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.

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.

Reflex control of sympathetic activity during simulated ventricular tachycardia in humans.

BACKGROUND: Ventricular tachyarrhythmias present a unique set of stimuli to arterial and cardiopulmonary baroreceptors by increasing cardiac filling pressures and decreasing arterial pressure. The net effect on the control of sympathetic nerve activity (SNA) in humans is unknown. The purpose of this study was to determine the relative roles of cardiopulmonary and arterial baroreceptors in controlling SNA and arterial pressure during ventricular pacing in humans. METHODS AND RESULTS: Two experiments were performed in which SNA and hemodynamic responses to ventricular pacing were compared with nitroprusside infusion (NTP) in 12 patients and studied with and without head-up tilt or phenylephrine to normalize the stimuli to either the arterial or cardiopulmonary baroreceptors in 9 patients. In experiment 1, the slope of the relation between SNA and mean arterial pressure was greater during NTP (-4.7+/-1.4 U/mm Hg) than during ventricular pacing (-3.4+/-1.1 U/mm Hg). Comparison of NTP doses and ventricular pacing rates that produced comparable hypotension showed that SNA increased more during NTP (P=0.03). In experiment 2, normalization of arterial pressure during pacing resulted in SNA decreasing below baseline (P<0.05), whereas normalization of cardiac filling pressure resulted in a greater increase in SNA than pacing alone (212+/-35% versus 189+/-37%, P=0. 04). Conclusions--These data demonstrate that in humans arterial baroreflex control predominates in mediating sympathoexcitation during ventricular tachyarrhythmias and that cardiopulmonary baroreceptors contribute significant inhibitory modulation.

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.

Atypical right atrial flutter patterns.

BACKGROUND: The purpose of our study was to define the incidence and mechanisms of atypical right atrial flutter. METHODS AND RESULTS: A total of 28 (8%) of 372 consecutive patients with atrial flutter (AFL) had 36 episodes of sustained atypical right AFL. Among 24 (67%) of 36 episodes of lower loop reentry (LLR), 13 (54%) of 24 episodes had early breakthrough at the lower lateral tricuspid annulus, whereas 11 (46%) of 24 episodes had early breakthrough at the high lateral tricuspid annulus, and 9 (38%) of 24 episodes showed multiple annular breaks. Bidirectional isthmus block resulted in elimination of LLR. A pattern of posterior breakthrough from the eustachian ridge to the septum was observed in 4 (14%) of 28 patients. Upper loop reentry was observed in 8 (22%) of 36 episodes and was defined as showing a clockwise orientation with early annular break and wave-front collision over the isthmus. Two patients had atypical right AFL around low voltage areas ("scars") in the posterolateral right atrium. CONCLUSIONS: Atypical right AFL is most commonly associated with an isthmus-dependent mechanism (ie, LLR or subeustachian isthmus breaks). Non-isthmus-dependent circuits include upper loop reentry or scar-related circuits.

Management of ventricular arrhythmias: a trial-based approach.

Sudden cardiac death accounts for approximately 300,000 deaths annually in the U.S., and most of these are secondary to ventricular tachycardia (VT) and fibrillation in patients with coronary artery disease. Most patients with cardiac death die before reaching the hospital, which brought about a tremendous amount of research focused at identifying patients at high risk. Several trials were initiated to test the effectiveness of various therapeutic measures in these high-risk patients. A history of myocardial infarction, depressed left ventricular function and nonsustained VT have all been identified as independent risk factors for future arrhythmic death. Similarly, patients with a history of sustained VT or a history of sudden cardiac death are a high-risk group and should be aggressively evaluated and treated. The purpose of this article is to discuss risk stratification and primary prevention of sustained ventricular arrhythmias. We also review the recent secondary prevention trials and discuss the options available in the management of patients with sustained ventricular arrhythmias.

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.

P-wave morphology during right atrial pacing before and after atrial flutter ablation--a new marker for success.

Fourteen patients with typical atrial flutter underwent pacing from the low lateral right atrium and the proximal coronary sinus in normal sinus rhythm before and after catheter ablation. During low lateral right atrial pacing, a positive change in P-wave morphology in the inferior leads was noted in every patient (n = 12) in whom bidirectional block was achieved; no recurrence was noted in any of these patients.

Interaction of a commercial heart rate monitor with implanted pacemakers.

Dry-electrode heart rate monitors allow display of heart rate by transmitting a signal to the receiving device, which typically is on the wrist or exercise machine, but due to the potential for electromagnetic interference, their use has been contraindicated in patients with pacemakers. In 12 patients, we found no adverse effect on pacemaker function; in addition, the monitors generally were accurate in measuring heart rate during pacing.

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.

Effects of repeated electrical defibrillations on cardiac troponin I levels.

Multiple endocardial countershocks applied during intraoperative endocardial implantable cardioverter-defibrillator testing for the purpose of defibrillation threshold determination resulted in detectable myocardial injury in 5 of 12 patients, as indicated by elevations in cardiac troponin I levels. This injury was not associated with acute changes on the surface electrocardiogram.

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.

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.

Intracardiac shunts resulting from transseptal catheterization for ablation of accessory pathways in otherwise normal hearts.

In a series of 14 patients undergoing transseptal catheterization for ablation of left-sided accessory pathways, hydrogen appearance time was used to detect left-to-right shunting after removal of the catheter. Six of the 12 patients who had no evidence of shunt before catheterization had evidence of shunting after the procedure.

Ischemia, metabolic disturbances, and arrhythmogenesis: mechanisms and management.

The development of ventricular arrhythmias is often a consequence of the interaction between structural abnormalities of the heart and transient disturbances in the electrophysiologic milieu. The critically ill patient is particularly susceptible to arrhythmias given the metabolic, ischemic, and neurohormonal stressors present in the intensive care unit. The significance of ventricular arrhythmias in the acute care setting is related to the presence of reversible causes and the extent of underlying heart disease. Long-term management of these patients is guided by an assessment of the risk for recurrent arrhythmias and the degree of left ventricular systolic dysfunction. In the absence of a reversible cause, symptomatic sustained arrhythmias are usually treated with an implantable cardioverter-defibrillator, a therapy that improves survival in this patient population. In many cases, however, proper long-term management of patients with ventricular arrhythmias is less clear, and the approach must be guided by a thorough understanding of the pathophysiology and the fundamental mechanisms of arrhythmogenesis.

Diagnostic approach to narrow complex tachycardia with VA block.

Narrow complex tachycardia with VA block is rare. The differential diagnosis usually consists of (1) junctional tachycardia (JT) with retrograde block; (2) AV nodal reentrant tachycardia (AVNRT) with proximal common pathway block; and finally (3) nodofascicular tachycardia using the His-Purkinje system for antegrade conduction and a nodofascicular pathway for retrograde conduction. Analysis of tachycardia onset and termination, the effect of bundle branch block on tachycardia cycle length, and the response to atrial and ventricular premature depolarization must be carefully done. Making the correct diagnosis is crucial as the success rate in eliminating the tachycardia will depend on tachycardia mechanism.

The effect of biphasic defibrillation on the immediate pacing threshold of a dedicated bipolar, steroid-eluting lead.

It is apparent that pacing threshold increases following an ICD shock, although the degree of change observed is dependent on the method used to assess pacing and the lead design used. We previously demonstrated a rise in postshock pacing threshold using a lead with integrated bipolar pacing in which the distal shocking coil also serves as the pacing anode. In this study, we sought to investigate whether the postshock pacing threshold increased significantly in an endocardial, steroid-eluting lead with dedicated bipolar pacing electrodes. Twenty patients (16 men, 4 women; median age 73, ejection fraction [EF] 0.17-0.58) were studied during pectoral ICD implantation (Medtronic active can model 7221Cx or 7223Cx with model 6932-65 lead). The diastolic pulse width pacing threshold at 1 or 2 V was determined. Pacing rate was set > or = 100/min at twice diastolic threshold output to assess pacing immediately following the first DFT test shock. For subsequent shocks, the output was adjusted to establish postshock thresholds as 1, 2, 3, or 4 times the diastolic threshold. The postshock threshold was defined as the output yielding 100% capture > or = 2.5 seconds following a shock. In 8 of 20 patients (ratio 0.40 +/- 0.11), a rise in the post-shock threshold was shown by failure of consistent capture when pacing at 2 times diastolic threshold > or = 2.5 seconds after a DFT test shock. Two of these patients failed at 3 times threshold, but none failed at 4 x threshold. Five of 12 patients with successful capture of 2 times threshold failed to capture at threshold. The postshock threshold increased by a mean factor of 2.83 +/- 0.83 in the group of patients with a threshold rise. Following ICD shock in an active can, steroid-eluting lead system with dedicated bipolar pacing, the post-shock threshold increases significantly. Our studies suggest a need for postshock pacing to be set at least 4 x threshold regardless of the lead design.

Initial experience with a high-impedance tined endocardial pacemaker lead: evidence for increased lead failure.

We report our initial clinical experience with a new tined ventricular endocardial pacemaker lead, the Medtronic model 5034. This lead has a reduced electrode tip size, which provides a higher impedance. Based on early evidence of elevation of pacing lead threshold, we compared our clinical experience with the performance of this lead with that of other similar models with larger surface area (Medtronic models 4024 and 5024). Of 17 implant procedures performed at our institution with the model 5034 lead, two (11.2%) developed high thresholds, versus 0% in 121 implant procedures with models 4024 or 5024 leads (p = 0.014). We conclude that there is evidence of increased failure caused by elevation of pacing threshold in this lead. This increased failure rate needs to be confirmed in a multicenter observational study or randomized trial.