Physiological changes during hemodialysis in patients with intradialysis hypertension.

Intradialysis hypertension is a frustrating complication among hemodialysis (HD) patients. This study was conducted to investigate the physiological changes during intradialytic hypertension. The beat-to-beat continuous heart rate, hematocrit (Hct) changes during HD, serum levels of nitric oxide, plasma levels of catecholamine, renin, endothelin (ET-1), cardiac output (CO), and peripheral vascular resistance (PVR) were measured before and after HD in patients prone to develop intradialysis hypertension (n = 30) and from age, sex-matched control HD subjects (n = 30). It was found that the baseline values of Hct, serum levels of nitric oxide, plasma levels of catecholamine, renin, and ET-1, CO, PVR, and power index (low frequency/high frequency ratios) of heart rate variability were not significantly different between the patients and control subjects. In the hypertension-prone group, the plasma levels of catecholamine, renin, and the serial measurements of power index, did not show significant changes. However, the patients showed a significant elevation of systemic vascular resistance (56.8 +/- 9.2% vs 17.7 +/- 9.5; P < 0.05), ET-1 (510.9 +/- 43.3 vs 276.7 +/- 30.1 pg/ml; P < 0.05) and a significant decrease of nitric oxide (NO)/ET-1 balance (0.018 +/- 0.003 vs 0.034 +/- 0.005; P < 0.05) at the end of HD compared with the control patients. It was found that the physiological changes in intradialysis hypertension patients were characterized by inappropriately increased PVR through mechanisms that did not involve sympathetic stimulation or renin activation but might be related with altered NO/ET-1 balance.

Transthoracic and transesophageal echocardiographic diagnosis of aneurysm of the sinus of Valsalva: a review of five year experience.

BACKGROUND: Aneurysms of the sinus of Valsalva (SVA) are uncommon congenital lesions. The clinical presentations vary from asymptomatic to progressive heart failure following rupture of the aneurysm into an adjacent cardiac chamber. Retrograde aortogram is the diagnostic tool of choice preoperatively. Recent studies have demonstrated that the SVA can be accurately diagnosed using transthoracic two-dimensional, and color Doppler flow mapping, even for surgical preparation without cardiac catheterization. We report our 5-year experience of transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) in the evaluation of SVA. METHODS: Eleven adult patients with SVA with or without rupture were studied using both TTE and TEE. All of the diagnoses were subsequently comfirmed by either cardiac catheterization or surgical findings. RESULTS: Aneurysms originated in the right coronary sinus (n = 9) and noncoronary sinus (n = 2); they ruptured into the right ventricle in 5 patients and the right atrium in 5 patients. An unruptured right SVA was noted in 1 patient. Both TTE and TEE could identify the site of the aneurysm, rupture sites, and the receiving chamber equally well. Co-existent cardiac lesions included 11 cases of valvular aortic regurgitation (mild in 7, moderate in 2 and severe in 2). Two cases of perimembranous type ventricular septal defect (VSD) and 6 cases of supracristal type VSD (including 1 case of tetraology of Fallot, 3 supracristal, 1 muscular and 1 subaortic) were noted. Three cases were complicated with valvular vegetations (1 aortic valve, 1 aortic and tricuspid valve and 1 aortic and pulmonic valve). One patient had patent ductus arteriosus and 2 patients had pulmonic valvular stenosis. CONCLUSIONS: TEE provides clearer definition for the detailed anatomy of the ruptured sac and co-existent cardiac lesions than TTE through high resolution and closer approach. We conclude that TEE is a powerful complementary diagnostic tool in the evaluation of patients with SVA. TEE also provides additionally useful information for guiding the surgical approach and for assessing the operative results even without cardiac catheterization.

Effect of nitric oxide on strophanthidin-induced ventricular tachycardia.

Nitric oxide (NO) has been demonstrated to have several effects on the heart. Through the stimulation of guanylate cyclase, NO increases cyclic GMP and decreases intracellular calcium. The purpose of this study was to evaluate the effects of NO on ventricular arrhythmia induced by strophanthidin in guinea pigs and dogs. In experiment 1, after strophanthidin-induced ventricular tachycardia, guinea pigs received different doses of L-arginine (0, 25, 50, 100, 200, and 400 mg/kg; n = 10 for each dose), 200 mg/kg L-arginine combined with 100 mg/kg N(G)-nitro-L-arginine methylester (L-NAME, n = 10), or 200 mg/kg D-arginine (n = 10). In experiment 2, after strophanthidin-induced ventricular tachycardia, dogs (n = 7) received 200 mg/kg L-arginine. By 12-lead ECG, monophasic action potentials in left and right ventricles were recorded throughout the study. In experiment 1, guinea pigs which received 200 mg/kg or 400 mg/kg L-arginine had greater incidences of ventricular tachycardia termination (60 and 80%, respectively) than those which received 0, 25, 50, and 100 mg/kg L-arginine (0, 0, 20, and 30%, respectively), those which received L-arginine with L-NAME (0%), and those which received D-arginine (0%). In experiment 2, 5 (71%) of the dogs had successful termination of ventricular tachycardia. These findings suggest that L-arginine was effective in treating strophanthidin-induced ventricular tachycardia in vivo and that the underlying mechanism is through a NO pathway.

Sudden changes in heart rate variability during the 1999 Taiwan earthquake.

Sympathovagal imbalance resulting from reactions to an earthquake was not prominent in patients who were taking beta-blockers.

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.

Alterations of heart rate variability after radiofrequency catheter ablation of focal atrial fibrillation originating from pulmonary veins.

BACKGROUND: Transient sinus bradycardia and hypotension have been reported as complications during radiofrequency (RF) ablation of focal atrial fibrillation (AF) originating from pulmonary veins (PVs). This study used heart rate variability (HRV) to evaluate the effects of focal PVs ablation on autonomic function. METHODS AND RESULTS: Thirty-seven patients with paroxysmal AF were referred for ablation. The study group included 30 patients who underwent transseptal ablation of PVs, and the control group included 7 patients who underwent the transseptal procedure without ablation. The mean sinus rate and time-domain (standard deviation of RR intervals and root-mean-square of differences of adjacent RR intervals) and frequency-domain (low frequency, high frequency, and low-frequency/high-frequency ratio) analyses of HRV were obtained by use of 24-hour Holter monitoring before and 1 week, 1 month, and 6 months after ablation. All the triggering points of AF were from PVs, and they were successfully ablated. Severe bradycardia and hypotension were noted during ablation of PVs in 6 patients (group IA); 24 patients without the above complication belonged to group IB. Compared with preablation values, a significant increase in mean sinus rate and low-frequency/high-frequency ratio and a significant decrease in standard deviation of RR intervals, root-mean-square of differences of adjacent RR intervals, low frequency, and high frequency were noted in groups IA and IB patients 1 week after ablation. The changes in HR and HRV recovered spontaneously in the 2 subgroups by 1 month later. These parameters of HRV did not change in the control group after the transseptal procedure. CONCLUSIONS: Transient autonomic dysfunction with alterations in HR and HRV occurred after ablation of focal AF originating from PVs.

Electropharmacologic characteristics of ventricular proarrhythmia induced by ibutilide.

The purpose of this study was to evaluate in vivo the proarrhythmic effects of ibutilide in dogs with or without ventricular hypertrophy. Fourteen dogs received repeated experiments both during the acute and chronic phases (8 weeks, with ventricular hypertrophy) of complete atrioventricular (AV) block. Twelve-lead ECG, monophasic action potentials in the left and right ventricle were recorded before and after each dose of ibutilide (0.01-0.08 mg/kg) during different ventricular rates. In these dogs, ibutilide increased QT interval, biventricular APD90, interventricular deltaAPD90 (difference between the left and right ventricular APD90), and QT dispersion, and induced early afterdepolarizations in a dose-dependent manner. The interventricular deltaAPD90, QT dispersion, and increases of QT interval were more pronounced during slower ventricular rates. There were greater QT interval, biventricular APD90 interventricular deltaAPD90, and QT dispersion values during chronic AV block than during acute AV block. Moreover, ibutilide can induce higher incidences of early afterdepolarizations and torsades de pointes [six (43%) of 14 versus 0 of 14; p < 0.05] during chronic AV block than during acute AV block. In conclusion, ibutilide can prolong ventricular repolarization and increase dispersion of ventricular repolarization in a dose-dependent and reverse rate-dependent manner. The high incidence of torsades de pointes in the dogs during chronic AV block suggests the importance of ventricular hypertrophy in the occurrence of ibutilide-induced proarrhythmia.

Effects of 17beta-estradiol on tachycardia-induced changes of atrial refractoriness and cisapride-induced ventricular arrhythmia.

INTRODUCTION: Gender difference is known to be associated with the occurrence of arrhythmia. However, the effects of female sex hormone on atrial electrophysiology, and on the occurrence of torsades de pointes (TdP) induced by cisapride have been unclear. METHODS AND RESULTS: Two experiments were included in this study. In experiment 1, effective refractory periods (ERPs) from five epicardial atrial sites were measured before and after rapid atrial pacing at 800 beats/min for 30 minutes in dogs with pretreatment of verapamil (n = 10), 17beta-estradiol (n = 10), or without pretreatment (n = 10, control group). In experiment 2, limb-lead ECG and monophasic action potentials in the left and right ventricles were recorded before and after each dose of cisapride (2 to 6 mg/kg) during different ventricular rates in dogs with (n = 9) and without (n = 14) concomitant administration of 17beta-estradiol (0.3 microg/kg). After 17beta-estradiol administration, there were greater atrial ERPs in the study dogs than in the control group. The atrial ERPs were shortened significantly after rapid atrial pacing, but the degree was greater in the control group than in the dogs pretreated with verapamil or 17beta-estradiol. Moreover, the recovery of atrial ERPs was faster in dogs pretreated with verapamil or 17beta-estradiol than in the control group. In experiment 2, cisapride prolonged the QT interval and biventricular APD90 and induced early afterdepolarizations (EADs) in a dose-dependent manner. However, dogs receiving cisapride combined with 17beta-estradiol had a greater increase of ventricular repolarization and a higher incidence of EADs than those receiving cisapride only. Moreover, dogs receiving cisapride combined with 17beta-estradiol (3/9, 33%) had a greater incidence of TdP than those receiving cisapride only (0/14, 0%, P < 0.05). CONCLUSIONS: 17beta-estradiol has a significant effect on atrial electrophysiology, which may be related to the prevention of atrial fibrillation. However, the high incidence of TdP in dogs receiving cisapride combined with 17beta-estradiol suggests that the female sex hormone is an important risk factor of cisapride-induced proarrhythmia.

Bezold-Jarisch-like reflex during radiofrequency ablation of the pulmonary vein tissues in patients with paroxysmal focal atrial fibrillation.

INTRODUCTION: Information is lacking about the occurrence of ablation-related proarrhythmic events during application of radiofrequency (RF) energy at the pulmonary veins in patients with paroxysmal focal atrial fibrillation. The purpose of this study was to assess the theoretical risk of reflex bradycardia and hypotension response during RF ablation of these regions rich in endocardial nerve terminals. METHODS AND RESULTS: Among the 40 consecutive patients (29 men, 11 women; mean age 65+/-12 years) with clinically documented frequent attacks of paroxysmal atrial fibrillation who underwent superior pulmonary vein ablation for left focal atrial fibrillation, 6 patients (15%) developed bradycardia-hypotension syndrome during energy delivery. A single atrial fibrillation trigger focus in the left or right superior pulmonary vein was found in 3 and 1 patients, respectively. Two patients had two trigger foci originating from the orifice or proximal part of both superior pulmonary veins. After RF current was applied for a period of 14+/-10 seconds, 2 patients developed junctional rhythm and sinus bradycardia, another 2 patients had profound sinus bradycardia, 1 patient had two episodes of sudden onset of complete AV block with resultant 9.5-second asystole, and 1 patient showed profound sinus bradycardia, transient AV block, and an 8-second asystole due to sinus arrest. Blood pressure fell when any substantial bradyarrhythmias occurred. All 6 patients were free of rhythm disturbances during the postablation follow-up period (mean 8+/-2 months). CONCLUSION: RF catheter ablation of the pulmonary vein tissues could evoke a variety of profound bradycardia-hypotension responses. The Bezold-Jarisch-like reflex might be the underlying mechanism.

Inducibility of atrial fibrillation during atrioventricular pacing with varying intervals: role of atrial electrophysiology and the autonomic nervous system.

INTRODUCTION: Patients receiving VVI pacemakers have a higher incidence of paroxysmal atrial fibrillation (AF) than those receiving DDD pacemakers. However, the mechanism behind the difference is not clear. The purpose of this study was to investigate whether atrial electrophysiology and the autonomic nervous system play a role in the occurrence of AF during AV pacing. METHODS AND RESULTS: The study population consisted of 28 patients who had (group I, n = 15) or did not have (group II, n = 13) AF induced by a single extrastimulus during pacing with different AV intervals. Atrial pressure, atrial size, atrial effective refractory periods, and atrial dispersion were evaluated during pacing with different AV intervals. Twenty-four-hour heart rate variability and baroreflex sensitivity also were examined. Atrial pressure, atrial size, effective refractory periods in the right posterolateral atrium and distal coronary sinus, and atrial dispersion increased as the AV interval shortened from 160 to 0 msec. During AV pacing, group I patients had greater minimal (52+/-17 vs 25+/-7 msec; P < 0.005) and maximal (76+/-16 vs 36+/-9 msec; P < 0.005) atrial dispersion than group II patients. The differences in atrial size and atrial dispersion among different AV intervals were greater in patients with AF than in those without AF. Baroreflex sensitivity (6.6+/-1.7 vs 3.9+/-1.0; P < 0.00005), but not heart rate variability, was higher in patients with AF than in those without AF. CONCLUSION: Abnormal atrial electrophysiology and higher vagal reflex activity can play important roles in the genesis of AF in patients receiving pacemakers.

Electrophysiological mechanisms and determinants of vagal maneuvers for termination of paroxysmal supraventricular tachycardia.

BACKGROUND: The vagal maneuvers used for termination of paroxysmal supraventricular reentrant tachycardia (PSVT) appear to involve more complex mechanisms than we have known, and further study should be done to explore the possible mechanisms. METHODS AND RESULTS: In this study, 133 patients with PSVT and 30 age- and sex-matched control subjects were included. We assessed the effects of different vagal maneuvers on termination of PSVT and compared baroreflex sensitivity and beta-adrenergic sensitivity between the patients with PSVT and control subjects. Out of 85 patients with atrioventricular reciprocating tachycardia (AVRT), vagal maneuvers terminated in 45 (53%). Of these, 28 (33%) terminated in the antegrade limb and 17 (20%) terminated in the retrograde limb. Out of 48 patients with atrioventricular nodal reentrant tachycardia (AVNRT), vagal maneuvers terminated the tachycardia in the antegrade slow pathway (14%) or in the retrograde fast pathway (19%). Baroreflex sensitivity was poorer but isoproterenol sensitivity test better in patients with AVNRT. Poorer antegrade atrioventricular node conduction properties and better vagal response determined successful antegrade termination of AVRT by vagal maneuvers. Poorer retrograde accessory pathway conduction property but better vagal response determined successful retrograde termination of AVRT. Better sympathetic and vagal response associated with poorer retrograde atrioventricular node conduction determined retrograde termination of AVNRT by the Valsalva maneuver. CONCLUSIONS: Both the vagal response and conduction properties of the reentrant circuit determine the tachycardia termination by vagal maneuvers. Improved understanding of the interaction of autonomic and electrophysiological mechanisms in maintaining or terminating PSVT may provide important insight into the pathophysiology of these two tachycardias.

Selective vagal denervation of the atria eliminates heart rate variability and baroreflex sensitivity while preserving ventricular innervation.

BACKGROUND: The purpose of this study was to test whether radiofrequency catheter ablation (RFCA) of 3 epicardial fat pads that resulted in efferent vagal denervation of the atria and sinus and atrioventricular nodes also denervated the ventricles. METHODS AND RESULTS: Vagal innervation of the ventricles was determined by measuring prolongation of ventricular effective refractory period induced by bilateral vagal stimulation (20 Hz, 10 V, 4 ms). Changes in heart rate variability (HRV) and baroreflex sensitivity (BRS) were also examined. We found that RFCA of the 3 epicardial fat pads vagally denervated the sinus and AV nodes and atria without affecting vagal innervation of the ventricles, indicating that efferent vagal fibers to the ventricles do not travel through the 3 epicardial fat pads. Parameters of time-domain variables decreased significantly; the total-power, high-frequency, and low-frequency components of frequency-domain variables decreased significantly; and the ratio of the low- and high-frequency components increased significantly after chronic vagal denervation. Vagally modulated sinus arrhythmia and BRS were also eliminated after chronic vagal denervation. These data also indicate that HRV and BRS represent vagal activity at the level of the sinus node and may not accurately reflect efferent vagal activity at the ventricular level. CONCLUSIONS: Selective vagal denervation of the sinus and AV nodes and atria decreased HRV and eliminated BRS while preserving ventricular innervation.

Intracardiac stimulation of human parasympathetic nerve fibers induces negative dromotropic effects: implication with the lesions of radiofrequency catheter ablation.

INTRODUCTION: The dromotropic effects of intracardiac parasympathetic nerve stimulation have not been well studied; furthermore, the effects of radiofrequency ablation lesions on parasympathetic nerve stimulation are not clear. METHODS AND RESULTS: Group I: intracardiac electrical stimulation in the right posteroseptal and anteroseptal areas under different stimulation strengths; group II: intracardiac electrical stimulation before and 10 minutes after intravenous propranolol; group III: intracardiac electrical stimulation before and 5 minutes after intravenous atropine. Among the 10 patients with AV nodal reentrant tachycardia (group IV) and the 10 patients with atrial flutter (group V), atrial fibrillation was induced before and after successful ablation, and intracardiac electrical stimulation in the right posteroseptal area was performed before and after successful ablation. The maximal response and complete decay of the response occurred within 2 to 6 seconds of initiation or termination of parasympathetic nerve stimulation. This negative dromotropic effect disappeared after atropine was administered, but not after propranolol. After successful ablation, parasympathetic stimulation still induced negative dromotropic effects. CONCLUSION: Electrical stimulation of parasympathetic nerve fibers near the posteroseptal and anteroseptal areas could induce a negative dromotropic effect, and this effect was preserved after successful radiofrequency ablation of slow pathway and isthmus conduction.

Characterization of low right atrial isthmus as the slow conduction zone and pharmacological target in typical atrial flutter.

BACKGROUND: Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown. METHODS AND RESULTS: Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length. CONCLUSIONS: The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.

Complex electrophysiological characteristics in atrioventricular nodal reentrant tachycardia with continuous atrioventricular node function curves.

BACKGROUND: Although typical atrioventricular nodal reentrant tachycardia (AVNRT) with discontinuous AV node function curves has been well studied, there has been a lack of any significant information about AVNRT without evidence of dual AV nodal pathway physiology during atrial extrastimulus testing or atrial pacing. METHODS AND RESULTS: Group 1 included 9 patients with continuous curves during atrial extrastimulus testing but without a jump (> or = 50 ms) of the atrial-His bundle (AH) interval during incremental atrial pacing. The maximal AH interval during atrial pacing (266 +/- 61 versus 168 +/- 27 ms, P = .007) or extrastimulus testing (290 +/- 60 versus 176 +/- 18 ms, P = .005) shortened significantly after ablation. Antegrade and retrograde AV node properties were similar before and after ablation. Group 2 included 14 patients with continuous curves and a jump of the AH interval during incremental atrial pacing. The atrial pacing cycle length with 1:1 AV conduction and effective refractory period (ERP) of the antegrade AV node increased significantly, whereas the maximal AH interval during atrial pacing (358 +/- 70 versus 203 +/- 28 ms, P = .001) or extrastimulus testing (338 +/- 75 versus 196 +/- 34 ms, P = .002) shortened significantly after ablation. Group 3 included 24 patients with discontinuous curves. The maximal AH interval during atrial pacing or extrastimulus testing and the ERP of the antegrade fast AV node shortened, whereas the ERP of the antegrade AV node increased significantly after ablation. The maximal AH interval before ablation, extent of decrease in maximal AH interval after ablation, ERP of the retrograde AV node before ablation, and tachycardia cycle length were significantly shorter in group 1 than groups 2 and 3. CONCLUSIONS: In AVNRT with continuous AV node function curves, dual AV nodal pathway physiology may or may not be demonstrated during atrial pacing. Significant shortening of the maximal AH interval during atrial pacing after radiofrequency ablation suggests successful elimination of AVNRT.

Efferent vagal innervation of the canine atria and sinus and atrioventricular nodes. The third fat pad.

BACKGROUND: The purpose of this study was to investigate the functional pathways of efferent vagal innervation to the atrial myocardium and sinus and atrioventricular (AV) nodes. METHODS AND RESULTS: Using vagally induced atrial effective refractory period shortening, slowing of spontaneous sinus rate, and prolongation of AV nodal conduction time as end points of vagal effects, we determined the actions of phenol and epicardial radiofrequency catheter ablation (RFCA) applied to different sites at or near the atrial myocardium to inhibit these responses. We found that efferent vagal fibers to the atria are located both subepicardially and intramurally or subendocardially. Most efferent vagal fibers to the atria appear to travel through a newly described fat pad located between the medial superior vena cava and aortic root (SVC-Ao fat pad), superior to the right pulmonary artery, and then project onto two previously noted fat pads at the inferior vena cava-left atrial junction (IVC-LA fat pad) and the right pulmonary vein-atrial junction (RPV fat pad) and to both atria. A few vagal fibers may bypass the SVC-Ao fat pad and go directly to the IVC-LA or RPV fat pad and then innervate the atrial myocardium. Vagal fibers to the sinus and AV nodes also converge at the SVC-Ao fat pad (a few fibers to the sinus node go directly to the RPV fat pad) before projecting to the RPV and IVC-LA fat pads. Long-term vagal denervation of the atria and sinus and AV nodes can be produced by RFCA of these fat pads and results in vagal denervation supersensitivity. Vagal denervation prevents induction of atrial fibrillation in this model. CONCLUSIONS: The newly described SVC-Ao fat pad receives most of the vagal fibers to the atria and sinus and AV nodes. Elimination of the fat pads with RFCA selectively vagally denervated the atria and sinus and AV nodes.

Electrophysiologic characteristics and radiofrequency catheter ablation in atrioventricular node reentrant tachycardia with second-degree atrioventricular block.

INTRODUCTION: Detailed electrophysiologic study of AV nodal reentrant tachycardia (AVNRT) with 2:1 AV block has been limited. METHODS AND RESULTS: Six hundred nine consecutive patients with AVNRT underwent electrophysiologic study and radiofrequency catheter ablation of the slow pathway. Twenty-six patients with 2:1 AV block during AVNRT were designated as group I, and those without this particular finding were designated as group II. The major findings of the present study were: (1) group I patients had better anterograde and retrograde AV nodal function, shorter tachycardia cycle length (during tachycardia with 1:1 conduction) (307 +/- 30 vs 360 +/- 58 msec, P < 0.001), and higher incidence of transient bundle branch block during tachycardia (18/26 vs 43/609, P < 0.001) than group II patients; (2) 21 (80.8%) group I patients had alternans of AA intervals during AVNRT with 2:1 AV block. Longer AH intervals (264 +/- 26 vs 253 +/- 27 msec, P = 0.031) were associated with the blocked beats. However, similar HA intervals (51 +/- 12 vs 50 +/- 12 msec, P = 0.363) and similar HV intervals (53 +/- 11 vs 52 +/- 12, P = 0.834) were found in the blocked and conducted beats; (3) ventricular extrastimulation before or during the His-bundle refractory period bundle could convert 2:1 AV block to 1:1 AV conduction. CONCLUSIONS: Fast reentrant circuit, rather than underlying impaired conduction of the distal AV node or infranodal area, might account for second-degree AV block during AVNRT. Slow pathway ablation is safe and effective in patients who have AVNRT with 2:1 AV block.

Results of radiofrequency ablation in patients with clinically documented, but noninducible, atrioventricular node reentrant tachycardia and orthodromic atrioventricular reciprocating tachycardia.

Among 1,281 patients with symptomatic supraventricular tachycardia, 34 patients (2.7%) with presumed diagnosis of atrioventricular node reentrant tachycardia and orthodromic atrioventricular reciprocating tachycardia did not have inducible tachycardia in the electrophysiologic laboratory. Application of radiofrequency energy to the presumed arrhythmogenic sites could achieve a high success rate, with a low recurrence rate in these patients.

Effect of high intensity drive train stimulation on dispersion of atrial refractoriness: role of autonomic nervous system.

OBJECTIVES: This study evaluated the effect of high intensity drive train (S1) stimulation on the atrial effective refractory period (ERP) and its relation to the autonomic nervous system. BACKGROUND: High intensity S1 stimulation was demonstrated to shorten the ventricular ERP and to increase dispersion of refractoriness. These effects may be due to local release of neurotransmitters. The response of the atrium and ventricle to neurotransmitters was different. The effects of high intensity S1 stimulation at the atrial tissue were evaluated. METHODS: Forty patients without structural heart disease were studied. In group 1, 20 patients, the atrial ERP was measured at 0, 7, 14, 21 and 28 mm away from the S1 site under both twice diastolic threshold and high intensity (10 mA) S1 stimulation. The same protocol was repeated after sequential administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In group 2, the other 20 patients, the atrial ERP was studied at three atrial sites (high lateral right atrium [HLRA], right posterior interatrial septum [RPS] and distal coronary sinus [DCS] with twice diastolic threshold and high intensity S1 stimulation at baseline and after sequential autonomic blockade. The three atrial sites were randomly assigned as the S1 location. RESULTS: In group 1, high intensity S1 stimulation shortened the atrial effective refractory period most prominently at the site of S1: (mean +/- SD) 13.3 +/- 6.4% (p < 0.001), 8.1 +/- 3.8% (p < 0.001), 4.8 +/- 4.3% (p < 0.001), 3.7 +/- 4.7% (p < 0.001) and 0.5 +/- 2.6% at 0, 7, 14, 21 and 28 mm from the S1 site, respectively. The effect of high intensity S1 stimulation was blunted with propranolol and autonomic blockade but persisted after atropine alone. High intensity S1 stimulation also increased dispersion of refractoriness (from 23 +/- 11 ms to 31 +/- 12 ms, p = 0.01), which was eliminated with autonomic blockade. In group 2, high intensity S1 stimulation had similar effects at different locations (ERP shortening of 10.8 +/- 2.7%, 10.8 +/- 2.2% and 12.2 +/- 4.6% at the HLRA, RPS and DCS, respectively). The responses to sequential autonomic blockade were similar to those in group 1. However, high intensity S1 stimulation at HLRA increased dispersion of refractoriness, but at DCS it reduced dispersion of refractoriness. CONCLUSIONS: High intensity S1 stimulation led to local shortening of the atrial ERP and increased dispersion of refractoriness. These effects were blunted with propranolol and autonomic blockade. High intensity S1 stimulation at the HLRA increased dispersion of atrial refractoriness, whereas the same stimulation at the DCS decreased dispersion of atrial refractoriness.

Electrophysiologic characteristics and radiofrequency catheter ablation of fast-slow form atrioventricular nodal reentrant tachycardia.

This study demonstrates that the fast-slow form of atrioventricular nodal reentrant tachycardia is usually catecholamine-sensitive and its electrophysiologic characteristics are significantly different from those of the slow-fast form. However, radiofrequency catheter ablation is a safe and effective treatment for patients with the fast-slow form of atrioventricular nodal reentrant tachycardia.