Influence of the site of stimulation on atrioventricular nodal refractory periods and the effect of verapamil

The refractory periods of the atrioventricular (AV) node appear dependent on the pattern of AV nodal input. In 21 superfused AV rabbit heart preparations stimulated from each of the 2 principal input regions, crista terminalis or atrial septum, the effect of changing the site of stimulation of the AV nodal refractoriness and the relative effect of verapamil on AV nodal refractoriness was determined. In 6 of 21 preparations the functional AV refractory curve became discontinuous only when stimulation was applied at the atrial septum and suggested dual AV nodal pathways (dual pathways group). In the 15 other preparations no interruption of the curve occurred with either crista terminalis or atrial septal stimulation (normal conduction group). In the normal conduction group, the difference in the effective refractory period of the AV node obtained by crista terminalis vs atrial septal stimulation was not significant (154 +/- 25 vs 150 +/- 28 ms). However, the functional refractory period was significantly longer with crista terminalis vs atrial septal stimulation (232 +/- 19 vs 239 +/- 19 ms, p less than 0.001). After verapamil administration, the effective and functional refractory periods during crista terminalis vs atrial septal stimulation were prolonged to 270 +/- 49 vs 285 +/- 55 ms (p less than 0.01) and 335 +/- 43 vs 351 +/- 41 ms (p less than 0.001), respectively. Thus, the difference in refractory periods associated with changing the stimulation site was exaggerated with verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ectopic left atrial rhythm that produces QRS changes in absence of Wolff-Parkinson-White syndrome

In an 18-year-old patient without manifest or concealed Wolff-Parkinson-White syndrome, spontaneous and paced left atrial impulses penetrated a left-sided AV nodal input and thereafter activated the ventricles in a normal fashion exclusively through the His-Purkinje system. On the other hand, sinus and paced right atrial impulses entered a right-sided atrioventricular nodal input that was completely dissociated from the left-sided input to subsequently activate the ventricles partly through Mahaim fibers and partly through the His-Purkinje system. The Mahaim fibers, which acted as "bystanders" during episodes of atrioventricular nodal reciprocating tachycardia, seemed to have extended from a "distal," common (right-sided) intranodal pathway (or "proximal" His bundle) to the right ventricle or, although this is less likely, to the right bundle branch. More studies are necessary to determine whether the association on the surface electrocardiogram of an ectopic slow left atrial rhythm with changes in QRS morphology (but not in QRS duration) always reflects the existence of Mahaim fibers.     

Demonstration of a Posterior Atrial Input to the Atrioventricular Node During Sustained Anterograde Slow Pathway Conduction

Objectives. This study sought to demonstrate electrophysiologic evidence for the existence of different anatomic atrial input sites of fast and slow conduction pathways in patients with dual atrioventricular (AV) node physiology.

Background. Although a separate posterior exit site exists for a retrograde slow AV node pathway, it remains unresolved whether a separate atrial input site into the AV node actually exists in patients with dual anterograde AV node pathway physiology.

Methods. In 10 patients with dual AV node pathway physiology, atrial pacing at three chosen drive cycle lengths (DCL1, DCL2 and DCL3) was performed at an anterior site (A) just above the His bundle recording site and at a posterior atrial site (P) just below the coronary sinus ostium. DCL3 was chosen as the one cycle length that resulted in a long AH interval consistent with slow pathway conduction. The stimulus to His bundle conduction times (SH) at both sites (SH_P and SH_A, respectively) and their differences (ΔSH = SH_P − SH_A) at each of the three drive cycle lengths were analyzed.

Results. The mean ± SD ΔSH values for DCL1 and DCL2 measured 9 ± 16 and 8 ± 18 ms, respectively, and the mean ΔSH value at DCL3 measured −34 ± 24 ms, which was significantly different from the mean ΔSH values at DCL1 and DCL2 (both p < 0.05).

Conclusions. The significant change in the ΔSH (SH_P − SH_A) value during slow pathway conduction could be accounted for by a corresponding shift of anterograde input from an anterior to a posterior entry site to the AV node. These findings support the notion that a separate anterograde entry site of the slow pathway does exist in patients with dual AV node pathway physiology.     

Dissociation of atrial electrograms by right and left atrial pacing in patients with atrioventricular reciprocating tachycardia

Seventeen patients had atrioventricular (AV) reciprocating tachycardia incorporating an AV bypass tract as the retrograde limb of the tachycardia circuit. High right atrial pacing during tachycardia dissociated the low septal right atrial electrogram in four of seven patients with a left free wall bypass tract, neither of two patients with a right free wall bypass tract, four of six patients with a posteroseptal bypass tract and both patients with an anteroseptal bypass tract. Pacing from the coronary sinus during tachycardia dissociated the atrial electrogram recorded at the os of the coronary sinus in no patient with a left free wall bypass tract, both patients with a right free wall bypass tract, two patients with a posteroseptal bypass tract and one patient with an anteroseptal bypass tract. These findings suggest two distinct inputs to the AV node, with the left-sided input being part of the tachycardia circuit in patients with a left free wall bypass tract and the right-sided input being part of the tachycardia circuit in patients with a right free wall bypass tract. However, in some patients with a septal bypass tract, neither the right- nor the left-sided atrial input appears to be a necessary link in the tachycardia circuit.     

Mechanisms underlying the reentrant circuit of atrioventricular nodal reentrant tachycardia in isolated canine atrioventricular nodal preparation using optical mapping

The reentrant pathways underlying different types of atrioventricular (AV) nodal reentrant tachycardia have not yet been elucidated. This study was performed to optically map Koch's triangle and surrounding atrial tissue in an isolated canine AV nodal preparation. Multiple preferential AV nodal input pathways were observed in all preparations (n=22) with continuous (73%, n=16) and discontinuous (27%, n=6) AV nodal function curves (AVNFCs). AV nodal echo beats (EBs) were induced in 54% (12/22) of preparations. The reentrant circuit of the slow/fast EB (36%, n=8) started as a block in fast pathway (FP) and a delay in slow pathway (SP) conduction to the compact AV node, then exited from the AV node to the FP, and rapidly returned to the SP through the atrial tissue located at the base of Koch's triangle. The reentrant circuit of the fast/slow EB (9%, n=2) was in an opposite direction. In the slow/slow EB (9%, n=2), anterograde conduction was over the intermediate pathway (IP) and retrograde conduction was over the SP. Unidirectional conduction block occurred at the junction between the AV node and its input pathways. Conduction over the IP smoothed the transition from the FP to the SP, resulting in a continuous AVNFC. A "jump" in AH interval resulted from shifting of anterograde conduction from the FP to the SP (n=4) or abrupt conduction delay within the AV node through the FP (n=2). These findings indicate that (1) multiple AV nodal anterograde pathways exist in all normal hearts; (2) atrial tissue is involved in reentrant circuits; (3) unidirectional block occurs at the interface between the AV node and its input pathways; and (4) the IP can mask the existence of FP and SP, producing continuous AVNFCs.     

Reduction of the pace polarization artefact for capture detection applications by a tri-phasic stimulation pulse.

This study investigated the ability to minimize pace polarization artefacts (PPA) by adjusting the post-stimulus pulse duration of a tri-phasic stimulation pulse. Adjustment of the stimulation pulse was enabled by downloading special study software into an already implanted pacemaker. Tests were performed in a total of 296 atrial leads and 311 ventricular leads. Both chronic and acute leads were included in the study. Statistically significant differences were found in the initial PPA (without any adjustment of the stimulus pulse) between atrial and ventricular leads. In addition, significant differences were observed among various lead models with respect to changes over time in the initial ventricular PPA. Successful PPA reduction was defined as a reduction of the PPA below 0.5 mV for atrial leads and below 1 mV for ventricular leads. Results show a success rate for ventricular and atrial PPA reduction of 97.8% and 98.7%, respectively. Threshold tests showed that after reduction of the PPA loss of ventricular capture can be reliably detected. However, atrial threshold tests showed many false positive evoked response detections. In addition, unexpectedly high evoked response amplitudes were observed in the atrium after reduction of the PPA. Results from additional measurements suggest that these high atrial evoked response amplitudes come from the influence of the input filter of the pacemaker.     

Bigeminal pulmonary vein ectopy suppressed by pulmonary vein isolation

A 58-year-old man with atrial fibrillation underwent pulmonary vein (PV) isolation (PVI). Bigeminal atrial premature beats persisted from the beginning of the PVI. The cardiac recordings from a basket catheter (BC) revealed the PV ectopic origin in the distal right superior PV. Successful PVI with the guidance of BC was confirmed by the appearance of concealed ectopy. Surprisingly, the PV ectopy completely disappeared immediately after the successful PVI. The findings suggest that the generation of PV trigger is sometimes dependent on left atrial input and that the underlying mechanism of the PV trigger may have been triggered activity or reentry.     

Ventricular response to atrial fibrillation: role of atrioventricular conduction pathways

Irregularity of the ventricular rhythm is a hallmark of patients with atrial fibrillation, yet the genesis of the irregularity is not yet fully understood. The role of the atrioventricular (AV) node in determining the irregularity of the ventricular response to atrial fibrillation was investigated by comparing the frequency distributions of the atrial (AA) and the ventricular (RR) intervals. Atrial electrograms and surface electrocardiographic leads were recorded during sustained atrial fibrillation in 12 patients with conduction over the AV node. The scaling factor (mean RR interval/mean AA interval) quantified the ability of the conduction pathway to scale the atrial input to a slower ventricular response and ranged from 2.55 to 5.92 (mean +/- SD 3.77 +/- 0.92). The coefficient of variation (SD/mean) measured the relative variability of the AA and RR interval distributions. The atrial and ventricular coefficients of variation were not significantly different (0.20 +/- 0.04 versus 0.21 +/- 0.03, p greater than 0.27). Similar recordings were analyzed in six patients with conduction over a accessory AV pathway. The scaling factor ranged from 1.54 to 2.46 (2.02 +/- 0.39) and, as was the case for patients with conduction over the AV node, the atrial and ventricular coefficients of variation did not significantly differ (0.24 +/- 0.08 versus 0.27 +/- 0.10, p greater than 0.6). For both groups of patients, ventricular variability and the maximal RR intervals were predicted by the product of the scaling factor and either atrial variability or maximal AA intervals, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in the pulmonary vascular input impedance in patients with atrial septal defect after surgical correction

In order to evaluate whether there is pulmonary vascular disease in patients with atrial septal defect (ASD), we used the pulmonary vascular input impedance to estimate the stiffness of the pulmonary vessels with before and after surgical intervention. Ten control subjects and 11 patients with ASD (9 operable and 2 inoperable) were examined. In preoperative patients the decreased total pulmonary resistance (Rin) and pulmonary vascular resistance appeared to open new parallel vascular channels with increased blood flow. Further, there were no significant differences in the pulmonary vascular input impedance spectrum and phase, and characteristic impedance among control subjects, preoperative and postoperative patients. Although distensibility of the pulmonary vascular wall in operable patients was similar to that in control subjects, an excessive elevation in Rin and input impedance modulus was observed in inoperable patients. The results demonstrate that the normal input impedance spectrum and phase in patients with ASD is predictive of a good prognosis after successful surgical correction.     

Ventricular pre-excitation disclosed by an episode of high-frequency atrial fibrillation: the role of frequency-dependent variations in the bundle of Kent conduction]

The presence of a ventricular pre-excitation, which becomes evident only during episodes of atrial fibrillation, is a very rare event. The authors report a case of ventricular pre-excitation revealed by an access of atrial fibrillation with high ventricular frequency and hemodynamic failure. The ventricular pre-excitation signs were not evident after the sinus rythm had been restored. The electrophysiological study has shown that such behaviour is not related to a different input of the stimulus in the bypass tract during the passage from the sinus rhythm to the atrial fibrillation, as other authors have recently suggested, but to rate-dependent variations of the conduction in the Kent bundle: in the bypass either a phase-4 block of the conduction is present, or a supernormal conduction.     

Nature of dual atrioventricular node pathways and the tachycardia circuit as defined by radiofrequency ablation technique.

OBJECTIVES. A comprehensive electrophysiologic study followed by selective radiofrequency ablation from three sites was performed in patients with atrioventricular (AV) node reentrant tachycardia to better delineate the nature of the tachycardia circuit. BACKGROUND. We postulated that the retrograde fast pathway is the anterior superficial group of transitional cells and the slow pathway is the compact node with its posterior input of transitional cells. Twenty-three consecutive patients were studied. In nine, the atria could be dissociated from the tachycardia by delivery of an atrial extrastimulus during tachycardia. METHODS. Radiofrequency ablation was performed with three approaches. The anterior approach was designed to interrupt the anterior superficial atrial input to the compact node, the posterior approach to interrupt the posterior atrial input to the compact node and the inferior approach to destroy the compact node itself. RESULTS. Selective ablation of the retrograde fast pathway was achieved in seven patients, six with the anterior and one with the inferior approach. Anterograde fast pathway conduction was not affected, whereas retrograde fast pathway conduction was either abolished or markedly depressed. None had induction of echoes or tachycardia after ablation. Selective ablation of the slow pathway was successful in 13 patients, 1 with anterior, 3 with posterior and 9 with inferior approaches. In these 13 patients, both anterograde and retrograde fast pathway conduction were not affected, the dual pathway physiology was abolished and the tachycardia was not inducible after ablation. Ablation of both the retrograde fast pathway and the slow pathway occurred with the inferior approach in three patients. CONCLUSIONS. We conclude that the retrograde fast pathway is likely to be the anterior superficial group of transitional cells, whereas the slow pathway is the compact node and its posterior input of transitional cells. A barrier seems to exist between the atrium and the tachycardia circuit. In a broad view of the AV node structure, the tachycardia circuit is confined to the node.     

Interrelationships between the autonomic nervous system and atrial fibrillation

Mechanisms responsible for atrial fibrillation are not completely understood but the autonomic nervous system is a potentially potent modulator of the initiation, maintenance, termination and ventricular rate determination of atrial fibrillation. Complex interactions exist between the parasympathetic and sympathetic nervous systems on the central, ganglionic, peripheral, tissue, cellular and subcellular levels that could be responsible for alterations in conduction and refractoriness properties of the heart as well as the presence and type of triggered activity, all of which could contribute to atrial fibrillation. These dynamic inter-relationships may also be altered dependent upon other neurohumoral modulators and cardiac mechanical effects from ventricular dysfunction and congestive heart failure. The clinical implications regarding the effects of the autonomic nervous system in atrial fibrillation are widespread. The effects of modulating ganglionic input into the atria may alter the presence or absence of atrial fibrillation as has been highlighted from ablation investigations. This article reviews what is known regarding the inter-relationships between the autonomic nervous system and atrial fibrillation and provides state of the art information at all levels of autonomic interactions.     

The role of electrical uncoupling in the genesis of atrioventricular conduction disturbance

The contribution of electrical uncoupling between the atrioventricular (A-V) nodal cells to the genesis of A-V nodal conduction disturbance was studied in isolated rabbit hearts. The electrical coupling was estimated by measuring the input resistance through a microelectrode. The A-V nodal conduction time was measured by recording atrial and His bundle electrograms (A-H interval).Treatment with ouabain (6.8 × 10^?7 m) for an hour increased the input resistance of the A-V nodal cells with a concomitant prolongation of the A-H interval. It also decreased the action potential amplitude, the maximal rate of depolarization, and the resting potential of these cells.High calcium perfusate containing 3.6 mm, 5.4 mm and 7.2 mm Ca increased the input resistance of the A-V nodal cells dose-dependently associated with a prolongation of the A-H interval. No significant change in the action potential configurations of the A-V nodal cells was caused by the high calcium perfusate.The increase in the input resistance of the A-V nodal cells under these conditions was considered to reflect an increase in the axial resistance which would cause a reduction in the electrical coupling. It is suggested that the reduction in the electrical coupling between the A-V nodal cells plays an important role in the genesis of the A-V nodal conduction disturbance caused by ouabain or high calcium perfusate.     

Rate-dependency of action potential duration and refractoriness in isolated myocytes from the rabbit AV node and atrium

During atrial fibrillation, ventricular rate is determined by atrioventricular nodal (AVN) conduction, which in part is dependent upon the refractoriness of single AVN cells. The aims of this study were to investigate the rate-dependency of the action potential duration (APD) and effective refractory period (ERP) in single myocytes isolated from the AV node and atrium of rabbit hearts, using whole cell patch clamping, and to determine the contribution of the 4-aminopyridine (4-AP)-sensitive current, I(TO1)to these relationships in the two cell types. AVN cells had a more positive maximum diastolic potential (-60+/-1 v-71+/-2 mV), lower V(max)(8+/-2 v 144+/-17 V/s) and higher input resistance [420+/-46 v 65+/-7 MOmega (mean+/-s.eP<0.05 n=9-33)], respectively, than atrial myocytes. Stepwise increases in rate from 75 beats/min caused activation failure and Wenckebach periodicity in AVN cells (at around 400 beats/min), but 1:1 activation in atrial cells (at up to 600 beats/min). Rate reduction from 300 to 75 beats/min shortened the ERP in both cell types (from 155+/-7 to 135+/-11 ms in AVN cells [P<0.05, n=6] and from 130+/-8 to 106+/-7 ms in atrial cells [P<0.05, n=10]). Rate increase from 300 to 480 and 600 beats/min shortened ERP in atrial cells, by 12+/-4% (n=8) and 26+/-7% (n=7), respectively (P<0.05). By contrast, AVN ERP did not shorten at rates >300 beats/min. In atrial cells, rate reduction to 75 beats/min caused marked shortening of APD(50)(from 51+/-6 to 29+/-6 ms, P<0. 05). 4-AP (1 m m) significantly prolonged atrial APD(50)at 75 beats/min (P<0.05, n=7), but not at 300 or 400 beats/min. In AVN cells, in contrast, there was less effect of rate change on APD, and 4-AP did not alter APD(50)at any rate. 4-AP also did not affect APD(90)or ERP in either cell type. In conclusion, a lack of ERP-shortening at high rates in rabbit single AVN cells may contribute to ventricular rate control. I(TO1)contributed to the APD(50)rate relation in atrial, but not AVN cells and did not contribute to the ERP rate relation in either cell type.     

Evidence against ANP as a natriuretic hormone during atrial distension

To determine whether natriuresis attributable to atrial natriuretic peptides (ANP) is obtained in response to atrial stretch after blockade of the afferent input and reflex diuresis from atrial receptors, urine flow and sodium excretion were measured in response to distension of a balloon in the left atrium with the vagi at 37 and 9 degrees C. It is known that during such a distension ANP plasma concentration is increased by the same amount whether or not the afferent vagal fibres are intact. In 11 chloralose anaesthetized dogs 22 distensions with the vagi at 37 degrees C increased urine flow 117.5% and increased sodium excretion 28.7%. In 11 distensions with the vagi at 9 degrees C, urine flow did not change but sodium excretion decreased significantly (-20.9%). Thus natriuresis could not be demonstrated in response to atrial stretch in anaesthetised dogs after blockade of the atrial receptor reflex. These results imply that under these conditions, in which ANP is reportedly released into plasma, ANP is not acting as a hormone. The results must call into question the suggestion that ANP is released into plasma in a concentration capable of causing a natriuresis as its normal physiological function.     

Electrophysiology of the Right Anterior Approach to the Atrioventricular Node:

Electrophysiology of Anterior AVN Input. Introduction: Previous reports have described electrophysiologic properties and rate-dependent responses in the transitional cell zone of the posterior AV nodal input (slow pathway). The purpose of this study was to investigate the electrophysiology of the anterior transitional cell zone (fast pathway) in vivo and in a Langendorff preparation perfused with a nonblood solution containing butanedionemonoxime to inhibit contraction. Methods and Results: In five anesthetized dogs, the His-bundle electrogram recorded from the aortic root included atrial activity in close proximity to the anterior limbus of the fossa ovalis. During decremental atrial pacing, the atrial potential exhibited amplitude alternans at a pacing cycle length (CL) of 135 ± 14 msec. In ten isolated pertused canine hearts, a bipctlar electrode catheter was positioned with its tip against the right anterior interatrial septum just superior to the tendon of Todaro. The AV Wenckebach CL (WCL) averaged 262 ± 21 msec. During further decreases in pacing CL, the bipolar atrial potential developed a 2:1 amplitude alternans (9/10 dogs) at CL = 168 ± 15 msec and then split into two components with subsequent 2:1 block between these components (10/10 dogs) at CL = 152 ± 19 msec. Radiofrequency ablation at this site in six dogs prolonged the stimulus to HB interval from 113 ± 19 to 151 ± 30 msec (P < 0.01) without changing the WCL, consistent with ablation of the fast AV nodal pathway. In six other isolated perfused canine hearts, an octapolar catheter (2-mm spacing) was positioned along the anterior limbus of the fossa ovalLs with the tip electrode located over the anterior portion (apex) of the triangle of Koch. The aforementioned 2:1 amplitude alternans occurred at a longer CL in the distal electrodes located at the tendon of Todaro than in the proximal electrodes at farther distances from the tendon of Todaro (185 ± 25 vs 171 ± 20 msec, P < 0.05), as did the 2:1 block between the two components (161 ± 18 vs 150 ± 18 msec, P < 0.05). Microelectrode recordings obtained adjacent to the catheter demonstrated 2:1 alternans and block patterns in the action potentials of transitional cells but not in atrial cells, which exhibited 1:1 conduction at all CL. Conclusions: The transitional cell zone in the anterior interatrial septum exhibits a specific rate-dependent, spatial gradient of conduction block, which can be recorded in bipolar electro-grams as well as microelectrode recordings. Electrophysiologic changes induced by radiofrequency ablation of this anterior atrial/transitional cell zone (corroborated by histology) provide strong presumptive evidence that this area constitutes all or a major part of the fast AV nodal pathway.     

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)     

Atrial compliance determines the nature of passive atrial stretch and plasma atrial natriuretic factor in the conscious dog.

STUDY OBJECTIVE--The aim was to measure changes in atrial wall function over a wide range of atrial filling pressures in order to determine the relationship governing the atrial stretch in vivo. DESIGN--Acute graded haemorrhage, 30 ml.kg-1, was used to reduce atrial stretch, and volume loading with 1000 ml saline was used to increase atrial stretch. EXPERIMENTAL MATERIAL--Awake mongrel dogs (n = 6) were instrumented for the measurement of left atrial appendage pressure and diameter; awake mongrel dogs (n = 4) were instrumented for measurement of left and right atrial appendage pressures and diameters. MEASUREMENTS AND MAIN RESULTS--During haemorrhage, left atrial pressure and diameter decreased progressively, and plasma atrial natriuretic factor fell from 44 (SEM 10) to 25(5) pg.ml-1 (p less than 0.05). Calculated left atrial wall stress and minute wall stress fell by 80(5.8)% and 72(15)% (p less than 0.05 from control). During volume expansion, however, atrial wall stress and minute wall stress markedly increased and plasma atrial natriuretic factor increased by more than 500%. The relationship between left atrial pressure and diameter was a typical exponential compliance curve during volume loading and haemorrhage for atrial systole, the A wave, and for atrial diastole, the V wave. During volume expansion right atrial pressure and diameter were also related exponentially. Left atrial passive stretch, as measured by V wave wall stress, increased more than right atrial stretch during volume loading. Changes in atrial filling in conscious dogs therefore result in typical exponential changes in atrial pressure and diameter in both atria. Plasma atrial natriuretic factor only increased at high filling pressures. The relationship between passive V wave minute wall stress and plasma atrial natriuretic factor also fitted an exponential curve. Thus when atrial filling was reduced, plasma atrial natriuretic factor fell by only 50% from control, while when atrial filling increased over the physiological range (up to 15 mm Hg left atrial pressure), it rose only to 100 pg.ml-1. CONCLUSIONS--Very high atrial appendage wall stresses are required to increase plasma atrial natriuretic factor markedly. Atrial stretch and the release of atrial natriuretic factor are non-linearly related. The stimulus for atrial natriuretic factor release is related to the exponential changes in atrial function due to the underlying atrial compliance relationship.     

阵发性心房颤动预测因素研究

目的　研究阵发性心房颤动 (PAF)的预测因素。方法　 PAF组 5 9例 ,对照组 31例。同步记录 12导联心电图 ,测量 P波离散度 (Pdis)、P波最大时限 (Pm ax) ;应用超声心动图测量左心房内径 ,计算左室心肌重量指数。结果　与对照组比较 ,PAF组 Pmax、Pdis、左房内径显著增大 (P<0 .0 1) ;Pmax与左房内径和左室心肌重量指数呈正相关 (r =0 .2 6 ,P <0 .0 5 ;r =0 .2 7,P <0 .0 5 ) ;结论　左房内径和 Pm ax为 PAF的独立预测指标 ,P波宽度与左房内径扩大和左室心肌重量指数增加有关。     

Impact of volume status on the incidence of atrial fibrillation following aortic arch repair

We evaluated the volume status of patients undergoing aortic arch repair to determine the impact of fluid balance on risk of postoperative atrial fibrillation (AF). From 1993, 445 patients who underwent total aortic arch repair were enrolled in this study. Patients who had AF preoperatively or died within the 10th postoperative day (POD) were excluded. Volumes administered (input) and eliminated (output) through all routes were recorded, and fluid balance (input minus output) was calculated intraoperatively, on the day of surgery, and PODs 1–2. The incidence of new onset of AF was 53.9% (240/445). Total input on POD 1 was greater in patients developing AF than in those not developing it (3 372 ± 90 vs 3 012 ± 79; P = 0.0036), as was net fluid balance on POD 1 as well (−806 ± 84 vs −558 ± 90; P = 0.050). Blood transfusion volume was greater in patients developing AF than in those not developing it on POD 1 (1 285 ± 89 vs 927 ± 74; P = 0.003) and POD 2 (405 ± 53 vs 227 ± 47; P = 0.015). Increased input volume and net fluid balance on POD 1 are associated with an increased risk of postoperative AF in patients undergoing aortic arch surgery.