A 2:1 AV rhythm: an adverse effect of a long AV delay during DDI pacing and its prevention by the ventricular intrinsic preference algorithm in DDD mode

A 91-year-old woman received a dual-chamber pacemaker for sick sinus syndrome and intermittently abnormal atrioventricular (AV) conduction. The pacemaker was set in DDI mode with a 350-ms AV delay to preserve intrinsic ventricular activity. She complained of palpitation during AV sequential pacing. The electrocardiogram showed a 2:1 AV rhythm from 1:1 ventriculoatrial (VA) conduction during ventricular pacing in DDI mode with a long AV interval. After reprogramming of the pacemaker in DDD mode with a 250-ms AV interval and additional 100-ms prolongation of the AV interval by the ventricular intrinsic preference function, VA conduction disappeared and the patient's symptom were alleviated without increasing unnecessary right ventricular pacing.     

Intermittent Pacemaker Syndrome: Revision of VVI Pacemaker to a New Cardiac Pacing Mode for Tachy-Brady Syndrome

A patient with tachy-brady syndrome manifested by paroxysmal atrial fibrillation and symptomatic sinus bradycardia and treated by VVI pacing developed pacemaker syndrome during episodes of ventricular pacing. His cardiac pacemaker was revised to a dual chamber system utilizing the new AV sequential DDI pacing mode which eliminated pacemaker-related tachycardias and totally abolished the pacemaker syndrome symptoms. There have been no further episodes of atrial fibrillation, possibly due to elimination of temporal dispersion of refractory periods during bradycardia. The propensity for atrial fibrillation has also been minimized by excluding competitive atrial stimulation during DVI pacing. The DDI mode provides the clinician increased utility and flexibility in the use of AV sequential pacing therapy.     

Effects of Different Pacing Modes on Left Ventricular Relaxation in Closed-Chest Dogs

Ventricular relaxation is an important determinant of ventricular filling; impaired relaxation may decrease cardiac output and stroke volume. Relaxation hos been shown to occur more quickly following beats with an increased extent of systolic fiber shortening. Since cardiac output and stroke volume are greater during atrioventricular (AV) sequential pacing than during ventricular pacing at identical heart rates, we reasoned that AV sequential pacing would improve relaxation. To assess this hypothesis we studied 11 dogs with chronic (1-3 months) complete heart block (CHB) induced by radiofrequency catheter ablation of the His bundle. Right and left heart pressures, thermodilution cardiac output, und single plane ventriculography were recorded during baseline rhythm (CHB), and VVI, and AV sequential pacing at a heart rate greater than the sinus rate. None had ventriculoatrial conduction. During AV sequential pacing, the AV interval was set at 150 msec. Cardiac output and stroke volume were significantly increased in the AV sequential compared to the VVI pacing mode. Left ventricular pressures, maximal positive and negative dP/dt, and the time constant (T) of isovolumic pressure decay were not different in the two modes. We conclude that despite increased stroke volume in the AV sequential pacing mode, relaxation is unchanged. We believe the lack of change in relaxation is due to nonuniform ventricular activation when depolarization is initiated at the right ventricular apex.     

Hemodynamic and symptomatic consequences of ventricular pacing

After implantation of a ventricular demand pacemaker (VVI), occasional patients continue to have dizziness, syncope, or near syncope ("pacemaker syndrome"). To identify patients in whom VVI pacing may have deleterious effects, we compared cuff blood pressure responses to VVI pacing with blood pressure responses to atrioventricular sequential pacing (DVI) or sinus rhythm in 50 consecutive patients. Patients with intact ventriculoatrial conduction had a much greater decrease in systolic blood pressure with VVI pacing (24 +/- 11 mm Hg) than those with ventriculoatrial dissociation (-4 +/- 15 mm Hg) (P less than 0.005). Patients who were in heart failure had a lesser decrease in blood pressure with VVI pacing than did those without failure (P less than 0.05); 13 of the 14 heart failure patients lacked ventriculoatrial conduction. Ten patients had symptomatic dizziness after VVI pacing; the incidence of symptoms was higher in patients with ventriculoatrial conduction (9 of 23) than in those without ventriculoatrial conduction (1 of 27) (P less than 0.003). We conclude that the presence of intact ventriculoatrial conduction appears to be a crucial determinant of the hemodynamic response to VVI pacing, and its presence may identify patients who are at risk for "pacemaker syndrome."     

Pacemaker Syndrome in a Patient with DDD Pacemaker for Long QT Syndrome

A patient with long QT syndrome was treated with beta blockers and had a permanent DDD pacemaker implanted. The lower rate was set to 85 beats/min because this provided the best shortening of QT interval at the lowest paced heart rate. The atrioventricular (AV) delay was programmed to 250 msec to allow native AV conduction. Patient returned complaining of symptoms suggestive of pacemaker syndrome. ECG during one of these episodes showed AV sequential pacing. Doppler echocardiography of hepatic vein flow suggested atrial contraction against a closed tricuspid valve. Endocardial electrogram telemetry demonstrated ventriculoatrial (VA) conduction with the retrograde atrial electrogram falling within the atrial refractory period and thus was not sensed. The following atrial stimulus did not capture because of the atrial refractoriness. Ventricular pacing proceeded after the programmed AV delay. Reprogramming the AV delay to 200 msec restored AV synchrony by allowing the atrial stimulus to capture by placing it outside of the refractory period of the atrium. No further symptoms reported during six months of follow-up.     

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.     

DDI Pacing in the Bradycardia-Tachycardia Syndrome

The bradycardia-tachycardia syndrome is a subgroup within the larger category of sinus node dysfunction. Pacing is often required to treat either the protracted asystolic spells following the spontaneous termination of a paroxysmal supraventricular tachyarrhythmia or to protect the patient from pharmacologically exacerbated bradycardias. While the optimal pacing mode for this subset of patients remains debatable, recent reports have favored the use of atrial ventricular sequential pacing with intact atrial sensing (DDI). This paper reports our experience with a series of 30 consecutive patients in whom the DDI mode was utilized as part of the management of this syndrome. DDI pacing has been demonstrated to be safe, extremely effective, and easy to use in this group of patients.     

A Double-Blind Study of Submaximal Exercise Tolerance and Variation in Paced Rate in Atrial Synchronous Compared to Activity Sensor Modulated Ventricular Pacing

To assess the variation in paced rate during everyday activity and the importance of atrioventricular synchronization (AV synchrony) for submaximal exercise tolerance, atrial synchronous (DDD) and activity rate modulated ventricular (VVI,R) pacing were compared in 17 patients with high degree AV block. The patients were randomly assigned to either mode and evaluated by treadmill exercise to moderate exertion and by 24-hour Holter monitoring after 2 months in the DDD and VVI,R modes, respectively. At the end of the study, the patients were programmed to the pacing mode corresponding to the preferred study period. During the treadmill test, the mean exercise time to submaximal exertion (Borg 5/10), exertion ratings and respiratory rate did not differ between pacing modes despite a significantly lower ventricular rate in the VVI,R mode. The atrial rate during VVI,R pacing was significantly higher than the ventricular rate, but did not differ from the ventricular rate during DDD pacing. There was a diurnal variation in paced rate in both pacing modes. Paced ventricular rate was, however, higher and variation in paced rate greater in DDD compared to VVI,R pacing. Nine patients preferred the DDD mode, three patients preferred the VVI,R mode, while five subjects did not express any preference. The results from this study indicate that the variation in paced rate during activity sensor-driven VVI,R pacing does not match that during DDD pacing neither during everyday activities nor during submaximal treadmill exercise. Nevertheless, no differences in exercise time, Borg ratings, and respiratory rate during submaximal exercise were found. Thus, for most patients with high degree AV block, DDD and VVI,R pacing seem equally satisfactory for submaximal exercise.     

Left Atrial Size and Wall Motion in Patients with Permanent Ventricular and Atrial Pacing

KUBICA, J., ET AL.: Left Atrial Size and Wall Motion in Patients with Permanent Ventricular and Atrial Pacing. It is well known that during permanent ventricular pacing atrial arrhythmias and embolic complications occur much more frequently in comparison to permanent atrial or sequential pacing. He-modynamic disturbances caused by ventriculoatrial conduction (VAC) are thought to be responsible for those complications. The aim of this study was to compare the left atrial size and its wall motion in three groups of patients with sick sinus syndrome. Group 1: 58 patients with VVI pacing and VAC observed (22 males, 36 females, aged 31–86, mean 62.3). Group 2: 43 patients with primary AAI pacing (13 males, 30 females, aged 27–74, mean 57.8). Group 3: 13 patients with AAI or DDD replacing the primary VVI mode due to pacemaker syndrome and/or heart failure, all with VAC present during VVI pacing (7 males, 6 females, aged 26–80, mean 59.8). Two-dimensional/M-mode echocardiography was performed in all these patients. In group 1 mean diastolic as well as mean systolic atrial diameters were significantly greater (p < 0.005) and wall motion significantly smaller (p < 0.005) in comparison to the other groups. Left atrial wall motion amounted to only 7.4% of the mean diastolic diameter in this group. Mean left atrial diastolic and systolic diameters and wall motion in patients with pacemakers preserving atrioventricular synchrony (group 2 and group 3) were almost identical and wall motion amounted to about 22% of the diastolic diameter in both these groups. We conclude that ventriculoatrial conduction leads to significant enlargement of left atrium and to the atrial wall-motion decrease. This predisposes to arrhythmias and embolic complications. Changes in atrial size and performance seem to be reversible with restoration of the physiological atrioventricular synchrony.     

Incidence of Atrial Fibrillation in Patients with Different Mode of Pacing. Long-term Follow-up

We evaluated the incidence of atrial fibrillation in 189 patients (92males, 97females, mean age 75 ± 12yrs, range 41–100yrs) with pacemaker, during a mean follow-up of 5.5yrs (range 1–24yrs). The indications for implant were: complete AV block (115pts), second degree Möbilz 2 AV block (51pts). bifascicular block (5pts). sick sinus syndrome (14pts), symptomatic bradycardia (4pts). The mode of stimulation considered were VVI (105pt), VVI rate responsive (21pts), single lead VDD (43pts), DDD (20pts). The occurrence of retrograde VA conduction in patients with VVI or VVI rate responsive pacing was also evaluated. Atrial fibrillation occurred in 40 pts (21%). The highest incidence was evidenced in patients with sick sinus syndrome (9pts, 64%), and in patients with VVI stimulation (28pts, 27%). On the contrary, the lowest incidence was found in single lead VDD stimulation (4pts, 9%). The patients with dual chamber pacing showed a relatively high incidence of the arrhythmia (5pts, 25%). Atrial fibrillation occurred in 9 out of 32 patients with retrograde VA conduction, and in 22 out of 94 patients without retrograde conduction (28% versus 23%, p=NS). In conclusion, it is confirmed that patients with sick sinus syndrome are at high risk for atrial fibrillation. Single lead VDD stimulation seems to be the better mode of pacing in preventing atrial fibrillation, while dual chamber pacing showed minor efficacy. The presence of retrograde VA conduction could not predict the occurrence of the arrhythmia.     

Pacemakers of the 1980s. An overview

Methods and devices for permanent cardiac pacing remained relatively stable for over two decades with use of the single-chamber ventricular demand (VVI) pacemaker. However, changes have occurred in the 1980s and are expected to continue with the availability of more advanced technology and with increasing knowledge about cardiac pacing. The physiologic benefit of the newer dual-chamber atrial synchronous (VDD) and fully automatic, universal (DDD) pacemakers over the VVI pacemaker in patients with permanent complete heart block and normal sinus node function has been established. These newer units not only reestablish atrioventricular synchrony but also are physiologically rate-responsive. The VDD pacemaker is expected to be phased out in favor of the DDD pacemaker. When the atrial rate or interval is lower than the lower rate limit, the VDD pacemaker functions as a VVI, whereas the DDD pacemaker functions as an atrioventricular sequential (DVI) pacemaker to maintain continuous atrioventricular synchrony. Contrary to general belief, patients with complete heart block and normal sinus node function may gain very little physiologic benefit, if any, from DVI pacing. The sinus node will compete with the pacemaker's atrial stimulation when the sinus rate is faster than the DVI pacemaker rate (which usually occurs during activity). Also, the ventricular pacing rate will not vary with physiologic change. The DVI and atrial demand (AAI) pacemakers have been used in some patients with sinus node dysfunction. Increasing exercise tolerance should not be expected in the majority of patients because they are not pacemaker-dependent during activity, ie, their heart rate is higher than the pacemaker rate. However, these pacemakers appear to help in eliminating pacemaker syndrome, which does not infrequently occur with VVI pacemakers. Patients with sinus node dysfunction but without atrioventricular block do not gain more physiologic benefit with a DDD than with a DVI pacemaker. Whether these patients have severe sinus node dysfunction all the time or adequate sinus node function most of the time during follow-up, the DDD pacemaker will function as a noncommitted DVI with atrial sensing (DDI). The early report of DVI pacemaker-induced atrial fibrillation during follow-up has been refuted by more recent works. If the DDD pacemaker is significantly more expensive than the DVI pacemaker, the latter type may be a good alternative for this condition.     

Inhibition of ventricular stimulation in patients with dual chamber pacemakers and prolonged AV conduction

Episodes of repetitive P wave undersensing have been described in dual chamber pacemakers due to automatic extension of the postventricular atrial refractory period (PVARP). Pacemaker stimulation was completely inhibited despite the presence of adequate P waves. This study sought to determine whether cycles of repetitive P wave undersensing occur even in the absence of PVARP extension. Two-hundred fifty-five patients were investigated after DDD or VDD pacemaker implantation for intermittent atrioventricular (AV) block. Forty-six episodes of repetitive atrial undersensing were found during 24-hour Holter ECG in nine patients. Pacemaker syndrome-like symptoms occurred. Episodes were elicited by atrial or ventricular premature contractions when (1) native AV conduction was present but considerably prolonged, (2) intrinsic sinus rate exceeded pacemaker intervention rate, and (3) native AV interval plus PVARP exceeded sinus cycle length. Programming of a particularly short AV interval and PVARP helped to reduce the incidence of repetitive P wave undersensing. Patients with dual chamber devices and prolonged native AV conduction are prone to develop episodes of output inhibition. Standard timing cycles may be inappropriate in these patients.     

Variable Effects of Adenosine on Retrograde Conduction in Patients with Atrioventricular Nodal Reentry Tachycardia

Adenosine has been demonstrated to reliably produce transient block of atrioventricular nodal (AVN) conduction, and has been advocated as a method of differentiating retrograde conduction via the atrioventricular node from accessory pathway conduction. However, the response of retrograde AVN to adenosine in patients with typical atrioventricular nodal reentry tachycardia (AVNRT) remains unclear. We evaluated 13 patients (mean age 45 ± 20 years) with typical AVNRT prior to AVN modification. During right ventricular pacing, a rapid bolus of adenosine (0.2 mg/kg; maximum 18 mg) was administered. Adenosine sensitivity, defined by transient ventriculoatrial block, was observed in six patients, while in seven patients ventriculoatrial conduction was unaffected. An adenosine bolus administered during sinus rhythm or atrial pacing resulted in antegrade atrioventricular block in all the adenosine resistant patients in whom this was performed (n = 6). Comparisons of AVN electrophysiological characteristics between the adenosine sensitive and adenosine resistant patients were performed. There was no difference with respect to ventriculoatrial effective refractory period, ventriculoatrial Wenckebach, AVNRT cycle length, and His to atrial echo interval in AVNRT. However, there was a trend toward a longer antegrade fast pathway ERP in the adenosine sensitive group (P = 0.07). Electrophysiological properties do not predict retrograde AVN adenosine sensitivity. Adenosine does not cause retrograde AVN block in all patients with AVNRT, and therefore cannot reliably distinguish between retrograde conduction via the AVN or an accessory pathway.     

Ventricular and Dual Chamber Pacing for Treatment of Carotid Sinus Syndrome

Thirty-nine consecutive patients with recurrent syncope and either cardioinhibitory or mixed type carotid sinus syndrome were studied to determine the efficacy of ventricular (VVI) pacing in 16, and dual chamber (DDD/DVI) in 23 patients. Only those patients affected by the isolated vasodepressor form were excluded. Follow-up lasted 12 ± 5 months. Symptoms were totally eliminated in 67% of patients and ameliorated with persistence of minor symptoms in 33%. All patients underwent an initial 2-month follow-up in the VVI mode. Evaluation of the 19 patients who remained symptomatic and the 20 who became asymptomatic with VVI pacing demonstrated that factors observed prior to pacemaker implant were related to failure of the VVI mode. These included symptomatic pacemaker effect (42% vs 0%), mixed carotid sinus syndrome (95% vs 65%), orthostatic hypotension (47% vs 15%), or ventriculoatrial conduction (68% vs 38%). In the 23 patients with dual chamber pacing, random 2 month comparisons were performed between VVI and DVI/DDD pacing. The dual chamber mode was preferred by 14 patients, none preferred the VVI mode and nine noted no difference. Comparison of the two groups found that the factors linked to DVI/DDD preference were symptomatic pacemaker effect (50% vs 0%), ventriculoatrial conduction (78% vs 44%), or orthostatic hypotension (50% vs 11 %). VVI pacing is efficacious in a high proportion of patients affected by cardioinhibitory or mixed carotid sinus syndrome. The identification of causes of VVI pacing failure allows determination of those who will benefit from VVI pacing and those who should have DVI/DDD. VVI pacing is suggested for the cardioinhihitory type with no symptomatic pacemaker effect and for the mixed type with no symptomatic pacemaker effect or orthostatic hypotension or ventriculoatrial conduction. Dual chamber pacing should be used in all other instances.     

Quality-of-Life in Patients Treated with Atrioventricular Synchronous Pacing Compared to Rate Modulated Ventricular Pacing: A Long-Term, Double-Blind, Crossover Study

To investigate whether the preservation of afrioventricular (AV) synchronization matters for quality-of-life during pacemaker treatment we assessed 17 consecutive patients with high degree AV block and preserved sinus node function in a double-blind, long-term crossover study. A questionnaire with regard to cardiovascular symptoms, sleep disturbances, cognitive functioning, physical ability, social interaction, emotional functioning, and self-perceived health was completed after 2 months of atrial synchronous (DDD) and rate modulated ventricular pacing (VVI,R), respectively. A significant improvement in shortness of breath, dizziness and palpitations as well as an improvement of cognitive functioning was observed during DDD pacing. Nine patients preferred the DDD mode and three the VVI,R mode. The remaining five patients did not express any preference. The preference for the DDD mode was explained by a significant reduction of cardiovascular symptoms and an improved self-perceived health, physical ability, and psychological well-being during DDD pacing. All differences in quality-of-life parameters between the two modes of pacing favored the DDD mode and no adverse effects of this mode were found. Thus, the maintenance of AV synchrony adds further symptomatic relief compared to rate increase alone. The results indicate that DDD pacing is the preferred mode of pacing in patients with high degree AV block and preserved sinus node function.     

Inappropriate Ventricular Blanking in a DDI Pacemaker

The DDI mode is a new pacing mode with potential advantages over DVI pacing. We describe anomalous post R wave ventricular pacing due to the presence of inappropriate ventricular blanking periods in a pacemaker programmed to the DDI mode. Although no adverse consequences were seen in our patients, potentially dangerous R-on-T pacing could occur, particularly if long atrioventricular delays are programmed. A method for eliminating this pacing anomaly is described. Patients programmed to the DDI mode with the pacemaker model described should be evaluated for post R wave ventricular pacing and corrective measures should be taken.     

A Case of Ventricular Undersensing in the DDI Mode: Cause and Correction

A case is presented that demonstrates a confusing problem of ventricular undersensing in the DDI pacing mode. Electrocardiographic monitoring of the patient after pacemaker implantation revealed intermittent ventricular channel outputs which appeared to be inappropriate. These occurred a period of time after the intrinsic R wave, equal to the programmed AV interval. This problem was caused by ventricular lead undersensing, which resulted when the patient's intrinsic rate was such that the intrinsic ventricular complex occurred during the ventricular blanking period. The problem was corrected by reprogramming the blanking period.     

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.     

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).     

Prospective Evaluation of Infrahisal Second-Degree AV Block Induced by Atrial Pacing in the Presence of Chronic Bundle Branch Block and Syncope

The value of nonfunctional infrahisal second-degree atrioventricular (AV) block induced by incremental atrial pacing was prospectively examined in 192 patients with chronic bundle branch block (BBB) and syncope. We compared 174 (91 %) patients with normal response to atrial pacing (Group I) to 18 (9%) patients with atrial pacing induced nonfunctional infrahisal second-degree AV block (Group II). Patients in group I had higher incidence of organic heart disease, ventricular tachycardia induction, and retrograde ventriculoatrial conduction (P < 0.001, P < 0.05, P < 0.01, respectively), while patients in group II had higher incidence of primary conduction disease and prolonged H-V intervals (P < 0.001, P < 0.01, and P < 0.001). During mean follow-up period of 65 ± 34 months for group I, and 68 ± 35 months for group II, a development of spontaneous second- or third-degree AV block was higher in group II (14/18 [78%]), than in group I (15/174 [9%]) (P < 0.001). The site of AV block was infrahisal in all patients in group II, and in 10 of 15 patients in group I. Because of the prophylactic pacing in all patients in group II, the incidence of sudden death was similar among the two groups, but patients in group I had higher incidence of cardiac death (P < 0.05). Conclusion: In patients with chronic BBB and syncope, a nonfunctional infrahisal AV block induced by incremental atrial pacing identified patients with particularly high risk of development of spontaneous infrahisal AV block. Therefore, permanent cardiac pacing is absolutely indicated in these patients.