Effect of P-wave timing during supraventricular tachycardia on the hemodynamic and sympathetic neural response.

BACKGROUND: Previous studies have shown the importance of the timing of atrial and ventricular systole on the hemodynamic response during supraventricular tachycardia (SVT). However, the reflex changes in autonomic tone during SVT remain poorly understood. METHODS AND RESULTS: Eleven patients with permanent dual-chamber pacemakers were enrolled in the study. Arterial blood pressure (BP), central venous pressure (CVP), and peripheral muscle sympathetic nerve activity (SNA) were recorded during DDD pacing at a rate of 175 bpm (cycle length 343 ms) with an atrioventricular (AV) interval of 30, 200 and 110 ms, simulating tachycardia with near-simultaneous atrial and ventricular systole, short-RP tachycardia (RPPR). Each pacing run was performed for 3 minutes separated by a 5-minute recovery period. All patients demonstrated an abrupt fall in BP, an increase in CVP, and an increase in SNA regardless of the AV interval. The decreases in SBP, DBP, and MAP and the increase in CVP were significantly less during long-RP tachycardia (AV interval 110 ms) than during the other 2 pacing modes (P:<0.05), and the increase in SNA in 7 of the 11 patients was significantly greater during closely coupled atrial and ventricular systole than during long-RP tachycardia (P:<0.05). CONCLUSIONS: These data suggest that the superior maintenance of hemodynamic stability during long-RP tachycardia is accompanied by reduced sympathoexcitation, which is primarily mediated by the arterial baroreceptors, with a modest cardiopulmonary vasodepressor effect.

Biventricular pacing decreases sympathetic activity compared with right ventricular pacing in patients with depressed ejection fraction.

BACKGROUND: Although there have been few studies in which the hemodynamic effects of right ventricular (RV) and left ventricular (LV) pacing were compared with those of biventricular (BV) pacing, the autonomic changes during these different pacing modes remain unknown. We hypothesized that BV pacing results in improved hemodynamics and a decrease in sympathetic nerve activity (SNA) compared with single-site pacing. METHODS AND RESULTS: Thirteen men with a mean ejection fraction of 0.28+/-0.7 were enrolled in the study. Arterial blood pressure (BP), central venous pressure (CVP), and SNA were recorded during 3 minutes of right atrial (RA)-RV, RA-LV, and RA-BV pacing at a rate 10 beats faster than sinus rhythm. BP was greater during LV (151+/-7/85+/-3 mm Hg) and BV (151+/-6/85+/-3 mm Hg) pacing than during RV pacing (146+/-7/82+/-3 mm Hg) (P:<0.05). There were no differences in CVP among all pacing modes (P:=0.27). SNA was significantly less (P:<0.02) during both LV (606+/-35 U) and BV (582+/-41 U) pacing compared with RV pacing (685+/-32 U) (P:<0.02). Although not statistically significant (P:=0. 08 to 0.14), there was a trend for patients with a narrow QRS to have a lower mean BP and higher SNA during LV pacing than during BV pacing (r=0.42 to 0.49). CONCLUSIONS: LV-based pacing results in improved hemodynamics and a decrease in SNA compared with RV pacing in patients with LV dysfunction regardless of the QRS duration.

Baroreflex gain predicts blood pressure recovery during simulated ventricular tachycardia in humans.

BACKGROUND: Despite similar degrees of left ventricular dysfunction and similar tachycardia or pacing rate, blood pressure (BP) response and symptoms vary greatly among patients. Sympathetic nerve activity (SNA) increases during sustained ventricular tachycardia (VT), and the magnitude of this sympathoexcitatory response appears to contribute to the net hemodynamic outcome. We hypothesize that the magnitude of sympathoexcitation and thus arterial baroreflex gain is an important determinant of the hemodynamic outcome of VT. METHODS AND RESULTS: We evaluated the relation between arterial baroreflex sympathetic gain and BP recovery during rapid ventricular pacing (VP) in patients referred for electrophysiological study. Efferent postganglionic muscle SNA, BP, and central venous pressure (CVP) were measured in 14 patients during nitroprusside infusion and during VP at 150 (n=12) or 120 (n=2) bpm. Arterial baroreflex gain was defined as the slope of the relationship of change in SNA to change in diastolic BP during nitroprusside infusion. Recovery of mean arterial pressure (MAP) during VP was measured as the increase in MAP from the nadir at the onset of pacing to the steady-state value during sustained VP. Arterial baroreflex gain correlated positively with recovery of MAP (r=0.57, P=0.034). No significant correlation between ejection fraction and baroreflex gain (r=0.48, P=0.08) or BP recovery (r=0.41, P=0.15) was found. When patients were separated into high versus low baroreflex gain, the recovery of MAP during simulated VT was significantly greater in patients with high gain. CONCLUSIONS: These data strongly suggest that arterial baroreflex gain contributes significantly to hemodynamic stability during simulated VT. Knowledge of baroreflex gain in individual patients may help the clinician tailor therapy directed toward sustained VT.

Increased sympathetic activity after atrioventricular junction ablation in patients with chronic atrial fibrillation.

OBJECTIVES: The aim of this study was to determine the changes in sympathetic nerve activity (SNA) after atrioventricular junction (AVJ) ablation in patients with chronic atrial fibrillation (AF). BACKGROUND: Polymorphic ventricular tachycardia (PMVT) has been reported after AVJ ablation in patients paced at a rate of < or =70 beats/min. We hypothesized that AVJ ablation results in sympathetic neural changes that favor the occurrence of PMVT and that pacing at 90 beats/min attenuates these changes. METHODS: Sympathetic nerve activity, 90% monophasic cardiac action potential duration (APD90), right ventricular effective refractory period (ERP) and blood pressure measurements were obtained in 10 patients undergoing AVJ ablation. Sympathetic nerve activity was analyzed at baseline and during and after successful AVJ ablation for at least 10 min. Data were also collected after ablation at pacing rates of 60 and 90 beats/min. The APD90 and ERP were measured before and after AV block during pacing at 120 beats/min. RESULTS: Sympathetic nerve activity increased to 134 +/- 16% of the pre-ablation baseline value (p < 0.01) after successful AVJ ablation plus pacing at 60 beats/min and decreased to 74 +/- 8% of baseline (p < 0.05) with subsequent pacing at 90 beats/min. Both APD90 and ERP increased significantly. CONCLUSIONS: 1) Ablation of the AVJ followed by pacing at 60 beats/min is associated with an increase in SNA. 2) Pacing at 90 beats/min decreases SNA to or below the pre-ablation baseline value. 3) Cardiac APD and ERP increase after AVJ ablation. The increase in SNA, along with the prolongation in APD, may play a role in the pathogenesis of ventricular arrhythmias that occur after AVJ ablation.

Initial energy for elective external cardioversion of persistent atrial fibrillation.

We conducted a prospective randomized study to determine the safety and efficacy rate of 3 commonly used energy levels (100, 200, and 360 J) for elective direct-current cardioversion of persistent atrial fibrillation. When compared with 100 and 200 J, the initial success rate with 360 J was significantly higher (14%, 39%, and 95%, respectively), and patients randomized to 360 J ultimately required less total energy and a lower number of shocks.

Effect of radiofrequency ablation on atrial mechanical function in patients with atrial flutter.

Atrial stunning, as assessed by left atrial appendage emptying and increased spontaneous echo contrast, is known to occur following direct-current cardioversion of atrial fibrillation (AF) and atrial flutter (AFI). Little is known on atrial mechanical function and the time course of atrial recovery following radiofrequency ablation of AFI. Fourteen patients undergoing radiofrequency ablation of persistent typical counterclockwise AFI were enrolled. Two-dimensional and pulse Doppler transesophageal echocardiography (TEE) were performed before ablation and immediately following restoration of sinus rhythm. Left atrial spontaneous echo contrast grades, left atrial appendage emptying fractions, and peak left atrial appendage emptying velocities were measured. Transthoracic echocardiography (TTE) was performed immediately after ablation, then repeated after 1 day, 1 week, and 6 weeks to measure peak transmitral velocities and percent atrial contribution to ventricular filling. Left atrial appendage emptying velocities decreased significantly following AFI termination (44 +/- 23 cm/s before ablation vs 25 +/- 14 cm/s after ablation, p = 0.01). Left atrial appendage emptying fractions also decreased significantly (0.48 +/- 0.1 preablation vs 0.34 +/- 0.17 postablation, p = 0.02). New spontaneous echo contrast developed in 4 patients (29%) after ablation. Four patients had complete atrial standstill after ablation, and 1 patient developed a new left atrial appendage thrombus. The percent atrial contribution to ventricular filling recovered progressively over 6 weeks with significant improvement in peak transmitral velocities at day 7. Thus, atrial stunning occurs after catheter ablation of AFI and may lead to rapid formation of thrombus in the left atrial appendage. Significant improvement in left atrial function occurs in 7 days.

Selective parasympathetic denervation following posteroseptal ablation for either atrioventricular nodal reentrant tachycardia or accessory pathways.

Baroreflex gain and coronary sinus norepinephrine and epinephrine levels were measured before and immediately after radiofrequency ablation in the posteroseptal region in 9 patients with atrioventricular nodal reentrant tachycardia or posteroseptal accessory pathways. Arterial baroreflex gain was significantly reduced after radiofrequency ablation (p = 0.046), whereas coronary sinus epinephrine and norepinephrine levels did not change significantly compared with preablation levels.

Arrhythmia discrimination using hemoglobin spectroscopy in humans.

BACKGROUND: Inappropriate therapies are frequently delivered by implantable cardioverter-defibrillators (ICDs). We have investigated muscle perfusion as a means of augmenting arrhythmia discrimination by using implanted near-infrared spectroscopy. OBJECTIVE: To evaluate hemodynamic stability by monitoring muscle perfusion from within the ICD pocket, in fresh tissue and inside the scar capsule on preexisting ICD generators, during induced cardiac arrhythmias, in humans. METHODS: The sensor was implanted on or under the pectoral muscle, during ICD defibrillation threshold testing. A microvascular oxygenation trend indicator (O2 Index) was computed during 74 induced ventricular fibrillation and 34 normal sinus rhythm episodes in 34 patients and also during 28 atrial and 90 ventricular overdrive pacing episodes as simulations of supraventricular and ventricular tachycardias, respectively. RESULTS: On average, the change in oxygenation, based on the O2 Index, was statistically significant (P <.003) from baseline within 3 seconds following cardiac arrest. An optimized O2 Index, used for detecting the hemodynamic trend, exhibited a decreasing trend during ventricular fibrillation (P <.0001) and was different from that during normal sinus rhythm (P <.0001). The sensitivity for the detection of ventricular fibrillation was 100%, and the specificity for the rejection of normal sinus rhythm was 82% in the presence of scar tissue on the optical sensor. For a 35-mm Hg drop in the mean arterial pressure as the threshold for hemodynamic instability, the specificity for the rejection of hemodynamically stable atrial and ventricular pacing episodes was 93% and 71%, respectively. CONCLUSION: An implantable near-infrared spectroscopic sensor may be useful for hemodynamic monitoring during cardiac arrhythmias to prevent inappropriate therapy.

Use of automated external defibrillators by a U.S. airline.

BACKGROUND: Passengers who have ventricular fibrillation aboard commercial aircraft rarely survive, owing to the delay in obtaining emergency care and defibrillation. METHODS: In 1997, a major U.S. airline began equipping its aircraft with automated external defibrillators. Flight attendants were trained in the use of the defibrillator and applied the device when passengers had a lack of consciousness, pulse, or respiration. The automated external defibrillator was also used as a monitor for other medical emergencies, generally at the direction of a passenger who was a physician. The electrocardiogram that was obtained during each use of the device was analyzed by two arrhythmia specialists for appropriateness of use. We analyzed data on all 200 instances in which the defibrillators were used between June 1, 1997, and July 15, 1999. RESULTS: Automated external defibrillators were used for 200 patients (191 on the aircraft and 9 in the terminal), including 99 with documented loss of consciousness. Electrocardiographic data were available for 185 patients. The administration of shock was advised in all 14 patients who had electrocardiographically documented ventricular fibrillation, and no shock was advised in the remaining patients (sensitivity and specificity of the defibrillator in identifying ventricular fibrillation, 100 percent). The first shock successfully defibrillated the heart in 13 patients (defibrillation was withheld in 1 case at the family's request). The rate of survival to discharge from the hospital after shock with the automated external defibrillator was 40 percent. A total of 36 patients either died or were resuscitated after cardiac arrest. No complications arose from use of the automated external defibrillator as a monitor in conscious passengers. CONCLUSIONS: The use of the automated external defibrillator aboard commercial aircraft is effective, with an excellent rate of survival to discharge from the hospital after conversion of ventricular fibrillation. There are not likely to be complications when the device is used as a monitor in the absence of ventricular fibrillation.