Revisiting right atrial isolation rationale for atrial fibrillation: functional anatomy of interatrial connections

Introduction

Direct catheter ablation for atrial fibrillation does not yield reproducible permanent control as for other atrial arrhythmias. Therefore, there is a need for an alternative intervention, i.e., left atrial exclusion, based on elective ablation of the interatrial connecting bundles.

Methods and results

We describe the “operative anatomy” of the three major interatrial connections: the Bachmann bundle, the coronary sinus bundle, and the left atrial-atrioventricular node connection, based on macroscopic dissections of human and porcine hearts and our previous experience. We identified the three right atrial attachments, with the coronary sinus (CS) and left atrial (LA)–atrioventricular (AV) nodal connection being most problematic for safe ablation.

Conclusions

To obtain a complete isolation of the left from the right atrium, all three connections must be ablated. The CS connection must be ablated distal to the ostium. If present, the LA–AV nodal connection can be safely ablated from the left atrium.     

Subcostal M-mode echocardiography of the right atrial wall in the diagnosis of cardiac arrhythmias

The M-mode echocardiogram of the right atrial (RA) wall can be easily recorded in each person from the subcostal location. In a normal RA wall motion pattern, atrial contraction is represented by a markedly prominent posterior motion. The presence or absence of atrial contractions in the subcostal RA wall echocardiogram, their amplitude, and their timing may help in the diagnosis of cardiac arrhythmias with the simultaneously recorded non-diagnostic electrocardiogram. Flat and hidden P waves can be accurately identified throughout the cardiac cycle. It is possible to distinguish between atrial, ventricular, and nodal premature beats and to recognize atrial fibrillation, atrial flutter, paroxysmal atrial tachycardia, paroxysmal atrial tachycardia with block, atrioventricular (AV) nodal tachycardia, and supraventricular tachycardias with aberrant ventricular conduction. The diagnosis of wandering pacemaker, AV dissociation, sinoatrial block, and AV block is facilitated. On the basis of study of 60 patients with various rhythm disturbances, it was concluded that analysis of the subcostal RA wall echocardiogram is a new, helpful noninvasive approach in the diagnosis of cardiac arrhythmias.     

Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion

Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second- or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac rhythm in atrial isomerism

Standard electrocardiograms from 126 consecutive patients with atrial isomerism were reviewed. Of 67 patients with left isomerism, 49 had sinus rhythm, 8 nodal rhythm and 10 atrioventricular (AV) block. Fifty-eight of 59 patients with right isomerism had sinus rhythm. Complete AV block was significantly more frequent in association with AV septal defect in left isomerism (5 of 45 patients) than in right isomerism (0 of 47 patients, p = 0.049). The P-wave axis was superior in 49% of patients with left isomerism but did not correlate with abnormalities of systemic or pulmonary venous connection. A significant shift of P-wave axis (more than 90 degrees) was seen on a subsequent electrocardiogram in 14 of 44 patients (32%) with left isomerism and 2 of 16 (13%) with right isomerism. Ambulatory electrocardiographic monitoring in 17 patients (14 with left isomerism) showed that only 4 had sinus rhythm throughout 24 hours. Only 1 patient with complete AV block received a permanent pacemaker. Despite the high incidence of electrocardiographic abnormalities, significant arrhythmias appear to be rare. The arrhythmias apparently do not influence the natural history of this condition or affect the outcome of palliative or corrective surgery. The prognosis is determined mainly or solely by the associated anatomic abnormalities.     

心电图J／R比值对下壁心肌梗死并发房室阻滞的预测价值

目的探讨急性下壁心肌梗死早期心电图表现对高度房室阻滞的预测价值以及与冠状动脉病变的关系。方法分析97例急性下壁心肌梗死患者早期心电图（下壁导联）J／R≥0．5的发生情况，部分病例结合冠脉造影结果，探讨其对房室阻滞的预测价值。结果27例（21．6％）在心肌梗死急性期发生二度以上房室阻滞。有房室阻滞者，心电图下壁导联J／R≥0．5多于无房室阻滞者（69．56％vs30．44％，p〈0．01）。冠状动脉造影显示，有房室阻滞者，右冠状动脉近中段的高度狭窄明显多于无房室阻滞者（100％vs58．33％）。结论急性下壁心肌梗死伴房室阻滞者的病损冠脉以右冠状动脉多见，下壁导联心电图J／R≥0．5对下壁心肌梗死合并房室阻滞的发生有一定的预测价值。     

Effect of sequential radiofrequency ablation lesions at fast and slow atrioventricular nodal pathway positions in patients with paroxysmal atrial fibrillation.

OBJECTIVE: To examine the hypothesis that the anatomic equivalents of the fast and slow pathways identified in patients with atrioventricular (AV) nodal tachycardia may be universal and represent the principal sites of atrial input into the normal compact AV node. METHODS: 15 patients undergoing complete AV junction ablation for paroxysmal atrial fibrillation were studied. Radiofrequency energy was delivered first in the anterior "fast pathway" position so as to prolong the atrium to bundle of His (AH) interval by over 50% of baseline (protocol 1) and then to the "slow pathway" position using the anatomical technique (protocol 2). RESULTS: Ablation protocol 1 resulted in prolongation of AH interval in all patients. Subsequent lesions at the level of the coronary sinus produced complete heart block in four patients, and in five caused a further increase in AH interval above that produced by protocol 1. Four of these latter patients developed complete block after delivery of RF energy slightly anterior to the level of the coronary sinus os, as did three further patients in whom ablation at the level of the coronary sinus had no effect. In four patients complete heart block could not be achieved by protocol 2. CONCLUSIONS: A discrete anterior "fast" pathway and a posterior "slow" pathway or network of posterior pathways form the principal inputs to the compact AV node in most patients with atrial fibrillation. The absence of dual AV nodal physiology in the majority of these patients may be related to the functional properties of the individual components of this posterior network.     

Ionic basis of a differential effect of adenosine on refractoriness in rabbit AV nodal and atrial isolated myocytes

OBJECTIVES: Firstly, to compare effects of adenosine on membrane potential and refractoriness in AV nodal and atrial cells. Secondly, to assess the contribution of the effects of adenosine on IKAdo and ICaL to its effects on the functional electrophysiological properties in the two cell types. METHODS: The whole cell patch clamp technique was used to record action potentials and ion currents in AV nodal and left atrial myocytes isolated enzymatically from rabbit hearts. RESULTS: Adenosine (10 microM) caused similar hyperpolarisation and shortening of the action potential duration (APD) in both cell types: maximum diastolic potential was hyperpolarised from -59 +/- 3 to -66 +/- 2 and from -70 +/- 2 to -76 +/- 2 mV (mean +/- SEM) and APD90 was shortened by 31 +/- 4 and 30 +/- 7% in AV nodal (n = 14) and atrial cells (n = 8), respectively. Adenosine shortened the effective refractory period (ERP) in atrial cells, from 124 +/- 15 to 98 +/- 14 ms (n = 8). In contrast, ERP in AV nodal cells was not significantly affected (112 +/- 13 vs. 102 +/- 12 ms, n = 14), and post-repolarization refractoriness was prolonged. By contrast, current injection, to induce an equal degree of hyperpolarisation to that produced by adenosine, shortened APD and ERP in both cell types, suggesting an additional action of adenosine in AV nodal cells. Adenosine (10 microM) did not affect peak ICaL in AV nodal cells, but significantly altered the biexponential time course of recovery of ICaL from inactivation. The proportion of recovery in the fast phase (time constant, tau = 102 +/- 10 ms) was reduced from 71 +/- 3 to 55 +/- 5%, with shift to the slow phase (tau = 858 +/- 168 ms), without altering tau in either phase. A similar effect of adenosine was seen in left atrial cells. CONCLUSION: Adenosine caused hyperpolarisation, APD-shortening and slowing of recovery of ICaL from inactivation, in both AV nodal and atrial cells, but prolonged post-repolarisation refractoriness in AV nodal cells only. This differential effect of adenosine on refractoriness in the two cell types could not be explained by effects on IKAdo, but may be due to slowed reactivation of ICaL, which is the predominant inward current in AV nodal but not left atrial cells.     

Gene dose-dependent atrial arrhythmias, heart block, and brady-cardiomyopathy in mice overexpressing A(3) adenosine receptors

OBJECTIVE: An increased expression of adenosine receptors is a promising target for gene therapy aimed at protecting the myocardium against ischemic damage, but may alter cardiac electrophysiology. We therefore studied the effects of heart-directed overexpression of A(3) adenosine receptors (A(3)ARs) at different gene doses on sinus and atrio-ventricular (AV) nodal function in mice. METHODS AND RESULTS: Mice with heart-specific overexpression of A(3)AR at high (A(3)(high)) or low (A(3)(low)) levels and their wild-type littermates were studied. Telemetric electrocardiogram (ECG) recordings in adult freely moving A(3)(high) mice showed profound sinus bradycardia resulting in either ventricular escape rhythms or an incessant bradycardia-tachycardia syndrome (minimal heart rate A(3)(high) 217+/-25*; WT 406+/-21 beats/min, all values as mean+/-S.E.M., n=7 per genotype, *p<0.05). Exercise attenuated bradycardia in A(3)(high) mice (maximal heart rate A(3)(high) 650+/-13*; WT 796+/-13 beats/min) and first-degree AV nodal block was present (PQ interval A(3)(high) 36+/-4*; WT 23+/-5 ms). Isolated hearts showed complete heart block (10/17 A(3)(high)* vs. 1/17 WT). Atrial bradycardia and AV block were already present 3 weeks after birth. Doppler echocardiography revealed atrial dysfunction and progressive atrial enlargement that was moderate at 3 and 8 weeks, and progressed at 12 and 21 weeks of age (all p<0.05 vs. WT). Atrial contractility and sarcoendoplasmic Ca(2+) ATPase (SERCA) 2a protein expression were reduced in isolated left A(3)(high) atria at the age of 14 weeks. Fibrosis was present in left A(3)(high) atria at 14 weeks, but not at 5 weeks of age. A(3)(low) mice had first-degree AV block without arrhythmias or structural changes. CONCLUSIONS: Heart-directed overexpression of A(3)AR resulted in gene dose-dependent AV block and pronounced sinus nodal dysfunction in vivo. Profound bradycardia heralded atrial and ventricular dilatation, dysfunction, and fibrosis. In contrast to A(1) adenosine receptors (A(1)AR), the effects of A(3)AR overexpression were attenuated during exercise. This may have implications for the physiology of sinus nodal regulation and for therapeutic attempts to increase the expression of adenosine receptors.     

Prevalence of atrial arrhythmia in 48 hypertensive patients: research of predictive criteria]

We studied atrial arrhythmias during a continue prospective work in 48 hypertensive patients referred to the OMS criteria. Hypertension was confirmed by a blood pressure ambulatory monitoring and stress testing blood pressure trend. All cardiovascular drugs were stopped at admission. Patients with associated valvular or coronary artery disease were excluded from analysis. In all patients, we realized a twelve lead-ECG, stress testing, 24 hour Holter monitoring, a blood pressure ambulatory monitoring, two-dimensional echocardiography with Doppler study and cardiac radio-nuclide angiography with diastolic function study. Atrial arrhythmias were considered significant if more than 100 premature atrial beats (PAB) and/or more than three successive PAB were present during Holter monitoring. Significant atrial arrhythmias were found in 39.5% of patients (group II, n = 19), not significant in 60.5% of patients (group I, n = 29). The duration of hypertension was longer in group II (140 vs 66 months, p < 0.05). There was no difference between the two populations considering left atrial size or blood pressure level. Furthermore, we were surprised to find a normal E/A ratio on mitral Doppler recording in patients with atrial arrhythmias (1.23 vs 0.9; p < 0.05). Others diastolic parameters didn't significantly differ. Left ventricular mass index was similar in the two groups but patients with atrial arrhythmias had more asymmetric hypertrophy (1.23 vs 1.13 septum/posterior wall ratio: p < 0.05). Conclusion: atrial arrhythmias in our study seem to be more dependent from duration of HTA and left ventricular asymmetric structure than from left atrial size.(ABSTRACT TRUNCATED AT 250 WORDS)     

Advanced early and late atrioventricular block in acute inferior wall myocardial infarction

Seventy-six patients with acute inferior acute myocardial infarction (AMI) and advanced atrioventricular (AV) block are described. According to pre-established ECG criteria and time of appearance of the advanced AV block, patients were divided into two groups. The early block group consisted of 31 patients who developed advanced AV block during the hyperacute ECG stage of AMI. Advanced AV block in these patients was characterized by early appearance, short duration, third-degree type block, poor response to atropine, and increased need for pacemaker therapy. The late block group consisted of 45 patients who developed advanced AV block during subsequent ECG stages of AMI. Advanced AV block in these patients was characterized by late appearance, longer duration, second-degree type block, positive response to atropine, and diminished need for pacemaker therapy. Morbidity and mortality also differed between both groups. Patients with early block had more syncope (32% vs 2%, p < 0.0001), more left heart failure (36 vs 7%, p < 0.005), and more cardiogenic shock (39% vs 2%, p < 0.001) than patients with late block. The mortality rate in the early block group was high (23%) and similar to that reported in the literature, whereas the mortality rate in the late block group was low (7%, p < 0.05) and similar to the mortality rate reported for acute inferior AMI without advanced AV block. These data identify a subgroup of patients with acute inferior AMI and advanced AV block, which accounts for the high mortality rate reported in this group of patients.     

Change in the retrograde atrial activation sequence following radiofrequency modification of the atrioventricular node: implications for the electrophysiologic circuit of a variant of atrioventricular nodal reentrant tachycardia

INTRODUCTION: Despite the great success in treating AV nodal reentrant tachycardia (AVNRT) with radiofrequency modification of the AV node, the dimensions of the electrophysiologic circuit of this arrhythmia remain unclear, and simple models fail to explain all tachycardia-related phenomena. METHODS AND RESULTS: We describe three unusual cases of supraventricular tachycardia (SVT). In all three cases, retrograde atrial activation during ventricular pacing or during SVT manifested local left atrial electrograms recorded from the coronary sinus preceding the septal atrial electrograms (eccentric activation), with earliest atrial activity at the lateral or posterolateral mitral annulus. Electrophysiologic maneuvers and observations were consistent with AVNRT as the mechanism in each case. In all cases, radiofrequency modification of the AV node eliminated inducible SVT and abolished dual pathway AV nodal physiology. The retrograde atrial activation sequence during ventricular pacing changed after ablation in each case, with septal atrial electrograms preceding left atrial electrograms recorded from the coronary sinus (concentric activation). CONCLUSION: The observations in these cases cannot be explained by the traditional model of slow, fast, and intermediate AV nodal pathways. A model incorporating a circuit close to the AV node with left atrial and coronary sinus connections is proposed.     

Cryoablation in pediatric atrioventricular nodal reentry: Electrophysiologic effects on atrioventricular nodal conduction

BACKGROUND: Cryoablation for treatment of atrioventricular nodal reentrant tachycardia (AVNRT) is safe and efficacious. Information on the effects of cryoablation on atrioventricular (AV) nodal conduction is limited. OBJECTIVES: The purpose of this study was to evaluate the effects of cryoablation on AV nodal conduction in pediatric patients with AVNRT. METHODS: We retrospectively analyzed electrophysiologic studies before and after successful cryoablation. Patients were divided into two groups: group 1 (n = 22, age 14 +/- 3 years) had baseline discontinuous atrial-to-His interval (AH) conduction curves; and group 2 (n = 13, age 12 +/- 4 years, P = .054) had continuous curves. RESULTS: At baseline, group 1 had longer measurements of maximal AH with A1A2, AV nodal effective refractory period, and AV block cycle length. Postcryoablation, both group 1 and group 2 showed decreases in maximal AH with A1A2 pacing or atrial overdrive pacing and in the finding of PR > or = RR with atrial overdrive pacing (group 1: 55% vs 5%, P < .001; group 2: 69% vs 0%, P < .001). A significant increase in overall AV effective refractory period and a decrease in AV block cycle length were found in group 1 but not group 2. Fifty percent of group 1 patients had complete abolition of slow pathway conduction. CONCLUSION: Successful cryoablation for treatment of AVNRT is associated with a reduction in PR > or = RR and with decreases in maximal AH with A1A2 pacing or atrial overdrive pacing. Further study is needed to determine the usefulness of these parameters for assessment of ablation efficacy or as proxies for AVNRT inducibility.     

Randomized comparison of two targets in typical atrial flutter ablation

Typical atrial flutter ablation has become anatomically guided to 2 separate sites within the isthmus at the inferior right atrium: (1) between the inferior vena cava and the tricuspid annulus (anterior side of the isthmus [A]), (2) between the eustachian crest, the coronary sinus ostium and tricuspid annulus (posterior side of the isthmus [P]). We prospectively compared ablation results at these sites in 72 consecutive patients. Patients were randomized in group P or A according to the initial target site. If ablation failed at 1 site after 15 radiofrequency (RF) pulses, the other side of the isthmus was targeted. Before 15 RF pulses, complete bidirectional isthmus block was achieved in 30 of 36 group A patients and in 25 of 36 group P patients, with similar mean RF pulses number, procedure time, and fluoroscopy time. After shifting to the other target, success was finally obtained at P in 2 of 6 group A patients, and at A in 8 of 11 group P patients before a maximum of 30 RF pulses. Among successful patients, number of RF pulses, procedure time, and fluoroscopy time were significantly lower in group A (7.2 +/- 5.4 vs 11.0 +/- 8.1 pulses, p = 0.03; 131 +/- 44 vs 163 +/- 66 minutes, p = 0.03; 31 +/- 19 vs 46 +/- 24 minutes, p = 0.01, respectively). Impairment of atrioventricular (AV) nodal conduction occurred in 5 patients only during ablation at P. AV block was transient in 4 patients and permanent in 1. Although atrial flutter ablation is equally effective at P and A, success seems easier to obtain when A is first targeted. Ablation at P is associated with a significant risk of AV block.     

Arrhythmias in Children Having a Single Left Superior Vena Cava and Minimal Structural Heart Disease

Background: The presence of a single left superior vena cava in the absence of complex congenital heart disease is uncommon, and, in the absence of hemodynamic consequences, it would not be expected to result in cardiovascular signs or symptoms. Single case reports and our anecdotal experience suggested to us that this anomaly is highly associated with cardiac arrhythmias.
Objective: We sought to describe the clinically important arrhythmias in a population of young patients having this anomaly.
Methods: A retrospective chart review was performed from all patients <20 years old and who were determined by echocardiography over an 11-year-period to have a single left superior vena cava and minor or no coexisting congenital heart defects. The prevalence of nonsinus pacemaker, age-corrected sinus rate percentile, and prevalence of brady- or tachyarrhythmias was compared with a control group of patients having bilateral superior vena cavae.
Results: Eight patients having a single left and 55 patients having bilateral superior vena cava(e) were identified. The existence of this anomaly tended to be associated with a lower age-corrected sinus rate percentile (17.5% vs 75%, P = 0.09), and was associated with a higher prevalence of arrhythmias (50% vs 7%, P = 0.014) compared with the control group. In the study group, one patient each had clinically relevant sinus node dysfunction, third-degree AV block, Wolff-Parkinson-White syndrome and atrial fibrillation, and AV nodal reentrant tachycardia.
Conclusion: Even in the absence of symptoms, patients found to have a single left superior vena cava should be monitored long-term for clinically important arrhythmias.     

Characterization of Sinoatrial Parasympathetic Innervation in Humans

INTRODUCTION: The response to sinoatrial parasympathetic nerve stimulation (shortened atrial refractoriness) was used to determine the atrial distribution of these nerve fibers in humans. We hypothesized that, in humans, parasympathetic nerves that innervate the sinoatrial node also innervate the right atrium and that the greatest density of innervation is near the sinoatrial nodal fat pad. METHODS AND RESULTS: Temporary epicardial wire electrodes were sutured in pairs in the sinoatrial nodal fat pad, high right atrium, and right ventricle by direct visualization during coronary artery bypass surgery in nine patients. Appropriate electrode placement was confirmed by electrically stimulating the fat pad in the operating room to prolong sinus cycle length by 50%. Experiments were performed in the electrophysiology laboratory 1 to 5 days after surgery. Programmed atrial stimulation was performed via an endocardial electrode catheter advanced to the right atrium. The catheter tip electrode was moved in 1-cm concentric zones around the epicardial wires by fluoroscopic guidance. Atrial refractoriness was determined in the presence and absence of sinoatrial parasympathetic nerve stimulation at each catheter site. In 8 of 9 patients, parasympathetic nerve stimulation reproducibly prolonged sinus cycle length by 50%. There was no effect on AV nodal conduction (no prolongation of PR interval) and no change in AV nodal refractoriness. Atrial effective refractory periods reproducibly shortened in response to parasympathetic nerve stimulation in 1-cm zones up to 3 cm surrounding the fat pad, by a mean (+/- SEM) of 26.6+/-4.3 msec (zone 1), 11.4+/-1.8 msec (zone 2), and 10.0+/-2.5 msec (zone 3), respectively (P = 0.0001). At distances > 3 cm from the fat pad, the effective refractory period did not shorten. CONCLUSION: Stimulation of parasympathetic nerves that innervate the sinoatrial node shortened atrial refractoriness in humans.     

Regular supraventricular tachycardias associated with idiopathic atrial fibrillation

The present study analyzed the recurrence rate of idiopathic atrial fibrillation (AF) after elimination by radiofrequency ablation of the substrate for a regular tachycardia. Forty consecutive patients with idiopathic AF and a history of regular palpitations or documented regular tachyarrhythmias were prospectively included. Regular tachyarrhythmias were induced in 82.5% of patients: atrial flutter (42.4% of the inducible arrhythmias), atrial tachycardia (24.2%), atrioventricular (AV) nodal reentry (18.2%), AV reentry through a concealed accessory pathway (9.1%), and AV nodal reentry associated with right atrial tachycardia (6.1%). Dual AV node physiology with single or dual AV node echoes was demonstrated in 6.1% of patients without inducible arrhythmias. During follow-up (92 +/- 11 months), AF recurred in 19.2% of patients after successful radiofrequency ablation and in 69.2% after unsuccessful or not performed procedures (p <0.05). Left atrial diameter did not change after successful ablation but increased significantly in the population without elimination of the substrate (initial diameter 37.5 +/- 2 mm, final diameter 46.4 +/- 3.2 mm; p <0.05). In conclusion, the systematic search for the substrate of regular tachyarrhythmias followed by their elimination by catheter ablation reduces the recurrence of idiopathic AF in patients with a history of regular palpitations or documented regular tachyarrhythmias.     

Phasic coronary blood flow velocity pattern and flow reserve in the atrium: regulation of left atrial myocardial perfusion

OBJECTIVES: The purpose of this study was to assess rest and stress atrial coronary blood flow (CBF) velocity and flow reserve. BACKGROUND: Because of the limitations of the methods used until now for assessing myocardial perfusion (MP) in the small mass of atrial tissue, data are lacking for human atrial MP. METHODS: Seventeen patients with suitable coronary anatomy underwent CBF velocity measurements with the use of a Doppler guide wire in the proximal left circumflex coronary artery (LCx) and left atrial circumflex branch (LACB), at baseline and after adenosine administration. All measurements were performed at resting heart rate and at 100 and 120 beats/min. RESULTS: Coronary blood flow velocity in the LACB showed a predominant systolic pattern in contrast to the diastolic pattern of the LCx. There was a disproportionate increase in baseline time-averaged peak coronary flow velocity (cm/s) between the LACB and LCx during the two levels of pacing-induced stress (16.8 +/- 5.5 vs. 16.2 +/- 5.1 at rest; 22.9 +/- 7.9 vs. 18.4 +/- 5.2 at 100 beats/min; and 27.1 +/- 8.0 vs. 20.4 +/- 5.1 at 120 beats/min; significant interaction, p < 0.001), but there were no significant differences in coronary flow reserve (CFR). CONCLUSIONS: Coronary blood flow in the left atrium is out of phase with that in the ventricular myocardium, showing a predominant systolic pattern. Although atrial and ventricular CFR show no significant differences at rest and with two levels of stress, the disproportionate increase in atrial blood flow velocity during stress indicates a peculiarity of atrial perfusion regulation.     

Irregularity of the ventricular rhythm during atrial fibrillation: effect of slow atrioventricular nodal pathway ablation.

BACKGROUND: The contribution of dual atrioventricular (AV) nodal pathway physiology to the irregularity of the ventricular rhythm during atrial fibrillation has not been clarified. HYPOTHESIS: This study was performed to assess the effects of slow AV nodal pathway ablation on the irregularity of the ventricular rhythm during atrial fibrillation. METHODS: Irregularity of the ventricular rhythm was quantified using analysis of heart rate variability. In 20 patients with AV nodal reentrant tachycardia, absolute heart rate variability during atrial fibrillation was quantified before and after slow AV nodal pathway ablation by the standard deviation of all NN intervals (SDNN). Relative heart rate variability was determined by computing the coefficient of variation, SDNN normalized for the standard deviation of the mean ventricular cycle length (MVCL-AF). RESULTS: The slope of the regression between MVCL-AF and SDNN was significantly more gradual after slow pathway ablation (slope 0.39 vs. 0.23, p < 0.001). Coefficient of variation increased in 12 patients with heart rates > 120 beats/min at baseline (18.6 +/- 3.9 vs. 22.1 +/- 2.7% MVCL-AF, p < 0.05), but decreased in 8 patients with heart rates < 120 beats/min at baseline (25.6 +/- 3.1 vs. 22.2 +/- 2.2% MVCL-AF, p = 0.05). Furthermore, coefficient of variation correlated with MVCL-AF only at baseline (slope 0.034, r = 0.66), but no relation was found after slow pathway ablation (slope 0, r = 0). CONCLUSIONS: Slow AV nodal pathway ablation alters the relation between absolute heart rate variability and mean ventricular rate during atrial fibrillation and eliminates cycle length dependency of relative heart rate variability. These data indicate that dual AV nodal pathway physiology contributes to the irregularity of the ventricular rhythm during atrial fibrillation.     

Development of sinus node disease in patients with AV block: implications for single lead VDD pacing

OBJECTIVE: To investigate the incidence of sinus node disease after pacemaker implantation for exclusive atrioventricular (AV) block. DESIGN: 441 patients were followed after VDD (n = 219) or DDD pacemaker (n = 222) implantation for AV block over a mean period of 37 months. Sinus node disease and atrial arrhythmias had been excluded by Holter monitoring and treadmill exercise preoperatively in 286 patients (group A). In 155 patients with complete AV block, a sinus rate above 70 beats/min was required for inclusion in the study (group B). Holter monitoring and treadmill exercise were performed two weeks, three months, and every six months after implantation. Sinus bradycardia below 40 beats/min, sinoatrial block, sinus arrest, or subnormal increase of heart rate during treadmill exercise were defined as sinus node dysfunction. RESULTS: Cumulative incidence of sinus node disease was 0.65% per year without differences between groups. Clinical indicators of sinus node dysfunction were sinus bradycardia below 40 beats/min in six patients (1.4%), intermittent sinoatrial block in two (0.5%), and chronotropic incompetence in five patients (1.1%). Only one of these patients (0.2%) was symptomatic. Cumulative incidence of atrial fibrillation was 2.0% per year, independent of the method used for the assessment of sinus node function and of the implanted device. CONCLUSIONS: In patients undergoing pacemaker implantation for isolated AV block, sinus node syndrome rarely occurs during follow up. Thus single lead VDD pacing can safely be performed in these patients.     

Intermittent Preexcitation and Mesothelioma of the Atrioventricular Node: A Hitherto Undescribed Entity

Mesothelioma of AV Node with WPW. This is the first documented case of spontaneous intermittent preexcitation associated with mesothelioma of the atrioventricular (AV) node. A 66-year-old male with recurrent atrial arrhythmias, palpitations, heart failure, and marked intra-atrial conduction defect that required a pacemaker died during sleep. Electrophysiologic study revealed left free-wall bypass tract with marked intra-atrial conduction defect and prolonged conduction across the bypass tract. With atrial pacing, high degrees of block were noted in the bypass tract. Serial section of the conduction system and both AV rims revealed two left posterior and lateral bypass pathways with patchy areas of fibrosis. A large mesothelioma (benign AV nodal tumor) almost completely replaced the AV node. In addition, there was marked fatty infiltration of the atria. In summary: (1) the intermittent preexcitation with prolonged conduction across the bypass tract and block with atrial pacing were probably related to the incomplete patchy degenerative changes in the bypass tract, and/or almost complete replacement of the AV node by the tumor; (2) the intra-atrial conduction defect was probably related to the replacement of the AV node by mesothelioma and/or the fatty infiltration of the atria: and (3) the paroxysmal atrial arrhythmias probably reflect the marked atrial pathology.