AV Pacing and LV Performance

Five patients with impaired left ventricular function (LV) and implanted AV sequential pacemakers underwent serial radionuclide angiograms. The goal was a non-invasive evaluation of the rapid changes in left ventricular performance elicited by rate, pacing mode and AV interval manipulation. End diastolic volume, end systolic volume, stroke volume and cardiac output were increased by AV sequential pacing in comparison with ventricular pacing at 70 beats per minute. No significant change in ejection fraction and blood pressure were noted with changing AV sequential pacing rates at usual pacing rates. Our data suggest that a short A V interval (150 ms) improved LV performance more than a long AV interval (250 ms). A non-invasive technique to optimize left ventricular performance on an acute basis by varying heart rate, AV interval and pacing mode with the implanted AV sequential pacemaker is feasible and may be useful in selective clinical situations.     

Hemodynamic Consequences of Atrioventricular and Ventriculoatrial Pacing

The effect of atrialventricular versus ventricular pacing and contraction were studied in seven open-chest dogs. Cardiac output, left ventricular, left atrial, right atrial and pulmonary artery pressures were recorded. The right or left ventricular apical areas were consistently superior as ventricular pacing sites.
Appearance of cannon A waves within the pre- or ejection period produced a significant decrease in left ventricular and systemic blood pressure, and cardiac output with a concomitant increase in right atrial, ventricular and pulmonary pressures. Prominent "v" waves were also observed during these periods.
Reducing the basic driving cycle length from 400 to 300 msec caused a marlted deterioration of all hemodynamic parameters with the appearance of mechanical alternans. Random VA conduction or ventricular pacing in the presence of com-plete AV and VA heart block appeared to offer a more favorable hemodynamic result than constant 1:1 VA conduction. It is concluded that maintenance of a physiologic AV interval permitting atrial contraction to appear outside of pre- or ejection period of ventricular systole is an important determinant or ventriculor function during cardiac pacing.     

Left Ventricular Function During Physiological Cardiac Pacing: Relation to Rate, Pacing Mode, and Underlying Myocardial Disease

The hemodynamic effects of cardiac pacing at different rates and in different modes were studied in 21 patients who were candidates for permanent pacemaker implantation. Nine of these had primary conduction disturbances (PCD), ten had ischemic heart disease (IHD), seven with additional cardiac failure (CHF), and two had hypertrophic cardiomyopathy (HCM). In patients with PCD, atrial (AOO) and AV sequential (DVI) pacing did not change systolic blood pressure and pulse pressure but ventricular (VVI) pacing caused a progressive fall in these measurements, especially as heart rate increased. Ventricular volume and stroke volume (counts) derived from radionuclide ventriculography (RVG) decreased progressively with higher pacing rates, especially during VVI pacing. Cardiac output was maintained during VVI pacing by the increase in heart rate; during AOO and DVI pacing, cardiac output increased. Similar but more marked differences were observed in patients with IHD and CHF and the changes were even greater in the patients with HCM. Left ventricular (LV) ejection fraction changed little with increasing heart rate in PCD but decreased progressively with the onset of ischemia in IHD and CHF. There was no difference in ejection fraction in the different pacing modes. Graphs related to LV contractility (end-systolic pressure-volume relations) showed that AOO pacing produced the highest and VVI pacing produced the lowest curves of myocardial contractility in all patient groups, except that at higher rates the AOO curve shifted down again in patients with IHD and CHF, presumably with the onset of myocardial ischemia. This study showed that physiological pacing produced the best hemodynamic results in all patient groups. Higher pacing rates should be avoided in patients with ischemic heart disease while VVI pacing should not be used in patients with HCM. Blood pressure and RVG studies during temporary pacing are useful in selecting the optimal pacing system in an individual patient when the clinical choice is not clear.     

VDD Pacing at Short Atrioventricular Intervals Does Not Improve Cardiac Output in Patients with Dilated Heart Failure

Atrial synchronous pacing with short, nonphysiologicai atrioventricular (AV) intervals has been reported to increase cardiac output in selected patients with severe dilated heart failure. The aim of this study was to determine the acute effect of atrial synchronous pacing with short AV intervals in a consecutive series of patients with dilated heart failure. Twelve patients with a mean ejection fraction of 21 %± standard error 2.5% were studied. Pacing catheters were placed in the high right atrium and right ventricular apex and a balloon flotation catheter in the pulmonary artery for measurement of cardiac output. Simultaneous transthoracic echocardiography was performed for measurement of left ventricular filling time and mitral regurgitation. In a randomized crossover design, measurements were made during VDD pacing at programmed AV intervals of 100 and 60 msec and during a control period in sinus rhythm. Left ventricular filling time increased at AV intervals of 100 and 60 msec (mean difference 37 ± 9 and 34 ± 11 msec, respectively, both P < 0.01 compared to control). Despite increases in ventricular filling time, stroke, and cardiac index declined with short atrioventricular intervals (at an AV interval of 60 msec, stroke index fell by 2.1 ± 0.5 mL/m², P < 0.05 and cardiac index by 125 ± 45 mL/m²; P = NS). Heart rate was unchanged at both AV intervals (78 ± 4.9 at control, 78 ± 5.2 at 100 msec and 79 ± 4.9 beats/min at 60 msec; P = NS). The decrease in stroke index at an AV Interval of 60 msec was inversely related to control left ventricular filling time (r = 0.74; P = 0.01) and ejection fraction (r = 0.69; P = 0.02) and directly related to heart rate (r = 0.77; P < 0.01). The change in stroke index at an AV delay of 60 msec was also inversely related to the change in mitral regurgitation induced by pacing (r = 0.84; P = 0.01). Thus, in a group of patients with stable dilated heart failure, atrial synchronous pacing with short AV intervals did not improve cardiac output. The change in cardiac output with pacing was inversely related to baseline left ventricular function and to the change in mitral regurgitation induced by pacing.     

Hemodynamic Findings During Sinus Rhythm, Atrial and AV Sequential Pacing Compared to Ventricular Pacing In a Dog Model

The hemodynamic responses of atrial lAF], atrioventricu-lar sequential (AVP) and ventricuJar pacing (VP) were compared to sinus rhythm (SfiJ in seventeen anesthetized dogs with intact AV conduction. The atrium and/or ventricle were paced at fixed rates above the control sinus rate. An AV interval shorter than normal conduction was selected to capture the ventricle. The changes of pulmonary capillary wedge pressure (PCWP, mmHg). mean aortic pressure (MAP, mmHg), cardiac output (CO, L/min), systemic vascular resistance (SVR, dynes/s/cm⁻⁵), left ventricular stroke work index (SWI) and mean systolic ejection rate (MSER, ml/s) during sinus rhythm, atrial pacing and atrio-ventricular sequential pacing (expressed in percentages of the individual values during ventricular pacing) were:
The importance of atrial systole for cardiac performance was clearly demonstrated in dogs with normally compliant hearts. In both atrial and atrioventricular sequential pacing compared to ventricular pacing there was a reduction of pulmonary capillary wedge pressure (PCWP) (p < 0.01) and systemic vascular resistance (SVR) (p < 0.01) despite an increase in cardiac output (CO). The lesser mean systolic ejection rate (MSER) found during atrioventricular sequential pacing compared to sinus rhythm and atrial pacing may be explained by the abnormal ventricular depolarization in this pacing mode; nevertheless, the mean systolic ejection rate was still greater than that found during ventricular pacing (p < 0.05).     

Long–Term Effect of VVI Pacing on Atrial and Ventricular Function in Patients with Sick Sinus Syndrome

We conducted a prospective, 6–month echocardiographic study on the effect of WI pacing on left atrial and ventricular function and dimensions in patients with sick sinus syndrome. Thirty nine patients (23 women and 16 men, aged 71.7 ± 9.2 years; 30 in sinus rhythm and 9 in atrial fibrillation) who had a WI pacemaker implanted because of sick sinus syndrome were recruited in the study. In 26 patients who presented with and remained in sinus rhythm, paced left ventricular ejection fraction and stroke volume were significantly decreased (71.4%± 11.8% to 67.0%± 13.6%, and 73.9 ± 29.0 cm³ to 66.3 ±21.1 cm³, respectively, P < 0.001 for both), whereas the paced diastolic dimension of the left atrium was significantly increased (3.2 ± 0.7 cm to 3.7 ± 0.9 cm, P < 0.001) at 6 months as compared with preimplantation. In nine patients with atrial fibrillation at implantation, paced left ventricular ejection fraction at follow–up was significantly decreased (67.7%±10.1% to 64.2%± 10.6%, P = 0.003), but paced stroke volume and left atrial diastolic dimension were not significantly changed (75.1 ± 25.6 cm³ to 79.0 ± 22.7 cm³, and 4.3 ±1.2 cm to 4.6 ±1.5 cm, P = NS for both) at follow–up. Cessation of pacing and restoration of sinus rhythm in 21 patients at follow–up did not result in any significant change of ejection fraction (67.5%± 10.2% to 67.6%± 9.7%, P = NS) whereas stroke volume was increased (59.1 ± 19.6 cm³ to 69.1 ± 22.3 cm³, P < 0.0001) in comparison with paced values. However, compared with preimplantation values, ejection fraction was significantly decreased (70.4%± 10.0% to 67.6%± 9.7%, P = 0.001), whereas stroke volume was not significantly changed (68.4 ± 22.3 cm³ to 69.1 ± 22.3 cm³, P = NS) during sinus rhythm at follow–up. In 14 of those patients, discontinuation of pacing resulted in a significant increase of left atrial fractional shortening (8.1 %± 1.7% to 20.1 %± 4.3%, P < 0.001) and significant increase of left atrial diastolic dimension compared with paced and preimplantation levels (3.8 ± 0.7 cm vs 3.6 ± 0.7 cm and 3.0 ± 0.5 cm, respectively, P < 0.001). Long–term WI pacing in patients with sick sinus syndrome results in increase of the left ventricular end–systolic dimension and permanent reduction of the left ventricular ejection fraction. In the left atrium, WI pacing causes an immediate reduction of the fractional shortening as well as long–term increase of the diastolic dimension.     

The Importance of the Left Atrioventricular Interval during Atrioventricular Sequential Pacing

During atrioventricular (AV) sequential pacing from the right heart, the interval between the left atrium and ventricle may vary from the programmed AV interval depending on the position of the atrial and ventricular electrodes and interatrial and interventricular conduction. The aim of this study was to determine the hemodynamic effects of altering the left AV interval while keeping the programmed AV interval constant. Four male and 17 female patients, aged 49 ± 15 years were studied. The left AV interval was measured by a catheter in the coronary sinus. Stroke volume and mitral flow were measured by simultaneous echo Doppler during AV sequential pacing from the right atrial appendage and right ventricular apex at programmed AV intervals of 100. 60, and 6 ms. The atrial catheter was then positioned on the atrial septum and the measurements repeated. With the atrial catheter in the right atrial appendage, interatrial activation time (118 ± 20 ms) was similar to interventricular activation time (125 ± 21 ms) and the left AV interval was almost identical to the programmed right AV interval. There was a significant correlation between interatrial and interventricular activation times (r = 0.8; P < 0.001). Positioning the atrial electrode on the septum decreased interatrial activation time by 39 ± 12 ms and increased the left AV interval by a similar amount. At a programmed AV interval of 60 ms, the left AV interval increased from 67 ± 15 ms to 105 ± 17 ms after the atrial catheter was repositioned from the appendage to the septum (P < 0.001). Compared to pacing from the right atrial appendage, atrial septal pacing increased mitral A wave velocity integral (2.8 ± 1.4 vs 4.4 ±1.7 cm at a programmed AV interval of 60 ms, P < 0.01), decreased E wave velocity integral (8.1 ± 2.2 vs 6.1 ± 2.4 cm, P < 0.001) but did not alter stroke volume (44.8 ± 10.6 vs 44.9 ± 10.1 mL). In contrast, a 40 ms decrease in the programmed right AV interval from 100 to 60 ms decreased stroke volume from 48.0 ± 10.0 to 44.9 ± 10.2 mL (P < 0.001). There was a strong relationship between interatrial and interventricular conduction so that patients with prolonged interatrial conduction still had equivalent left and right AV intervals during atrioventricular sequential pacing from the right atrial appendage and right ventricular apex. Positioning the atrial electrode on the septum decreases interatrial activation time and increases the left AV interval by about 40 ms but has minimal hemodynamic effect in patients without heart failure.     

Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial-Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy

HETTRICK, D.A., et al .: Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy. The role of atrial lead location in cardiovascular function in the presence of impaired ventricular dysfunction is unknown. We tested the hypothesis that left atrial (LA) and left ventricular (LV) hemodynamics are affected by alterations in AV delay and are influenced by atrial pacing site in dogs with dilated cardiomyopathy. Dogs   (n = 7)   were chronically paced at 220 beats/min for 3 weeks to produce cardiomyopathy and then instrumented for measurement of LA, LV end diastolic pressure (LVEDP) and mean arterial pressure (MAP), LA volume, LV short-axis diameter, and aortic and pulmonary venous blood flow. Hemodynamics were measured after instrumentation and during atrial overdrive pacing from the right atrial appendage (RAA), coronary sinus ostium (CSO) and lower LA lateral wall (LAW). The AV node was then ablated, and hemodynamics were compared during dual chamber AV pacing (right ventricular apex) from each atrial lead location at several AV delays between 20 and 350 ms. Atrial overdrive pacing from different sites did not alter hemodynamics. Cardiac output (CO), stroke volume, LVEDP, MAP and +dLVP/dt demonstrated significant (P < 0.05) variation with AV delay during dual chamber pacing. CO was higher during LAW pacing than RAA and CSO pacing (   2.3 ± 0.4   vs   2.1 ± 0.3   vs   2.0 ± 0.3 l/min   , respectively) at an AV delay of 120 ms. Also, MAP was higher in the LAW than RAA and CSO (   65 ± 9   vs   59 ± 9   vs   54 ± 11 mmHg   , respectively) at an AV delay of 350 ms. Atrial lead location affects indices of LV performance independent of AV delay during dual chamber pacing in dogs with cardiomyopathy. (PACE 2003; 26[Pt. I]:853–861)     

Short-Term and Long-Term Changes of Left Ventricular Volumes During Rate-Adaptive and Single-Rate Pacing

To evaluate the adaptation of the heart to exercise during pacing, 15 patients with permanent endocardial pacemakers were studied; nine patients had atrioventricular universal (DDD) pacemakers (Symbios 7005) and six patients had activity detecting rate-responsive ventricular (VVIR) pacemakers (Activitrax 8403). Left ventricular function in each patient during rate variable pacing was compared to ventricular function during VVI single-rate pacing. End-systolic and end-diastolic volume changes during exercise were measured by radionuclide angiography and the amount of volume change was used to assess left ventricular function. Both short-term (within 4 hours) and long-term measurements (after at least 4 weeks) were made at rest and at 50% of the maximal exercise capacity in DDD or VVIR mode and were compared with VVI single-rate pacing. All patients, when changed from DDD or VVIR mode to VVI single-rate pacing showed a significant increase of the end-diastolic volume during exercise, which increased even more after long-term VVI pacing. During long-term rate variable pacing, there was no increase of the end-diastolic volume during exercise. DDD or VVIR pacing initially showed a substantial increase of the end-systolic volume during exercise combined with a decrease of left ventricular ejection fraction, suggesting a decrease of the left ventricular contractility. After 4 weeks, contractility improved both with DDD and VVIR pacing. We conclude that short-term DDD and VVIR pacing induces a temporary impairment of left ventricular function that improves after 4 weeks, whereas long-term VVI pacing is associated with left ventricular dilatation even at moderate levels of exercise.     

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.     

Nonphysiological Left Heart AV Intervals as a Result of DDD and AAI "Physiological" Pacing

DDD and AAI pacemakers are considered physiological, since they preserve atrioventricular (AV) synchrony. Artificial pacing, however, is performed largely from right heart chambers, causing aberrant depolarization pathways. Pacing at the right atrial appendage (RAP) is known to delay left atrial contraction due to interatrial conduction time (IACT), and right ventricular (RV) apical pacing (RVP) delays left ventricular (LV) contraction due to interventricular conduction time (TVCT). These delays may render the left heart AV intervals (LAV) either too short or too Jong, thus affecting LV systolic function. The purpose of this study was to evaluate the actual LAV intervals during conventional, right heart AAI and DDD pacing. Resulting LAV intervals were compared to programmed AV values during all DDD pacing modalities. Ten patients with DDD and six patients with AAI pacemakers were studied. IACT was measured from the atrial spike to the onset of left P wave, as recorded by an esophageal lead. Systolic time intervals were measured using either a carotid pulse tracing or a densitogram (photoplethysmography). LV function was appraised by measuring rate-corrected LV ejection time (LVETc). IVCT was measured indirectly as the lengthening of LV preelection period (PEPJ caused by RV pacing, as compared to normal depolarization pathway. Intrinsic‘ACT and IVCT were considered zero. Right heart AV intervals (RAV) were measured from surface ECG and LAVs were calculated according to the following equations: Sinus Rhythm: LAV = RAV; Atrial Pace 4- Ventricular Sense: LAV= RAV ? IACT; Atrial Sense + Ventricular Pace: LAV = RAV + IVCT; Sequential AV Pace: LAV = RAV ? IACT + IVCT, Results: 1. IACT: mean = 73 msec, range: 35–130; IVCT: mean = 50 msec, range: 44–100. 2. Compared to RAVs, LAVs were either too short or too long (?130 to + 300 msec: P < 0.001 J in RAP 4- RVS and RAS + RVP. Conclusions: 1. LAV differed significantly from RAV during AP + VS and AS + VP. 2. “Physiological” RAV intervals in DDD and AAI may cause nonphysiological LAV, possibly affecting LV function. 3. IACT and IVCT should be accounted for when programming DDD PM to provide physiological LAV.     

The Effect of Ventricular Activation Sequence on Cardiac Performance During Pacing

The aim of this study was to evaluate the importance of a normal ventricular activation pattern for cardiac performance. In nine mongrel clogs, atrial pacing was compared to AV synchronous pacing at three different A V delays (150, 100, and 60 nis). In six dogs, proximal septal AV synchronous pacing was compared to apical A V synchronous pacing at three different A V delays. AV synchronous pacing was performed after RF induced complete heart block. Hemodynarnics were evaluated by assessment of positive and negative dP/dt, cardiac output, and left ventricular and pulmonary pressures. Atrial pacing was superior to AV synchronous pacing with respect to positive and negative dP/dt and cardiac output. This difference was present at all AV delays. Proximal septal pacing was associated with a higher positive and negative dP/dl compared to apical pacing at all AV delays. Left ventricular activation time was significantly shorter during proximal septal pacing than during apical pacing (88 ± 4 vs 115 ± 4 ms, P < 0.001). We conclude that atrial and proximal septal pacing improves cardiac function and shortens the ventricular activation time compared to apical AV synchronous pacing independent of the AV interval.     

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.     

心室起搏管理功能对房室传导阻滞患者的近期疗效观察

目的观察具备心室起搏管理（MVP）功能的起搏器（Adapta）在Ⅱ度或间隙性Ⅲ度房室传导阻滞患者的近期效果。方法29例患者入选,分别置入具有MVP功能的Adapt起搏器（实验组,n=17）和其他类型双腔起搏器（对照组,n=12）。并分别在置入前和置入后1、3个月进行随访。随访中观察上述两组的右室起搏比例、心功能（纽约心功能分级、血脑钠肽）、左房内径、左室舒张末内径、左室射血分数等变化。结果置入双腔起搏器（Adapta）术后1个月及3个月,与对照组比较,实验组心室起搏比例明显降低（39．89％±41．21％vs96．48％±3．52％;40．91％±43．49％vs94．53％±4．62％,P均〈0．05）。其他指标两组间无明显差异。结论起搏器心室起搏管理功能可以在短期内降低心室起搏比例。     

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.     

Adverse effects of long-term right ventricular apical pacing and identification of patients at risk of atrial fibrillation and heart failure

In patients needing a pacemaker (PM) for bradycardia indications, the amount of right ventricular (RV) apical pacing has been correlated with atrial fibrillation (AFib) and heart failure (HF) in both DDD and VVI mode. RV pacing was linked with left ventricular (LV) dyssynchrony in almost 50% of patients with PM implantation and atrioventricular (AV) node ablation for AFib. In patients with normal systolic function needing a PM, apical RV pacing resulted in LV ejection fraction (LVEF) reduction. These negative effects were prevented by cardiac resynchronization therapy (CRT). Algorithms favoring physiological AV conduction are possible useful tools able to maintain both atrial and ventricular support and limit RV pacing. However, when chronic RV pacing cannot be avoided, it appears necessary to reconsider the cut-off value of basic LVEF for CRT. In HF patients, RV pacing can induce greater LV dyssynchrony, enhanced by underlying conduction diseases. In this context, a more deleterious effect of RV pacing in implantable cardioverter-defibrillator (ICD) patients with low LVEF can be expected. In some major ICD trials, DDD mode was correlated with increased mortality/HF. This negative impact was attributed to unnecessary RV pacing >40-50%, virtually absent in VVI-40 mode. However, some data suggest that avoiding RV pacing may also not be the best option for patients requiring an ICD. In patients with impaired LV function, AV synchrony should therefore be ensured. The best pacing mode in ICD patients with HF should be defined on an individual basis.     

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%.     

心室起搏对老年房颤患者超声心动图指标的影响

【目的】采用超声心动图来评价老年高龄房颤患者安置心脏起搏器前后各项心功能指标的变化。【方法】128例慢性房颤患者分为两组,对照组不安装心脏起搏器,起搏组予装·心脏起搏器,入选时及三年后所有患者均行超声心动图检查,记录并比较左室每搏量（SV）、心输出量（CO）、左室射血分数（LVEF）、左室舒张末期内径（LVEDD）、心脏指数（CI）及心率（HR）等指标。【结果】起搏组CO、CI及HR较对照组升高,且差异有统计学意义（P〈0．05）;SV、LVEF较对照组降低,LVEDD较对照组升高,但差异无统计学意义（P〉0．05）。两组患者治疗前后心脏结构指标无显著性改变（P〉0．05）。【结论】老年高龄的房颤患者安装心脏起搏器后CO和CI显著增加,费用并不昂贵,且在心脏起搏器使用年限内患者的生活质量得到了提高。     

The Effect of VVI Pacing and Resultant Atrioventricular Dyssynchrony on Segmental Volumes

Left and right ventricular volumes were monitored simultaneously in four anesthetized dogs by intracardiac impedance ventriculography during normal sinus rhythm, spontaneous ventricular rhythm, and VVI and VDD pacing. Cardiac output was found to increase with VVI pacing rate but remained somewhat lower than normal sinus or VDD values. The dissynchronous atrial contraction was found to distort the volume waveforms but had little effect on right ventricular volumes. Left atrial contraction had the greatest impact on left ventricular filling at near normal AV delays. Cardiac output during VDD pacing was found to be a maximum at 170 msec and decreased in three of four dogs at 220 msec. Examination of volume waveforms during "filling" indicates that the right ventricle is dominated by passive filling while the left ventricle demonstrates a large active or "fast" filling phase.     

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.