Beneficial effects of biatrial pacing on cardiac function in patients with bradycardia -- tachycardia syndrome.

BACKGROUND: Biatrial (BiA) pacing prevents atrial fibrillation. By an unknown mechanism. The purpose of this study was to use Doppler echocardiography to evaluate the hemodynamic effects during BiA pacing. METHODS AND RESULTS: The subjects were 7 patients with bradycardia - tachycardia syndrome with an implanted pacemaker. Atrial pacing sites were the right atrial appendage (RAA) and coronary sinus. P wave duration during BiA pacing (123 +/-16 ms) was significantly shorter than during either RAA pacing (167+/-19 ms, p<0.05) or sinus rhythm (148+/-12 ms, p<0.05). Doppler echocardiography revealed a greater cardiac output during BiA pacing than during RAA pacing (4.1+/-1.1 vs 3.5+/-0.7 L/min, p=0.042). The Doppler waveform of transmitral flow indicated that the left ventricular contraction interrupted the atrial filling wave during RAA pacing. The interval between the end of the atrial filling wave of transmitral flow and the mitral valvular closing sound was significantly increased by BiA pacing compared with RAA pacing (56+/-65 vs 40+/-57 ms, p=0.047). CONCLUSION: Cardiac hemodynamics were improved by BiA pacing and reduction of left atrial load may be one of the mechanisms.     

Pulmonary vein flow analysis by transoesophageal echocardiogr phy in patients with chronic atrial fibrillation; 1 year follow-up after cardioversion.

AIMS: Left and right upper pulmonary vein flow can be adequately recorded by transoesophageal Doppler echocardiography. The aim of this study was to investigate whether analysis of the pulmonary venous flow velocity pattern can predict the long-term maintenance of sinus rhythm after successful cardioversion of chronic atrial fibrillation. METHODS AND RESULTS: Thirty-six consecutive patients, aged 53+/-9 years, with chronic atrial fibrillation of 5.33+/-2 months duration, were subjected to transoesophageal Doppler echocardiography to record left and right upper pulmonary venous flow, 24 h and 3 months following successful cardioversion. One year following cardioversion, 12 patients (33.3%) were in sinus rhythm (sinus rhythm group) while the remaining 24 patients were in atrial fibrillation (atrial fibrillation group). At 24 h following cardioversion, biphasic systolic forward flow in the left and/or right upper pulmonary venous flow velocity was detected in 10 patients of the sinus rhythm group and in four patients of the atrial fibrillation group (P<0001). The systolic fraction was significantly higher in the sinus rhythm group, 0.48+/-0.04 and 0.39+/-0.06, P<0.001 for the left upper pulmonary venous flow, and 0.52+/-0.05 and 0.41+/-0.04, P<0.001 for the right upper pulmonary venous flow, respectively. In patients who displayed a biphasic systolic forward flow and in whom the right upper pulmonary venous flow systolic fraction was higher than 0.50 at 24 h post-cardioversion, the probability of maintenance of sinus rhythm at 1 year exceeded 95%. CONCLUSION: The detection of a biphasic systolic forward flow in the pulmonary venous flow velocity, and of a right upper pulmonary vein systolic fraction higher than 0.50 as early as 24 h following cardioversion of chronic atrial fibrillation, identifies patients who will remain in sinus rhythm 1 year after cardioversion.     

Atrial septal pacing to resynchronize atrial contraction and improve atrial transport function

OBJECTIVES: Atrial septal pacing via a trans-septal breakthrough site within the right atrial septum can shorten global atrial activation time, resulting in significant reduction of recurrence of atrial fibrillation events. This study examined whether this pacing method will lead to resynchronization of atrial contraction and its benefit on hemodynamic function can be maintained for 24 months. METHODS: Thirty patients with atrial fibrillation and delayed atrial conduction were enrolled (17 males, 13 females, mean age 73 +/- 7 years). Trans-septal breakthrough site within the right atrial septum was identified through pacing from the dorsal left atrium. Continuous atrial septal pacing at the trans-septal breakthrough site was performed for 24 months. Time difference (TD) between right and left atrial contractions was measured during atrial septal pacing and sinus rhythm by pulse Doppler echocardiography of the trans-tricuspid (P-At) and mitral (P-Am) blood flows (TD = P-Am - P-At). RESULTS: The atrial lead was screwed near the fossa ovalis in 29 of 30 patients. Atrial septal pacing yielded significantly shorter P wave duration (101.9 +/- 10.4 vs 139.6 +/- 14.7 msec, p < 0.001), leading to significant reduction of TD in atrial contraction (-8.8 +/- 10.0 vs 29.8 +/- 13.6 msec, p < 0.001)as compared to sinus rhythm. Both shorter P wave duration and reduced TD during atrial septal pacing remained statistically significant during the follow-up period as compared to sinus rhythm. Both left atrial diameter and A to E ratio of filling waves at mitral valve were significantly decreased at 12 months and remained decreased at 24 months. CONCLUSIONS: Atrial septal pacing at the trans-septal breakthrough site can resynchronize atrial contraction and results in improved hemodynamic effects during 24 months of follow-up.     

Alpha-receptor constriction induced by atrial fibrillation during maximal coronary dilatation

Summary The mechanism of coronary vasoconstriction induced by atrial fibrillation during maximal coronary dilatation was studied in 19 chloralose-urethane anesthetized dogs. Maximal coronary dilatation was achieved by carbochromene (5 mg/kg i.v.) or dipyridamole (0.2 mg/kg i.v.) Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Atrial fibrillation was compared with rhythmic atrial pacing at similar heart rates (207±12 vs. 204±12 beats/min). During maximal coronary dilatation, coronary resistance was 0.38±0.05 mm Hgxminx100 g/ml (RU) at sinus rhythm, 0.41±0.06 RU at atrial pacing, and 0.52±0.07 RU at atrial fibrillation, that was significantly (p<0.005) higher than during sinus rhythm and atrial pacing. Accordingly, coronary oxygen extraction was 14±1% at sinus rhythm, 17±1% at atrial pacing (p<0.005 vs. sinus rhythm) and 27±2% at atrial fibrillation (p<0.001 vs sinus rhythm and atrial pacing). Beta-adrenoceptor blockade with propranolol (1 mg/kg i.v.) did not prevent this coronary vasoconstrictive effect. Following alpha-blockade with phenoxybenzamine (10 mg/kg i.v.), however, coronary resistance was 0.52±0.08 RU during sinus rhythm, 0.54±0.10 RU during atrial pacing and 0.57±0.09 RU during atrial fibrillation. The data suggest coronary vasoconstriction induced by atrial fibrillation mediated by an alpha-adrenoceptor mechanism.Supported by a grant from the Deutsche Forschungsgemeinschaft, Bonn, F.R.G.     

Effect of Bachmann's bundle pacing on atrial fibrillation: electrophysiologic assessment

BACKGROUND: It has recently been reported that simultaneous multisite atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus (CS) pacing are useful for preventing the induction of atrial fibrillation (AF). HYPOTHESIS: We investigated whether a simple pacing approach via BB could reduce the induction of AF by extrastimuli (S2) from the right atrial appendage (RAA). METHODS: Programmed electrical stimulation was performed from the RAA and the area of BB at the superior aspect of the atrial septum, and bipolar recordings were obtained from the RAA, BB, and CS in 14 patients. RESULTS: In five patients, AF was induced with critically timed RAA-S2 delivered during RAA pacing. However, AF was not induced in any patient when RAA-S2 was delivered during BB pacing. The duration of the P wave during BB pacing was significantly shorter than that during RAA pacing and sinus rhythm (BB 80 +/- 16 ms vs. RAA 106 +/- 36 ms vs. sinus rhythm 100 +/- 24 ms, p < 0.05). The intra-atrial conduction time to the distal coronary sinus (CSd) caused by early S2 at the RAA was significantly reduced by BB pacing (BB 114 +/- 22 ms vs. RAA 157 +/- 35 ms, p < 0.001). CONCLUSION: Bachmann's bundle pacing reduces atrial conduction time caused by RAA-S2 and may be useful for preventing the induction of AF.     

Effect of gender on atrial electrophysiologic changes induced by rapid atrial pacing and elevation of atrial pressure

INTRODUCTION: The incidence of atrial fibrillation is greater in men than in women, but the reasons for this gender difference are unclear. The purpose of this study was to evaluate the effects of gender on the atrial electrophysiologic effects of rapid atrial pacing and an increase in atrial pressure. METHODS AND RESULTS: Right atrial pressure and effective refractory period (ERP) were measured during sinus rhythm and during atrial and simultaneous AV pacing at a cycle length of 300 msec in 10 premenopausal women, 11 postmenopausal women, and 24 men. The postmenopausal women were significantly older than the premenopausal women (61 +/- 8 years vs 34 +/- 10 years; P < 0.01). During sinus rhythm, mean atrial ERP in premenopausal women was shorter (211 +/- 19 msec) than in postmenopausal women and age-matched men (242 +/- 18 msec and 246 +/- 34 msec, respectively; P < 0.05). Atrial ERPs in all patients shortened significantly during atrial and simultaneous AV pacing. However, the degree of shortening during atrial pacing (43 +/- 8 msec vs 70 +/- 20 msec and 74 +/- 21 msec; P < 0.05) and during simultaneous AV pacing (48 +/- 16 msec vs 91 +/- 27 msec and 84 +/- 26 msec; P < 0.05) was significantly less in premenopausal women than in postmenopausal women or age-matched men. CONCLUSION: The results of this study demonstrate a significant gender difference in atrial electrophysiologic changes in response to rapid atrial pacing and an increase in atrial pressure. The effect of menopause on the observed changes suggests that the gender differences may be mediated by the effects of estrogen on atrial electrophysiologic properties.     

Effects of altered site of electrical activation on myocardial performance during inotropic stimulation

The effects of altering the site of electrical activation on responses to isoproterenol (ISO) and treadmill exercise were examined in mongrel dogs instrumented for long-term measurement of left ventricular pressure, left ventricular dP/dt, coronary blood flow, cardiac output, left ventricular diameters, and mean arterial pressure and O2 content in the coronary sinus and aorta. During spontaneous rhythm, 0.2 micrograms/kg/min ISO increased heart rate by 90 +/- 7 beats/min, left ventricular dP/dt by 2479 +/- 301 mm Hg/sec, cardiac output by 3.5 +/- 0.9 liters/min, coronary blood flow by 30.4 +/- 3.9 ml/min, and myocardial oxygen consumption (MVO2) by 3.91 +/- 0.84 ml/min. During right atrial pacing at 193 +/- 7 beats/min, the effects of ISO were not different from the effects during spontaneous rhythm, with the exception of a lesser increase in coronary blood flow and lesser reductions in coronary resistance and left ventricular end-diastolic diameter and pressure. During right ventricular pacing at an identical rate, ISO increased left ventricular dP/dt (1140 +/- 158 mm Hg/sec) and cardiac output (2.2 +/- 0.5 liters/min) significantly less (p less than .025) than during either sinus rhythm or right atrial pacing, while MVO2 rose to a higher value. During right ventricular pacing the changes in mean arterial pressure and left ventricular end-diastolic diameters with ISO were not significantly different from those during right atrial pacing. Treadmill exercise induced significantly smaller (p less than .025) increases in left ventricular dP/dt during right ventricular pacing as compared with during either right atrial pacing or sinus rhythm, while MVO2 rose to a higher value.(ABSTRACT TRUNCATED AT 250 WORDS)     

Coronary sinus pacing initiates counterclockwise atrial flutter while pacing from the low lateral right atrium initiates clockwise atrial flutter: Analysis of episodes of direct initiation of atrial flutter

Introduction: Rapid atrial pacing in sinus rhythm may directly induce atrial flutter without provoking intervening atrial fibrillation, or initiate atrial flutter indirectly, by a conversion from an episode of transient atrial fibrillation provoked by rapid atrial pacing. The present study was performed to examine whether or not the direct induction of clockwise or counterclockwise atrial flutter was pacing-site (right or left atrium) dependent. Methods and Results: We analyzed the mode of direct induction of atrial flutter by rapid atrial pacing. In 46 patients with a history of atrial flutter, rapid atrial pacing with 3 to 20 stimuli (cycle LENGTH = 500 − 170 ms) was performed in sinus rhythm to induce atrial flutter from 3 atrial sites, including the high right atrium, the low lateral right atrium, and the proximal coronary sinus, while recording multiple intracardiac electrograms of the atria. Direct induction of atrial flutter by rapid atrial pacing was a rare phenomenon and was documented only 22 times in 15 patients: 3, 11, and 8 times during stimulation, respectively, from the high right atrium, low lateral right atrium, and the proximal coronary sinus. Counterclockwise atrial flutter (12 times) was more frequently induced with stimulation from the proximal coronary sinus than from the low lateral right atrium (8 vs 1, P = .0001); clockwise atrial flutter (10 times) was induced exclusively from the low lateral right atrium (P = .0001 for low lateral right atrium vs proximal coronary sinus, P = .011 for low lateral right atrium vs high right atrium). Conclusions: Direct induction of either counterclockwise or clockwise atrial flutter was definitively pacing-site dependent; low lateral right atrial pacing induced clockwise, while proximal coronary sinus pacing induced counterclockwise atrial flutter. Anatomic correlation between the flutter circuit and the atrial pacing site may play an important role in the inducibility of counterclockwise or clockwise atrial flutter.     

Effect of experimentally induced atrial fibrillation on coronary circulation in dogs

The influence of atrial fibrillation on coronary circulation was studied in 21 anesthetized open-chest dogs. Atrial fibrillation was induced either by local application of acetylcholine (10% in normal saline) on the left atrial appendage or by electric stimulation (2-7 volts, 2 ms, 50 Hz). When atrial fibrillation was induced (n = 10), mean aortic pressure fell and heart rate rose significantly; coronary blood flow (CBF) remained unchanged (78 +/- 6 vs. 75 +/- 5 ml/min X 100 g) while coronary vascular resistance (CVR) (1.16 +/- 0.05 vs. 0.87 +/- 0.07 [m Hg X min X 100 gl/ml [RU], p less than 0.0001) and sinus oxygen saturation (26 +/- 2 vs. 22 +/- 1%, p less than 0.05) decreased. Following the application of carbochromen (5 mg/kg in 3 min i.v.) resulting in maximal coronary dilatation, atrial fibrillation resulted in a reduction in CBF (311 +/- 48 vs. 205 +/- 30 ml/min X 100 g, p less than 0.01) and coronary sinus oxygen saturation (65 +/- 6 vs. 42 +/- 6%, p less than 0.01), while CVR (0.27 +/- 0.03 vs. 0.37 +/- 0.04 RU, p less than 0.0001) was 38 +/- 8% (p less than 0.0005) higher during atrial fibrillation than at sinus rhythm. When hearts were paced to a rate which was identical to the average heart rate at atrial fibrillation (n = 11), CBF (92 vs. 125 +/- 14 ml/min X 100 g, p less than 0.001) and sinus oxygen saturation (24 +/- 2 vs. 30 +/- 2%, p less than 0.0025) were higher and CVR (1.16 +/- 0.11 vs. 0.97 +/- 0.10 RU, p less than 0.0005) lower than during atrial fibrillation; during maximal coronary dilatation by carbochromen, pacing also resulted in a higher CBF (233 +/- 24 vs. 168 +/- 16 ml/min X 100 g, p less than 0.0005) and sinus oxygen saturation (70 +/- 3 vs. 57 +/- 2%, p less than 0.0005), while CVR (0.25 +/- 0.02 vs. 0.46 +/- 0.02 RU, p less than 0.0005) was lower than during atrial fibrillation. Thus atrial fibrillation results in a decrease in coronary vascular resistance but an increase in coronary oxygen extraction. When heart rate is controlled, the vasoconstrictor effect of atrial fibrillation becomes unmasked. Coronary vasoconstriction during atrial fibrillation appears to be greater during maximal coronary dilatation than during control.     

Stunning of the left atrium after pharmacological cardioversion of atrial fibrillation

INTRODUCTION: Stunning of the left atrium and atrial appendage is a well known but not fully clarified phenomenon observed during the cardioversion of atrial fibrillation regardless of the cardioversion method attempted. AIM: To assess the effects of propafenone and amiodarone on left atrium and left atrial appendage contractility. METHODS: Forty patients with paroxysmal atrial fibrillation (20 females, 20 males), aged 60-83 (mean 72.0+/-10.1) years, were enrolled into the study. Half of these patients had sinus rhythm restored by the administration of oral propafenone (150-300 mg) and the remaining 20 patients were treated with intravenous amiodarone (150-450 mg). The control group consisted of 20 patients (10 females, 10 males) aged 52-78 (mean 61.2+/-9.3) years with sinus rhythm and no history of atrial fibrillation. All the patients had a transthoracic (TTE) and transesophageal (TEE) echocardiography performed while still in the AF, before drug administration and 1 hour after sinus rhythm restoration. RESULTS: All haemodynamic parameters of the left atrium measured after the sinus rhythm restoration were significantly worse when compared with the control group. Left atrial fractional shortening and total atrial fraction were significantly lower after propafenone than amiodarone (8.6+/-3.6% vs 11.7+/-5.5%, p<0.05; and LA FC 16.2+/-5.3% vs 23.3 (+/-6.3)% respectively, p<0.05). Doppler echocardiographic parameters included in the analysis such as mitral flow and superior left pulmonary vein flow were significantly lower in the sinus rhythm restoration group than in the control group. Among them the end-diastolic mitral flow velocity amplitude and flow velocity integral as well as the maximum pulmonary retrograde velocity were significantly worse in the group treated with propafenone than in patients receiving amiodarone. All the atrial appendage Doppler velocity parameters were significantly reduced after the sinus rhythm restoration in both groups. In the patients treated with propafenone, values of these parameters were significantly decreased compared with the patients receiving amiodarone. CONCLUSIONS: Successful pharmacological cardioversion of atrial fibrillation causes the left atrium and left atrial appendage contractility impairment similar to that observed with other methods of the sinus rhythm restoration. Following the AF cardioversion the level of left atrial stunning is higher in the patients treated with propafenone than in subjects receiving amiodarone.     

Haemodynamics of induced atrial fibrillation: a comparative assessment with sinus rhythm, atrial and ventricular pacing

The haemodynamics and myocardial lactate consumption during induced atrial fibrillation (AF) were studied in 10 patients with paroxysmal AF. Their mean age (+/- SD) was 61 +/- 5 years and none had clinical evidence of ischaemic or rheumatic heart disease. Compared with sinus rhythm, the onset of AF was associated with a reduction in systolic blood pressure (152 +/- 13 mmHg) in AF vs 169 +/- 23 mmHg in sinus rhythm, P less than 0.01). There was no consistent change in cardiac output at the onset of AF compared with sinus rhythm, but the cardiac output was lower compared with regular atrial pacing at rates similar to those of induced AF (3.85 +/- 0.76 vs 4.38 +/- 0.89 l min-1, P less than 0.02). Compared with sinus rhythm or rate-matched atrial pacing, AF was associated with an elevated pulmonary arterial pressure (24.2 +/- 5.6 mmHg in AF vs 17.9 +/- 14.4 mmHg in sinus rhythm, P less than 0.01) and pulmonary arterial wedge pressure (18.6 +/- 5.6 vs 9.7 +/- 3.9 mmHg, P less than 0.01). The haemodynamic changes during AF were similar to those seen during regular ventricular pacing at an equivalent rate, although the latter was associated with a lower systolic blood pressure (152 +/- 13 mmHg in AF vs 136 +/- 25 mmHg in ventricular pacing, P less than 0.05) and higher right atrial pressure (8.2 +/- 4.4 vs 11.5 +/- 7.5 mmHg respectively, P less than 0.05), presumably due to the deleterious effects of cannon 'a' waves.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of acute atrial fibrillation on the vasodilator reserve of the canine atrium

Acute atrial fibrillation appreciably alters atrial physiology by increasing atrial blood flow and atrial oxygen consumption. To determine the effects of atrial fibrillation on atrial vasodilator reserve atrial fibrillation was produced in dogs by electrical atrial stimulation. Reactive hyperaemic responses were measured using Doppler crystals fixed to the sinus node artery and to an adjacent right ventricular branch artery during sinus rhythm, after 20 minutes of atrial fibrillation, and after systemic administration of chromonar (a potent coronary dilator) during atrial fibrillation. During sinus rhythm the peak to resting blood flow velocity ratio after a 20 s occlusion of the sinus node artery was 3.2(1) (mean(SEM)). A 20 s occlusion of a right ventricular branch artery during sinus rhythm resulted in a significantly larger response (5.9(0.7). The repayment to debt area ratio in response to a 20 s occlusion was 1.1(0.2) for the sinus node artery but 3.9(1.0) for a right ventricular branch. During atrial fibrillation the peak to resting velocity ratio was substantially decreased in the sinus node artery (2.3(0.6)) but was not significantly changed in the right ventricular branch (4.4(0.6)). Atrial fibrillation plus chromonar abolished reactive hyperaemia in both the sinus node artery and the right ventricular branch vessel. Right atrial blood flow (microspheres) increased from 45(4) in sinus rhythm to 106(19) ml X min-1 X 100 g-1 in atrial fibrillation and to 208(22) ml X min-1 X 100 g-1 after chromonar administration during atrial fibrillation. Thus the quantitative characteristics of coronary reactive hyperaemia in the right atrium were substantially different from those in the right ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reversal of electrical remodeling after cardioversion of persistent atrial fibrillation

INTRODUCTION: In animals, atrial fibrillation results in reversible atrial electrical remodeling manifested as shortening of the atrial effective refractory period, slowing of intra-atrial conduction, and prolongation of sinus node recovery time. There is limited information on changes in these parameters after cardioversion in patients with persistent atrial fibrillation. METHODS AND RESULTS: Thirty-eight patients who had been in atrial fibrillation for 1 to 12 months underwent electrophysiologic testing 10 minutes and 1 hour after cardioversion. At 1 week, 19 patients still in sinus rhythm returned for repeat testing. Reverse remodeling of the effective refractory period was not uniform across the three atrial sites tested. At the lateral right atrium, there was a highly significant increase in the effective refractory period between 10 minutes and 1 hour after cardioversion (drive cycle length 400 ms: 204 +/- 17 ms vs 211 +/- 20 ms, drive cycle length 550 ms: 213 +/- 18 ms vs 219 +/- 23 ms, P < 0.001). The effective refractory period at the coronary sinus and distal coronary sinus did not change in the first hour but had increased by 1 week. The corrected sinus node recovery time did not change in the first hour but was shorter at 1 week (606 +/- 311 ms vs 408 +/- 160 ms, P = 0.009). P wave duration also was shorter at 1 week (135 +/- 18 ms vs 129 +/- 13 ms, P = 0.04) consistent with increasing atrial conduction velocity. CONCLUSION: The atrial effective refractory period increases, sinus node function improves, and atrial conduction velocity goes up in the first week after cardioversion of long-standing atrial fibrillation in humans. Reverse electrical remodeling of the effective refractory period occurs at different rates in different regions of the atrium.     

Effect of heart rate on left ventricular diastolic transmitral flow velocity patterns assessed by Doppler echocardiography in normal subjects

Although a number of factors, including age and ventricular loading, are known to influence the pattern of left ventricular (LV) filling as depicted by Doppler echocardiographic transmitral flow velocities, few and conflicting data are available regarding the influence of heart rate (HR). Therefore, 20 volunteers (mean age 30 years) were evaluated with pulsed-wave Doppler echocardiography, performed with the sample volume placed at the mitral anulus level in the apical 4-chamber projection. Transmitral flow measurements comprised peak and integrated early passive (E) and late atrial (A) filling velocities and the slope of velocity decline from peak E filling. Measurements were recorded during baseline (sinus rhythm, mean 70 beats/min) and during transesophageal atrial pacing (mean 88 beats/min). LV end-diastolic dimension, mean arterial pressure and PR interval (corrected for pacing-induced delay in interatrial conduction time) were unchanged during pacing versus baseline measurements. Peak and integrated E filling velocities averaged 0.59 +/- 0.09 m/s and 6 +/- 1 cm, respectively, at baseline and were not significantly greater at the higher HR. In contrast, baseline peak and integrated A velocities averaged 0.37 +/- 0.06 m/s and 2.3 +/- 0.7 cm, respectively, but were significantly greater at the higher HR (0.5 +/- 0.07 m/s and 3.2 +/- 1.1 cm, respectively [p less than 0.003 vs baseline for each]). Further analysis of a subgroup of 9 subjects for whom Doppler measurements were available at 3 HRs (sinus 70; pacing 80 and 90) yielded strong evidence for a linear relation between HR and peak A velocity (A = 0.008 HR - 0.21, with p less than 0.0001 for significance of the linear trend).(ABSTRACT TRUNCATED AT 250 WORDS)     

Identification of pulmonary vein potentials by differential site atrial pacing in patients with paroxysmal atrial fibrillation: enhanced detection by pulmonary vein pacing

INTRODUCTION: Pulmonary vein (PV) isolation may cure paroxysmal atrial fibrillation (PAF); however, identification of PV potentials may be difficult in sinus rhythm. Studies have suggested that atrial pacing may improve the identification of PV potentials. METHODS AND RESULTS: In 25 consecutive patients who underwent PV isolation for PAF, the results of pacing from the distal PV, distal and proximal coronary sinus, and high right atrium compared to sinus rhythm were analyzed to determine the most effective pacing site for identification of PV potentials. The percentage of confirmed PV potentials and the longest interval between atrial and PV potentials in each PV were compared during differential site pacing and sinus rhythm. PV potentials were confirmed in 63 (82%) of 77 PVs that could be mapped during the complete pacing protocol and during sinus rhythm. Distal PV pacing identified significantly more PV potentials (left upper pulmonary vein [LUPV] 100%, left lower pulmonary vein [LLPV] 84%, right upper pulmonary vein [RUPV] 80%, right lower pulmonary vein [RLPV] 53%) compared to other pacing sites and sinus rhythm. Among atrial pacing sites, those ipsilateral to the PV being mapped were the most effective for identifying PV potentials. The intervals between atrial and PV potentials were significantly longer during distal PV pacing than pacing at other sites (LUPV 81.6 +/- 26.2 ms, LLPV 61.4 +/- 26.1 ms, RUPV 59.7 +/- 33.2 ms, RLPV 39.7 +/- 26.7 ms). CONCLUSION: (1) Distal PV pacing was most effective for identifying PV potentials. (2) The interval between atrial and PV potentials was longest during distal PV pacing.     

Evaluation of hepatic venous flow patterns using a pulsed Doppler technique

Evaluation of hepatic venous flow patterns was attempted by pulsed Doppler echocardiography. Subjects were 80 patients including those with dilated cardiomyopathy, old myocardial infarction, angina pectoris, pulmonary hypertension, constrictive pericarditis, tricuspid regurgitation (TR), lone atrial fibrillation, and post-cardiac surgery. Eleven normal subjects served as controls. The mean age was 53.0 +/- 12.4 years. Most of the TR patients had atrial fibrillation. Patients with aortic regurgitation and significant mitral regurgitation were excluded. Afterload stress by angiotensin II infusion was performed in 51 subjects, mainly for those with ischemic heart disease, cardiomyopathy and the normal controls. Hepatic venous flow patterns included double-peaked flow signals toward the right atrium, and the relationship between systolic (S) and diastolic flow velocities (D) was expressed as the velocity ratio [S/(S+D)]. A reversed flow during atrial systole was expressed as an "A wave" and that between the S and D waves, as an "O wave". Systolic flow velocity was less than diastolic flow velocity in cases with atrial fibrillation and the post-surgical cases. The velocity ratio was greater than 0.5 in nearly all patients with normal sinus rhythm, and less than 0.5 in cases with atrial fibrillation and the post-surgical cases. In the former, systolic flow velocity was less than diastolic flow velocity after defibrillation, in spite of restoration of normal sinus rhythm. These findings indicate that systolic flow velocity was influenced by atrial relaxation; diastolic flow velocity, by ventricular diastolic function. The A wave was increased in cases with pulmonary hypertension and A wave velocity in the hepatic vein correlated with systolic pulmonary artery pressure. In cases with tricuspid regurgitation, reversed flows were detected during ventricular systole both in normal sinus rhythm and in atrial fibrillation. After infusions of angiotensin II the velocity ratio increased in cases with dilated cardiomyopathy and in normal controls (p less than 0.01). The hepatic venous flow pattern after infusion in the former was characterized by dominant systolic and diminished diastolic flow velocities with a consequent increase in the velocity ratio toward 1.0, while a change in the ratio was less marked in normal controls. In conclusion, analysis of the hepatic venous flow pattern by pulsed Doppler echocardiography is very useful for evaluating cardiac function. A marked increase in the velocity ratio after angiotensin II infusion suggests decreased cardiac function.     

Further evidence of localized posterior interatrial conduction delay in lone paroxysmal atrial fibrillation.

AIMS: Prolongation of interatrial conduction time has been reported in patients with paroxysmal atrial fibrillation (PAF). The study objective was to localize the region of the conduction delay in patients with lone PAF. METHODS AND RESULTS: Twenty-one patients with lone PAF and 23 patients with AV nodal re-entrant tachycardia ablation without history of PAF (control group) were recruited. Endocardial recordings were made during sinus rhythm and programmed atrial stimulation. The authors measured the interatrial conduction time, the 'right-sided' conduction time between the high lateral right atrium and the proximal coronary sinus (RA-CSp), and the 'left-sided' conduction time between the proximal and the distal coronary sinus (CSp-LA). During sinus rhythm, the interatrial conduction time was longer in the PAF group (103 +/- 19 vs 86 +/- 12 ms, P<0.01) due to delay of right-sided conduction (RA-CSp was 74 +/- 20 vs 56 +/- 10 ms, P<0.01). During programmed stimulation at the distal coronary sinus, the maximal RA-CSp time was also longer in the PAF group (110 +/- 47 vs 69 +/- 16 ms, P<0.05). No differences in CSp-LA time were observed. CONCLUSION: This study supports the role of posterior septal right atrial conduction disturbances in the genesis of lone PAF.     

Atrial lead placement in the right atrial appendage during recent or chronic arrhythmia

An atrial arrhythmia could be encountered during the atrial lead implantation. The lead placement must subsequently be delayed after restitution of the sinus rhythm or completely abandoned. The authors investigate the atrial lead placement during atrial arrhythmia and the lead performance at 6-month follow-up. The study population was 65 patients aged 78.5 years, 42 males and 28 structural heart diseases. They were implanted for sick sinus syndrome (n=14), atrioventricular block (n=44), infra-hisian conduction abnormality (n=7) in association with an atrial fibrillation (63.1%), an atrial flutter (24.6%) or an atrial tachycardia (12.3%). The onset of the arrhythmia was < or = 7 days (47.7%) or > 7 days (52.3%). An atrial lead was placed in the right atrial appendage under fluoroscopic control. If the sinus rhythm was not restored at 1 month, an electrical cardioversion was performed. The per-implantation atrial signal amplitude was 2.2+/-1.5 mV (range 0.5 mV to 7 mV). Sinus rhythm was restored in 54 patients. At 1 month, one patient was in an incessant atrial fibrillation. The 53 patients in sinus rhythm had a good atrial lead performance. Out of 46 patients who completed the 6-month follow-up, 4 had an arrhythmia recurrence. The 42 patients in sinus rhythm had a good atrial lead performance. At 1 and 6-month follow-up, the atrial pacing threshold (1.1+/-0.7 V vs 1.2+/-1.0 V, ns) and the atrial signal amplitude (2.1+/-1.0 mV and 2.1+/-0.9 mV, ns) were stable. Comparing the patients with a recent or a chronic arrhythmia, the pacing thresholds (1.2+/-1.1 V vs 1.14+/-0.8 V, ns), the atrial signal amplitudes (2.17+/-0.9 mV vs 2.05+/-0.9 mV, ns) and the proportion of satisfactory pacemaker performance in DDD(R) mode for the patients in sinus rhythm (100% vs 100%, ns) did not statistically differ between the two groups at 6 months. In conclusion, the placement of an atrial lead in the right atrial appendage during an atrial arrhythmia is feasible with a good lead performance at 6 months in sinus rhythm regardless the onset time of the arrhythmia and provides a satisfactory atrial-based pacing with the preservation of the atrioventricular synchrony.     

Reversal of atrial electrical remodeling following cardioversion of long-standing atrial fibrillation in man.

BACKGROUND: In animal studies, atrial fibrillation has been shown to shorten the atrial refractory period and impair its rate adaptation. However, little is known about the effects of chronic atrial fibrillation on atrial electrophysiology and its recovery course in humans. METHODS AND RESULTS: Nineteen patients, mean age 64 +/- 14 years, with chronic atrial fibrillation of more than six months duration were included in this study. All of them were successfully converted to sinus rhythm with an external defibrillator. Atrial effective refractory periods at right atrial appendage and distal coronary sinus were determined with five pacing cycle lengths (300, 400, 500, 600 and 700 ms) at 30 min after cardioversion and once a day for four days. The atrial conduction properties, including P wave duration of surface ECG, and right and left atrial conduction times, were also measured at the same time interval. Twenty age-matched patients without a history of atrial tachyarrhythmia were evaluated as controls. In comparison with controls, chronic atrial fibrillation significantly shortened the atrial effective refractory period, impaired its rate adaptation response, especially at distal coronary sinus, and depressed the conduction properties of atria. The atrial conduction properties did not change during the four-day follow-up period; however, the atrial effective refractory period was gradually prolonged and its rate adaptation response improved after restoration of sinus rhythm. CONCLUSIONS: In humans, chronic atrial fibrillation significantly shortened the atrial effective refractory period, and impaired its rate adaptation response. Restoration and maintenance of sinus rhythm could reverse these electrophysiological changes.     

Interstudy variability of coronary flow reserve. Influence of heart rate, arterial pressure, and ventricular preload

To define the long-term variability of serial coronary flow reserve (CFR) measurements in humans and to evaluate the influence of changes in heart rate, mean arterial pressure, and left ventricular preload on CFR, 45 patients with normal left ventricular function (38 cardiac allograft recipients, five patients with normal coronary arteries, and two patients with minimal coronary artery disease [less than 50% diameter stenosis]) were studied. CFR (ratio of peak hyperemic [h] to resting [r] coronary blood flow velocity [CBFV]) was measured with a 3F coronary Doppler catheter and intracoronary papaverine. Initial CFR measurements were highly correlated with repeat measurements obtained 11 +/- 0.6 months later (r = 0.95; mean absolute difference, 0.3 +/- 0.1; n = 17). Differences in CFR between studies were related to changes in heart rate (r = 0.61, p = 0.01) but not to changes in mean arterial pressure (r = 0.25, p = 0.33). To define the effects of rapid changes in heart rate, mean arterial pressure, and preload on CFR, these variables were altered by atrial pacing, handgrip exercise, and volume expansion, respectively. Atrial pacing produced a rate-related increase in rCBFV but did not change hCBFV. Consequently, CFR was significantly reduced as heart rate was increased progressively from 76 +/- 2 in sinus rhythm (4.5 +/- 0.2) to 100 (3.8 +/- 0.2, p less than 0.05, n = 32) to 120 beats/min (3.2 +/- 0.1, p less than 0.05, n = 7). Despite a 19 +/- 2 mm Hg rise in mean arterial pressure during handgrip exercise, CFR was unchanged from baseline (3.7 +/- 0.3 vs. 3.7 +/- 0.4, p = NS, n = 7) because rCBFV rose proportionally with hCBFV. When pulmonary capillary wedge pressure was increased from 9 +/- 1 to 16 +/- 1 mm Hg after volume expansion, CFR was significantly decreased (from 3.8 +/- 0.2 to 2.9 +/- 0.2, p less than 0.05, n = 9) because rCBFV was increased while hCBFV remained unchanged. Hence, serial CFR measurements in humans are highly reproducible in the absence of conditions known to affect resting or hyperemic coronary blood flow. Increases in heart rate or preload reduced CFR because rCBFV was increased while hCBFV was unchanged. In contrast, changes in mean arterial pressure did not alter CFR. Proper interpretation of CFR measurements should take into account the hemodynamic conditions at which they are obtained.