Effects of Atrial, Ventricular, and Atrioventricular Sequential Pacing on Coronary Flow Reserve

KOLETTIS, T.M., et al .: Effects of Atrial, Ventricular, and Atrioventricular Sequential Pacing on Coronary Flow Reserve . Experimental animal data have indicated that altered left ventricular depolarization sequence as a result of right ventricular pacing may diminish coronary blood flow in the distribution of the left anterior descending coronary artery. To further investigate this, we compared the effects of atrial, ventricular, and atrioventricular (AV) sequential pacing on coronary flow reserve. Twenty-seven patients (24 male, mean age 55 ± 7 years) with normal left anterior descending coronary arteries were studied. Coronary flow reserve was calculated as the ratio of mean flow velocity at maximal coronary vasodilatation to mean flow velocity at baseline. The study consisted of two parts. In the first part, AV sequential pacing was compared to atrial pacing at the same rate; coronary flow reserve did not differ significantly between the two pacing modes (14 patients, 4.85 ± 1.88 vs 5.47 ± 1.55, respectively, P > 0.05). In the second part, all three pacing modalities were compared; coronary flow reserve was significantly higher during ventricular compared to AV sequential pacing, but not significantly different compared to atrial pacing (3.69 ± 1.42 vs 2.90 ± 0.86 vs 3.11 ± 0.89, respectively, P < 0.05). This difference was secondary to a significant decrease in mean baseline velocity during ventricular pacing, while mean velocity during hyperemia was comparable between the three pacing modes. It is concluded that AV sequential pacing does not appear to exert a significant effect on coronary flow reserve. Ventricular pacing, however, may lower resting coronary blood velocity in some patients, without affecting maximal coronary blood velocity, resulting in a higher coronary flow reserve.     

Effect of Ventricular Pacing on Coronary Blood Flow in Patients with Normal Coronary Arteries

Although ventricular pacing is thought to produce impairment of left ventricular function by altering the sequence of ventricular activation and AV dyssynchrony, little is known about the effect of ventricular pacing on coronary blood flow. We measured coronary blood flow and coronary flow reserve in the left anterior descending coronary artery during sinus rhythm, and during both atrial and ventricular pacing at a rate of 100 ppm in 14 patients with normal coronary arteries. The double product increased significantly during both types of pacing. Coronary arterial diameter during ventricular pacing significantly increased compared to that during both sinus rhythm and atrial pacing. Coronary flow velocity during ventricular pacing was significantly lower compared to that during both sinus rhythm and atrial pacing. Coronary blood flow increased significantly during atriai pacing (30.7%± 12.1%; P < 0.001), but not significantly during ventricular pacing (23.6%± 47.0%; P = ns). While coronary flow re-serve during both atrial (3.9 ± 1.3) and ventricular pacing (3.8 ± 0.9) was lower compared to its value during sinus rhythm (4,5 ± 1.5), the difference was not significant. There was a significant positive correlation between the coronary flow reserve during sinus rhythm and the increase of coronary blood flow during ventricular pacing (R²= 0.78; P < 0.001). We concluded that an increase in coronary blood flow during ventricular pacing is not a common finding regardless of the increase in metabolic demand. The increase of coronary blood flow during ventricular pacing was less in patients with a reduced coronary flow reserve. These findings suggest that preservation of AV synchrony and the presence of a normal sequence of ventricular activation may play an important role in preserving coranary blaod flow in this subset of patients.     

Beat-to-Beat Variability in Stroke Volume During VVI Pacing as Predictor of Hemodynamic Benefit from DDD Pacing

To determine whether the magnitude of Beat-to-Beat variability in stroke volume (SVJ during VVI pacing can predici hemodynamic benefit from DDD pacing, we undertook Doppier recordings of systolic and diastolic LV flow during VVI and DDD pacing in 20 patients (age 54 ± 9 years)with DDD pacemakers implanted due to AV block. SV increased by 19%± 10% from VVI to DDD (P < 0.01). This increase was greater (29%± 9%)in patients with a ratio of early (E)/late (A) filling < 1 compared to those with E/A > 1 (10%± 9%) (P < 0.001). Beat-to-Beat variability in SV was greater in VVI (13%± 8%)compared to DDD (4%± 1%) (P < 0.001). Patients with E/A < 1 showed greater Beat-to-Beat variability in SV during VVI pacing (19 ± 6%)compared to those with E/A > 1 (8%± 4%) (P < 0.001). Beat-to-Beat variability in SV during VVI pacing correlated with both percent change in SV from VVI to DDD (r = 0.89, P < 0.001)and E/A (r = -0.71, P < 0.001). In conclusion, patients with E/A < 1 derive greater hemodynamic benefit at rest from DDD pacing compared with E/A > 1. In addition, patients with complete AV block who show large variations in SV during VVI pacing may obtain greater hemodynamic benefit at rest from DDD pacing than patients with small variations.     

The Hemodynamic Importance of Atrial Systole: A Function of the Kinetic Energy of Blood Flow?

The relative importance of atrial systole on left ventricular filling was investigated at rest and during exercise in 25 patients with dual chamber pacemakers. The mean blood flow velocity over the atrial valve, the velocities of the rapid filling phase (E), the active filling phase (A), and the E/ A ratio were determined for pulsed Doppler-echocardiography. The patients were first examined at rest during AV sequential pacing (DVI) at 70 and 104 beats/mm. The investigation was subsequently repeated during atrial synchronous pacing (VDD) at rest and during supine submaximal exercise at workloads adjusted to achieve heart rates corresponding to those during DVI pacing. The mean blood flow velocity at rest did not differ between DVI and VDD pacing at 70 beats/mm (0.46 vs 0.49 m/sec). When (he resting heart rate was increased to 104 beats/min (DVI) the mean blood flow velocity increased to 0.56 msec (P < 0.001). At a corresponding heart rate during exercise (VDD) the velocity increased to 0.70 msec (P < 0.001). At a resting heart rate of 70 beats/min the E/A ratio (n = 14) did not differ significantly between DVI and VDD pacing. With an increased resting heart rate (DVI) the E/A ratio decreased from 0,94 ± 0.45 to 0.78 ± 0.18; NS. When the heart rate increased during exercise (VDD) the E/A ratio increased from 0.75 ± 0.14 to 0.97 ± 0.16; P < 0.001. There was a positive correlation between the increase of the mean blood flow velocity and the increase of the E/A ratio during exercise (r = 0.69, P < 0,01). No such correlation was found when the heart rate was changed at rest. Thus, the importance of atrial systole on ventricular filling diminishes during exercise in accordance with increasing blood flow velocity, which by physical principles is related to the kinetic energy. The relative importance of atrial systole is hence inversely correlated to the kinetic energy of the blood flow.     

Evolution of Atrial Signals from a Single Lead VDD Pacemaker

The atrial sensing capabilities of a new single pass lead VDD pacing system (Pacesetter AddVent) were assessed in a prospective multicenter study of 101 implants during the period July 1994 through March 1996. The pacing lead (Pacesetter AV Plus) has a unique quadripolar 4-in-line connector and uses a pair of ring electrodes with an interelectrode spacing of 12 mm for atrial sensing. The mean age of the patients (51 men) was 73 years (range 19–91). Seventy-five patients had complete heart block; the others had 2:1 AV block. Wide variations were found in signal amplitude: mean P wave amplitude, measured over four cycles in the supine position, was 2.4 ± 1.9 mV at implant, dropping to 1.9 ± 1.7 mV predischarge, and remaining constant at follow-up but with a narrower range. Holter monitoring was undertaken in 24 patients, with a total of 550 monitored hours. Mean AV synchrony was 98.2%± 4.6% (excluding premature ventricular contractions), with 20 patients (83%) showing > 99% AV synchrony, with atrial sensing at 0.1 mV where needed. No oversensing was observed in any patient. There was a low incidence of atrial fibrillation (2%) and sinus bradycardia (0%). The findings show that the range of atrial signals, although wide initially, converges over the first year and remains adequate for reliable AV synchronous pacing.     

Evaluation of atrial thrombus formation and atrial appendage function in patients with pacemaker by transesophageal echocardiography

BACKGROUND: Physiologic pacing is claimed to be superior to ventricular pacing in as much as it entails lower risk of atrial fibrillation, stroke, and atrial remodeling. There are few data on the relation between atrioventricular (AV) synchrony and atrial clot formation. Utilizing transesophageal echocardiography (TEE), this study sought to evaluate the effect of AV synchrony loss on left atrial physiology, atrial stasis, and clot formation. METHODS: We conducted a cross-sectional study on patients with both AV and ventricular pacing with left ventricular ejection fraction (LVEF) >30%. TEE enabled us to explore atrial and pacing leads thrombi and measure left atrial appendage (LAA) flow velocity. RESULTS: A total 72 patients (mean age, 65 +/- 11.7) were enrolled in the study. The pacing mode was VVI in 53% and AV sequential in 47% of patients. LVEF (mean +/- SD; %) was 53.3 +/- 6.2% in ventricular pacing mode and 52.2 +/- 6.6 in physiologic pacing mode. Thrombus formation on pacing lead (<10 mm in 97% of patients) was observed in 32% of all the patients (23% in patients with AV sequential pacing mode and 39% with VVI mode). Left atrial appendage flow velocity (LAA-FV) was significantly higher among the patients with AV sequential pacing mode (49.44 +/- 18 cm/s vs 40.94 +/- 19.4 cm/s, P value = 0.02). LAA-FV >40 cm/s was detected in 60% of the patients, 60% of whom were in physiologic mode. Left atrial size was significantly larger among the patients with VVI pacing mode (42.3 +/- 2.3 mm vs 37.79 +/- 4.5 mm, P = 0.001). Multivariate analysis showed no relation between LAA-FV and age, hypertension, diabetes mellitus, left atrial size, and left ventricular function. Only one patient had right atrial clot. There was no thrombus in the ventricles and atrial appendage. CONCLUSION: Long-term loss of AV synchrony induced by VVI pacing is associated with the impairment of LAA contraction. Thrombus formation in the LAA is not increased by VVI pacing in patients with relatively good left ventricular (LV) function and sinus rhythm.     

Comparison of Ventricular Function in Atrial Rate Adaptive Versus Dual Chamber Rate Adaptive Pacing During Exercise

The hemodynamic effects of two different pacing modes—rate adaptive atrial (AAIR) versus dual chamber (DDDR) pacing—were assessed in 12 patients with DDDR pacemakers during upright bicycle exercise first-pass radionuclide angiography using a multiwire gamma camera with tantalum-178 as a tracer. All patients had sinus node disease with intact AV conduction. Patients exercised to the same heart rate in random order in these two different pacing modes, AAIR and DDDR with AV delay (of 100 msec) selected to maintain 100% ventricular capture. Cardiac output in creased significantly above baseline values during exercise in both pacing modes: 154 ± 41% (mean ± SEM, P = 0.002) with AAIR, versus 95 ± 24% (P = 0.004) with DDDR (P = NS between the two modes). The peak filling rate, likewise, increased in both pacing modes (2.3 ± 0.21 end-diastolic volumes/sec to 3.8 ± 0.31 end-diastolic volumes/sec in AAIR [P = 0.0004] and 2.2 ± 0.18 end-diastolic volumes/sec to 3.4 ± 0.27 end-diastolic volumes/sec in DDDR [P = 0.0008]). LV ejection fraction was normal at rest (60 ± 4%, SEM) and did not significantly change with submaximal exercise in either pacing mode (both 56%, P = NS). No significant changes in end-diastolic volume or stroke volume indexes occurred with exercise in either pacing mode. Our study demonstrates that in patients with normal resting LV function, AAIR and DDDR pacing are equally effective in attaining appropriate increases in cardiac output and LV filling during exercise.     

A New Dual-Chamber Pacing Mode to Minimize Ventricular Pacing

Despite the low long-term incidence of high-degree atrioventricular (AV) block and the known negative effects of ventricular pacing, programming of the AAI mode in patients with sinus node dysfunction (SND) remains exceptional. A new pacing mode was, therefore, designed to combine the advantages of AAI with the safety of DDD pacing. AAIsafeR behaves like the AAI mode in absence of AV block. First- and second-degree AV blocks are tolerated up to a predetermined, programmable limit, and conversion to DDD takes place in case of high-degree AV block. From DDD, the device may switch back to AAI, provided AV conduction has returned. The safety of AAIsafeR was examined in 43 recipients (70 ± 12-year old, 24 men) of dual chamber pacemakers implanted for SND or paroxysmal AV block. All patients underwent 24-hour ambulatory electrocardiographic recordings before hospital discharge and at 1 month of follow-up with the AAIsafeR mode activated. No AAIsafeR-related adverse event was observed. At 1 month, the device was functioning in AAIsafeR in 28 patients (65%), and the mean rate of ventricular pacing was 0.2%± 0.4%. Appropriate switches to DDD occurred in 15 patients (35%) for frequent, unexpected AV block. AAIsafeR mode was safe and preserved ventricular function during paroxysmal AV block, while maintaining a very low rate of ventricular pacing. The performance of this new pacing mode in the prevention of atrial fibrillation will be examined in a large, controlled study.     

Adequacy of Pacing Rate During Exercise in Rate Responsive Ventricular Pacing

Our objective was to determint; the adequate pacing rate during exercise in ventricular pacing by measuring exercise capacity, cardiac output, and sinus node activity. Eighteen patients with complete AV block and an implanted pacemaker underwent cardiopulmonary exercise tests under three randomized pacing rates: fixed rate pacing (VVJ) at 60 beats/min and ventricular rate-responsive pacing (VVIR) programmed to attain a heart rate of about 110 beats/min ar 130 beats/min (VVIR 110 and VVIR 130, respectively) at the end of exercise. Compared with VVI and VVIR 130, VVIR 110 was associated with an increased peak oxygen uptake(VVIR 110:20.3 ± 4.5 vs VVI: 16.9 ± 3.1; P < 0.01; and VVIR 130: 19.0 ± 4.1 mL/min per kg, respectively; P < 0.05) and a higher oxygen uptake at anaerobic threshold (15.3 ± 2.7, 12.7 ± 1.9; P < 0.01, and 14.6 ± 2.6 mL/min per kg; P < 0.05). The atrial rate during exercise expressed as a percentage of the expected maximal heart rate was lower in VVIR 110 than in VVI or VVIR 130 (VVIR 110: 75.9%± 14.6% vs VVI: 90.6%± 12.8%; P < 0.01; VVIR 110 vs VVIR 130: 89.1%± 23.1%; P < 0.05). There was no significant difference in cardiac output at peak exercise between VVIR 110 and VVIR 130. We conclude that a pacing rate for submaximal exercise of 110 beats/min may be preferable to that of 130 beats/min in respect to exercise capacity and sympathetic nerve activity.     

Effect of Short Atrioventricular Delay on Cardiac Output

RONASZEKI, A., ET AL.: Effect of Short Atrioventricular Delay on Cardiac Output. Short atrioventricular (AV) delay modifies late diastolic filling dynamics. The effect of this change on cardiac output [CO) was studied in closed chest, AV blocked canine preparations (N: 10), during AV sequential pacing (80 bpm). CO (thermodilution technique) and transmitral flow velocity (TMFV, pulsed-wave Doppler) were measured and compared (paired t-test) on the basis of TMFV pattern, when atrial contraction (A wave) started just after early diastolic transmitral flow deceleration [PR:219 ± 25 ms, mean ± SD) and when A wave occurred at the end of late diastole and shortened due to the next ventricular contraction (PR: 56 ± 11 ms). The short AV delay resulted in 12.0 ± 5.9% decrease of CO, reflecting the interrupted late diastolic atrial transport. Properly timed atrial contraction is necessary for optimal AV sequential pacing.     

Atrial Septal Pacing: A Method for Pacing Both Atria Simuhaneously

By pacing both atria simultaneously, one could reliably predict and optimize left-sided AV timing without concern for IACT. With synchronous depolarization of the atria, reentrant arrhythmias might be suppressed. We studied four male patients (73 ± 3 years) with paroxysmal atrial fibrillation and symptomatic bradyarrhythmias using TEE and fluoroscopy as guides; a standard active fixation screw-in lead (Medtronic model #4058) was attached to the interatrial septum and a standard tined lead was placed in the ventricle. The generators were Medtronic model 7960. The baseline ECG was compared to the paced ECG and the conduction time were measured to the high right atrium, distal coronary sinus and atrial septum in normal sinus rhytbm, atrial septal pacing, and AAT pacing. On the surface ECG, no acceleration or delay in A V conduction was noted during AAI pacing from the interatrial septum as compared with normal sinus rhythm. The mean interatrial conduction time for all 4 patients was 106 ± 2 ms; the interatrial conduction time measured during AAT pacing utilizing the atrial septal pacing lead was 97 ± 4 ms (P = NS). During atrial septal pacing, the mean conduction time to the high right atrium was 53 ± 2 ms. The mean conduction time to the lateral left atrium during atrial septal pacing, was likewise 53 ± 2 ms. We conclude that it is possible to pace both atria simultaneously from a single site using a standard active fixation lead guided by TEE and fluoroscopy. Such a pacing system allows accurate timing of the left-sided AV delay.     

The Effect of Posture on the Response to Atrioventricular Synchronous Pacing in Patients with Underlying Cardiovascular Disease

In order to determine whether the hemodynamic benefit of atrioventricular synchronous pacing is maintained in the upright position, 14 patients with dual chamber pacemakers were paced in VVI mode and DDD mode in both the supine and standing position. The hemodynamic response was assessed by measuring the velocity time integral derived from the pulsed-wave Doppler signal in the left ventricular outflow tract during VVI pacing and dual chamber pacing at three different AV delays (125, 200, 250 ms). In the supine position, the velocity time integral during VVI pacing was 14.6 ± 3.0 cm and this increased during DDD pacing at all three AV delays (17.7 ± 3.3, 17.9 ± 3,0, 17.5 ± 3.5 cm). In the upright position, the velocity time integral during VVI pacing was 12.9 ± 3.5 cm and this increased with DDD pacing (15.5 ± 3.3, 15. 1 ± 4.0, 15.1 ± 3.9 cm). It was concluded that although stroke volume decreases when assuming the upright position, the beneficial response to dual chamber pacing is maintained and equals that observed in the supine position.     

Hemodynamically optimized temporary cardiac pacing after surgery for congenital heart defects

Disturbance of normal AV synchrony and dyssynchronous ventricular contraction may be deleterious in patients with otherwise compromised hemodynamics. This study evaluated the effect of hemodynamically optimized temporary dual chamber pacing in patients after surgery for congenital heart disease. Pacing was performed in 23 children aged 5 days to 7.7 years (median 7.3 months) with various postoperative dysrhythmias, low cardiac output, and/or high inotropic support and optimized to achieve the highest systolic and mean arterial pressures. The following four pacing modes were used: (1) AV synchronous or AV sequential pacing with individually optimized AV delay in 11 patients with first- to third-degree AV block; (2) AV sequential pacing using transesophageal atrial pacing in combination with a temporary DDD pacemaker for atrial tracking and ventricular pacing in three patients with third-degree AV block and junctional ectopic tachycardia, respectively, who had poor signal and exit block on atrial epicardial pacing wires; (3) R wave synchronized atrial pacing in eight patients with junctional ectopic tachycardia and impaired antegrade AV conduction precluding the use of atrial overdrive pacing; (4) Atrio-biventricular sequential pacing in two patients. Pressures measured during optimized pacing were compared to baseline values at underlying rhythm (13 patients with first-degree AV block or junctional ectopic tachycardia) or during pacing modes commonly used in the given clinical situation: AAI pacing (1 patient with slow junctional rhythm and first-degree AV block during atrial pacing), VVI pacing (2 patients with third-degree AV block and exit block and poor sensing on epicardial atrial pacing wires) and dual-chamber pacing with AV delays set to 100 ms (atrial tracking) or 150 ms (AV sequential pacing) in 7 patients with second- to third-degree AV block and functional atrial pacing wires. Optimized pacing led to a significant increase in arterial systolic (mean) pressure from 71.5 +/- 12.5 (52.3 +/- 9.0) to 80.5 +/- 12.2 (59.7 +/- 9.1) mmHg (P < 0.001 for both) and a decrease in central venous (left atrial) pressure from 12.3 +/- 3.4 (10.5 +/- 3.2) to 11.0 +/- 3.0 (9.2 +/- 2.7) mmHg (P < 0.001 and < 0.005, respectively). In conclusion, several techniques of individually optimized temporary dual chamber pacing leading to optimal AV synchrony and/or synchronous ventricular contraction were successfully used to improve hemodynamics in patients with heart failure and selected dysrhythmias after congenital heart surgery.     

Modulation of the Arterial Coronary Blood Flow by Asynchronous Activation with Ventricular Pacing

This study aims to test the assumptions that: (1) coronary arterial flow is attenuated in an early activated region by ventricular pacing; (2) asynchronous mechanical activation caused by ventricular pacing under controlled perfusion pressure and intact coronary tone is associated with reduced coronary flow compared to atrial pacing; and (3) abolishment of vascular tone under controlled perfasion pressure diminishes the expected difference in blood flow between atrial and ventricular pacing. Blood flow velocity (BFV) in the left anterior descending (LAD) and the left circumflex arteries (CFX) and a wall thickening index were measured in 14 open-chest dogs under normal conditions, and constant perfasion pressure. Four pacing sites were used: right atrium (RAJ, mid-right ventricle (RVyJ, mid-left ventricle (LVp), and left ventricular apex (Apex. Pacing modes were either sequential ventriculoatrial (VA) (protocol A, n = 7), or sequential atrioventricalar (AV) (protocol B, n = 7), with a shorter AV difference (30 msec) than normal. Residis: BFV was decreased in the LAD during HV and Apex, pacingby 9.7%-12.9% versas LV^p and by 1.6%-14.6% versus LV^p (P < 0.05). No BFV variations were observed in the CFX. Flow velocity conductance (FVC = mean blood flow velocity divided by the mean aortic pressure) was higher by 16%-28% in the CFX for the three ventricular pacing sites versus the airial pacing, and higher by 14.1%± 6.1% only in LV_p versus RA_p pacing in the LAD (P < 0.05). Wall thickening index reduced during ventricular pacing in all three ventricular sites by 50%-64% (P < 0.05) compared to atrial pacing. Under constant perfusion pressure, LAD blood flow decreased with ventricular pacing as compared to right atrial pacing; this was particularly pronounced during the diastolic phase (16.6%?45.5%, P < 0.02). Normalized oscillatory flow amplitude (OFA.J was reduced in RVy, pacing compared to RA_p and LV_p pacing (16.2 ± 3.5 and 21.7%± 4.1%, respectively, P < 0.03). The variations in blood flow and OFAn disappeared with adenosine-mediated maximum vasodilatation. Summary; (1) Mean and phasic flows are reduced in the early activated LAD region by ventricular pacing (RV_p, Apex. (2) Under controlled perfusion pressure and intact vascular tone, ventricular pacing compromises blood flow compared with atrial pacing. (3) This effect disappears when vascular tone is eliminated by intracoronary injection of adenosine, suggesting that the coronary autoregulation is responsible for some of the effects.     

Efficacy of Ventricular Rate Stabilization by Right Ventricular Pacing During Atrial Fibrillation

To assess the effect of right ventricular pacing on rate regularity during exercise and daily life activities, 16 patients with sinoatrial disease and chronic atrial fibrillation (AF) were studied. Incremental ventricular pacing was commenced at 40 beats/min until > 95% of ventricular pacing were achieved during supine, sitting, and standing. Thirteen patients also underwent randomized paired submaximal exercise tests in either a fixed rate mode (VVI) or a ventricular rate stabilization (VRS) mode in which the pacingrate was set manually at 10 beats/min above the average AF rate duringthe last minute of each exercise stage. The pacing interval for rate regularization was shortest during standing (692 ± 26 ms) compared with either supine or sitting (757 ± 30 and 705 ± 26 ms, respectively, P < 0.05). During exercise, VRS pacing significantly increased the maximum rate (119 ± 5.2 vs 106 ± 4.2 ms, P < 0.05), percent of ventricular pacing (85%± 5% vs 23%± 7%, P < 0.05), rate regularity index (5.8%± 1.6% vs 13.4%± 1.9%, P < 0.05), and maximum level of oxygen consumption (12.4 ± 0.5 vs 11.3 ± 0.5 ml/kg, P < 0.05) compared with VVI pacing. There was no change in oxygen pulse or difference in symptom scores in this acute study between the two pacing modes. It is concluded that right ventricular pacing may significantly improve rate regularity and cardiopulmonary performance in patients with chronic AF. This may be incorporated in a pacing device for rate regularization of AF using an algorithm that is rate adaptive to postural and exercise stresses.     

Interatrial Conduction During Cardiac Pacing

DDD pacemakers sense and pace right-sided cardiac chambers. The relationship of atrial to ventricular systole on the left side of the heart is of importance for systemic hemodynamics. Effective atrioventricular synchrony is partially determined by interatrial conduction time (IACT). At the time of DDD pacemaker implantation, interatrial conduction was measured using an intraesophageal pill electrode in 25 patients who were on no cardiac medications. Mean interatrial conduction time for all patients prolonged from 95 ± 18 ms during sinus rhythm to 122 ± 30 ms during right atrial pacing (p < 0.001). In 16 patients with P wave duration < 110 ms interatrial conduction prolonged from 85 ± 10 ms during sinus rhythm to 111 ± 9 ms during right atrial pacing (p < 0.01) compared to 114 ± 20 ms prolonging to 111 ± 19 ms (p < 0.01] in 9 patients with P wave duration > 110 ms. In each patient, while atrioventricular conduction prolonged with incremental right atrial pacing, interatrial conduction times did not vary. Interatrial conduction prolongs from baseline during atrial pacing and remains constant at all paced rates from 60–160 heats per minute. In addition to longer interatrial conduction times during sinus rhythm, patients with electrocardiographic P wave prolongation have longer interatrial conduction times during right atrial pacing than do normals (p < 0.0001). Based on interatrial conduction times alone, the AV interval during DDD cardiac pacing should be approximately 25 ms longer during AV pacing as compared to atrial tracking.     

Effect of Dual Chamber Atrioventricular Sequential Pacing on Coronary Flow Velocity in a Patient with Hypertrophic Obstructive Cardiomyopathy

Effects of dual chamber A V sequential pacing on coronary flow velocity, especially systolic reversal flow, were tested in a patient with hypertrophic obstructive Cardiomyopathy. AV sequential pacing with shorter AV delays reduced the systolic reversal flow in the coronary artery, and improved the pressure gradient of the left ventricular outflow tract.     

Comparison of Resting Hemodynamic Indices and Exercise Performance During Atrial Synchronized and Asynchronous Ventricular Pacing

Resting hemodynamic indices and exercise tolerance were measured during atrial synchronized (VAT) and asynchronous ventricular pacing (VOO) in 35 patients with implanted pacemakers which could be externally programmed to function in either pacing mode. Cardiac output and mean systemic arterial pressure were significantly greater during VAT pacing (VAT: 4.5 ± 1.21 /min, 115 ± 28 mmHg; VOO: 3.7 ± 0.8 1/min 105 ± 25 mmHg respectively), although there was no difference in pulmonary artery end-diastolic pressure. Maximal exercise performance was assessed using the Bruce protocol in both pacing modes. Neither the patient nor the supervising physician was aware of the preselected pacing mode; a second physician monitored the electrocardiogram and blood pressure but influenced the point of exercise termination only if a potentially dangerous arrhythmia or hypotension occured. Blood pressure responses were superior and atrial rates lower during VAT pacing, In all but five patients, exercise tolerance was improved by VAT pacing. This amounted to 33 percent or more in 23/35 patients. This improvement was shown to be maintained in the 20 patients who had repeat exercise tests several weeks later. Ventricular arrhythmias, hypotension, and lightheadedness frequently complicated exercise during asynchronous pacing but occurred rarely with atrial synchronized pacing. Resting hemodynamic indices did not predict the extent of improvement gained by physiological pacing.     

Regional Wall Motion During Pacing for Hypertrophic Obstructive Cardiomyopathy

In order to assess the influence of right ventricular stimulation on LV contraction sequence in hypertrophic obstructive cardiomyopathy (HOCM), we performed a regional wall-motion analysis of the left ventricle by comparing normal His-Purkinje activation to pacing from the right ventricular apex. In 9 patients (5 males and 4 females, mean age 61 ± 9 years) assessed after a mean pacing period of 12 weeks (range 7–24 weeks), AV sequential pacing induced a 52% reduction in maximal pressure gradient from 76 ± 36 to 40 ± 28 mmHg (P < 0.01) as determined by Doppler examination. Regional wall-motion analysis of the left ventricle was computed from digitized two-dimensional echocardiographic images by means of the area shrinking method. Pacing induced a significant reduction of total septal area shrinking from 25%± 17% to 12%± 17% (P < 0.005). A tendency toward paradoxical septal motion was observed in one patient only. The apex showed no significant variation. A 6% increase in area shrinking was observed at the posterior wall and lateral free wall, from 38%± 13% to 43%± 10% (P < 0.05). Pacing did not significantly alter the global ejection fraction. A direct correlation between the magnitude of subaortic pressure gradient reduction and that of septal motion changes was found in a majority of patients. In conclusion, dual chamber pacing reduces septal wall motion in patients with HOCM obstructive cardiomyopathy. Tins might be one of the mechanisms involved in the reduction of LV outflow tract obstruction.     

Single Lead VDD Pacing: Multicenter Study

Optimal treatment for patients with AV block and normal sinoatrial node (SA) function entails atrial sensing and ventricular pacing (VDD mode). Single-lead VDD pacing preserves AV synchrony, precludes the need to insert two leads, and makes the implanter's work simpler and quicker. Our objectives were to verify the performance of the Thera(tm) VDD pacing system (Medtronic, Inc., Minneapolis, MN, USA), and evaluate the effectiveness of its atrial sensing and its ventricular sensing and pacing. In 165 patients, 150 adults (mean age 62 ± 18 years) and 15 children (mean age 7 ± 5 years) with 1°–3° AV block and normal SA node function, a Thera VDD system (Models 8948 or 8968) was implanted. Intraoperative ventricular electrical measurements were not significantly different from those of VVI pacemakers. The mean amplitude of the atrial signal during implantation was 4.1 ± 1.9 mV. Optimal atrial signals during implantation were usually obtained in the mid or lower part of the right atrium by using a special technique. Adequate atrial measurements remained stable throughout 24 months. There was no difference between serial measurements of atrial signal amplitudes at predischarge and during follow-up visits. Reposition of the lead was done in 2 patients (1.4%), and reprogramming to VVI in 7 patients: due to atrial fibrillation in 3 (1.8%) and due to atrial undersensing in 4 patients (2.4%). Thera VDD pacing is reliable and easy to manage with dependable atrial sensing and ventricular pacing. The survival rate of VDD pacing at 2 years was 96%.