blockade of the alpha 1 -adrenoceptor by DL-017 contributes to reduction of arterial pressure. The antihypertensive effect without reflex tachycardia and loss of autoregulation of cerebral blood flow makes DL-017 suitable for chronic long-term treatment of hypertension.

Pulsatility of ascending aorta and restenosis after coronary angioplasty in patients >60 years of age with stable angina pectoris.

A recent study has demonstrated that the pulsatility of the ascending aorta is a strong predictive factor for restenosis after coronary angioplasty. However, whether the pulsatility of the ascending aorta is still a significant predictor for restenosis in elderly patients with a stiffer aorta is unknown. We investigated the relation between arterial pulsatility in the ascending aorta and restenosis after coronary angioplasty in patients aged > 60 years. Eighty-seven consecutive patients (80 men, aged 72.5 +/- 5.1 years) with stable angina were included. Before angioplasty, the arterial systolic, diastolic, and mean pressure waveforms of the ascending aorta were measured. We used fractional pulse pressure (PPf, the ratio of pulse pressure to mean pressure) and pulsatility index (PI, the ratio of pulse pressure to diastolic pressure) to estimate the pulsatility of the ascending aorta. Angiographic restenosis occurred in 39 patients. Pulse pressure, PPf, and PI were significantly higher in patients with restenosis after coronary angioplasty (restenosis vs without restenosis: pulse pressure, 77.6 +/- 12.2 vs 66.1 +/- 15.4 mm Hg [p < 0.001]; PPf, 0.80 +/- 0.09 vs 0.69 +/- 0.11 [p < 0.001]; PI, 1.19 +/- 0.20 vs 0.98 +/- 0.21 [p < 0.001]). After multivariate stepwise adjustment of risk factors of restenosis and using receiver-operating characteristic analysis, the odds ratio (OR) of restenosis was: pulse pressure > 66 mm Hg, OR 5.88 (95% confidence interval [CI] 2.17 to 15.93); PPf > 0.72, OR 13.71 (95% CI 4.81 to 39.05); PI > 1.06, OR 13.56 (95% CI 4.67 to 39.38). Moreover, among patients aged > 70 years (n = 60), the predictive values of PPf and PI were even higher than those in patients aged < or = 70 years (n = 27). Thus, in elderly patients with stable angina, the pulsatility of the ascending aorta is a powerful predictor of restenosis after coronary angioplasty.

Effects of cavotricuspid isthmus ablation on atrioventricular node electrophysiology in patients with typical atrial flutter.

BACKGROUND: The atrial musculature in the cavotricuspid isthmus is a part of posterior inputs to the AV node. In patients with typical atrial flutter, effects of radiofrequency ablation of this isthmus on AV node conduction are still unknown. METHODS AND RESULTS: This study included 16 patients with clinically documented typical atrial flutter. Group 1 had 8 patients without and group 2 had 8 patients with dual AV nodal pathway physiology. Electrical pacing from the interatrial septum and low right atrium was performed to evaluate antegrade AV node function before and after ablation of the cavotricuspid isthmus. In group 1, the AV node conduction properties were similar before and after ablation. In group 2, the AV node Wenckebach cycle length and maximal AH interval during low right atrium (356+/-58 versus 399+/-49 ms, P=0.008; 303+/-57 versus 376+/-50 ms, P=0.008) and interatrial septum (365+/-62 versus 393+/-59 ms, P=0.008; 324+/-52 versus 390+/-60 ms, P=0.008) pacing were significantly longer after ablation. Elimination of the slow pathway after ablation was noted in 2 patients, including 1 with AV nodal reentrant echo beats. CONCLUSIONS: Radiofrequency ablation of the cavotricuspid isthmus was effective in eliminating typical atrial flutter without injury of antegrade fast AV node conduction. The atrial musculature in the cavotricuspid isthmus significantly contributed to the slow AV node conduction.

Acquired pulmonary vein stenosis after radiofrequency catheter ablation of paroxysmal atrial fibrillation.

INTRODUCTION: Elimination of the initiating focus within the pulmonary vein (PV) using radiofrequency (RF) catheter ablation is a new treatment modality for treatment of drug-refractory atrial fibrillation. However, information on the long-term safety of RF ablation within the PV is limited. METHODS AND RESULTS: In 102 patients with drug-refractory atrial fibrillation and at least one initiating focus from the PV, series transesophageal echocardiography was performed to monitor the effect of RF ablation on the PV. There were 66 foci in the right upper PV and 65 foci in the left upper PV. Within 3 days of ablation, 26 of the ablated right upper PVs (39%) had increased peak Doppler flow velocity (mean 130+/-28 cm/sec, range 106 to 220), and 15 of the ablated left upper PVs (23%) had increased peak Doppler flow velocity (mean 140+/-39 cm/sec, range 105 to 219). Seven patients had increased peak Doppler flow velocity in both upper PVs. No factor (including age, sex, site of ablation, number of RF pulses, pulse duration, and temperature) could predict PV stenosis after RF ablation. Three patients with stenosis of both upper PVs experienced mild dyspnea on exertion, but only one had mild increase of pulmonary pressure. There was no significant change of peak and mean flow velocity and of PV diameter in sequential follow-up studies up to 16 (209+/-94 days) months. CONCLUSION: Focal PV stenosis is observed frequently after RF catheter ablation applied within the vein, but usually is without clinical significance. However, ablation within multiple PVs might cause pulmonary hypertension and should be considered a limiting factor in this procedure.

Beneficial effect of HCL-31D in murine models of endotoxaemia.

We evaluated the effect of HCL-31D, a novel cAMP-specific phosphodiesterase inhibitor, on the induction of inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma)-treated rat aortic smooth muscle cells (RASMC) and on survival in a murine model of severe endotoxaemia. Treatment of cultured RASMC with LPS and IFN-gamma resulted in an increase of nitrite, tumour necrosis factor (TNF-alpha) production and induction of iNOS mRNA. However, incubation with HCL-31D (1 approximately 50 microM) for 24 h caused significant attenuation of nitrite and TNF-alpha formation as well as iNOS mRNA induction in a dose-dependent manner but no effect on iNOS activity in RASMC. In addition, administration of HCL-31D (5 mg/kg, i.p.) resulted in that the increase of both plasma nitrate and TNF-alpha levels induced by LPS in vivo was significantly reduced in LPS-treated rats. Treatment of conscious mice with a high dose of LPS (60 mg/kg, i.p.) to ICR mice resulted in a 24-h survival rate of only 10%. However, administration of HCL-31D (5 mg/kg, i.p. at 0 h and 6 h after LPS) improved the 24-h survival to 50%, indicating that HCL-31D has a beneficial effect in murine model endotoxaemia. These effects may be mainly due to inhibition of TNF-alpha formation and of the induction of iNOS. We proposed that the elevation of cAMP levels by HCL-31D may be involved in the prevention of TNF-alpha formation and iNOS induction.

Pulmonary vein dilation in patients with atrial fibrillation: detection by magnetic resonance imaging.

INTRODUCTION: The positive relationship between left atrial (LA) size and atrial fibrillation (AF) is well recognized; however, there is little information on the association of pulmonary vein (PV) diameter and AF. The purpose of this study was to investigate by magnetic resonance angiography the change of PV and LA size in patients with no history of AF, patients with paroxysmal AF (PAF), and patients with chronic AF (CAF). METHODS AND RESULTS: The study included 47 patients. Group I included 15 patients with normal sinus rhythm and no history of documented AF. Group II included 24 patients with drug-refractory PAF who underwent electrophysiologic study and radiofrequency ablation of PV foci. Group III included 8 patients with CAF who were converted to sinus rhythm by external electrical cardioversion. Age and concomitant heart diseases were similar among the three groups. We measured the diameter of each PV at its junction with the LA in addition to LA dimensions by gadolinium-enhanced magnetic resonance angiography with three-dimensional reconstruction. Significant dilation of both superior PVs (P < 0.01) and transverse diameter of LA (P < 0.01) was seen in the three groups. There were no significant changes of both inferior PVs, corrected PV (PV/LA) diameter, or longitudinal diameter of LA among the three groups. Only 28% patients showed arrhythmogenic foci from the largest PV. CONCLUSION: Significant dilation of both superior PVs with simultaneous LA enlargement was demonstrated i

Prolonged fractionation of paced right atrial electrograms in patients with atrial flutter and fibrillation.

OBJECTIVES: This study investigated the extent of fractionation of paced right atrial electrograms in patients with and without paroxysmal atrial flutter (AFL) or atrial fibrillation (AF). BACKGROUND: Slow conduction through nonuniform anisotropic atrial muscles, represented by fractionated electrograms, may favor the generation of atrial tachyarrhythmias. METHODS: This study included 10 control patients (Group 1), 8 patients with documented paroxysmal AFL (Group 2) and 10 patients with documented paroxysmal AF (Group 3). Five electrode catheters were placed in the different sites of the right atrium and one catheter was positioned at the coronary sinus ostium. Atrial pacing from one site was done by a constant drive train with an extrastimulus inserted every fourth beat while recording at the other five sites was performed. The delay of each fractionated potential in the high-pass filtered atrial electrogram in response to extrastimulation was determined and used to construct conduction curves of delay versus the S1S2 interval. RESULTS: The mean increase in electrogram duration between a coupling interval of 350 ms and 10 ms above atrial refractoriness was significantly greater in Groups 2 and 3 compared with that in Group 1 (8.5 +/- 2.5 vs. 11.0 +/- 2.7 vs. 5.9 +/- 2.3 ms, respectively, p < 0.001). The mean S1S2 interval at which delay increased suddenly was also longer in Groups 2 and 3 compared with Group 1 (326 +/- 9 vs. 343 +/- 12 vs. 307 +/- 17 ms, respectively, p < 0.001). CONCLUSIONS: Increased delays in the individual potential of the fractionated atrial electrograms may be related to the development of AFL and AF.

Electrophysiologic characteristics in initiation of paroxysmal atrial fibrillation from a focal area.

OBJECTIVES: We investigated the electrophysiologic characteristics in the initiation of paroxysmal atrial fibrillation (PAF) from a focal area. BACKGROUND: The electrophysiologic characteristics in the initiation of PAF are still not clear. METHODS: The study group consisted of 77 patients (M/F = 65/12, age 66 +/- 12 years) with frequent episodes of PAF; we analyzed: 1) 15 cycle lengths of electrical activity before the onset of atrial fibrillation (AF); 2) coupling interval (CI) of the first ectopic beat just before the initiation of AF; and 3) the prematurity of an ectopic beat (prematurity index [PI] = CI/mean of preceding 15 cycle lengths). RESULTS: A total of 111 episodes of sustained AF were identified. Two patterns of AF initiation were observed: group I (59/111, 53%) included the episodes preceded by cycle length oscillation, and group II (52/111, 47%) included the episodes initiated by a single ectopic beat with preceding cycle length relatively constant. The PI of group I episodes was significantly greater than that of group II (0.41 +/- 0.12 vs. 0.34 +/- 0.10, p < 0.01). The CI (267 +/- 54 ms vs. 217 +/- 55 ms, p < 0.05), AF1 (194 +/- 36 ms vs. 153 +/- 37 ms, p < 0.05) and PI (0.49 +/- 0.13 vs. 0.37 +/- 0.11, p < 0.01) of the AF episodes from the superior vena cava (SVC) were significantly longer and greater than those of AF episodes from pulmonary veins (PVs). CONCLUSIONS: In patients with PAF originating from PVs or the SVC, two major initiating patterns were found. Moreover, the electrophysiologic characteristics in the initiation of AF originating from the SVC were also different from those of AF initiating from the PVs.

Mechanism of spontaneous transition from typical atrial flutter to atrial fibrillation: role of ectopic atrial fibrillation foci.

Paroxysmal AF has been known to be initiated by ectopic beats, especially in the pulmonary veins (PVs), and radiofrequency catheter ablation could cure it. We considered that the spontaneous transition from typical atrial flutter to AF also could be initiated by ectopic beats. Twenty patients (18 men, mean age 66 +/- 14 years) with episodes of spontaneous transition from typical atrial flutter to AF were included in this study. They underwent detailed mapping of both atria. All the patients had spontaneous AF initiated by ectopic beats, and all of them had typical atrial flutter and spontaneous transition from typical atrial flutter (12 patients with counterclockwise atrial flutter and 8 patients with clockwise atrial flutter) to AF. The transition was initiated by ectopic beats from the PVs (17 foci, 85%), crista terminalis (2 foci, 10%), and superior vena cava (1 focus, 5%). After successful ablation of AF foci, typical atrial flutter was induced again, but no spontaneous transition was found after at least 10 minutes of observation. We concluded that paroxysmal AF and spontaneous transition from typical atrial flutter to AF were initiated by ectopic beats, and successful catheter ablation of the ectopic foci can eliminate paroxysmal AF and spontaneous transition from typical atrial flutter to AF.

Mechanisms of transition between double paroxysmal supraventricular tachycardias.

INTRODUCTION: Coexistence of double tachycardias in one patient has been infrequently reported. Furthermore, the mechanisms of transition between double paroxysmal supraventricular tachycardias have not been well studied. METHODS AND RESULTS: Thirty-five patients with two paroxysmal supraventricular tachycardias were studied. Group IA consisted of 3 patients with spontaneous transition between AV reciprocating tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT). Group IB consisted of 13 patients without spontaneous transition between AVRT and AVNRT. Group IIA consisted of 5 patients with spontaneous transition between AVNRT and atrial tachycardia (AT). Group IIB consisted of 14 patients without spontaneous transition between AVNRT and AT. The absolute values of differences between the two tachycardia cycle lengths were significantly smaller in patients with than in those without transition between the two tachycardias (25+/-8 msec vs 90+/-46 msec, P < 0.05, IA vs IB; 21+/-25 msec vs 99+/-57 msec, P < 0.01, IIA vs IIB). The cutoff point of 25 msec had 80% positive predictive value for transition between the two tachycardias. Transition between two tachycardias occurred due to a spontaneous premature atrial complex (30%), conduction block at one limb of tachycardia (20%), or tachycardia-induced tachycardia (50%). Absence of transition between two tachycardias might be explained by the absence of a spontaneous premature atrial complex, longer cycle length of the first tachycardia, larger difference between two tachycardia cycle lengths, or induction of each tachycardia under different situations. CONCLUSION: Double supraventricular tachycardias with similar tachycardia cycle lengths are vulnerable to transition between different tachycardias.

Role of right middle pulmonary vein in patients with paroxysmal atrial fibrillation.

INTRODUCTION: Elimination of the ectopic foci from pulmonary veins (PVs) has proved to be a curative therapy for focal atrial fibrillation (AF). However, information about the importance of the right middle PV (RMPV) in initiation of AF and radiofrequency ablation of AF is limited. METHOD AND RESULTS: Forty-three patients (34 men and 9 women; age 65+/-12 years) with drug-refractory paroxysmal AF underwent electrophysiologic study and catheter ablation for treatment of AF. Three-dimensional magnetic resonance angiography (MRA) of the PVs and left atrium (LA) was performed to determine the anatomic patterns of RMPV. Diameter of PV ostium was measured at the junction of the LA and each PV. MRA findings showed the following: (1) 36 (84%) of 43 patients had a discrete RMPV; (2) there are three drainage patterns of RMPV, including joining the proximal part (<1 cm from the ostium) of the right superior PV (RSPV), joining the right inferior PV (RIPV), and a separate RMPV ostium in the LA wall; and (3) the ostial diameter of RMPV was significantly smaller than RSPV and RIPV (P < 0.01). Electrophysiologic studies demonstrated that five AF foci arose from RMPV. The coupling interval between the ectopic beat of AF and sinus beat was longer in RMPV than RSPV (262+/-45 msec vs 212+/-47 msec; P = 0.043). All AFs from RMPV were ablated successfully. PV stenosis or AF recurrence from RMPV was not found during follow-up of 10+/-4 months. CONCLUSION: RMPV was detected by MRA in >80% of paroxysmal AF patients. Ectopy from RMPV can initiate AF, and radiofrequency ablation of RMPV foci is feasible and safe.

Differentiating the ligament of Marshall from the pulmonary vein musculature potentials in patients with paroxysmal atrial fibrillation: electrophysiological characteristics and results of radiofrequency ablation.

It was reported that paroxysmal atrial fibrillation (PAF) can be initiated by ectopic atrial beats originating from the pulmonary vein (PV) or left atrial tract (LAT) within the ligament of Marshall (LOM). The aim of this study was to differentiate the LAT from the PV potentials, and to investigate the results of radiofrequency ablation guided by these potentials. Ten patients (age 60 +/- 12 years) with PAF who had a recording of double potentials (DPs) in or around the left PV were included. Group I had five patients with the second deflection of DPs (D2) due to activation of the LAT, and Group II had five patients with D2 due to activation of the PV musculature. There were no significant difference in the isoelectric interval between DPs, the activation time, and amplitude of D2 between Groups I and II. During distal coronary sinus (CS) pacing, the CS ostium (CSO) to D2 interval was shorter compared with that during sinus rhythm in Group I (39 +/- 19 vs 71 +/- 25 ms, P = 0.04), but was longer in Group II (96 +/- 16 vs 44 +/- 19 ms, P = 0.04). During ectopic activation, three patients in Group I, but no Group II patients, had transformation of recorded DPs into triple potentials. Radiofrequency ablation guided by the earliest activation of the LAT potential was performed with transient suppression of PAF, but ablation guided by the earliest activation of the PV potentials had a high success rate in eliminating PAF. In conclusion, differentiating the LAT from the PV potentials for initiation of PAF is feasible by an electrophysiological approach, and may be important for radiofrequency ablation of PAF.

Pulmonary vein electrogram characteristics in patients with focal sources of paroxysmal atrial fibrillation.

INTRODUCTION: The major source of ectopic beats initiating paroxysmal atrial fibrillation (AF) is from pulmonary veins (PVs). However, the electrogram characteristics of PVs are not well defined. METHODS AND RESULTS: Group I consisted of 129 patients with paroxysmal AF. Group II consisted of 10 patients with a concealed left-sided free-wall accessory pathway. All group I patients had spontaneous AF initiated by ectopic beats, including 169 ectopic foci originating from the PVs. We analyzed PV electrograms from the 169 ectopic foci during sinus beats and ectopic beats. During AF initiation, most (70%) ectopic beats showed PV spike potential followed by atrial potential; 16% of ectopic beats showed PV fragmented potential followed by atrial potential; and 14% showed fusion potentials. The coupling interval between the sinus beat and the ectopic beat was significantly shorter in the inferior PVs than in the superior PVs (171 +/- 48 msec vs 222 +/- 63 msec, P = 0.001) and was significantly shorter in the distal foci than in the ostial foci of PVs (206 +/- 52 msec vs 230 +/- 56 msec, P = 0.01). The incidence of conduction block in the PVs during AF initiation was significantly higher in the inferior PVs than in the superior PVs (12/24 vs 37/145, P = 0.03) and was significantly higher in the distal foci than in the ostial foci of PVs (43/121 vs 6/48, P = 0.04). The maximal amplitude of PV potential was significantly larger in the left PVs than in the right PVs, and the maximal duration of PV potential was significantly longer in the superior PVs than in the inferior PVs during sinus beats in both group I and II patients. CONCLUSION: PV electrogram characteristics were different among the four PVs. Detailed mapping and careful interpretation are the most important steps in ablation of paroxysmal AF originating from PVs.

Effect of phenylephrine on focal atrial fibrillation originating in the pulmonary veins and superior vena cava.

OBJECTIVES: This study was aimed at evaluating the effects of phenylephrine infusion on the occurrence of focal atrial fibrillation (AF). BACKGROUND: Paroxysmal AF can be initiated by ectopic atrial beats originating in the pulmonary vein (PV) or superior vena cava (SVC). The effect of change in autonomic tone on this focal AF is unknown. METHODS: This study included 12 patients with frequent bursts of AF documented by 24-h Holter monitoring. The number and coupling interval of spontaneous ectopic activity and bursts of AF were evaluated for 1 min before and after phenylephrine (2 to 3 microg/kg) injection. RESULTS: After detailed mapping, four patients had a focus located in the left superior PV, six in the right superior PV and two in the SVC. In 10 patients with AF foci originating in the PVs, the frequency of ectopic activity (19.5 +/- 27.4 vs. 11.4 +/- 22.9 beats/min, p = 0.059) was reduced as well as AF bursts (14 +/- 3 vs. 1.8 +/- 2.7 bursts/min, p = 0.005) before versus after phenylephrine injection; the minimal coupling interval of ectopic activity and AF bursts became longer compared with baseline. The maximal percent increase in sinus cycle length after phenylephrine injection was significantly greater in patients with complete suppression of AF compared with those with partial suppression (43 +/- 19 vs. 14 +/- 5%, p = 0.01). However, no significant effect of phenylephrine on AF originating in the SVC was found. CONCLUSIONS: Change in autonomic tone induced by phenylephrine injection was effective in suppressing focal AF originating in the PVs but not in the SVC.

Radiofrequency catheter ablation of atrial fibrillation initiated by spontaneous ectopic beats.

Several reports have demonstrated that most paroxysmal atrial fibrillation is initiated by ectopic beats from a focal area, and radiofrequency catheter ablation can effectively cure atrial fibrillation. Although most of the ectopic beats originate from the orifices of the pulmonary veins or from the myocardial sleeves in the pulmonary veins, ectopic beats can also originate from superior vena cava, crista terminalis, coronary sinus, ligament of Marshall, or left atrial posterior free wall. Owing to the potential risk and complexity of catheter ablation, the ideal candidates should have frequent episodes and drug refractory paroxysmal atrial fibrillation.

Atrial tachycardias originating from the atrial septum: electrophysiologic characteristics and radiofrequency ablation.

INTRODUCTION: The characteristics of atrial tachycardia (AT) have varied widely among different reports. The anatomic locations of ATs may bias the results. We propose that septal ATs and free-wall ATs have different characteristics. METHODS AND RESULTS: One hundred forty-one patients with AT underwent electropharmacologic study, endocardial mapping, and radiofrequency ablation. Forty-nine (34.7%) patients had septal AT originating from the anteroseptal, mid-septal, and posteroseptal areas. Tachycardia cycle length was similar between septal AT and free-wall AT (367 +/- 46 msec vs 366 +/- 58 msec, P > 0.05). More patients with septal AT required isoproterenol to facilitate induction (44.9% vs 31.5%, P <.0.05). Septal AT was more sensitive to adenosine than free-wall AT (84.4% vs 67.8%, P < 0.05). Only posteroseptal AT showed a positive P wave in lead V1 and negative P wave in all the inferior leads (II, III, aVF). Radiofrequency catheter ablation had a comparable success rate for septal AT and free-wall AT (96% vs 95%) without impairment of AV conduction. During follow-up of 49 +/- 13 months (range 17 to 85), the recurrence rate was similar for septal AT and free-wall AT (3.2% vs 4.6%, P = 0.08). CONCLUSION: Septal AT has electrophysiologic characteristics that are distinct from those of free-wall AT. Catheter ablation of the septal AT is safe and effective.

Predicting the arrhythmogenic foci of atrial fibrillation before atrial transseptal procedure: implication for catheter ablation.

INTRODUCTION: Use of endocardial atrial activation sequences from recording catheters in the right atrium, His bundle, and coronary sinus to predict the location of initiating foci of atrial fibrillation (AF) before an atrial transseptal procedure has not been reported. The purpose of the present study was to develop an algorithm using endocardial atrial activation sequences to predict the location of initiating foci of AF before transseptal procedure. METHODS AND RESULTS: Seventy-five patients (60 men and 15 women, age 68 +/- 12 years) with frequent episodes of paroxysmal AF were referred for radiofrequency ablation. By retrospective analysis, characteristics of the endocardial atrial activation sequences of right atrial, His-bundle, and coronary sinus catheters from the initial 37 patients were correlated with the location of initiating foci of AF, which were confirmed by successful ablation. The endocardial atrial activation sequences of the other 38 patients were evaluated prospectively to predict the location of initiating foci of AF before transseptal procedure using the algorithm derived from the retrospective analysis. Accuracy of the value <0 msec (obtained by subtracting the time interval between high right atrium and His-bundle atrial activation during atrial premature beats from that obtained during sinus rhythm) for discriminating the superior vena cava or upper portion of the crista terminalis from the pulmonary vein (PV) foci was 100%. When the interval between atrial activation of ostial and distal pairs of the coronary sinus catheter of the atrial premature beats was <0 msec, the accuracy for discriminating left PV foci from right PV foci was 92% in the 24 foci from the left PVs and 100% in the 19 foci from the right PVs. CONCLUSION: Endocardial atrial activation sequences from right atrial, His-bundle, and coronary sinus catheters can accurately predict the location of initiating foci of AF before transseptal procedure. This may facilitate mapping and radiofrequency ablation of paroxysmal AF.

Initiation of atrial fibrillation by ectopic beats originating from the superior vena cava: electrophysiological characteristics and results of radiofrequency ablation.

BACKGROUND: The superior vena cava (SVC) has cardiac musculature extending from the right atrium. However, no previous study in humans has given details regarding the ectopic foci that initiate paroxysmal atrial fibrillation (PAF), which may originate from the SVC. METHODS AND RESULTS: A total of 130 patients with frequent attacks of PAF initiated by ectopic beats were included. Eight patients (6%) had spontaneous AF initiated by a burst of rapid ectopic beats from the SVC (located 19+/-7 mm above the junction of the SVC and right atrium), which was confirmed by multiplane angiographic and intracardiac echocardiographic visualization and was marked by a sharp SVC potential preceding atrial activity. During initial repetitive discharges, the group with SVC ectopy had a higher incidence of intravenous conduction block than the group with pulmonary vein ectopy (75% versus 37%; P=0.03). The activation time of the earliest intracardiac ectopic activities relative to ectopic P wave onset was significantly shorter in the SVC ectopy than the pulmonary vein ectopy group (37+/-15 versus 84+/-32 ms; P<0. 001). After 5+/-3 applications of radiofrequency energy, AF was eliminated. SVC angiography after ablation revealed a local indentation of the venous wall in one patient. Two patients manifested coexisting sinus rhythm and a "focal" fibrillating activity confined inside the SVC after radiofrequency ablation. During a follow-up period of 9+/-3 months, all 8 patients were free of antiarrhythmic drugs, without tachycardia recurrence or symptoms of SVC obstruction. CONCLUSIONS: Ectopic beats initiating PAF can originate from the SVC. A radiofrequency current delivered to eliminate these ectopies is a highly effective and safe way to prevent PAF.