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We describe a patient who underwent radiofrequency (RF) catheter ablation of symptomatic atrial fibrillation. After left atrial (LA) catheter ablation and pulmonary vein isolation, a macro-reentrant atrial tachycardia (AT) with a critical isthmus at the mitral isthmus was induced by incremental atrial pacing from the coronary sinus. Extensive RF energy applications from endocardial sites using ablation catheters with 4 mm- and 8 mm- tips resulted in no discrete potentials being recorded from the endocardial sites of the isthmus, but the tachycardia could not be terminated. However, discrete potentials were recorded within the CS, and epicardial RF energy applications from the CS eliminated the tachycardia. Thus, mapping in the CS is useful for detecting residual conduction at epicardial sites along the mitral isthmus. RF catheter ablation within the CS should be considered when no distinct electrograms are recorded after extensive ablation from the endocardial sites and when distinct electrograms are recorded within the CS.

Objectives: The goal of this study was to describe the prevalence and ablation of coronary sinus (CS) arrhythmias after left atrial ablation for atrial fibrillation (AF)., Background: The CS has been implicated in a variety of supraventricular arrhythmias., Methods: Thirty-eight patients underwent mapping and ablation of atypical flutter that developed during (n = 5) or after (n = 33) ablation for AF. Also included were two patients with focal CS arrhythmias that occurred during an AF ablation procedure. A tachycardia was considered to be originating from the CS if the post-pacing interval in the CS matched the tachycardia cycle length and/or if it terminated during ablation in the CS., Results: Among the 33 patients who developed atypical flutter late after AF ablation, 9 (27%) were found to have a CS origin. Overall, 16 of the 40 patients in this study had a CS arrhythmia. The tachycardia was macro-re-entrant in 14 patients (88%) and focal in two patients. Radiofrequency ablation with an 8-mm-tip catheter was successful in 15 patients (94%) without complication. In eight patients (50%), > or = 45 W was required for successful ablation. Thirteen of the 15 patients (87%) with a successful ablation acutely remained arrhythmia-free during 5 +/- 5 months of follow-up., Conclusions: The musculature of the CS serves as a critical component of the re-entry circuit in approximately 25% of patients with atypical flutter after ablation for AF. The CS may also generate focal atrial arrhythmias that may play a role in triggering and/or maintaining AF. Catheter ablation of these arrhythmias in the CS can be performed safely.

Objective: The purpose of the present study was to develop an experimental model of inappropriate sinus tachycardia (IST) by injecting a catecholamine into a fat pad containing autonomic ganglia (AG) innervating the sinus node (SN)., Methods: Initial protocols in 3 groups of pentobarbital anesthetized dogs consisted of (1) slowing the heart rate (HR) by electrical stimulation of AG in the fat pad; (2) the effect of intravenous injection of epinephrine (0.1-0.3 mg) on the HR and systolic blood pressure (BP); (3) the response of SN rate to intravenously injected isoproterenol (1 microgm/kg). These studies established a reference for the response to epinephrine injection (mean dose 0.2 +/- 0.9 mg, n = 14) into the fat pad at the base of the right superior pulmonary vein (RSPV). ECG leads, right atrial and His bundle electrograms, BP and core body temperature were continuously monitored., Results: Epinephrine, injected into the fat pad, caused a significant increase in heart rate (HR, average: 211 +/- 11/min, p < 0.05 compared to control) but little change in systolic BP, 149 +/- 10 mmHg, p = NS (Group I, N = 8). The tachycardia lasted >30 minutes. Ice mapping and P wave morphology showed the tachycardia origin in the SN in 6/8 and in the crista terminalis (CT) in 2. Injection of 0.4 cc of formaldehyde into the FP restored HR (159 +/- 16) toward baseline (154 +/- 18). In Group II (N = 6), the same regimen induced a significant increase in both HR and systolic BP (194 +/- 17/min and 230 +/- 24 mmHg, respectively) compared to control values (143 +/- 23/min, 162 +/- 24 mmHg) which lasted for > 30 minutes. Ice mapping and P wave morphology showed that the pacemaker was in the SN (1), overlying the CT (2), or atrioventricular junction (2). Formaldehyde (0.4 cc) injected into the FP restored both HR and systolic BP toward baseline values (148 +/- 29/min and 152 +/- 24 mmHg, p = NS) and prevented, slowing of the HR by electrical stimulation of the AG; moreover, the same dose of epinephrine injected intravenously increased HR and SBP but only for 2-5 minutes; Isoproterenol (1 microg/kg) injected intravenously induced essentially the same increase in sinus rate after AG ablation as in the control state (194 +/- 15/min vs 193 +/- 23/min, p = NS)., Conclusion: Experimental IST is mainly localized in the SN or CT. Ablation of the AG terminates IST without impairing the SN response to an adrenergic challenge.

Objective: Biventricular pacing has demonstrated improvement in cardiac function in treating congestive heart failure (CHF). Two different operative strategies (coronary sinus vs. epicardial stimulation) for left ventricular (LV) pacing were compared., Methods: Since April 1999, a total of 86 patients (pts, age: 63+/-10 years) with depressed systolic LV function (mean ejection fraction 24+/-9%), left bundle-branch-block (mean QRS 182+/-22 ms) and congestive heart failure NYHA III or higher were enrolled. For biventricular stimulation coronary sinus (CS) leads were placed in 79 pts. Nine of these devices were converted to surgical epicardial LV-leads, because of CS-lead failure. In 7 patients epicardial LV-leads were initially implanted surgically, accounting for a total of 16 pts with surgical placed epicardial steroid-eluting LV-leads. For these, a limited left-lateral thoracotomy (7+/-4 cm) was used. Thirty-three (38%) pts had an indication for a defibrillator. The mean follow-up time was 16.4+/-15.4 months (0.1-45 months), representing 107.1 patient-years., Results: In the biventricular pacing mode, QRS duration decreased to 143+/-16 ms (P<0.001). Threshold capture of the CS-leads increased significantly compared to surgically placed epicardial leads (18 month control: 2.2+/-1.4V/0.5 ms vs. 0.7+/-0.3V/0.5 ms), which had no increase in threshold (P<0.001). At the 18 month follow-up 7 CS-leads had a threshold of >4V/0.5 ms vs. epicardial leads which were under 1.1V/0.5 ms, except for one (1.8V/0.5 ms). After CS-lead implantation 25 LV-lead related complications occurred, (failed implantation, CS-dissection, loss of pacing capture, diaphragm stimulation or lead dislodgment), vs. one dislodgement after surgical epicardial lead placement (P<0.05). Correct lead positioning (obtuse marginal branch area) was achieved in all surgical epicardial placements but only in 70% with CS-leads (P<0.03). In the follow up period, 9 pts died (4 cardiac related). Heart transplantation was necessary in 4 pts due to deterioration of the cardiomyopathy., Conclusions: Surgical epicardial lead placement revealed excellent long-term results and a lower LV-related complication rate compared to CS-leads. Although, the approach via limited thoracotomy for biventricular pacing is associated with 'more surgery', it is a safe and reliable technique and should be considered as an equal alternative.

We and others have demonstrated that impaired arterial baroreceptor reflex (ABR) function is one of the major causes of hypertension-associated end organ damage. The goal of this study was to clarify the potential neuro-humoral mechanisms responsible for impaired ABR-induced end organ damage. The sino-aortic denervated (SAD) rat was used as an animal model of ABR dysfunction. One-week SAD rats were characterized by hypertension, tachycardia, increased norepinephrine content, and decreased beta-endorphin and leu-enkephalin content in hypothalamus and medulla oblongata, and increased plasma levels of arginine-vasopressin. In 18-week SAD rats, the 24-hour average arterial pressure, heart rate, beta-endorphin, and leu-enkephalin content in hypothalamus and medulla oblongata and plasma levels of arginine-vasopressin and angiotensin II were not different from those measured in ABR-intact rats. However, blood pressure variability and angiotensin II content in kidney and left ventricle increased. When exposed to chronic stress, exaggerated changes in arterial pressure, blood pressure variability, the levels of central norepinephrine, beta-endorphin and leu-enkephalin, plasma arginine-vasopressin and angiotensin II, and tissue angiotensin II were found in 18-week SAD rats. These data indicate that a long-term impairment of ABR leads to chronic activation of central noradrenergic neurons and tissue renin-angiotensin system, and that stress induces exaggerated responses of neuro-humoral factors and hemodynamics in SAD rats. Thus, if the present results hold true for humans, one can expect abnormal neurotransmitter/neuromodulator responses to environmental insults in patients with impaired ABR function.

Transient sinus node dysfunction has been demonstrated by noninvasive methods following the maze procedure for atrial fibrillation (AF). However, extensive data from invasive electrophysiological studies have not been previously reported. Thirty-seven patients, mean age 54 +/- 10 years, underwent the maze (III) procedure. Electrophysiological studies with recordings of SNRT, CSNRT, AVN-ERP, point of Wenckebach block, AH, PA, and HV interval, were performed preoperatively and 6 and 15 months postoperatively. Induction of atrial flutter/AF was attempted postoperatively. Based on electrophysiological study evaluation, the maze (III) procedure did not cause permanent damage to the sinus node in any patient with a documented normal sinus node function preoperatively (CSNRT max 541 +/- 210 vs 587 +/- 437 ms, P = 0.26). Postoperative AV node function was normal in all patients with a documented normal AV node function before surgery. One patient had an iatrogenic third degree AV block. There was no difference in PA or HV interval after surgery. Sustained atrial tachyarrhythmias could be induced in 5 patients, of whom 4 developed permanent AF/atrial flutter late after surgery. At late follow-up, (mean 45 months), 27 (73%) patients were in sinus rhythm, 5 (13%) patients had permanent pacing, and 5 patients had recurrent AF requiring His bundle ablation (n = 2) or medical treatment (n = 3). Based on electrophysiological studies, the maze (III) procedure does not cause permanent damage to the sinus or AV nodes or to the right atrial and His-Purkinje conduction systems. Electrophysiological study evaluation may predict the need for postoperative pacemaker. Induction attempts of atrial arrhythmias may predict future recurrences and guide therapeutic efforts.

The heart's pacemaker, the sinoatrial node, does not consist of a group of uniform sinoatrial node cells embedded in atrial muscle. Instead, it is a heterogeneous tissue with multiple cell types and a complex structure. Evidence suggests that from the periphery to the center of the sinoatrial node, there is a gradient in action potential shape, pacemaking, ionic current densities, connexin expression, Ca2+ handling, myofilament density, and cell size. This complexity may be necessary for the sinoatrial node to pacemake under diverse conditions, drive the more hyperpolarized atrial muscle, and resist proarrhythmic perturbations.

The aims of present study were to verify the topography of the intracardiac nerve subplexuses (INS) by using electrophysiological methods, its relations with sinoatrial (SA) node function and to investigate possibility of selective surgical SA node denervation. Fifteen mongrel dogs of either sex weighing 8 to 15 kg were used for electrophysiological studies. Both cervical vagosympathetic trunks were isolated and crushed by tight ligatures. Nervus subplexuses destructions were performed by cryocoagulation in three zones located around the right superior vena cava: ventral, lateral and dorsal. The sinus rhythm, SA node function recovery time, AV node conductivity, AV node and atrial effective refractory period were measured. Five experiments in each of three zones were performed. Experimental data show that destruction of the epicardial nerves has different effect on electrophysiological parameters. After destruction of the anterior zone of the right atrium the sinus rhythm decreased on an average by 11.6%; SA node function recovery time prolonged by 7.2%; AV node conductivity decreased by 13.1%; AV node effective refractory period prolonged by 12.9% and atrial effective refractory period, by 10.9 %. Measurements of electrophysiological parameters after intravenous injection of atropine sulphate show that sinus rhythm decreased on an average by 23.4%; SA node function recovery time increased by 9.1%; the conductivity of AV node decreased by 10.2%; AV node effective refractory period prolonged by 15.4% and atrial effective refractory period, by 13.2%. After destruction of the intracardiac nerves of the lateral zone, the sinus rhythm decreased by 15.7%; SA node function recovery time increased by 16.3%; AV node conductivity decreased by 8.3%; AV node effective refractory period and atrial effective refractory period prolonged by 11.9% and 10.0%, respectively. After the atropine sulphate intravenous injection, the sinus rhythm decreased on an average by 7.1%, SA node function recovery time prolonged by 7.1%, AV conductivity decreased by 9.1%, AV node effective refractory period increased by 12.4%, and atrial effective refractory period prolonged by 12.5%. After destruction of the nerves in the dorsal zone the changes of electrophysiological parameters were opposite to those obtained after destruction of the nerve tracts in the anterior or lateral zones: the sinus rhythm increased on an average by 4.3%; SA node function recovery time shortened by 8.8%; AV conductivity increased by 9.7%; AV node and atrial effective refractory period decreased by 12.3% and 12.1%, respectively. After intravenous atropine sulphate infusion, sinus rhythm decreased on an average by 8.3%; SA node function recovery time prolonged by 9.6%; AV node conductivity decreased by 5%; AV node and atrial effective refractory period prolonged by 4.2% and 5.2%, respectively. The average changes of electrophysiological parameters before and after INS destruction shows that cryocoagulation of ventral and lateral zones eliminates the effects of sympathetic tone to SA and AV nodal activity. Cryocoagulation of dorsal zone eliminates the effects of nervus vagus to both nodal structures. These findings shows the possibility alter or correct SA node function by making selective surgical SA node denervation.

Background: The aim of this study was to explore the characteristics and mechanisms of the cardiovascular effects of cocaine in dilated cardiomyopathy., Methods and Results: We studied the cardiovascular responses to acute intravenous cocaine (1 mg/kg) in 8 conscious, chronically instrumented dogs before and after the development of dilated cardiomyopathy induced by rapid ventricular pacing. To help elucidate the role of altered baroreflex function in mediating the cardiovascular effects of cocaine, we also studied responses in 3 conscious, chronically instrumented dogs that had undergone surgical sinoaortic baroreceptor denervation. Cocaine produced greater increases in heart rate (+57 +/- 8% from 112 +/- 5 beats/min versus +28 +/- 3% from 100 +/- 4 beats/min; P <.01), first derivative of left ventricular pressure (+30 +/- 5% from 1,714 +/- 147 mm Hg/sec versus +15 +/- 3% from 3,032 +/- 199 mm Hg/sec; P <.01), coronary vascular resistance (+28 +/- 5% from 2.3 +/- 0.3 mm Hg/mL/min versus +11 +/- 5% from 2.2 +/- 0.3 mm Hg/mL/min; P <.05) and plasma norepinephrine concentration (+130 +/- 31% from 462 +/- 102 pg/mL versus +86 +/- 32% from 286 +/- 77 pg/mL; P <.05) in dogs with dilated cardiomyopathy as compared to controls. In addition, responses were much more rapid in onset following the development of dilated cardiomyopathy. Chronotropic and inotropic responses to cocaine were similarly rapid and exaggerated in dogs after baroreceptor denervation., Conclusions: Cocaine produces rapid and exaggerated chronotropic, inotropic, and coronary vasoconstrictor responses in conscious dogs with pacing-induced dilated cardiomyopathy. Alterations in arterial baroreflex function may play a role in these observations, which in turn may underlie the clinically observed association between cocaine and heart failure.

Background: Elevated awake resting heart rate (HR) has been shown to be a major risk factor for cardiovascular disease. Since coronary ischaemic events appear to peak during transition from sleep to awake HR, we sought to determine whether the degree of diurnal HR fluctuation (dHRV) is an independent predictor of coronary and peripheral atherogenesis. In this study, we varied both baseline HR and dHRV using sino-atrial node ablation (SNA) in a primate model of diet-induced atherogenesis and determined the degree of plaque formation relative to both HR parameters., Methods: HR was recorded continuously for 6 months by an implantable intraaortic sensor/transmitter in 17 active unrestricted male cynomolgus monkeys. In nine monkeys, SNA was employed to create a wide spectrum of dHRV, and the power amplitude of dHRV was determined for the daily HRV cycle with power spectral analysis. After a 6-month diet induction period, percent coronary and carotid stenosis, intimal thickness and area were quantitated in each animal., Results: Total serum cholesterol and mean HR were no different between high ( n= 10) and low ( n= 7) dHRV groups (866 mg% vs. 740 mg%, P> 0.2 and 130 +/- 22 and 115 +/- 13, P> 0.1, respectively). Percent carotid stenosis was markedly greater in both high HR and dHRV animals ([HR], 54 +/- 19 vs. 35 +/- 10, P< 0.04) and ([dHRV], 54 +/- 17 vs. 32 +/- 10, P< 0.01). Significant increases in all measures of coronary atherogenesis were found in high dHRV animals when compared with those with low dHRV (percent stenosis: 48% +/- 22 vs. 23% +/- 16, P< 0.02), (lesion area: 1.2 +/- 0.8 vs. 0.3 +/- 0.3, P< 0.02), and (intimal thickness: 0.3 +/- 0.1 vs. 0.1 +/- 0.1, P< 0.01), respectively. While there was a trend towards greater coronary atherogenesis in animals with high HR, this did not reach statistical significance., Conclusion: Elevated HR and dHRV are both associated with enhanced experimental atherosclerotic plaque formation. However, a greater degree of carotid and coronary atherogenesis is observed in animals with high dHRV. These findings suggest that elevated dHRV is a stronger predictor for susceptibility to atherogenesis than elevated HR alone. Such a relationship may be attributed to the potential role of dHRV in modulating the frequency of adverse near wall haemodynamic forces, which have been shown to induce atherosclerotic plaques. Lowering of dHRV in humans by exercise or pharmacological agents may have a beneficial role in retarding atherosclerotic plaque induction, progression and complication.

The outcome of surgical repair of sinus venosus atrial septal defect was reviewed retrospectively. The operation was performed on 44 children aged 8 to 163 months, between April 1985 and November 1998. Median cardiopulmonary bypass and aortic crossclamp times were 58 minutes (range, 29 to 141 minutes) and 29 minutes (range, 4 to 67 minutes), respectively. Use of blood products decreased from 4.5 units per patient in the first period (1985 to 1989) to 0.6 units in the last period (1995 to 1998). Median intensive care and hospital stays were 2 days (range, 1 to 12 days) and 6 days (range, 4 to 16 days), respectively. There was 1 early death (2.3%). Complications included reexploration for bleeding in 2 patients (4.5%) and for superior vena cava obstruction in 1 (2.3%), and arrhythmias in 3 (6.8%), which required a pacemaker in one. During follow-up of 15 to 176 months, 83.8% of patients were in sinus rhythm. One required angioplasty for superior vena cava stenosis, hemodynamically insignificant residual shunt was found in 3, and mild superior vena cava stenosis in 3. Repair of sinus venosus atrial septal defect carries a low mortality and morbidity, but long-term follow-up is needed to monitor potential sinus node dysfunction and superior vena cava stenosis.

Introduction: Parasympathetic activity predominates over sympathetic activity not only with respect to heart rate but also with respect to the pacemaker location in the dog heart. After we removed the parasympathetic neural elements in the sinoatrial (SA) fat pad in the right atrium, we observed that cervical vagus stimulation did not decrease the atrial rate, but it did suppress the increase in rate evoked by sympathetic stimulation. We determined whether the pacemaker rate and location were affected by presynaptic or postsynaptic mechanisms., Methods and Results: We determined the earliest activation site by means of isochronic activation mapping of the right atrium of open chest, anesthetized dog hearts. An electrode array, which consisted of 48 unipolar electrodes, was used to record atrial activation. This array covered the three main pacemaker regions, including the SA node region. After parasympathetic nerve fibers in the SA fat pad had been denervated, vagus stimulation at 10 and 30 Hz did not decrease the heart rate, but it attenuated the increase in heart rate evoked by sympathetic stimulation or isoproterenol. Vagus stimulation at 10 Hz during sympathetic stimulation did not shift the earliest activation site from the superior pacemaker region to the SA node region in 11 of 18 experiments. However, vagus stimulation at 10 Hz during isoproterenol infusion shifted the earliest activation site to the SA node region in 11 of 13 experiments. More intense vagus stimulation during combined sympathetic stimulation or isoproterenol infusion shifted the earliest activation site to the SA node or the inferior pacemaker region in 15 of 18 and in all experiments, respectively., Conclusion: The results suggest that activation of parasympathetic elements not located in the SA fat pad attenuates the increase in heart rate and the shift in pacemaker location evoked by sympathetic activation. The sympathetic and parasympathetic effects interact at presynaptic and postsynaptic sites in the dog heart.

Introduction: Striated myocardial connections between the venous wall of the coronary sinus (CS) and the left atrium have been described in humans. This aim of this study was to investigate the conduction properties and potential arrhythmogenicity of CS and left atrial myocardial connections in patients with and patients without paroxysmal atrial fibrillation (PAF)., Methods and Results: Thirty-eight patients with PAF, 52 patients with other arrhythmias, and 44 patients without arrhythmia underwent catheter mapping of the CS from the distal superoposterior part to the ostium. Catheterization of the superoposterior CS was feasible in 21, 32, and 25 subjects in the three groups, respectively (P = 0.82). Discrete double potentials or fractionated electrograms were recorded during proximal CS or right atrial pacing in 14 (66.7%), 11 (34.4%), and 5 (20.0%) patients, respectively (P = 0.004). In 29 patients, double or fractionated potentials were recorded at the distal superoposterior CS, in 3 at the mid-CS, and in 4 at the ostium. Spontaneous or induced atrial ectopy and/or tachyarrhythmias were recorded in 18 (85.7%), 12 (37.5%), and 2 (8.0%) patients in the three groups, respectively (P < 0.001) and originated from the CS in 6, 3, and 0 patients, respectively (P = 0.010)., Conclusion: Recording of double potentials is possible within the CS, particularly at its distal superoposterior part, near the left superior pulmonary vein. Their prevalence is higher in patients with PAF than in subjects with other or no arrhythmias, and their presence denotes possible sources or substrate for atrial arrhythmia.

Introduction: A novel sustained inward Na+ current i(sv), which sensitive to Ca2+-antagonists and potentiated by beta-adrenergic stimulation, has been described in pacemaker cells of rabbit, guinea pig, and rat sinoatrial node, as well as rabbit AV node. Although i(st) has been suggested to be an important pacemaker current, this has never been tested experimentally because of the lack of a specific blocker. In this study, we address the role of i(st) in the pacemaker activity of the sinoatrial node cell using computer models., Methods and Results: The newly developed models of Zhang et al. for peripheral and central rabbit sinoatrial node cells and models of Noble and Noble, Demir et al., Wilders et al., and Dokos et al. for typical rabbit sinoatrial node cells were modified to incorporate equations for i(st). The conductance g(st) was chosen to give a current density-voltage relationship consistent with experimental data. In the models of Zhang et al. (periphery), Noble and Noble, and Dokos et al., in which i(st) was smaller or about the same amplitude as other inward currents, i(st) increased the pacemaking rate by 0.6%, 2.2%, and 0.8%, respectively. In the models of Zhang et al. (center), Demir et al., and Wilders et al., in which i(st) was larger than some other inward ionic currents, i(st) increased the pacemaking rate by 7%, 20%, and 14%, respectively., Conclusion: i(st) has the potential to be a regulator of pacemaker activity, although its importance will depend on the amplitude of i(st) relative to the amplitude of other inward currents involved in pacemaker activity.

Introduction: Depression of sinus node function occurs in dogs and in patients after cessation of atrial flutter and fibrillation. We tested whether transient atrial pacing might produce similar changes in humans., Methods and Results: We studied the impact of short-term rapid atrial pacing, simulating atrial tachyarrhythmias, on sinoatrial conduction time (SACT) and corrected sinus node recovery time (CS-NRT) in 10 patients undergoing electrophysiologic study. None had recognizable structural heart disease, history of atrial fibrillation or flutter, autonomic dysfunction, or any tachycardia for at least 24 hours before study. All cardiac drugs were discontinued >5 half-lives prior to study. No patient had significant hypotension during atrial stimulation. SACT and CSNRT were measured at baseline, and sinus node reset zone was determined. Right atrial pacing was performed for 10 to 15 minutes, after which SACT and CSNRT were measured again. Both parameters increased significantly, from 423+/-208 msec to 491+/-214 msec and from 80+/-50 msec to 96+/-53 msec, respectively (P = 0.02 and P < 0.001, respectively)., Conclusion: Rapid atrial pacing for only 10 to 15 minutes, simulating transient atrial tachyarrhythmias, alters sinus node function in humans. Additional studies are needed to evaluate the mechanism, but the clinical implication is that even transient episodes of atrial tachyarrhythmias can cause sinus node remodeling in patients.

A giant coronary aneurysm arising from the sinus node artery is reported. Diagnosis of this lesion by computed tomography and angiography is illustrated. The operative management is described. "Off-pump" aneurysmectomy was successfully performed. The role of occlusion test of the aneurysm inflow tract is emphasized.

Dilation of the coronary sinus is mostly a congenital lesion. As acquired lesion it was found to be associated with poor left ventricular function. In the present case an angiographic diagnosed posterior left ventricular aneurysm was during surgery found to be a dilated coronary sinus. Preoperative left ventricular function was normal.

Inappropriate sinus tachycardia and postural orthostatic tachycardia are ill-defined syndromes with overlapping features. Although sinus node modification has been reported to effectively slow the sinus rate, long-term clinical response has not been adequately assessed. Furthermore, whether patients with postural orthostatic tachycardia would benefit from sinus node modification is unknown. The study prospectively assessed the short- and long-term clinical outcomes of seven consecutive female patients with postural orthostatic tachycardia syndrome and inappropriate sinus tachycardia who were treated with sinus node modification. The study was conducted in a tertiary care center. The electrophysiological and clinical responses were prospectively assessed as defined by autonomic function testing, including Valsalva maneuver, deep breathing, tilt table testing, and quantitative sudomotor axonal reflex testing. Among the study population (mean age was 41+/-6 years), 5 (71%) patients had successful sinus node modification. At baseline, heart rates were 101+/-12 beats/min before modification and 77+/-9 beats/min after modification (P = 0.001). With isoproterenol, heart rates were 136+/-9 and 105+/-12 beats/min (P = 0.002) before and after modification, respectively. The mean heart rate during 24-hour Holter monitoring was also significantly reduced: 96+/-9 and 72+/-6 beats/min (P = 0.005) before and after modification, respectively. Despite the significant reduction in heart rate, autonomic symptom score index (based on ten categories of clinical symptoms) was unchanged before (15.6+/-4.1) and after (14.6+/-3.6) sinus node modification (P = 0.38). Sinus rate can be effectively slowed by sinus node modification. Clinical symptoms are not significantly improved after sinus node modification in patients with inappropriate sinus tachycardia and postural orthostatic tachycardia. A primary subtle autonomic disregulation is frequently present in this population. Sinus node modification is not recommended in this patient population.

In a series of 35 consecutive patients, the presence of a permanent pacemaker appears to be a strong risk factor for developing superior vena cava syndrome after radiofrequency modification of the sinus node. Treatment of this complication with balloon venoplasty is as effective as surgical repair.

Catheter ablation orientated on the induction of a functional intraatrial block within the posterior isthmus of the tricuspid annulus has been shown to effectively abolish atrial flutter. In order to improve and simplify the current technique, a strategy based on an electrode catheter for combined right atrial and coronary sinus mapping and stimulation was explored prospectively. Twenty-four consecutive patients referred for catheter ablation of recurrent type I atrial flutter were included. A steerable 7 Fr catheter (Medtronic/Cardiorhythm) composed of two segments with 20 electrodes was used for right atrial and coronary sinus activation mapping and stimulation. Multiple steering mechanisms allowing intubation and positioning of the distal part within the coronary sinus were incorporated into the device. Adequate positioning of the mapping catheter was achieved solely via a transfemoral approach in all patients after 7.7 +/- 4.6 minutes, providing stable electrogram recordings during the entire ablation procedure. Radiofrequency current ablation (16.3 +/- 9.6 pulses) caused a significant bidirectional increase of the mean intraatrial conduction times via the posterior isthmus irrespective to the stimulation interval. Significant changes of intraatrial conduction properties were induced during ablation in 22 of 24 patients (bidirectional block: n = 18, unidirectional block: n = 3, conduction delay: n = 1, unchanged conduction: n = 2). Following ablation atrial flutter was noninducible in all patients. Twenty-two of 24 patients (92%) remained free of atrial flutter episodes during a follow-up of 12.5 +/- 5.7 months. Two of six patients without a bidirectional conduction block had a recurrence of atrial flutter. Atrial flutter ablation guided by the induction of an intraatrial conduction block can be effectively performed with this novel strategy for combined mapping of the posterior tricuspid isthmus, including coronary sinus and right atrial free wall. This transfemoral approach has a high accuracy with respect to the detection of radiofrequency current-induced changes of intraatrial conduction patterns.

Introduction and Objectives: The MAZE procedure was developed as a surgical approach to the management of patients with atrial fibrillation refractory to medical treatment. This study seeks to identify the risk and benefits of adding the MAZE procedure in patients with atrial fibrillation undergoing surgery for underlying organic cardiac disorders., Material and Methods: Since november 1993, we have performed 10 interventions with the MAZE procedure, for the treatment of refractory atrial fibrillation. The indication to perform the technique was systemic embolism in 5 patients, contraindication for the anticoagulant treatment in two cases and no response to antiarrhythmic treatment in 5 cases. Two patients had more than one indication. In all the cases another surgical procedure was performed, 5 replacements of mitral valve, a mitral repair, one tricuspid repair and tree repairs of an atrial septal defect., Results: Soon after surgery 9 patients were in sinus rhythm, and one in atrial fibrillation. Four patients needed atrial pacing during the first days. One patient required a pacemaker due to symptomatic sinus bradycardia. During the first 3 months, 4 patients had episodes of paroxysmal atrial fibrillation and flutter. One patient died suddenly one month after surgery. Seven patients have completed two years of follow-up, and are in stable sinus rhythm, in functional class I and free of antiarrhythmic drugs. All of them have echocardiographic evidence of mechanical activity in both atria. Left atrium had been reduced from 5.3 +/- 0.7 cm to 4.5 +/- 0.7 cm (p < 0.05). No patient has presented new embolic events., Conclusions: The MAZE procedure is a good choice in selected patients with atrial fibrillation refractory to medical treatment, or a precedent of systemic embolism. However, several problems can complicate the patient's course.

This article reports the early and late results of a patient in whom radiofrequency current was used to ablate an incessant inappropriate sinus tachycardia. During successful radiofrequency application there was a sudden change of rate and subsequent emergence of a stable rhythm with the same sinus node P wave characteristics. During follow-up, normal cardiac cycles were still present after six months of the procedure, although the patient still complained of palpitations, suggesting no correlation with the heart rate.

Prerequisite for successful radiofrequency catheter ablation on tachycardias is the exact mapping during the electrophysiologic study. The new mapping system CARTO allows a three-dimensional color-coded electroanatomic map of impulse propagation using electromagnetic technology. Mapping of sinuatrial activation in the right atrium of 11 patients represents the first clinical experience with this new system. The physiological activation sequence could be determined in all patients three-dimensionally, and the sinus node could be localized as a physiological activation focus with interindividual variability only in the sagital plane without complications. The nonfluoroscopic mapping system allows high resolution visualization of electrical activity and may therefore improve precision and simplify the determination of the arrhythmogenic substrate during tachycardias for successful catheter ablation.

Recent clinical studies have reported a beneficial effect of fluoxetine, a serotonin reuptake inhibitor, in patients with severe refractory orthostatic hypotension. The present study was undertaken to investigate the effect of fluoxetine in orthostatic hypotension occurring during Parkinson's disease on both blood pressure values and number of clinical symptoms during orthostatic procedure evaluated using a validated clinical rating scale. In a pilot study performed in fourteen patients with idiopathic Parkinson's disease plus orthostatic hypotension, fluoxetine hydrochloride (20 mg orally daily during one month) significantly reduced the fall in systolic blood pressure [-33 +/- 21 (SD) mmHg before fluoxetine vs -22 +/- 19 mmHg after fluoxetine, P = 0.03] elicited by standing without modifying heart rate. The drug also significantly reduced the number of postural symptoms occurring during the orthostatic procedure [2.9 +/- 1.5 (SD) before fluoxetine vs 1.2 +/- 1.3 after fluoxetine, P = 0.006]. A similar pattern of response was obtained in an experimental model of neurogenic orthostatic hypotension obtained in chronically sino-aortic denervated dogs submitted to an 80 degrees head-up tilt test procedure under chloralose anaesthesia. Fluoxetine did not change plasma noradrenaline levels. This pilot study suggests a slight but clinically significant effect of fluoxetine on both hemodynamic parameters and clinical symptoms in parkinsonian patients suffering from orthostatic hypotension.

Objective: The transseptal superior approach can offer an excellent view of the mitral valve but the incision almost always transects the sinus node artery. The purpose of this study was to evaluate the sinus node function after mitral operation by this approach., Patients and Methods: We reviewed the electrocardiograms of 76 patients who underwent mitral valve operations either via transseptal superior approach or via right lateral atriotomy. Nine patients who maintained the sinus rhythm for more than one year after surgery via the transseptal superior approach were selected for electrophysiological study to evaluate the sinus node function., Results and Conclusions: Postoperative electrocardiographic and electrophysiological studies revealed that the sinus node function after the transseptal superior approach was relatively well maintained for more than one year after the operation. The influence of the transseptal superior approach on the sinus node function in the mid-term postoperative period was apparently mild and did not cause a serious problem. However, some of the patients did show abnormal data in terms of sino-atrial conduction time and intrinsic heart rate. Therefore, further follow-up of the sinus node function is necessary in patients who underwent mitral surgery through the transseptal superior approach.

Background: Cardiac angiotensin AT1 receptors have been found in several animal species. In-vitro studies performed on cardiac preparations have shown that angiotensin II (ANG II) exerts a positive inotropic effect; however, in-vivo results have allowed no definitive conclusion to be drawn. The reasons behind these controversial results remain unknown, and could originate both from different experimental conditions and from the techniques used to assess myocardial contractility., Objective: To investigate, by means of echocardiographic measurements, whether ANG II, administered to intact and to sinoaortic denervated isoflurane-anesthetized rabbits, was able to directly increase myocardial contractility., Methods: The effect of ANG II on cardiac contractility was assessed with the use of simultaneous pressure measurements and Doppler-echocardiographic recordings. Specifically, we used both the relationship between the left ventricular end-systolic wall stress and the velocity of heart-rate-corrected circumferential fiber shortening (VCFC) and the maximum rate of rise of the ventricular pressure as indices of changes in myocardial contractility. Cardiac contractility was evaluated both in intact and in chronically sinoaortic denervated isoflurane-anesthetized rabbits under basal conditions and after ANG II infusion (50 ng/kg per min)., Results: After ANG II infusion, increases in mean arterial blood pressure, left ventricular end-diastolic diameter and pressure were observed both in intact and in chronically sinoaortic denervated rabbits. The left ventricular end-systolic wall stress (a function of the mean arterial pressure and chamber size) and the maximum rate of rise of the ventricular pressure rose markedly in rabbits of both groups, whereas the VCFC decreased significantly. However, when compared the VCFC under ANG II infusion with that calculated at the same level of left ventricular afterload under basal conditions, we observed that ANG II infusion induced no significant change in VCFC either in intact of in chronically sinoaortic denervated rabbits., Conclusion: Our results indicate that administration of ANG II to isoflurane-anesthetized rabbits induces a marked rise in ventricular pre- and after-loads and exerts no significant effect on the cardiac contractility. In light of this, it is reasonable to assume that the short-term increase in arterial blood pressure can be ascribed mainly to the increase in peripheral arterial resistance.

Background: Inappropriate sinus tachycardia (IST) is a rare form of supraventricular arrhythmia. It can cause disabling symptoms and may be refractory to medical treatment. In symptomatic drug refractory patients, sinus node excision or total ablation of the sinus node with permanent pacemaker implantation was the only therapeutic option. Recently, radiofrequency (RF) modification of the sinus node has been reported to be an effective treatment for this condition., Aim: To present our experience with sinus node modification using RF energy in the management of IST., Methods: Between 1989 to 1996 three patients (two females and one male), aged 28-36 years were diagnosed with symptomatic IST. All had failed multiple drugs and hence underwent sinus node modification using RF. In the first two patients, the site of RF application was guided by anatomical landmarks using fluoroscopy to localise the presumed most superior portion of the crista terminalis and also the earliest site of atrial activation. In the third patient, a 20 pole electrode catheter was used to map the crista terminalis and guide the ablation. Success was defined by 20-30% reduction in the heart rate with normal atrial activation sequence after ablation., Results: The three patients described here had IST by clinical, electrocardiographic and electrophysiological criteria and were refractory to multiple antiarrhythmic drugs. The number of RF applications were 11, 15, and three applied at the site of earliest atrial activation for the control of heart rates. Patient 3 had a early recurrence at one month and underwent repeat sinus node modification (five RF applications). All three patients who underwent RF modification of the sinus node had a successful outcome. The procedure was uncomplicated and the patients remain asymptomatic during follow up (20, 12 and three months) with satisfactory control of heart rate, although one patient requires atenolol which was previously ineffective., Conclusions: RF modification of the sinus node is feasible and effective for IST, and should be the treatment of choice in patients refractory to medical therapy.

The aim of this study was to determine the effectiveness of the 'corridor' procedure when added to mitral valve replacement in restoring and maintaining sinus rhythm in patients with chronic atrial fibrillation resulting from rheumatic mitral valve disease. Twenty-two patients with rheumatic mitral valve disease and chronic atrial fibrillation with fast, irregular ventricular response were divided into two groups. In the first group (n = 12), mitral valve replacement was combined with sinus node-AV node isolation ('corridor'): in the second, control group (n = 10), mitral valve replacement was performed through the left atriotomy. The effectiveness of the 'corridor' procedure on heart rhythm was analysed by: (i) 24-h Holter monitoring performed before and during 72 h after surgery, at hospital discharge, and 2 months later; and (ii) postoperative electrophysiological studies using temporary epicardial wires on each isolated atrial compartment. Immediately after surgery and in the following 2 months, heart rate variability analysis showed significantly lower hourly ventricular rates and rate variations in the 'corridor' group compared with those of the control group (P < 0.01). A significant difference was also found when comparing postoperative to preoperative findings in the corridor group (P < 0.05). In the control group, however, no significant differences (P > 0.05) were found concerning pre- and postoperative ventricular rate variations. At hospital discharge, nine of 12 patients with 'corridor' procedure were in sinus rhythm. Control patients remained in atrial fibrillation with irregular ventricular rate. The 'corridor' procedure, when added to mitral valve replacement, prolonged surgery, but led to restoration and long-term maintenance of sinus rhythm in 75% of patients with chronic atrial fibrillation and rheumatic mitral valve disease.

Autonomic control of atrial rate was evaluated in anesthetized dogs by electrical stimulation of stellate ganglia and/or cervical vagi before and after the intrinsic cardiac right atrial ganglionated plexus (RAGP) was injected with the nicotinic blocker hexamethonium or the membrane stabilizing chemical lidocaine, or the RAGP was surgically removed. Injections of lidocaine or hexamethonium into or surgical removal of the RAGP eliminated the bradycardia elicited by vagal stimulation without reducing the tachycardia induced by stellate stimulation. Yet, after surgical ablation of the RAGP, the tachycardia induced by sympathetic stimulation was still reduced by 94% by parasympathetic stimulation. After injections of hexamethonium or lidocaine into the RAGP were administered, the sympathetically induced tachycardia was reduced by 39 and 85%, respectively, by parasympathetic stimulation. After RAGP ablation, when atrial rate was increased by infusion of beta-adrenergic agonists, parasympathetic stimulation reduced atrial rate by 13%. Sinoatrial (SA) nodal parasympathectomy, produced by disrupting the RAGP, eliminates direct vagal control of the SA node while leaving prejunctional parasympathetic projections to sympathetic afferents innervating the SA node intact.

As the treatment of inappropriate sinus tachycardia, beta-adrenoreceptor blockade therapy is the most common method for pharmacological heart rate control, but it is occasionally limited by side effects of the drugs, especially in patients with cardiac dysfunction. On the other hand, cryoablation or surgical exclusion of the sinus node have not been accepted generally for their necessity of permanent pacemaker implantation. Modification of the sinus node function is a new method of nonpharmacological treatments, although the skillfull and troublesome technique is required. In this study, the efficacy and safety of laser sinus node modification without electrophysiological technique were investigated as a new simplified method. In six mongrel dogs, the laser-tissue interactions by epicardial Nd-YAG laser irradiation were investigated by measuring the diameter and the depth of the irradiated lesions. Laser irradiations were performed from the head to the tail on the sinus node areas directed only by terminal groove for the visual landmark without electrophysiological technique until about 25% decrease in heart rate occurred in other six open-chest dogs.

The biatrial approach to exposing the mitral valve during surgery has the potential for improving visualization of the valve with minimal cardiac manipulation. This procedure, involving a right atriotomy and an extended transseptal incision, may isolate the sinus node from its normal blood supply and autonomic innervation. Thirty-eight consecutive patients undergoing this procedure were examined. Twenty-two of these patients (58%) were admitted in normal sinus rhythm and 15 (40%) were in atrial fibrillation (AF) or atrial flutter. Of the 22 patients admitted in normal sinus rhythm, only 3 patients remained in this rhythm at discharge. Fourteen of the 22 patients were discharged in a slow, low atrial rhythm. All of the patients admitted in AF were discharged in AF. Of the 14 patients discharged in a low atrial rhythm, the rhythm persisted in eleven patients (80%) at a mean of 6-month follow-up. The routine use of this transseptal approach to mitral valve surgery needs further assessment in light of the predictable loss of the sinus mechanism.

Sinus node tachycardia is an uncommon cause of paroxysmal supraventricular tachycardia. Of those patients who were referred to our clinic for electrophysiologic evaluation and catheter ablation, four patients (1 male, 3 female) were found to have sinus node tachycardia. The diagnosis of sinus node tachycardia required all of the following: The P-wave during sinus rhythm had to be similar to the P-wave during the tachycardia, the atrial activation sequence during sinus rhythm and tachycardia had to be similar, the origin of the tachycardia had to be in the high right atrium. In one patient the tachycardia was incessant. The other three patients had paroxysmal sinus node tachycardia that could be induced by programmed atrial stimulation. No patient had overt cardiac disease. One patient had an inducible av nodal reentrant tachycardia and one patient had a second atrial tachycardia originating from the basal right atrium. Activation mapping during tachycardia was performed in all patients. Local atrial activation at the site of successful ablation preceded the P-wave in the surface electrocardiogram by 54 +/- 43 ms. In three patients the interval from the local atrial activation at the site of successful catheter ablation to the onset of the signal from the high right atrium (HRA) ranged from 25 ms to 125 ms, in one patient the signal from the high right atrium was the earliest recorded signal during tachycardia. In all patients the tachycardia was terminated with the application of radiofrequency current. Two to a maximum of 12 radiofrequency current applications were necessary; complications were not observed. In all patients a second electrophysiologic study was performed 8 +/- 2 weeks after successful catheter ablation; no patient had inducible sinus node or atrial tachycardia. During a follow-up of 5 +/- 2 months, no patient had a recurrence of sinus node tachycardia or required antiarrhythmic medication. It is concluded that catheter ablation in patients with sinus node tachycardia is an effective and safe treatment.

Background: Radiofrequency catheter ablation is the treatment of choice for patients with paroxysmal supraventricular tachycardias refractory to medical therapy. However, in symptomatic patients with inappropriate sinus tachycardia resistant to drug therapy, catheter ablation of the His' bundle with permanent pacemaker insertion is currently applied. We evaluated the safety and efficacy of radiofrequency modification of the sinus node as alternative therapy for patients with inappropriate sinus tachycardia., Methods and Results: Sixteen patients with disabling episodes of inappropriate sinus tachycardia refractory to drug therapy (4.2 +/- 0.3 drug trials) underwent either total sinus node ablation or sinus node modification. The region of the sinus node was identified as the region of earliest atrial activation in sinus rhythm during electrophysiological study. This region was further defined by use of intracardiac echocardiography (ICE) in 9 patients, in whom it was found that an ablation catheter could be guided reliably and maintained on the crista terminalis. Radiofrequency energy was delivered during tachycardia between either a standard 4-mm or custom 10-mm thermistor-imbedded catheter tip and a skin patch. Total sinus node ablation was performed successfully in all 4 patients in whom it was attempted and was characterized by a junctional escape rhythm. Sinus node modification was successfully achieved in all 12 patients in whom it was attempted and was characterized by a 25% reduction in the sinus heart rate. For the group as a whole, exercise stress testing after ablation revealed a gradual chronotropic response, with a significant reduction in maximal heart rate (132.8 +/- 6.5 versus 179.5 +/- 3.6 beats per minute [bpm]; P < .001) without evidence of an exaggerated heart rate response to a light workload (103.0 +/- 4.1 versus 139.5 +/- 3.5 bpm; P < .001). Twenty-four-hour ambulatory ECG monitoring revealed a significant decrease in maximal heart rate and mean heart rate after ablation (167.2 +/- 2.6 versus 96.7 +/- 5.0 bpm, P < .001, and 125.6 +/- 5.0 versus 54.1 +/- 5.3 bpm, P < .001, respectively). There was a significant decrease in the number of applications of radiofrequency energy required in patients undergoing modification of the sinus node when guided by ICE compared with fluoroscopy alone (3.6 +/- 0.8 versus 10.4 +/- 2.1; P < .01) as well as a decrease in fluoroscopy time (33.0 +/- 9.5 versus 58.5 +/- 8.4 minutes). After a mean follow-up period of 20.5 +/- 0.3 months, there were no recurrences of inappropriate sinus tachycardia in patients who underwent a total sinus node ablation. However, 2 patients who had a total sinus node ablation subsequently required permanent pacing because of symptomatic pauses, and 1 patient developed an ectopic atrial tachycardia. After a mean follow-up of 7.1 +/- 1.7 months, there were two recurrences of inappropriate sinus tachycardia in patients who underwent sinus node modification. However, no significant bradycardia or pauses were observed. Complications encountered during the study included 1 patient who developed transient right diaphragmatic paralysis and another patient who developed transient superior vena cava syndrome., Conclusions: Sinus node modification is feasible in humans and should be considered as an alternative to complete atrioventricular junctional ablation for patients with disabling inappropriate sinus tachycardia refractory to medical management. Sinus node modification may be aided by ICE.

Background: The sinus P wave arises from a pacemaker complex distributed along the crista terminalis. We investigated the feasibility of modification of sinus pacemaker function using graded applications of radiofrequency energy along the crista terminalis in dogs to achieve sinus rate control., Methods and Results: Modification of sinus pacemaker function (30 +/- 5% reduction in intrinsic heart rate with retention of a normal P-wave axis) was performed in 11 dogs (group 1). Total sinus pacemaker ablation (> 50% reduction in intrinsic heart rate with development of a low ectopic atrial or a junctional rhythm) was performed in 4 dogs (group 2). Intracardiac echocardiography was used to identify the crista terminalis as an anatomic marker of sinus node location. Sinus pacemaker modification caused a significant decrease in intrinsic heart rate (31% reduction, P < .001), heart rate responsiveness to isoproterenol (30% reduction, P < .0001), and average (20% reduction, P = .0002) and maximal (22% reduction, P = .0007) heart rates during 24-hour Holter monitoring. In 6 of the 11 animals, the targeted rate reduction of 30 +/- 5% was accurately achieved (mean, 31.6 +/- 4.3%; P < .001), and in the other 5, significant reduction of intrinsic heart rate was achieved but with greater variation (28.0 +/- 17.3%, P < .005). Corrected sinus node recovery time was not prolonged. After modification, earliest activation was mapped to the crista terminalis inferior to the lesion in all animals. In long-term follow-up (3.7 +/- 1.0 months), effects were maintained. After total sinus pacemaker ablation, junctional and low atrial escape pacemakers were unstable., Conclusions: This study demonstrates the feasibility of modification of sinus pacemaker function for sinus rate control using catheter-based radiofrequency ablation guided by intracardiac echocardiography. This can be done while pacemaker stability and attenuated responsiveness to autonomic influences are preserved. Intracardiac echocardiography accurately defined the crista terminalis and provided a reliable means to anatomically localize catheter position in relation to the sinus node.

Background: Subsidiary atrial pacemakers assume control after sinoatrial (SA) node excision, and anesthetic-catecholamine interactions can produce severe bradycardia during isoflurane anesthesia. We hypothesized that epinephrine enhances atrial, atrioventricular junctional, and ventricular dysrhythmias after SA node excisions in dogs and that inhalation anesthetics would facilitate such dysrhythmias., Methods: In eight dogs, SA nodes were excised and epicardial electrodes implanted at the atrial appendages, at the His bundle, and along the sulcus terminalis. Site of the earliest atrial activation and incidences of nonatrial beats were determined in the conscious state, with methylatropine, with epinephrine, and during halothane, isoflurane, or enflurane anesthesia., Results: After SA node excision, a stable, regular subsidiary atrial pacemaker rhythm resulted. Epinephrine and halothane shifted the site of earliest activation to more remote atrial sites. Epinephrine-induced ventricular escape was increased by all anesthetics tested, but atropine prevented ventricular escape. Epinephrine-induced His bundle (atrioventricular junctional) and premature ventricular beats were increased by halothane and enflurane. After SA node excision, ventricular escape occurred as a result of epinephrine-anesthetic interactions, especially during anesthesia with isoflurane., Conclusions: In dogs with excised SA nodes, anesthetic-catecholamine interaction facilitates ventricular escape, His bundle dysrhythmias, and premature ventricular beats. In addition, halothane and enflurane, more than isoflurane, facilitate ectopic ventricular tachydysrhythmias with epinephrine. Compared to intact dogs, dogs with excised SA nodes may be more susceptible to epinephrine anesthetic dysrhythmias. If findings can be extrapolated to humans, intrinsic SA node dysfunction may facilitate severe cardiac dysrhythmias with inhalation anesthetics and catecholamines.

Background: Management of patients with sinus node dysfunction must consider the stability of subsidiary pacemakers during anesthesia and treatment with antimuscarinic or sympathomimetic drugs. Baroreflex regulation of atrial pacemaker function is known to contribute to the interactions between inhalation anesthetics and catecholamines. Sinoatrial (SA) node excision can be a model for intrinsic SA node dysfunction. Subsidiary atrial pacemakers are expected to emerge after SA node excision, but they may respond differently to humoral and neural modulation. Isolated and combined effects of epinephrine and methylatropine should help characterize subsidiary pacemaker function during anesthesia with halothane, isoflurane, and enflurane., Methods: In eight dogs, SA nodes were excised and epicardial electrodes implanted at the atrial appendages, the His bundle, and along the sulcus terminalis. Spontaneous pacemaker automaticity and subsidiary atrial pacemaker recovery time were measured in the conscious state, in the presence of methylatropine, with 1 and 2 micrograms.kg-1.min-1 epinephrine and during 1.25 and 2 MAC halothane, isoflurane, and enflurane., Results: After SA node excision, a stable and regular subsidiary atrial pacemaker rhythm emerged. Each anesthetic prolonged subsidiary atrial pacemaker recovery times. This prolongation was greater in the presence of methylatropine. Without methylatropine, isoflurane and enflurane, but not halothane, further enhanced the baroreflex-mediated negative chronotropic effects of epinephrine, whereas with methylatropine, each anesthetic reduced the direct positive chronotropic effects of epinephrine., Conclusions: Halothane, isoflurane, and enflurane have significant depressant effects on the spontaneous and epinephrine-altered automaticity of subsidiary atrial pacemakers. Depression of subsidiary atrial pacemaker automaticity was most apparent in dogs with muscarinic blockade.

Radiofrequency catheter modification of the sinus node for persistent inappropriate sinus tachycardia has not been previously reported. This article describes a patient in whom radiofrequency current was used to ablate an incessant automatic tachycardia focus mapped to the region of the sinus node, where a discrete multicomponent electrogram demonstrating earliest atrial activation was recorded. A transient junctional rhythm developed immediately after ablation, with rapid subsequent emergence of a stable rhythm having normal sinus nodal characteristics.

An important factor in the efficient and successful completion of the ablation procedure is the design characteristics of the mapping/ablation catheters. These procedures are often hampered by the inability to maneuver the catheter to the desired location, in part because the catheters only have a single plane deflection capability and are not designed for the specific cardiac anatomical structures that contain the arrhythmogenic substrate. Single and Biplane Deflectable Catheters: Using measurements taken from six normal human cadaver hearts, ablation catheter design characteristics are presented for posterior, posterior septal, lateral, and posterior lateral pathways for retrograde and transseptal approaches. Three catheter designs based on anatomical characteristics were also evaluated. Pigtail Catheter: This catheter adapts to the atrial side of the mitral ring and improves positioning and stability for mapping and ablation of left-sided accessory pathways. Loop Catheter: This catheter is positioned at the perivalvular tricuspid ring and provides simultaneous mapping and ablation capabilities without the need to move the catheter or the need for additional catheters. Rotating Tip Catheter: The tip of this catheter is made up of three elongated teeth, which were curved 120 degrees apart into the rotating tip electrode. This electrode was designed to negotiate the surfaces of the atrial and intraventricular chambers. It is capable of discrete movements and has a large electrode-tissue contact area for the ablation of atrial and ventricular arrhythmias. Catheter designs presented in this article are based on the ability of the catheter to adapt to the anatomical location of the arrhythmogenic tissue as well as the maneuverability of the catheter's mapping and ablation electrodes. An anatomical approach to the design of ablation catheter technology is likely to reduce the x-ray radiation exposure for patient and operator, and may further increase the success rate of the procedure.

Objectives: This study evaluates 1) the safety and efficacy of catheter delivery of radiofrequency current to eliminate sustained sinoatrial node reentrant tachycardia; 2) the incidence of sinoatrial node reentrant tachycardia in the current group of patients undergoing electrophysiologic study for paroxysmal supraventricular tachycardia; and 3) the association of sinoatrial node reentrant tachycardia with other tachyarrhythmias., Background: Sustained sinoatrial node reentrant tachycardia is an uncommon cause of paroxysmal supraventricular tachycardia that is reported to occur infrequently in conjunction with other arrhythmias. Although pharmacologic and surgical therapies are available, there is limited information with regard to catheter ablation of sinoatrial node reentrant tachycardia., Methods: Ten patients with sustained sinoatrial node reentrant tachycardia underwent electrophysiologic study and radiofrequency current ablation. Patients were followed up for 9.2 +/- 6.0 months., Results: Of 343 consecutive patients referred for electrophysiologic evaluation of paroxysmal supraventricular tachycardia, 11 (3.2%) were found to have inducible sustained sinoatrial node reentrant tachycardia. Nine of the 11 patients had other associated arrhythmias, including atrioventricular (AV) node reentrant tachycardia (6 patients), AV reciprocating tachycardia (2 patients), ectopic atrial tachycardia (2 patients) and bundle branch reentrant tachycardia (1 patient). In 10 patients, direct ablation of sinoatrial node reentrant tachycardia was attempted and was successful in all (confidence interval for failure 0-0.26). Sinoatrial node reentrant tachycardia was eliminated with a median of four radiofrequency current applications (range 1 to 10) at 20 to 30 W. Successful ablation site characteristics during sinoatrial node reentrant tachycardia included 1) atrial activation > or = 35 ms (mean 44 +/- 8 ms) before the onset of the surface P wave, 2) atrial activation > or = 20 ms (mean 28 +/- 6 ms) before the onset of high right atrial activation, and 3) significantly prolonged and fractionated electrograms (mean duration 87 +/- 21 ms). No complications were encountered, and there have been no recurrences of sinoatrial node reentrant tachycardia., Conclusions: Sinoatrial node reentrant tachycardia may be effectively and safely treated with radiofrequency current ablation at the site of earliest atrial activation.