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Pacing Rate (pacing + rate)
Selected AbstractsClinical Evaluation of a Pacemaker Algorithm That Adjusts the Pacing Rate During Sleep Using Activity VariancePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2000FIRAT DURU DURU, F., et al.: Clinical Evaluation of a Pacemaker Algorithm That Adjusts the Pacing Rate During Sleep Using Activity Variance. Even though rate responsive pacemakers are able to regulate pacing rates based on sensor activity, they are set with a minimum rate that is not adjusted to provide rate decreases during sleep. The aim of this study was to evaluate the performance of the "Sleep Rate" feature, as compared to patient diaries and a validated method that identifies sleep from wrist actigraphy. In 19 patients (15 men; age 69 ± 8 years) with Pacesetter Trilogy DR+ pacemakers, the base rate and the sleep rate were set to 80 and 50 ppm, respectively. When the patients returned 2 days later, data recorded by the pacemaker and wrist actigraph were analyzed to find the agreement in corresponding sleep/wake periods. In 17 (89%) patients, the pacemaker went into the sleep mode. The total sleep time derived from actigraphy significantly exceeded the time during which the pacemaker was in sleep mode (1156.8 ± 83.4 vs 307.3 ± 77.2 minutes). Frequent reversions out of the sleep mode limited the total sleep time derived from the pacemaker. Cumulative analysis of the pacemaker data showed that the maximum time in the sleep mode was 78 minutes, and exceeded 1 hour in six instances, 30 minutes in 32 instances, and 15 minutes in 83 instances. Epoch by epoch comparisons revealed a good agreement (93.6 ± 1.8%) during wakefulness between the corresponding actigraph and pacemaker epochs. However, only 24.6 ± 3.7% of the corresponding epochs during sleep were identical, and the overall agreement was 54.4 ± 3.7%. Except for one patient who reported palpitations, patients did not suffer from a pacemaker rate change. The Sleep Rate feature provides rate reduction during sleep, while assuring rapid frequency response during physical activity. However, the current algorithm does not allow long periods of slow pacing rate during continuous sleep, possibly due to its conservative design and the presence of movement arousals, which has to be improved in future generation algorithms. [source] Preserving Normal Ventricular Activation Versus Atrioventricular Delay Optimization During Pacing: The Role of Intrinsic Atrioventricular Conduction and Pacing RatePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2000IVAN ILIEV ILIEV The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 ± 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal A V delay in the DDD mode and comparison between AAI and DDD with optimal A V delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (AHI) was 282 ± 68 ms for rate 70/min and 330 ± 98 ms for rate 90/min (P < 0.01). The optimal A V delay was 159 ± 22 ms, A V delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16%± 9%. At rate 70/min the patients with ARI , 270 ms had higher AFTVI in AAI than in DDD (0.214 ± 0.05 m vs 0.196 ± 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI(0.192 ± 0.03 m vs 0.166 ± 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 ± 0.03 m vs 0.162 ± 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 ± 0.05 m vs 0.173 ± 0.05 mP < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 ± 0.05 m vs 0.158 ± 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate. [source] Cardiac and coronary function in the Langendorff-perfused mouse heart modelEXPERIMENTAL PHYSIOLOGY, Issue 1 2009Melissa E. Reichelt The Langendorff mouse heart model is widely employed in studies of myocardial function and responses to injury (e.g. ischaemia). Nonetheless, marked variability exists in its preparation and functional properties. We examined the impact of early growth (8, 16, 20 and 24 weeks), sex, perfusion fluid [Ca2+] and pacing rate on contractile function and responses to 20 min ischaemia followed by 45 min reperfusion. We also assessed the impact of strain, and tested the utility of the model in studying coronary function. Under normoxic conditions, hearts from 8-week-old male C57BL/6 mice (2 mm free perfusate [Ca2+], 420 beats min,1) exhibited 145 ± 2 mmHg left ventricular developed pressure (LVDP). Force development declined by ,15% (126 ± 5 mmHg) with a reduction in free [Ca2+] to 1.35 mm, and by 25% (108 ± 3 mmHg) with increased pacing to 600 beats min,1. While elevated heart rate failed to modify ischaemic outcome, the lower [Ca2+] significantly improved contractile recovery (by >30%). We detected minimal sex-dependent differences in normoxic function between 8 and 24 weeks, although age modified contractile function in males (increased LVDP at 24 versus 8 weeks) but not females. Both male and female hearts exhibited age-related reductions in ischaemic tolerance, with a significant decline in recovery evident at 16 weeks in males and later, at 20,24 weeks, in females (versus recoveries in hearts at 8 weeks). Strain also modified tolerance to ischaemia, with similar responses in hearts from C57BL/6, 129/sv, Quackenbush Swiss and FVBN mice, but substantially greater tolerance in BALB/c hearts. In terms of vascular function, baseline coronary flow (20,25 ml min,1 g,1) was 50,60% of maximally dilated flows, and coronary reactive and functional hyperaemic responses were pronounced (up to 4-fold elevations in flow in hearts lacking ventricular balloons). These data indicate that attention to age (and sex) of mice will reduce variability in contractile function and ischaemic responses. Even small differences in perfusion fluid [Ca2+] also significantly modify tolerance to ischaemia (whereas modest shifts in heart rate do not impact). Ischaemic responses are additionally strain dependent, with BALB/c hearts displaying greatest intrinsic tolerance. Finally, the model is applicable to the study of vascular reactivity, providing large responses and excellent reproducibility. [source] A self-regulating TCP acknowledgment (ACK) pacing schemeINTERNATIONAL JOURNAL OF NETWORK MANAGEMENT, Issue 3 2002James Aweya We describe in this paper a new TCP ACK pacing scheme that dynamically tunes its behavior to account for variations or changes in the network load. The scheme does not require the knowledge of when TCP is in the slow-start or congestion avoidance phase to determine the proper ACK pacing rate. Copyright © 2002 John Wiley & Sons, Ltd. [source] Temporary Epicardial Ventricular Stimulation in Patients with Atrial Fibrillation: Acute Effects of Ventricular Pacing Site on Bypass Graft FlowsJOURNAL OF CARDIAC SURGERY, Issue 4 2009Navid Madershahian M.D. This study aimed to evaluate the optimal epicardial ventricular pacing site in patients with AF following coronary artery bypass surgery (CABG). Methods: In 23 consecutive patients (mean age = 69.2 ± 1.9 years, gender = 62% male, ejection fraction [EF]= 50.4 ± 2.1%) monoventricular stimulations (VVI) were tested with a constant pacing rate of 100 bpm. The impact of ventricular pacing on bypass graft flow (transit-time flow probe) and pulsatility index (PI) were measured after lead placement on the mid paraseptal region of the right (RVPS) and the left (LVPS) ventricle, on the right inferior wall (RVIW), and on the right ventricular outflow tract (RVOT). In addition, hemodynamic parameters were measured. Patients served as their own control. Results: Comparison of all tested pacing locations revealed that RVOT stimulation provided the highest bypass grafts flows (59.9 ± 6.1 mL/min) and PI (2.2 ± 0.1) when compared with RVPS (51.3 ± 4.7 mL/min, PI = 2.6 ± 0.2), RVIW (54.0 ± 5.1 mL/m; PI = 2.4 ± 0.2), and LVPS (53.1 ± 4.5 mL/min; PI = 2.3 ± 0.1), respectively (p < 0.05). When analyzing patients according to their preoperative LV function (group I = EF > 50%; group II = EF < 50%), higher bypass graft flows were observed with RVOT pacing in patients with lower EF (p = n.s.). Conclusions: Temporary RVOT pacing facilitates optimal bypass graft flows when compared with other ventricular pacing sites and should be the preferred method of temporary pacing in cardiac surgery patients with AF. Especially in patients with low EF following CABG, RVOT pacing may improve myocardial oxygen conditions for the ischemic myocardium and enhance graft patency in the early postoperative period. [source] Atrial Fibrillation in the Goat Induces Changes in Monophasic Action Potential and mRNA Expression of Ion Channels Involved in RepolarizationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2000HUUB M.W. VAN DER VELDEN PH.D. MAP Changes and Ion Channel Expression in Goat AF. Introduction: Sustained atrial fibrillation (AF) is characterized by a marked shortening of the atrial effective refractory period (AKRP) and a decrease or reversal of its physiolonic adaptation to heart rate. The aim of the present study was to investigate whether the AF-induced changes in AKKP in the goat are associated with changes in the atrial monophasic action potential (MAP) and whether an abnormal expression of specific ion channels underlies such changes. Methods and Results: Following thoracotomy, MAPs were recorded from the free wall of the right atrium hoth before induction of AF (control) and after cardioversion of sustained AF (>2 months) in chronically instrumented goats. In control goats. MAP duration at 80% repolarization (MAPD80) shortened (P < 0.01) from 132 ± 4 msec during slow pacing (400-msec interval) to 86 ± 10 msec during fast pacing (180 msec). After cardioversion of sustained AF, the MAPD80, during slow pacing was as short as 67 ± 5 msec (electrical remodeling). Increasing the pacing rate resulted in prolongation (P = 0.02) of the MAPD80 to 91 ± 6 msec. Also. MAPD20 (20% repolarization) shortened (P = 0.05) from 32 ± 4 msec (400 msec) to 14 ± 7 msec (180 msec) in the control goats, whereas it prolonged (P = 0.03) from 20 ± 3 msec (400 msec) to 33 ± 5 msec (180 msec) in sustained AF, mRNA expression of the L-type Ca2+ channel ,1c gene and Kv1.5 potassium channel gene, which underlie Ica, and Ikur respectively, was reduced in sustained.AF compared with sinus rhythm hy 32% (P = 0.01) and 45% (P < 0.01). respectively. No significant changes were found in the mRNA levels of the rapid Na+ channel, the Na+/Ca2+ exchanger, or the Kv4.2/4.3 channels responsible for I10. Conclusion: AF-induced electrical remodeling in the goat comprises shortening of MAPD and reversal of its physiologic rate adaptation. Changes in the time course of reploarization of the action potential are associated with changes in mRNA expression of the , subunit genes of the L.-type Ca2+ channel and the Kvl.5 potassium channel. [source] Rapid Ventricular Pacing for Catheter Interventions in Congenital Aortic Stenosis and Coarctation: Effectiveness, Safety, and Rate Titration for Optimal ResultsJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 1 2010CHETAN MEHTA M.B.B.S. Introduction: Infants and children with congenital aortic stenosis and coarctation of the aorta can be treated by catheter intervention. There are several pharmacological and mechanical techniques described to overcome the balloon movement; none, however, have proved entirely satisfactory. An alternative method to achieve balloon stability is the use of rapid ventricular pacing. We describe our experience with titrating the pacing rate and the use of this technique. Methods: A retrospective review of database was performed, to identify patients who underwent transcatheter intervention with rapid ventricular pacing. Invasive systemic pressures were documented with a catheter in the aorta. Rapid ventricular pacing was initiated at the rate of 180 per minute and increased by increments of 20 per minute to a rate required to achieve a drop in systemic pressure by 50% and a drop in pulse pressure by 25%. The balloon was inflated only after the desired pacing rate was reached. Pacing was continued until the balloon was completely deflated. Results: Thirty patients were identified, 29 of whom had interventions with rapid ventricular pacing. Balloon valvuloplasty of aortic valve was performed on 25 patients while 4 patients had stenting for coarctation by this technique. The rate of ventricular pacing required ranged from 200 to 260 per minute with a median rate of 240. Balloon stability at the time of intervention was achieved in 27 patients. Conclusion: Rapid ventricular pacing is a safe and effective method to provide transient decrease in cardiac output at the time of transcatheter interventions to achieve balloon stability. (J Interven Cardiol 2010;23:7,13) [source] Microdislodgment of Ventricular Pacing Lead Undetectable During Rapid Pacing One Year After ImplantationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2003YUKO CHINUSHI CHINUSHI, Y., et al.: Microdislodgment of Ventricular Pacing Lead Undetectable During Rapid Pacing One Year After Implantation. A 71-year-old woman had undergone valvular heart surgery in 1981, and implantation of a permanent ventricular pacemaker for ventricular pauses during atrial fibrillation in 2001. One year after pacemaker implantation, she complained of faintness. When pacing at 100 beats/min the pacemaker functioned properly. However, pacing and sensing failure was detected at a pacing rate of 60 beats/min. At rapid pacing rates, the lead tip was in closer contact with the endocardium, and its microdislodgment was undetectable. The symptoms have resolved since the lead was repositioned. (PACE 2003; 26:787,788) [source] Clinical Evaluation of a Pacemaker Algorithm That Adjusts the Pacing Rate During Sleep Using Activity VariancePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2000FIRAT DURU DURU, F., et al.: Clinical Evaluation of a Pacemaker Algorithm That Adjusts the Pacing Rate During Sleep Using Activity Variance. Even though rate responsive pacemakers are able to regulate pacing rates based on sensor activity, they are set with a minimum rate that is not adjusted to provide rate decreases during sleep. The aim of this study was to evaluate the performance of the "Sleep Rate" feature, as compared to patient diaries and a validated method that identifies sleep from wrist actigraphy. In 19 patients (15 men; age 69 ± 8 years) with Pacesetter Trilogy DR+ pacemakers, the base rate and the sleep rate were set to 80 and 50 ppm, respectively. When the patients returned 2 days later, data recorded by the pacemaker and wrist actigraph were analyzed to find the agreement in corresponding sleep/wake periods. In 17 (89%) patients, the pacemaker went into the sleep mode. The total sleep time derived from actigraphy significantly exceeded the time during which the pacemaker was in sleep mode (1156.8 ± 83.4 vs 307.3 ± 77.2 minutes). Frequent reversions out of the sleep mode limited the total sleep time derived from the pacemaker. Cumulative analysis of the pacemaker data showed that the maximum time in the sleep mode was 78 minutes, and exceeded 1 hour in six instances, 30 minutes in 32 instances, and 15 minutes in 83 instances. Epoch by epoch comparisons revealed a good agreement (93.6 ± 1.8%) during wakefulness between the corresponding actigraph and pacemaker epochs. However, only 24.6 ± 3.7% of the corresponding epochs during sleep were identical, and the overall agreement was 54.4 ± 3.7%. Except for one patient who reported palpitations, patients did not suffer from a pacemaker rate change. The Sleep Rate feature provides rate reduction during sleep, while assuring rapid frequency response during physical activity. However, the current algorithm does not allow long periods of slow pacing rate during continuous sleep, possibly due to its conservative design and the presence of movement arousals, which has to be improved in future generation algorithms. [source] A Prospective Randomized-Controlled Trial of Ventricular Fibrillation Detection Time in a DDDR Ventricular DefibrillatorPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2000KENNETH A. ELLENBOGEN Implantable cardioverter defibrillators (ICDs) with dual chamber and dual chamber rate responsive pacing may offer hemodynamic advantages for some ICD patients. Separate ICDs and DDDR pacemakers can result in device to device interactions, inappropriate shocks, and underdetection of ventricular fibrillation (VF). The objectives of this study were to compare the VF detection times between the Ventak AV II DR and the Ventak AV during high rate DDDR and DDD pacing and to test the safety of dynamic ventricular refractory period shortening. Patients receiving an ICD were randomized in a paired comparison to pacing at 150 beats/min (DDD pacing) or 175 beats/min (DDDR pacing) during ICD threshold testing to create a "worst case scenario" for VF detection. The VF detection rate was set to 180 beats/min, and VF was induced during high rate pacing with alternating current. The device was then allowed to detect and treat VF. The induction was repeated for each patient at each programmed setting so that all patients were tested at both programmed settings. Paired analysis was performed. Patient characteristics were a mean age of 69 ± 11 years, 78% were men, coronary artery disease was present in 85%, and a mean left ventricular ejection fraction of 0.34 ± 0.11. Fifty-two episodes of VF were induced in 26 patients. Despite the high pacing rate, all VF episodes were appropriately detected. The mean VF detection time was 2.4 ± 1.0 seconds during DDD pacing and 2.9 ± 1.9 seconds during DDDR pacing (P = NS). DDD and DDDR programming resulted in appropriate detection of all episodes of VF with similar detection times despite the "worst case scenario" tested. Delays in detection may be seen with long programmed ventricular refractory periods which shorten the VF sensing window and may be avoided with dynamic ventricular refractory period shortening. [source] Preserving Normal Ventricular Activation Versus Atrioventricular Delay Optimization During Pacing: The Role of Intrinsic Atrioventricular Conduction and Pacing RatePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2000IVAN ILIEV ILIEV The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 ± 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal A V delay in the DDD mode and comparison between AAI and DDD with optimal A V delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (AHI) was 282 ± 68 ms for rate 70/min and 330 ± 98 ms for rate 90/min (P < 0.01). The optimal A V delay was 159 ± 22 ms, A V delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16%± 9%. At rate 70/min the patients with ARI , 270 ms had higher AFTVI in AAI than in DDD (0.214 ± 0.05 m vs 0.196 ± 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI(0.192 ± 0.03 m vs 0.166 ± 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 ± 0.03 m vs 0.162 ± 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 ± 0.05 m vs 0.173 ± 0.05 mP < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 ± 0.05 m vs 0.158 ± 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate. [source] Successful Treatment of Severe Orthostatic Hypotension with Cardiac Tachypacing in Dual Chamber PacemakersPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2000HARUHIKO ABE Orthostatic hypotension is an evolving and disabling disease usually observed in elderly patients with dramatic consequences on morbidity, mortality, and impairing the quality of life. We studied the effects of the pacing rate and AV interval on the blood pressure drop in the upright position in two patients with previously implanted pacemakers for sinus node dysfunction. Although the AV interval did not affect the blood pressure drop in the upright position, tachypacing at 100 paces/min improved it dramatically and prevented syncope. Cardiac tachypacing is a useful therapeutic option in severe refractory Orthostatic hypotensive patients, especially those with chronotropic incompetence. [source] Treatment for Mechanical Valve Thrombosis in the Right Heart: Combined Pharmacological and Mechanical ThrombolysisARTIFICIAL ORGANS, Issue 8 2010Shigeaki Aoyagi Abstract We report clinical results of combined pharmacological and mechanical thrombolysis for mechanical prosthetic valve thrombosis (PVT) in the right heart. Between January 1992 and December 2008, combined thrombolysis, which consisted of an intravenous infusion of urokinase together with mechanical disruption of thrombus in a prosthetic valve by temporarily increasing the cardiac pacing rate, was performed in three patients with four cases of mechanical PVT in the right heart. The prosthetic valve in all three patients was a bileaflet mechanical valve, and was located in the tricuspid position in two patients and in the pulmonary position in the remaining patient. PVT was diagnosed by echocardiography and cineradiography. Thrombolysis was successful in all four cases in the three patients, and no hemorrhagic complications or clinically symptomatic pulmonary embolisms were observed. Mechanical disruption of thrombus using a pacemaker appears to be an effective adjunctive modality to thrombolysis with fibrinolytic agents for PVT in the right heart. Combined pharmacological and mechanical thrombolysis may improve success rates and reduce the time required for thrombolysis of PVT. [source] Regional variations in action potential alternans in isolated murine Scn5a+/, hearts during dynamic pacingACTA PHYSIOLOGICA, Issue 2 2010G. D. K. Matthews Abstract Aim:, Clinical observations suggest that alternans in action potential (AP) characteristics presages breakdown of normal ordered cardiac electrical activity culminating in ventricular arrhythmogenesis. We compared such temporal nonuniformities in monophasic action potential (MAP) waveforms in left (LV) and right ventricular (RV) epicardia and endocardia of Langendorff-perfused murine wild-type (WT), and Scn5a+/, hearts modelling Brugada syndrome (BrS) for the first time. Methods:, A dynamic pacing protocol imposed successively incremented steady pacing rates between 5.5 and 33 Hz. A signal analysis algorithm detected sequences of >10 beats showing alternans. Results were compared before and following the introduction of flecainide (10 ,m) and quinidine (5 ,m) known to exert pro- and anti-arrhythmic effects in BrS. Results:, Sustained and transient amplitude and duration alternans were both frequently followed by ventricular ectopic beats and ventricular tachycardia or fibrillation. Diastolic intervals (DIs) that coincided with onsets of transient (tr) or sustained (ss) alternans in MAP duration (DI*) and amplitude (DI,) were determined. Kruskal,Wallis tests followed by Bonferroni-corrected Mann,Whitney U -tests were applied to these DI results sorted by recording site, pharmacological conditions or experimental populations. WT hearts showed no significant heterogeneities in any DI. Untreated Scn5a+/, hearts showed earlier onsets of transient but not sustained duration alternans in LV endocardium compared with RV endocardium or LV epicardium. Flecainide administration caused earlier onsets of both transient and sustained duration alternans selectively in the RV epicardium in the Scn5a+/, hearts. Conclusion:, These findings in a genetic model thus implicate RV epicardial changes in the arrhythmogenicity produced by flecainide challenge in previously asymptomatic clinical BrS. [source] Mechanisms for Discordant AlternansJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2001MARI A. WATANABE M.D., Ph.D. Discordant Alternans Mechanism.Introduction: Discordant alternans has the potential to produce larger alternans of the ECG T wave than concordant alternans, but its mechanism is unknown. Methods and Results: We demonstrate by one- and two-dimensional simulation of action potential propagation models that discordant alternans can form spontaneously in spatially homogeneous tissue through one of two mechanisms, due to the interaction of conduction velocity and action potential duration restitution at high pacing frequencies or through the dispersion of diastolic interval produced by ectopic foci. In discordant alternans due to the first mechanism, the boundaries marking regions of alternans with opposite phase arise far from the stimulus site, move toward the stimulus site, and stabilize. Dynamic splitting of action potential duration restitution curves due to electrotonic coupling plays a crucial role in this stability. Larger tissues and faster pacing rates are conducive to multiple boundaries, and inhomogeneities of tissue properties facilitate or inhibit formation of boundaries. Conclusion: Spatial inhomogeneities of electrical restitution properties are not required to produce discordant alternans. [source] Microdislodgment of Ventricular Pacing Lead Undetectable During Rapid Pacing One Year After ImplantationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2003YUKO CHINUSHI CHINUSHI, Y., et al.: Microdislodgment of Ventricular Pacing Lead Undetectable During Rapid Pacing One Year After Implantation. A 71-year-old woman had undergone valvular heart surgery in 1981, and implantation of a permanent ventricular pacemaker for ventricular pauses during atrial fibrillation in 2001. One year after pacemaker implantation, she complained of faintness. When pacing at 100 beats/min the pacemaker functioned properly. However, pacing and sensing failure was detected at a pacing rate of 60 beats/min. At rapid pacing rates, the lead tip was in closer contact with the endocardium, and its microdislodgment was undetectable. The symptoms have resolved since the lead was repositioned. (PACE 2003; 26:787,788) [source] Clinical Evaluation of a Pacemaker Algorithm That Adjusts the Pacing Rate During Sleep Using Activity VariancePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2000FIRAT DURU DURU, F., et al.: Clinical Evaluation of a Pacemaker Algorithm That Adjusts the Pacing Rate During Sleep Using Activity Variance. Even though rate responsive pacemakers are able to regulate pacing rates based on sensor activity, they are set with a minimum rate that is not adjusted to provide rate decreases during sleep. The aim of this study was to evaluate the performance of the "Sleep Rate" feature, as compared to patient diaries and a validated method that identifies sleep from wrist actigraphy. In 19 patients (15 men; age 69 ± 8 years) with Pacesetter Trilogy DR+ pacemakers, the base rate and the sleep rate were set to 80 and 50 ppm, respectively. When the patients returned 2 days later, data recorded by the pacemaker and wrist actigraph were analyzed to find the agreement in corresponding sleep/wake periods. In 17 (89%) patients, the pacemaker went into the sleep mode. The total sleep time derived from actigraphy significantly exceeded the time during which the pacemaker was in sleep mode (1156.8 ± 83.4 vs 307.3 ± 77.2 minutes). Frequent reversions out of the sleep mode limited the total sleep time derived from the pacemaker. Cumulative analysis of the pacemaker data showed that the maximum time in the sleep mode was 78 minutes, and exceeded 1 hour in six instances, 30 minutes in 32 instances, and 15 minutes in 83 instances. Epoch by epoch comparisons revealed a good agreement (93.6 ± 1.8%) during wakefulness between the corresponding actigraph and pacemaker epochs. However, only 24.6 ± 3.7% of the corresponding epochs during sleep were identical, and the overall agreement was 54.4 ± 3.7%. Except for one patient who reported palpitations, patients did not suffer from a pacemaker rate change. The Sleep Rate feature provides rate reduction during sleep, while assuring rapid frequency response during physical activity. However, the current algorithm does not allow long periods of slow pacing rate during continuous sleep, possibly due to its conservative design and the presence of movement arousals, which has to be improved in future generation algorithms. [source] |