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Intracavitary electrogram (IEGM) is a useful tool in the interpretation of difficult pacemaker electrograms. A case of 320 ms P-V spike interval on the surface ECG despite a 110 ms programmed sensed AV delay is presented. Atrial IEGM revealed atrial tachycardia with a significant atrial conduction delay.
We describe a case of abnormal right atrial (RA) conduction in a patient with atrial tachycardia (AT) but no history of structural heart disease or cardiac surgery. Following ablation of AT, the patient experienced typical atrial flutter (AFL) and a postcardioversion ECG suggestive of low atrial rhythm. Repeat EPS and three-dimensional electroanatomic activation mapping showed unusual RA activation during SR. This case illustrates the possibility that abnormal intraatrial conduction may lead to unusual patterns of activation in the RA which can serve as a necessary substrate for the initiation and maintenance of macro-reentry circuits.
BACKGROUND: Radiofrequency (RF) catheter ablation is the procedure of choice for the potential cure of atrioventricular nodal reentrant tachycardia (AVNRT) with high success rates. We hypothesed that as a result of the close proximity of Koch's triangle and low inter-atrial septal fibers, the RF ablation applied at this region may result in prolongation of inter-atrial conduction time (IACT). METHODS: RF ablation of AVNRT was performed by conventional technique. IACT was measured before and 20 minutes after RF ablation during sinus rhythm. Number of ablations given and duration of ablation were noted. RESULTS: The study group was consisted of 48 patients (36 [75%] female, 12 [25%] male, mean age 43.4 +/- 14. 5 years). RF ablation was successful in all patients. Mean RF time was 4. 0 +/- 3. 3 minutes and mean number of RF was 11. 9 +/- 9, 8. The mean IACT was 70.1 +/- 9.0 ms before ablation and 84.9 +/- 12.7 ms after ablation, which demonstrated a significant prolongation (p<0.001). The prolongation of IACT was very well correlated with the number of (r=0.897, p<0.001) and duration of RF (r=0.779; p<0.001). CONCLUSIONS: RF ablation of AVNRT results in prolongation of IACT. The degree of prolongation is associated with the duration and number of RF ablations given. The relationship between this conduction delay and late arrhythmogenesis need to be evaluated.
A haemodynamic and M mode echocardiographic study of 57 patients hospitalised for chronic, symptomatic 2nd or 2rd degree AV block was carried out after 3 periods of pacing, each lasting 2 hours : 1) sequential AV pacing ( SAV ) with a 200 ms delay, considered as the mode of reference; 2) sequential ventriculo-atrial pacing ( SVA ) with the same sequential delay, recreating equivalent conditions of 1/1 ventriculo-atrial conduction (VAC); 3) ventricular pacing (V) recreating complete AV dissociation ( CAVD ). The pacing rate was the same for each patient (89 +/- 9/min). In comparison with SAV , SVA caused much worse haemodynamic changes than V : large increases in mean atrial pressures (+161% and +64% in RAP and PCP respectively); "canon" atrial A waves which were poorly tolerated (mean amplitude 14 mmHg and 18 mmHg on the RA and PCP waves respectively); in some cases, a large fall in blood pressure was observed due to the failure of systemic resistances to increase and compensate for the constant decrease in pump function (mean reduction of 23% of cardiac index; 29% of LV work index). These changes are much more pronounced in diseased than in healthy hearts, especially in the presence of mitral or tricuspid regurgitation. Echocardiography showed the main cause of these haemodynamic changes to be a reduction in ventricular filling with significant reductions in LV systolic and diastolic dimensions, changes in the mitral valve echos (reduction in the opening and closing velocities, delayed closure), probably related to a decrease in transvalvular blood flow, and decreased regional contractility of the interventricular septum. These observations justify an increase in the indications of modes of pacing maintaining permanent atrio-ventricular sequence (VVI pacing at slow rates; AAI pacing, DVI or DDD pacing in cases of abnormal AV conduction with VAC, especially in cases of sick sinus syndrome with permanent bradycardia). These modes of pacing are particularly beneficial when the electrical abnormality is associated with a decompensated cardiac lesion, or with decreased ventricular compliance or mitral regurgitation.
A patient with the sick-sinus syndrome was evaluated because of symptomatic deterioration after insertion of a ventricular demand pacemaker. Clinical features of the ventricular pacemaker syndrome were recognized and confirmed by electrophysiological and hemodynamic studies. Phase analysis--a new technique for detecting patterns of cardiac emptying from gated cardiac blood-pool scintigrams--demonstrated a pattern consistent with 1:1 ventriculo-atrial conduction. Phase analysis of the gated cardiac blood-pool scintigram may be useful in the assessment of patients with ventricular demand pacemakers who complain of fatigue and effort intolerance.
BACKGROUND: Vascular endothelial growth factors (VEGFs) and their receptors are essential regulators of vasculogenesis and angiogenesis in both embryos and adults. One of the factors with a still unknown physiological function is VEGF-B, which is expressed in many tissues, including the heart. METHODS AND RESULTS: Mice carrying a targeted deletion in the VEGF-B gene were developed. In VEGF-B(-/-) animals, no gross abnormalities were observed in organs that normally show high expression of VEGF-B, such as the heart, muscle, and kidney. Analysis of heart function by ECG showed that adult VEGF-B(-/-) mice have an atrial conduction abnormality characterized by a prolonged PQ interval. VEGF- or basic fibroblast growth factor-induced corneal angiogenesis was similar in normal and VEGF-B(-/-) mice. CONCLUSIONS: VEGF-B seems to be required for normal heart function in adult animals but is not required for proper development of the cardiovascular system either during development or for angiogenesis in adults.
A 82-years-old man, symptomatic for fatigue and lypothymia, was referred to our centre in order to evaluate the opportunity of a permanent pacemaker insertion. A 12-lead ECG was described as a Mobitz type II second-degree atrioventricular block with 2:1 conduction. This surface ECG revealed some sinus beats with normal AV conduction, everyone followed by a bizarre, non-conducted P' wave, inscripted in the previous T wave. The Holter ECG showed a sinus rhythm with a mean rate of 70 beats/minute: during the night and at 06:39 pm of the following day, ECG strip showed some sinus beats, everyone followed by an atrial non-conducted ectopic beat, characterized by prematurity and abnormal shape (P' wave), that appears as a small deformation on the preceding T wave. At the beginning and the end of the strip we can estimate respectively 9 and 4 sinus beats, that represent the normal rhythm of this patient. So, it is possible to compare the normal P-P interval (P-P = 0.84 sec) to the shorter P-P' interval (P-P = 0.40 sec) and make the correct diagnosis of non-conducted atrial bigeminy simulating a second-degree AV block with 2:1 conduction.
BACKGROUND: Abnormalities of the terminal force of the P wave in Lead V1 (ptf-V1) and dispersion of corrected atrial repolarization (Ta-TcD) are believed to represent interatrial conduction defect. METHODS AND RESULTS: To determine whether atrial conduction disturbance correlates with cardiac allograft rejection, we analyzed 249 twelve-lead-electrocardiograms, echocardiograms, hemodynamic parameters, and endomyocardial biopsys from 137 patients with heart transplantation. Both ptf-V1 and Ta-TcD were significantly increased in patients with severe, moderate, and mild rejection. In 22 patients, significant increases of the ptf-V1 and Ta-TcD were observed before positive histological findings, and significantly correlated with severity of rejection during 5- week to 1-year follow-up. Increase of 0.030 mm x sec in ptf-V1 or 0.040 s1/2 in Ta-TcD indicated cardiac rejection > or =1B with sensitivity of 88 and 83%, specificity of 85 and 77%, respectively. CONCLUSION: These results suggest that the ptf-V1 and Ta-TcD might be an adjunct to detect rejection and reduce the number of surveillance EMB.
In 14 patients with symptomatic sinus node dysfunction--sinus bradycardia, sino-atrial exit block, or sinus arrest--electrophysiological studies were performed before implantation of a pacemaker. In 8 patients incremental high right atrial pacing showed AV-nodal Wenckebach at pacing rates equal to or above 130/min (group I); in 6 patients AV-nodal Wenckebach was reached at pacing rates less than 130/min (group II). During ventricular pacing at a rate 10-15% faster than the existing sinus rate, ventriculo-atrial (VA) conduction was present in all patients of group I, while VA conduction was present in only 2 patients of group II (p less than 0.05). Patients with symptomatic sinus node dysfunction but with intact AV conduction frequently show VA conduction during ventricular pacing and thus are particularly at risk for developing a pacemaker syndrome when a ventricular demand (VVI) pacemaker is implanted. This complication can be avoided by atrial demand (AAI) pacing or AV sequential (DVI) pacing. When adequate experience has been gathered with AV universal (DDD) pacemakers, the indications for selection of a pacemaker in patients with symptomatic sinus node dysfunction will probably change.
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INTRODUCTION: Advancing age is an independent risk factor for atrial fibrillation (AF), which is considered to be initiated by ectopic triggers and maintained by an arrhythmogenic substrate. It is not known whether substrate changes produce this age-related increase in propensity toward AF. We addressed the hypothesis that advancing age is associated with changes in biatrial electrophysiology even in patients with no history of atrial arrhythmias. METHODS AND RESULTS: Patients with left-sided accessory pathways and requiring routine electrophysiological studies were recruited. Electroanatomic mapping was performed in the left and right atria of 23 patients (age ranging from 17 to 75 years) with structurally normal hearts and no history of AF during sinus rhythm and pacing. Unlike previous studies, a trigonometric method was used to quantify wavefront propagation velocities (WPV) precisely in the direction of propagation. Refractoriness was measured at 2 cycle lengths, at three different atrial sites. Both right (r =-0.77, P < 0.0001) and left (r =-0.79, P < 0.001) atrial WPV demonstrated strongly inverse correlation with age. Furthermore, left and right WPVs were highly correlated (r = 0.66, P < 0.01), with velocities being 6.4 +/- 2.2 cm/sec higher in the right atria (P < 0.01). Refractoriness was significantly correlated with increasing age only at the septum (r = 0.53, P < 0.01). Left atrial wavelength was inversely correlated with increasing age (r =-0.56, P = 0.03). P wave duration was associated with age (r = 0.42, P = 0.04) and left atrial size (r = 0.44, P = 0.04) but not atrial WPV. CONCLUSION: Aging human atria demonstrate progressive decline in WPV and increase in septal refractoriness. These age-related changes in biatrial electrophysiology are likely to be important factors in the age-related increase in AF prevalence.
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In studies to ascertain the basis of dynamic changes in the P wave, bipolar epicardial potentials were recorded from multiple atrial electrodes in dogs. One hundred to 120 activation times were displayed by a digital computer and used to construct atrial isotemporal activation sequence maps. Changes in heart rate or beat-to-beat cycle length were induced by vagal stimulation or infusion of autonomic mediating drugs. Changes in cycle length were associated with dynamic changes in the atrial activation sequence and surface P-wave. A conspicuous finding was that epicardial atrial depolarization began at three widely separated locations. These three points were consistently present in all animals and were generally located at the 12, 3, and 6 o'clock positions of the superior vena cava-right atrial junction. The dynamic changes in P waves and atrial activation sequence which accompanied the changes in cycle length were due to sudden shifts in the point of earliest activity between the three early sites. Asymmetric atrial depolarization with more rapid conduction along the crista terminalis, superior interatrial band, and pectinate muscles was present in all dogs. Although the anisotropic atrial geometry played an important role in the asymmetric conduction, the widely distributed onset of activity contributed significantly to the uneven spread. The multiple points of origin of the atrial wavefront might be explained by either a trifocal, distributed pacemaker or the epicardial exits of three specialized pathways conducting an impulse emanating from a single focus. These data explain the dynamic variation in P-wave morphology in normal hearts and also imply a relationship between the altered origin of atrial depolarization, atypical P waves, brady- or tachyarrhythmias, and heart rate control.
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Five patients with second degree intraatrial block are presented. The first three cases had a sick sinus syndrome with sinus bradycardia, broad P waves and episodes of atrial flutter or fibrillation. In these patients a Wenckebach phenomenon could bei elicited by atrial stimulation at a critical driving rate between the stimulated site and the recording electrode. In the first patient this conduction disturbance was obtained at several right atrial stimulation sites. The block could be elicited in the other two patients only in a limited area of the right atrium respectively only by left atrial pacing. In the remaining two patients an atrial tachycardia with block was observed. The intraatrial conduction disturbance was manifested as an exit block around the ectopic pacemaker. In one patient the tachycardia was induced by digitalis intoxication. In the other patient no etiologic factor of the tachycardia could be found. While the first three patients presented intraatrial conduction disturbances already in sinus rhythm, the last two cases showed after recovery from the atrial tachycardia P waves of normal duration and configuration.
BACKGROUND: Interaction between wave fronts in the right and left atrium may be important for maintenance of atrial fibrillation, but little is known about electrophysiological properties and preferential routes of transseptal conduction. METHODS AND RESULTS: Eighteen patients (age 44+/-12 years) without structural heart disease underwent right atrial electroanatomic mapping during pacing from the distal coronary sinus (CS) or the posterior left atrium. During distal CS pacing, 9 patients demonstrated a single transseptal breakthrough near the CS os, 1 patient in the high right atrium near the presumed insertion of Bachmann's bundle and 1 patient near the fossa ovalis. The mean activation time from stimulus to CS os was 48+/-15 ms compared with 86+/-15 ms to Bachmann's bundle insertion (P<0.01) and 59+/-23 ms to the fossa ovalis (P=NS and P<0.01, respectively). During left atrial pacing, the earliest right atrial activation was near Bachmann's bundle in 5 and near the fossa ovalis in 4 patients. The activation time from stimulus to CS os was 70+/-15 ms compared with 47+/-16 ms to Bachmann's bundle (P<0.01) and 59+/-25 ms to the fossa ovalis (P=NS). Whereas the total septal activation time was not significantly different during CS pacing compared with left atrial pacing (41+/-16 versus 33+/-17 ms), the total right atrial activation time was longer during CS pacing (117+/-49 versus 79+/-15 ms; P<0.05). CONCLUSIONS: Three distinct sites of early right atrial activation may be demonstrated during left atrial pacing. These sites are in accord with anatomic muscle bundles and may have relevance for maintenance of atrial flutter or fibrillation.
To investigate the effects of autonomic nerve activation on electrophysiological properties of ischemic atrial myocardium, experiments were performed in 10 open chest adult dogs anesthetized with xylazine and alpha-chloralose. Ischemia was created in the right atrial free wall by ligation of one or more branches of the right coronary artery. Bipolar electrograms were recorded from multiple sites in the ischemic and non-ischemic zones. The atria were paced at 400 ms and 180 ms to assess conduction properties. One hour after ligation, delayed activation, electrogram fractionation, and electrogram alternans were observed in the ischemic zone. All local conduction abnormalities were heart rate dependent in that they were only observed at a pacing cycle length of 180 ms. The average duration of ischemic zone electrograms was significantly prolonged from 17.7+/-1.6 ms to 26.4+/-1.6 ms (P<0.001). Right and left vagal stimulation significantly shortened the electrogram duration in the ischemic zone from 26.4+/-1.6 ms to 19.7+/-1.1 ms (P<0.01) and 20.0+/-1.1 ms (P<0.01), respectively. Ischemia-induced electrogram alternans was eliminated completely. During right and left stellate stimulation, electrogram duration was not altered and alternans was still present. In conclusion, vagal stimulation in this canine model improves local conduction in ischemic myocardium in the right atrium. This effect may be mediated by a reversal of the ischemia-induced membrane depolarization and a shortening of refractoriness in the atrium during vagal activation.