Plasma ANP and Cyclic GMP Levels Versus Left Ventricular Performance at Different AV Delays in AV Sequential Pacing

Eleven resting patients with an implanted DDD pacemaker were studied. After 30 minutes of AV sequentiai pacing at a rate of 80 beats/min with three consecutive atrioventricular delays (AVDs; 100, 150, and 200 msec) peripheral venous blood was drawn for further analyses by specific radioimmunoassays of atrial natriuretic peptide (ANP) and the ANP second messenger, cyclic guanosine monophosphate (cGMP). Relative changes in left ventricular (LV) stroke volume following alterations of AVD were assessed by means of pulsed-Doppler echocardiography through measurement of LV outflow time-velocity integrals (TVI). The optimal AVD (oA VD) was defined in individual patients as that which was associated with the greatest TVI and with improvement over both other AVDs of more than 4%. The oA VD was found in nine patients. For these nine patients no significant differences in either plasma ANP or cGMP between various AVDs were observed. However, we found such differences with respect to values measured at oAVD; both ANP and cGMP levels were lowest at oAVD. Pooling together the data obtained in 11 patients at three AVDs, a positive correlation between ANP and cGMP levels was found (r = 0.7, P < 0.0001. n = 33). Moreover, changes of plasma ANP and cGMP induced by every A VD increment of 50 msec were also correlated (r = 0.6, P < 0.01, n = 22). It is concluded that in AV sequential pacing at rest piasma ANP reaches minimal levels at the AVD, which provides the best LV performance. Although levels of cGMP changed in parallel with those of ANP, low relative values of cGMP differences may limit the usefulness of cGMP assays in optimization of the AVD.     

Influence of AV Synchrony on the Plasma Levels of Atrial Natriuretic Peptide (ANP) in Patients with Total AV Block

ANP was determined in 13 patients with DDD pacemakers due to total AV block, at rest and during bicycle ergometry under both pacing modes, DDD and VVI (7O/min). Under DDD pacing, the mean ANP level (normal range 5-95 pg/mL) at rest was 36 +/- 18 pg/mL (mean +/- SD) and increased significantly by the factor of 3.5 to 1 27 pg/mL during exercise (p less than 0.01). By just changing the pacing mode to VVI, the ANP levels rose to 73 +/- 28 pg/mL (p less than O.0 1) at rest (= 203% of DDD resting level) and to 216 +/- 184 pg/mL (= 170% of DDD peak level) during exercise P less than 0.01). These results show that under AV synchronous pacing, the ANP levels we generally lower. A possible explanation for this increased release of ANP during asynchronous VVI pacing is the acute increase of the atrial wall tension which occurs when the atria contacts during the systole against closed AV valves.     

Atrial Natriuretic Peptide During Different Pacing Modes in a Comparison with Hemodynamic Changes

The study investigates the response of atrial natriuretic peptide (ANP) to different cardiac pacing modes in comparison with hemodynamic changes. Ten patients underwent Swan-Ganz catheterization during pacemaker implant. Atrioventricular and ventricular pacing were performed consecutively at three pacing rate levels (80, 100, and 110 ppm). Blood samples were taken from the pulmonary artery for ANP determination, both basally and at the end of each pacing period. Concomitantly, mean pulmonary capillary wedge pressure (PCWP) and mean pulmonary artery pressure (PAP) were measured. Cardiac output (CO) was determined by thermodilution both basally and during the 110 ppm steps. During atrioventricular pacing, whereas no significant changes were observed for ANP, PCWP and PAP, CO increased significantly (P less than 0.0005). At the beginning of ventricular pacing hemodynamic parameters and ANP levels were comparable with those of baseline conditions. During subsequent ventricular pacing PCWP and ANP increased significantly at the 110 ppm rate step (P less than 0.05). PAP did not change significantly, whereas CO decreased in all cases (P less than 0.01). A positive correlation was observed between ANP and PCWP during ventricular (P less than 0.001), but not atrioventricular pacing. The results, while confirming the hemodynamic advantages of atrioventricular pacing, point to a major stimulation of ANP secretion during ventricular pacing. This fact, together with the observed drop in CO and the correlation between ANP and PCWP, suggest that the increase of ANP in ventricular pacing may be the expression of a compensatory mechanism to the hemodynamic disadvantages of atrioventricular asynchrony.     

Effect of Different AV Delays on Left Ventricular Diastolic Function and ANF Levels in DDD Paced Hypertensive Patients During Daily Activity and Exercise

Fifteen hypertensive patients (13 men) with left ventricular hypertrophy, mean age 69 6 5 years, having complete heart block and paced in the DDD mode, were studied by two-dimensional and Doppler echo in 100 and 200 ms atrioventricular delays. ANF plasma levels were measured at rest and at peak exercise, during pacing with the two different atrioventricular delays. ANF plasma levels were significantly higher at pacing with long atrioventricular delays (200 ms), at rest (152.47 6 12.38 pg/mL vs 119 6 12.38 pg/mL, P, 0.001) and at exercise (180.93 6 11.51 vs 123.67 6 16.24 pg/mL, P, 0.0001). ANF plasma levels were significantly increased at exercise, compared to those at rest during pacing with the two different atrioventricular delays, but we found a more pronounced increase of ANF levels (from 152.47 6 10.49 pg/mL to 180.93 6 11.51 pg/mL), when the atrioventricular delays was set to 200 ms (P, 0.0001). A significant decrease of isovolumic relaxation time (from 123.33 6 20.5 to 105.33 6 11.06 ms, P, 0.001) was observed, during pacing with the short atrioventricular delays. Moreover, the peak early (E) to peak atrial (A) velocity ratio (E/A) was declined (from 0.89 6 0.7 to 0.57 6 0.18, P, 0.05). We also noticed that patients with small left ventricles exhibit greater increase in ANF plasma levels during DDD pacing with long atrioventricular delays (r 5 20.792, P 5 0.000). In conclusion, left ventricular diastolic function of our patients seems to be improved during DDD pacing with short (100 ms) atrioventricular delays, as it was expressed by echocardiographic and hormonal measurements.     

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).     

Failure to Sense P Waves During DDD Pacing

ECG tracings of three patients in whom AV universal (DDD) pacemakers were implanted intermittently demonstrated dropped P waves. In one patient, true atrial undersensing was present; in the others, sensing of the atrial electrode was appropriate, but sensing of sinus P waves was intermittently blocked by normal pacemaker operation. In this report we discuss the electrocardiographic diagnosis of atrial undersensing in order to avoid unnecessary reinterventions.     

Atrial Natriuretic Factor Release During Exercise in Patients Successively Paced in DDD and Rate Matched Ventricular Pacing

Dual chamber pacemakers were implanted in nine patients with permanent second or third degree AV block feight had complete retrograde block). Two identical exercise tests were performed after at least 1 month after implantation. During the first test (T₁) the pacemaker was programmed to the DDD mode and heart rates were recorded every 15 to 30 seconds during exercise and 30 minutes after exercise. Following 30 minutes of rest, the implanted pacemaker was programmed to the VVT mode and driven by an external pacemaker via a skin electrode. The second exercise test (T₂) was then performed and the rate of the external pacemaker was progressively changed to reproduce exactly the rate observed during T₁ at the same exercise stress. Atrial natriuretic factor (ANF) levels were determined at rest, at regular intervals during exercise, and 30 minutes after exercise. ANF levels and release were statistically higher during rate matched ventricular, than DDD pacing. It is concluded that preservation of AV synchrony reduces ANF release induced by heart rate acceleration during exercise.     

The Effect of DDD Pacing on Ergospirometric Parameters and Neurohormonal Activity in Patients with Hypertrophic Obstructive Cardiomyopathy

This study examined the acute and long-term effects of DDD pacing on ergospirometric parameters and neurohormonal activity in patients with hypertrophic obstructive Cardiomyopathy (HOCM). We studied eight patients (five males), aged 56 ± 7 years, with HOCM refractory to drugs. In all patients a DDD pacemaker was implanted and programmed with an atrioventricular (AV) delay that insured full ventricular activation. The patients underwent echocardiographic examination and exercise stress testing before and 3 days, 3 months, and 12 months after pacemaker implantation. Oxygen consumption was measured at the anaerobic threshold (VO_2AT) and peak exercise (pVO₂). Atrial natriuretic peptide (ANP) and cyclic adenosine monophosphate (c-AMP) levels were measured concomitantly. Left ventricular outflow tract (LVOT) pressure gradient decreased significantly from 70 ± 18 to 25 ± 12 mmHg (P < 0.05) 3 days after pacing and remained unchanged at 3 and 12 months. pVO₂ and VO_2AT increased significantly, from 20.1 ± 3 to 23.4 ± 3 mL/kg/min and from 16 ± 3 to 17.8 ± 2 mL/kg/min, respectively (P < 0.05). This improvement continued up to 3 months, and then remained stable until the end of the 12-month follow-up period. ANP levels decreased at 3 days from 85.4 ± 5.7 to 75.4 ± 7.3 fmol/mL (P < 0.05), and remained unchanged over the 12 months. c-AMP levels did not change significantly after the onset of pacing. DDD pacing in patients with HOCM not only reduces the LVOT pressure gradient but also causes a significant early and long-term improvement in exercise capacity and neurohormonal profile.     

Cardiac Output Versus Pacing Rate at Rest and with Exercise in Dogs with AV Block

To achieve maximum benefit from exercise (rate)-responsive pacing in subjects with sinus node dysfunction and AV block, it is necessary to determine the pacing rate (HR) which produces maximum cardiac output (CO) under specified exercise conditions. However, the CO-HR relationship for exercise has not been systematically investigated. To permit determination of the optimum HR, CO was measured at rest and with exercise for different pacing rates. Seven dogs with complete AV block and permanently implanted ventricular pacemakers were exercised on a treadmill for 5 min at each of four pacing rates (55, 76, 101, 116/min) and at two constant exercise levels (225 and 560 kg.m/min). CO was determined by impedance cardiography during the resting state preceding exercise and during a brief period (10-20 s) immediately after exercise, and was expressed as a percent of the CO determined at rest with HR = 55/min. A three-phase pattern of CO versus HR appears to exist for exercise as for rest. For exercise, starting from a low HR, CO increases markedly; a "plateau" is reached during which moderate increase in CO is achieved by increasing HR. At very rapid pacing rates, CO may actually decrease with further increase in HR. The results of this study suggest that a subject-specific optimum HR exists for each constant exercise level. Moreover, the methodology employed in the study is applicable to the identification of optimum HR for any exercise (rate)-responsive pacemaker.     

Plasma Levels of Natriuretic Peptides During Ventricular Pacing in Patients with a Dual Chamber Pacemaker

The mechanism(s) responsible for the release of brain natriuretic peptide (BNP), a cardiac hormone of ventricular origin, are still not completely understood. We measured plasma atrial natriuretic peptide (ANP) and BNP in 15 subjects (10 men, mean age 67 ± 3 years) with a dual chamber pacemaker and unimpaired heart function during ventricular pacing, which is known to induce an increase in atrial pressure and plasma ANP concentration. Under ECC monitoring, all subjects received sequential atrioventricular pacing for 30 minutes and ventricular pacing for 30 minutes, at the same rate of 80 beats/min. Arterial pressure and plasma BNP and ANP levels were measured every 10 minutes throughout the study. Ventricular pacing led to atrioventricular dissociation in eight subjects and to retrograde ventriculo-atrial conduction in seven. Arterial pressure remained unchanged in all subjects. In the group with atrioventricular dissociation, plasma ANP increased from 10.14 ± 0.58 to 16.72 ± 0.92 fmol/mL at the 60th minute (P < 0.0001), whereas plasma BNP did not change at all (fiom 1.26 ± 0.07 to 1.16 ± 0.09 fmol/mL). In the group with retrograde conduction, plasma ANP concentration doubled (fiom 10.95 ± 1.66 to 21.40 ± 1.51 fmol/mL, P < 0.0001), BNP increased 1.5-fold (from 1.16 ± 0.06 to 1.64 ± 0.14 fmol/mL, P < 0.001), and the ANP: BNP ratio augmented fiom 10:1 to 13.4:1. These results indicate that the release of ANP and BNP is regulated by different mechanisms, supporting the view that there is a dual natriuretic peptide system, comprising ANP fiom the atria and BNP fiom the ventricles.     

Evaluation of Asynchronous Left Ventricular Relaxation by Doppler Echocardiography During Ventricular Pacing with AV Synchrony (VDD): Comparison with Atrial Pacing (AAI)

The effect of right ventricular pacing on left ventricular relaxation was studied in 13 patients (age 62 ± 3 years), with the atrial sensing ventricular pacing mode (VDD). A control group of similar age (64 ± 4 years) consisted of 11 patients with atrial pacing (AAI). The timing of events was determined in both groups at similar R-R intervals (921 ± 77 ms vs 967 ± 37 ms). The loading conditions as estimated by peak systolic wall stress (afterload) and end-diastolic left ventricular dimensions (preload) were approximately the same in both groups. The ratio of late to early filling velocities were similar in both groups. Dominant changes were: increased preejection period (142 ± 13 ms vs 95 ± 15 ms); and higher velocities of isovolumic relaxation flow (60 ± 34 cm/s vs 25 ± 4 cm/s) in patients with ventricular pacing. The isovolumic relaxation time was longer in patients with VDD pacing (127 ± 14 ms vs 108 ± 12 ms). Anterior systolic interventricular septal motion (paradoxal motion) was recorded in nine patients with VDD pacing and in none of the patients with AAI pacing. Isovolumic relaxation flow was detected during atrial pacing in five (45%) patients and in 13 (100%) patients during atrial sensing ventricular pacing, indicating asynchronous left ventricular relaxation. This data shows that VDD pacing compared to atrial pacing resulted in an altered activation pattern of the left ventricle, associated with delayed onset, asynchronous contraction with interventricular septal motion abnormalities and prolonged asynchronous left ventricular relaxation with abnormal motion manifested by the presence of isovolumic relaxation flow.     

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.     

Influence of Pacing Mode and Rate on Peripheral Levels of Atrial Natriuretic Peptide (ANP)

The effect of acute modifications of pacing mode and rate on plasma ANP levels was evaluated. ANP was determined in ten resting patients with DDD pacemakers due to binodal disease or intermittent second-and third-degree AV block. At 82/minute pacing rate the ANP plasma levels (normal range 2 to 30 fmol/mL) corresponded to those under AAI (4.05 +/- 2.10 fmol/mL) and DDD (4.18 +/- 2.02 fmol/mL) pacing, but increased significantly (P 0.05) during VVI pacing (6.96 +/- 3.70 fmol/mL). Acceleration of DDD stimulation frequency from 82 to 113/minutes led to significant increase of ANP levels by the factor of three in all chosen AV delays. The lowest ANP plasma levels were measured at 175 msec AV delay under 82/minute pacing rate in DDD mode. Under 113/minutes the differences of ANP concentration after variations of AV delays were less pronounced. The influences of altered atrial pressure and tension on ANP release are discussed to account for changes in ANP plasma levels following different modes and rates of pacemaker stimulation.     

Intrapatient Comparison Between Chronic VVIR and DDD Pacing 'In Patients Affected by High Degree AV Block Without Heart Failure

MENOZZI, C., ET AL.: Intrapatient Comparison Between Chronic VVIR and DDD Pacing in Patients Affected by High Degree AV Block Without Heart Failure. In patients affected by high degree AV block without preexisting congestive heart failure there is no definite demonstration that DDD pacing gives real clinical advantages in respect to VVIR pacing. We performed an intrapatient, long-term study between the two pacing modes in 14 high degree AV block patients, using the Medtronic Synergyst 7027 dual chamber pacemaker, who could be programmed alternatively in DDD or VVIR mode. After a 4-week run-in period following the pacemaker implant, patients completed a randomized, double-blind, cross-over study to compare the effect of 6-week period VVIR and DDD pacing on symptoms and cardiovascular parameters. A semiquantitative score scale was used to quantify the symptoms of general well-being, palpitations, dizziness, pulsating sensation in the neck or abdomen, shortness of breath at rest and during effort, chest pain, and NYHA classification. The sum of symptom scores was 10.4 ± 6.7 in VVIR period and 4.6 ± 2.7 in DDD period (p < 0.001); five patients (36%) crossed over early from VVIR to DDD because of intolerable symptoms; overall, eight patients preferred the DDD mode and no one preferred the VVIR. Cardiac output at rest (echo-Doppler method) was 4.7 ± 1.4 versus 5.7 ± 1.6 liter/min (p < 0.01), body weight was 65.9 ± 6.6 versus 64.9 ± 6.1 kg (p < 0.02), atrial natriuretic peptide was 236 ± 112 versus 198 ± 110 pg/mL (p < 0.01), respectively, during VVIR and DDD modes. Effort tolerance was similar with the two modes of pacing (68 ± 15 vs 70 ± 18 watt/min). In conclusion, hemodynamic advantages of atrial synchronization reflect a better quality of life for the patients even if an individual variability exists.     

Noninvasive Beat-to-Beat Arterial Blood Pressure Measurement During VVI and DDD Pacing: Relationship to Symptomatic Benefit from DDD Pacing

To noninvasively assess the hemodynamic effects of VVI and DDD pacing modes we measured beat-to-beat arterial blood pressure during VVI and DDD pacing in 30 patients with complete heart block (CHB), using fingertip photoplethysmography. Of these patients, 15 undertook a double-blind cross-over comparison of the symptomatic effects of VVI versus DDD pacing to determine the relationship between blood pressure changes and the occurrence of symptoms suggestive of the pacemaker syndrome during ventricular pacing. Mean (SD) systolic blood pressure was 11.7 (15.4) mmHg lower during VVI pacing compared to DDD pacing (P < 0.0005). The mean (SD) beat-to-beat variability of systolic blood pressure was 5.20 (2.87%) in VVI mode versus 2.12 (1.07%) in DDD mode (P < 0.0000005). In comparison with DDD pacing, the excess of symptoms experienced by patients during VVI pacing did not correlate with the change in mean systolic blood pressure, but was significantly correlated with the increase in beat-to-beat systolic blood pressure variation during VVI pacing (r = 0.58, P = 0.024). We conclude that noninvasive measurement of fingertip arterial beat-to-beat blood pressure is a rapid and simple method of assessing the hemodynamic effect of VVI pacing. Beat-to-beat blood pressure variability was related to symptomatic intolerance of VVI pacing and may have potential utility as an aid to diagnosis or as a predictor of pacemaker syndrome.     

Sympathetic Nervous System Response to Dynamic Exercise in Complete AV Block Patients Treated with AV Synchronous Pacing with Fixed AV Delay or with Auto-AV Delay

IGAWA, O., ET AL.: Sympathetic Nervous System Response to Dynamic Exercise in Complete AV Block Patients Treated with AV Synchronous Pacing with Fixed AV Delay or with Auto-AV Delay. To investigate the sympathetic nervous system (SNS) responses and circulatory responses to exercise in eight patients (five male and three female) with complete atrioventricular block (CAVB) treated with atrio-ventricular (AV) synchronous pacing, a symptom-limited, multistaged treadmill stress test was performed, and plasma norepinephrine (NE) and circulatory parameters were measured at rest, at peak exercise, and in the recovery period. The eight patients were tested using the fixed AV interval (150 or 156 msec). Their exercise tolerance was generally poor. In all measured points, plasma NE levels were significantly higher in the eight study patients than those in the 12 normal subjects (eight male and four female). Systolic blood pressure (SBP) of CAVB patients elevated significantly after exercise compared to that at peak exercise. Heart rate (HR) responses of CAVB patients were characterized by their poor increase at peak exercise. These results suggest that some latent cardiac dysfunction continues in the CAVB patients however satisfactorily the AV synchronous pacing might perform. AV synchronous pacing with three different kinds of auto-atrioventricular delay (auto-AVD) was applied to three of the eight patients. In each AVD mode, a treadmill stress test was performed repeatedly according to the same protocol. Plasma NE concentrations under the condition with fixed AVD at peak exercise increased compared to those under the other two conditions with auto-AVD. These findings suggest that AV synchronous pacing with auto-AVD WQS better than that with fixed AVD during exercise. Plasma NE response to exercise seems to be a useful indicator for evaluating the condition of patients treated with DDD pacemakers and their adaptation for cardiac function.     

Exercise Induced Sympathetic Influences Do Not Change Interatrial Conduction Times in VDD and DDD Pacing

Using telemetry, right atrial electrogram (RA), and marker channel of atrial sense events (M_A) in combination with the left atrial electrogram (LA), recorded by a filtered bipolar esophageal lead, interatrial conduction during submaximal exercise and at rest was examined in 46 DDD pacemaker patients. The RA-LA and M_A-LA conduction times measured in the presence of atrial sensing (VDD) as well as the conduction time S_A-LA from atrial stimulus (S_A) to LA, determined during atrial pacing (DDD) were found to be individual constants independent of exercise induced sympathetic influences. Thus, having determined an optima! mechanical interval (LA-LV)_mech/opt from left atrium to ventricle by other methods, the optimal AV delay for DDD as well as for VDD operation can be calculated by the sum of the appropriate interatrial conduction time (S_A-LA, respectively M_A-LA) and the (LA-LV)_mech/opt interval. Due to the constant S_A-LA and M_A-LA, the difference between these two values (AV delay correction interval) is a constant as well, which remains unchanged during exercise. Therefore, in selecting the rate responsive AV delay, only hemodynamic and not electrophysiologica] measurements need to be considered.     

Quality-of-Life During DDD and Dual Sensor VVIR Pacing

Twenty-one patients (mean age 68 ± 8 years) with dual-sensor (QT + activity) DDDR pacemaker were randomly assigned to a crossover, double-blind study in order to evaluate their quality-of-life scores. All pacemakers were implanted for sick sinus syndrome (8 patients) or complete heart block (13 patients). The pacemakers were randomly programmed to VVIR or DDD pacing modes for 2-week periods and then the pacing mode was switched for another 2-week period. At the end of each period, the quality-of-life was evaluated by a questionnaire with regard to cardiovascular symptoms, physical activity, psychosocial and emotional functioning, and self-perceived health. Nineteen questions were scored 0–5 points each. Significant improvement in the mean total quality-of-life score (20.5 ± 14.9 vs 34.8 ± 17.4) as well as in dyspnea on effort, dizzy spells, palpitation, sweating, fatigue, lethargy, emotional functioning, and self-perceived health was observed during DDD compared to VVIR pacing. No question was scored in favor of VVIR pacing mode. Significant improvements during DDD pacing was demonstrated in all subgroups of patients (sick sinus syndrome, chronotropically competent and incompetent patients, and patients with high degree AV block). Eighteen patients preferred DDD pacing mode, while only one preferred WIR pacing mode. Two remaining patients expressed no preference. The results suggest that DDD pacing offers better quality-of-life than dual sensor VVIR pacing in all subgroups of patients commonly indicated for pacemaker implantation.     

Is DDD Pacing Superior to VVI,R? A Study on Cardiac Sympathetic Nerve Activity and Myocardial Oxygen Consumption at Rest and During Exercise

Rate responsive ventricular pacing (VVI,R) has been demonstrated to equal atrial synchronous ventricular pacing (DDD) with regard to hemodynamics and exercise tolerance. Whether the two modes are also comparable, with regard to cardiac metabolic effects, is not yet dear. We assessed central hemodynamics, cardiac sympathetic nerve activity fcardiac norepinephrine overflow), and myocardial oxygen consumption in 16 patients treated with rate responsive atrial synchronous ventricular pacemakers (DDD,R), due to high degree AV block. The study was performed at rest and during supine exercise at two workloads (30 ± 12 and 68 ± 24 watts, respectively) during VDD and rate matched VVI pacing (VVI_m). Ventricular rates at rest and during both workloads were almost identical. Cardiac output at rest tended to be higher in the VDD mode, due to a slightly higher stroke volume. Central pressures including right atrial pressure and pulmonary capillary wedge pressure were similar in the pacing modes. The coronary sinus blood flow, the coronary sinus arteriovenous oxygen difference, and the myocardial oxygen consumption did not differ between the two pacing modes. Cardiac norepinephrine overflow was similar in the two pacing modes, at rest or during exercise. Thus, we found no significant differences between VDD and VVI_m pacing with regard to central hemodynamics, cardiac sympathetic nerve activity (cardiac norepinephrine overflow), or myocardial oxygen consumption either at rest or during moderate exercise.     

Failure of Plasma Atrial Natriuretic Peptide Levels to Increase During Exercise in Patients with Chronic Atrial Fibrillation

It is generally accepted that plasma atrial natriuretic peptide release occurs secondary to atrial stretch. The influence of coordinated atrial contraction (AC) upon this process is not fully appreciated. The aim of the study was to determine the importance of coordinated AC upon peripheral atrial natriuretic peptide levels (α-hANP) during exercise. Peripheral α-hANP levels were measured at rest and during exercise in 12 patients with complete heart block (CHB) and permanent rate responsive pacemakers. Seven patients had coordinated AC and five had chronic atrial fibrillation (AE). Each patient performed three treadmill exercise tests. Maximal inspired oxygen volume (VO₂ max) was determined during test 1. Tests 2 and 3 were performed to 70% VO₂ max, the pacemaker being programmed to either VVI or VVIR mode. Plasma α-hANP was measured using a two-site immunoradiometric assay. At rest there was a small but significant difference between the two patient groups: AF 60.2 pg/mL versus AC 97.6 pg/mL; P = 0.03. During exercise in the AC patients, there was a significant increase in α-hANP levels, in VVIR mode, to 238.4 pg/mL, and in VVI mode, to 207.9 pg/mL, P = 0.002 and 0.003, respectively. In those patients with chronic AF, there was no significant rise or fall in α-hANP levels in either pacing mode, VVIR 65.2 pg/mL, VVI 46.6 pg/mL. Previous workers have suggested that α-hANP release by nonfunctioning atria is normal. We have shown that the presence of coordinated AC is required for the release of α-hANP during exercise in patients with CHB, and that this appears to be independent of ventricular rate.