Atrioventricular Ring Research Articles

Ionic mechanisms of regional action potential heterogeneity in the canine right atrium.

Atrial action potential heterogeneity is a major determinant of atrial reentrant arrhythmias, but the underlying ionic mechanisms are poorly understood. To evaluate the basis of spatial heterogeneity in canine right atrial repolarization, we isolated cells from 4 regions: the crista terminalis (CT), appendage (APG), atrioventricular ring (AVR) area, and pectinate muscles. Systematic action potential (AP) differences were noted: CT cells had a "spike-and-dome" morphology and the longest AP duration (APD; value to 95% repolarization at 1 Hz, 270+/-10 ms [mean+/-SEM]); APG and pectinate muscle cells had intermediate APDs (180+/-3 and 190+/-3 ms, respectively; P<0.001 versus CT for each), with APG cells having a small phase 1; and AVR cells had the shortest APD (160+/-4 ms, P<0.001 versus other regions). The inward rectifier and the slow and ultrarapid delayed rectifier currents were similar in all regions. The transient outward K+ current was significantly smaller in APG cells, explaining their small phase 1 and high plateau. L-type Ca2+ current was greatest in CT cells and least in AVR cells, contributing to their longer and shorter APD, respectively. The E-4031-sensitive rapid delayed rectifier K+ current was larger in AVR cells compared with other regions. Voltage- and time-dependent current properties were constant across regions. We conclude that myocytes from different right atrial regions of the dog show systematic variations in AP properties and ionic currents and that the spatial variation in ionic current density may explain AP differences. Regional variation in atrial ionic currents may play an important role in atrial arrhythmia generation and may present opportunities for improving antiarrhythmic drug therapy.

The 1997 Grüntzig Lecture. 1967-1997: thirty years of cardiac arrhythmias.

I had the good fortune of doing my cardiology training in the 1960s in the Wilhelmina Gasthuis, the University of Amsterdam. Headed by professor Dirk Durrer (Fig. 1), the department of cardiology was a hive of activity, unravelling the electrical activity of the heart. Durrer, who was an original thinker, an inspiring leader, and an outstanding teacher, had assembled a group of physicians including Drs Hans Buller, Bart Dekker, Gerrit Freud, Michiel Janse, Frits Meijler and Rudolf van Dam, who were all actively involved in seeking insight into basic processes governing cardiac excitation and the genesis of cardiac arrhythmias. The cooperation between cardiology and medical physics was of enormous significance in Amsterdam. Professor Henk van der Tweel in his Department of Medical Physics played a key role in the development of instruments for stimulating the heart and recording its electrical activity. In 1967 Durrer and Roos revealed that the earliest ventricular epicardial activation during sinus rhythm occurred close to the atrioventricular ring. This was demonstrated in a patient with the WolffParkinson-White syndrome (WPW), who was operated upon in Leiden by Professor Brom because of an atrial septal defect. The question then arose, how could the arrhythmias be reproduced? In 1933, Wolferth and Wood suggested that there may be two atrioventricular (AV) connections in the WPW syndrome. This would make it possible for arrhythmias to occur by using a circuit with anterograde AV conduction over one connection and retrograde (ventriculo-atrial) conduction over the other. Durrer and Roos’ epicardial activation map of the patient with WPW proved the existence of a second AV connection. This prompted the development of a versatile stimulator by the Department of Medical Physics (Professor Van der Tweel, Dr Jan Strackee and Leo Schoo), which would allow programmed electrical stimulation of the heart with such accuracy that the hypothesis of a circus movement tachycardia could be tested.

Value of epicardial potential maps in localizing pre-excitation sites for radiofrequency ablation. A simulation study

Using computer simulations, we systematically investigated the limitations of an inverse solution that employs the potential distribution on the epicardial surface as an equivalent source model in localizing pre-excitation sites in Wolff-Parkinson-White syndrome. A model of the human ventricular myocardium that features an anatomically accurate geometry, an intramural rotating anisotropy and a computational implementation of the excitation process based on electrotonic interactions among cells, was used to simulate body surface potential maps (BSPMs) for 35 pre-excitation sites positioned along the atrioventricular ring. Two individualized torso models were used to account for variations in torso boundaries. Epicardial potential maps (EPMs) were computed using the L-curve inverse solution. The measure for accuracy of the localization was the distance between a position of the minimum in the inverse EPMs and the actual site of pre-excitation in the ventricular model. When the volume conductor properties and lead positions of the torso were precisely known and the measurement noise was added to the simulated BSPMs, the minimum in the inverse EPMs was at 12 ms after the onset on average within cm of the pre-excitation site. When the standard torso model was used to localize the sites of onset of the pre-excitation sequence initiated in individualized male and female torso models, the mean distance between the minimum and the pre-excitation site was cm for the male torso and cm for the female torso. The findings of our study indicate that a location of the minimum in EPMs computed using the inverse solution can offer non-invasive means for pre-interventional planning of the ablative treatment.

Accuracy of single-dipole inverse solution when localising ventricular pre-excitation sites: simulation study.

Different factors are investigated that may affect the accuracy of an inverse solution that uses a single-dipole equivalent generator, in a standardised inhomogeneous torso model, when localising the pre-excitation sites. An anatomical model of the human ventricular myocardium is used to simulate body surface potential maps (BSPMs) and magnetic field maps (MFMs) for 35 pre-excitation sites positioned on the epicardial surface along the atrioventricular ring. The sites of pre-excitation activity are estimated by the single-dipole method, and the measure for the accuracy of the localisation is the localisation error, defined as the distance between the location of the best-fitting single dipole and the actual site of pre-excitation in the ventricular model. The findings indicate that, when the electrical properties of the volume conductor and lead positions are precisely known and the 'measurement' noise is added to the simulated BSPMs and MFMs, the single-dipole method optimally localises the pre-excitation activity 20 ms after the onset of pre-excitation, within 0.71 +/- 0.28 cm and 0.65 +/- 0.30 cm using BSPMs and MFMs, respectively. When the standard torso model is used to localise the sites of onset of the pre-excitation sequence initiated in four individualised torso models, the maximum errors are as high as 2.6-3.0 cm (even though the average error, for both the BSPM and MFM localisations, remains within the 1.0-1.5 cm range). In spite of these shortcomings, it is thought that single-dipole localisations can be useful for non-invasive pre-interventional planning.

Spatial resolution of body surface potential maps and magnetic field maps: a simulation study applied to the identification of ventricular pre-excitation sites.

The spatial resolution of body surface potential maps (BSPMs) and magnetic field maps (MFMs) is investigated by means of an anatomically accurate computer model of the human ventricular myocardium. BSPMs and MFMs are calculated for the simulated activation sequences initiated at 35 pre-excitation sites located along the atrioventricular (AV) ring of the epicardium. Changes in the BSPMs and MFMs corresponding to different pre-excitation sites are quantified in terms of the correlation coefficient r. The spatial resolution (selectivity) for a given pre-excitation site is defined as the half-distance between those neighbouring locations at which morphological features of maps, in terms of r, become distinct (r < 0.95). It is found that, at 28 ms after the onset of pre-excitation and with no noise added, this distance +/- SD, for all sites along the AV ring for the 117-lead BSPMs, is 0.83 +/- 0.32 cm, and for the 64-lead and 128-lead MFMs it is 1.54 +/- 0.84 cm and 1.15 +/- 0.43 cm, respectively. The findings suggest that, when features of non-invasively recorded electrocardiographic and magnetocardiographic map patterns are used for identifying accessory pathways in patients suffering from WPW syndrome, BSPMs are likely to provide more detailed information for guiding the ablative treatment than MFMs. For some sites MFMs provide more information. Both modalities may provide additional assistance to the cardiologist in locating the site of the accessory pathway.

Atrial conduction abnormalities in patients with systemic progressive sclerosis.

Atrial abnormalities in patients with progressive systemic sclerosis have not been evaluated in terms of intra-atrial conduction. We hypothesized that a delay in atrial conduction in these patients might produce diastolic abnormalities as well as atrial arrhythmias. To evaluate the atrial function of patients with progressive systemic sclerosis by using echocardiography to measure the intra-atrial electromechanical activation coupling interval. Twenty patients with progressive systemic sclerosis were assessed by Doppler echocardiography. Twenty age-matched healthy controls were also evaluated. Two-dimensional guided M-modes of ventricular long axes were recorded using simultaneous phono- and electrocardiograms of the apical four chamber view at the right lateral, septal and left lateral sites of the atrioventricular rings. Transmitral and tricuspid pulsed Doppler flow velocities were also recorded. Filtered P wave duration was measured on the signal averaged ECG to determine the duration of atrial electrical activation. There was a delay in P on the electrocardiogram (P) at the onset of atrial contraction on long axis M-modes at all three atrioventricular ring sites in patients with progressive systemic sclerosis as compared with controls (P-right; 56 +/- 13 vs 47 +/- 10 ms, P-septal; 74 +/- 14 vs 55 +/- 10 ms, and P-lateral; 93 +/- 16 vs 72 +/- 11 ms, P < 0.01). Inter-atrial conduction time [(P-lateral)-(P-right)] was delayed in patients with progressive systemic sclerosis, compared with healthy controls (37 +/- 15 vs 25 +/- 6 ms, P < 0.01). Mitral A waves acceleration and deceleration times were also decreased in the patients. The interval was prolonged between P to the onset and the peak of the A wave in transmitral flow. Duration of the filtered P wave was significantly prolonged in progressive systemic sclerosis as compared with controls (124 +/- 12 ms vs 106 +/- 8 ms, P < 0.01). PQ intervals, E waves and acceleration and deceleration times did not differ significantly in progressive systemic sclerosis vs, controls. The A wave acceleration rate on transmitral flow (peak A wave velocity/acceleration time) showed a significant correlation with inter-atrial conduction delay (r = 0.55, P < 0.01). Intra-atrial electromechanical coupling intervals were delayed in patients with progressive systemic sclerosis. Thus, the mechanical late diastolic filling time due to atrial contraction in the total diastolic phase was severely limited, and this resulted in a restricted mitral A wave. We should therefore evaluate patients with progressive systemic sclerosis for significant atrial abnormalities.

Distribution of PGP 9.5, TH, NPY, SP and CGRP immunoreactive nerves in the rat and guinea pig atrioventricular valves and chordae tendineae.

The distribution of nerves immunoreactive to protein gene product 9.5 (PGP 9.5), tyrosine hydroxylase (TH), neuropeptide Y (NPY), substance P (SP) and calcitonin gene related peptide (CGRP) antisera was investigated in the atrioventricular valves of the Sprague-Dawley rat and the Dunkin-Hartley guinea pig using confocal and epifluoresence microscopy. No major differences were noted between the innervation of the mitral and tricuspid valves in either species. For all antisera the staining was more extensive in the guinea pig valves. Two distinct nerve plexuses separated by a 'nearly nerve free' zone were identified in both species with each antiserum tested. This was most apparent on the anterior cusp of the mitral valve. The major nerve plexus extends from the atrioventricular ring through the basal, intermediate and distal zones of the valves towards the free edge of the valve cusp. These nerve bundles, arranged as primary, secondary and tertiary components, ramify to the free edge of the valve and extend to the attachment of the chordae. They do not contribute to the innervation of the chordae tendineae. The second, minor chordal plexus, runs from the papillary muscles through the chordae tendineae and passes parallel to the free edge of the cusp. The nerves of this minor plexus are interchordal, branching to terminate mainly in the distal zone, free edge of the valve cusp and adjacent chordae tendineae. Some interchordal nerve fibres loop from a papillary muscle up through a chorda, along the free edge and pass down an adjacent chorda into another papillary muscle. The nerve fibres of the major and minor plexuses intermingle although no evidence was found for interconnectivity between them. In the distal zone between the major plexus which extends from the base of the valve and the minor chordal plexus there is a zone completely free of nerves staining with antisera to TH and NPY. Occasional nerves which stained positive for PGP 9.5, SP and CGRP immunoreactivities crossed this 'nearly nerve free zone' passing either from the chordal/free edge nerves to the intermediate and basal zones or vice versa. An additional small nerve plexus which displayed immunoreactivity to CGRP antiserum extended from the atrioventricular ring into the basal zone of the valve cusp. Not all chordae tendineae displayed immunoreactive nerve fibres. It is concluded that the innervation patterns of the sensory and sympathetic neurotransmitters and neuropeptides examined in the atrioventricular valves of the rat and guinea pig are ubiquitous in nature. The complexity of the terminal innervation network of the mammalian atrioventricular valves and chordae tendineae may contribute to the complex functioning of these valves in the cardiac cycle.

Body surface potential mapping of simulated retrograde P waves around the atrioventricular ring in the dog

Body surface potential mapping of simulated retrograde P waves around the atrioventricular ring in the dog

P wave morphology during atrial pacing along the atrioventricular ring: ECG localization of the site of origin of retrograde atrial activation

P wave morphology during atrial pacing along the atrioventricular (AV) ring was evaluated to develop electrocardiographic (ECG) criteria for identifying the site of origin of the atrial activation wave during reentrant supraventricular tachycardia. Because P wave morphology changes as the pattern of atrial activation changes, the P wave should show characteristic morphologies during reentrant supraventricular tachycardia with use of either accessory AV pathways or the AV node for retrograde atrial activation. In 14 patients, 12-lead ECGs were recorded during bipolar atrial pacing at sites in the coronary sinus vein (along the mitral annulus) and along the atrial endocardium of the tricuspid annulus. P wave morphology was graded for each lead at each site. Sensitivity, specificity, and predictive value of ECG criteria for left versus right and anterior versus posterior atrial pacing sites were evaluated. Data were obtained from 14 sites along the AV ring, including 71 recordings at 6 sites in the coronary sinus vein and 94 recordings at 8 sites along the tricuspid annulus. These recordings were further divided into 54 anterior sites and 80 posterior sites, as well as 62 recordings along the right free wall and 32 recordings along the right atrial septum. The predictive value of a positive P wave in lead I indicating right atrial site of origin was 98.9%, and that for a negative or isoelectric P wave in lead I indicating a left atrial site of origin was 94.6%. Negative P wave in leads II, III, and aVF indicated a posterior site of origin, with a predictive value of 91.2%. The predictive value of a negative or isoelectric P wave in lead V 1 indicating a right atrial free wall site was 87.5%. Thus, P wave morphology can be used to localize the site of origin of the atrial depolarization wave to a region along the AV ring.

Non-invasive detection of left atrial mechanical failure in patients with left ventricular disease.

To define patients with left atrial mechanical failure and identify its echocardiographic, physiological, and clinical associations. Prospective study with cross sectionally guided M mode and Doppler echocardiograms, and with apexcardiograms, electrocardiograms, and phonocardiograms. Tertiary cardiac referral centre. 10 patients with left atrial mechanical failure and 20 healthy controls of similar age. 10 patients with left atrial mechanical paralysis were identified among 4036 adults over a 1 year interval. Nine were in sinus rhythm and one had a DDD pacemaker. Left atrial mechanical activity was absent on M mode echocardiograms of the left sided atrioventricular ring and the aortic root. A Doppler A wave on transmitral flow and a clearly defined A wave on the left ventricular apexcardiogram were also absent, though evidence of right atrial mechanical movement was present in nine patients. Mean (SD) age was 63 (19) years and six were men. Nine had left ventricular disease and one had undergone extensive resection of the left atrium. Abnormal measurements of left ventricular end diastolic dimension (62 (13) mm), fractional shortening (15 (6)%), isovolumic relaxation time (19 (12) ms), left atrial size (45 (10) mm), and transmitral Doppler E wave deceleration time (110 (35) ms) were recorded. Left atrial mechanical failure may be present in patients with left ventricular disease despite normal sinus rhythm. Normal atrial activation on 12 lead electrocardiogram suggests it is primarily mechanical in origin. The possibility of left atrial mechanical failure must be considered when Doppler patterns of transmitral flow are used to assess left ventricular diastolic function.

Atrial electromechanical sequence in normal subjects and patients with DDD pacemakers.

To assess the effect of right atrial appendage pacing on atrial electromechanical interrelations in patients with DDD pacemakers. Prospective study by M mode echocardiogram, Doppler echocardiogram, and apexcardiogram, along with electrocardiogram and phonocardiogram. Tertiary cardiac referral centre. 20 patients with DDD pacemakers and 20 age matched normal controls. Age, RR interval, atrial size, left ventricular size, and fractional shortening were similar in the two groups. Atrial electromechanical delay (the time from the onset of P wave or atrial pacing spike on ECG to the onset of atrial contraction on M mode echogram) was 68 (SD 7) ms at the lateral site of right atrium, 82 (9) ms at the central fibrous body, 93 (11) ms at the lateral site of left atrium in normals. In patients with DDD pacing, however, this delay increased to 85 (22) ms, 117 (23) ms, and 138 (25) ms respectively (all P < 0.01). Interatrial mechanical delay (the time from the onset of right atrial motion to the onset of the left) increased from 25 (6) ms in normal controls to 53 (18) ms in patients (P < 0.01). Intra-atrial mechanical dispersion (the time from the earliest to the latest onset of regional atrial motion around the atrioventricular ring) in the right atrium increased from 6 (2) ms in normals to 19 (2) ms in patients (P < 0.01), but it remained unchanged in the left atrium (6 (2) ms in normal controls v 7 (2) ms in patients, P > 0.05). Peak atrial shortening rate was not different between the two groups. Differences of atrial electromechanical activity between the two groups were also reflected on Doppler echocardiogram and apexcardiogram. Right atrial appendage pacing disturbs the normal coordinate sequence of right atrial mechanical activity and leads to a striking and variable increase in intra-atrial conduction time as well as in interatrial conduction time. Left atrial contraction remains synchronous although the timing of the start of its contraction was delayed. These values can be determined in individual patients to allow optimal setting of DDD pacemakers.

Right ventricular filling in dilated cardiomyopathy.

To assess right ventricular filling in dilated cardiomyopathy. 32 patients with dilated cardiomyopathy and 24 healthy controls. Stroke distances were measured by pulsed Doppler echocardiography at left ventricular outflow and left and right ventricular inflow. The inflow tract dimensions of both ventricles and the outflow tract dimension of the left ventricle were measured from two dimensional images. Right and left sided atrioventricular (AV) ring excursions were measured by M mode echocardiography at the tricuspid and mitral rings. Stroke volume was derived as stroke distance multiplied by left ventricular outflow tract area. Total stroke distances were calculated as the sum of AV valve Doppler stroke distances and ring excursion. The effective orifice areas of the two AV valves were thus defined as stroke volumes divided by total stroke distance. Total tricuspid stroke distance was normally less than mitral (6.0 (1.7) v 7.6 (1.7) cm, P < 0.05), implying that effective orifice area of the tricuspid valve was consistently greater (6.6 (1.6) v 4.5 (0.8) cm2, P < 0.01). Total tricuspid ring excursion was normally more than mitral (2.30 (0.30) v 1.62 (0.22) cm, P < 0.01). Total tricuspid stroke distance in dilated cardiomyopathy was also less than mitral (7.8 (2.4) v 9.7 (2.8) cm, P < 0.05). Tricuspid stroke distance was significantly increased in patients with dilated cardiomyopathy compared with that in healthy controls (P < 0.05 v controls), though stroke volume was much smaller (26 (10) v 63 (11) ml, P < 0.01) so that tricuspid effective orifice area was reduced to less than half normal (2.7 (1.2) cm2, P < 0.01). Total tricuspid ring long axis excursion was more than mitral (1.37 (0.6) v 0.74 (0.21) cm, P < 0.01). Right ventricular end diastolic inflow dimension was increased compared with that in healthy controls (3.9 (0.7) v 2.8 (0.5) cm, P < 0.01), correlating inversely with tricuspid effective orifice area (r = -0.71, P < 0.01). Total tricuspid ring excursion was bimodally distributed as a low amplitude group (less than 1.6 cm, n = 23) and a high amplitude group (more than 1.6 cm, n = 9), in which the interval P2 to onset of tricuspid flow was much longer (100 (35) v 50 (14) ms, P < 0.01). Enlargement of the right ventricular inflow tract in dilated cardiomyopathy, especially to more than 5 cm, is accompanied by a progressive decrease in effective tricuspid orifice area, sometimes to less than 1 cm2 and increased inflow velocities. Right ventricular relaxation was incoordinate in 28% of the patients studied. These disturbances of right ventricular filling are likely to compromise overall cardiac function independently of left ventricular disease.

Architecture of atrial musculature in humans.

To investigate the gross arrangement of the principal muscular bundles of the two atria, and to suggest how it may contribute to contraction and spread of atrial excitation. A prospective analysis based on anatomical examination of adult human hearts. A national heart and lung institute and a tertiary referral centre for cardiac disease. 9 normal postmortem human hearts. Dissection of atrial muscles with macrophotography. RESUltS--The atrial walls consist of circumferential and longitudinal muscular bundles, the former being arranged at the base of the atria with the latter predominating in the parietal walls. The muscular bundles in the right atrium are larger than those in the left. The main muscles forming the right atrial wall are the terminal crest and terminal pectinate muscles. The terminal crest, the most obvious muscle, is arranged longitudinally with its pectinate muscles connecting to the musculature of the atrioventricular vestibule. No structure resembling the terminal crest is seen in the left atrium. Instead the left atrial wall is composed of intermingled series of muscles, chief of these being the interatrial band and the septoatrial bundle. The former is arranged circumferentially at the atrial base, while the latter is mainly longitudinal. The wall of the right atrium is not of uniform thickness because of the presence of the terminal crest and its pectinate muscles on its internal surface. By contrast, the left atrial wall is much more uniform and its average thickness is greater than that of the right atrium. The rim of the oval fossa is the most important muscular structure on the septal surface and is formed by the infolded atrial walls. The other principal muscles of the atria attach to it, so that the rim provides mechanical support for overall movement of the atrial walls. Comparison of the gross arrangement of the atrial musculature with earlier echocardiographic measurements showed that this arrangement of the muscle explains movement of the atrioventricular ring and overall atrial contraction, and provides a suitable substrate for preferential conduction. The anatomical features of the atrial musculature explain the known facts concerning atrial contraction and preferential conduction.

Terminal diversification of the myocyte lineage generates Purkinje fibers of the cardiac conduction system

The rhythmic contraction of the vertebrate heart is dependent on organized propagation of electrical excitation through the cardiac conduction system. Because both muscle- and neuron-specific genes are co-expressed in cells forming myocardial conduction tissues, two origins, myogenic and neural, have been suggested for this specialized tissue. Using replication-defective retroviruses, encoding recombinant beta-galactosidase (beta-gal), we have analyzed cell lineage for Purkinje fibers (i.e., the peripheral elements of the conduction system) in the chick heart. Functioning myocyte progenitors were virally tagged at embryonic day 3 of incubation (E3). Clonal beta-gal+ populations of cells, derived from myocytes infected at E3 were examined at 14 (E14) and 18 (E18) days of embryonic incubation. Here, we report that a subset of clonally related myocytes differentiates into conductile Purkinje fibers, invariably in close spatial association with forming coronary arterial blood vessels. These beta-gal+ myogenic clones, containing both working myocytes and Purkinje fibers, did not incorporate cells contributing to tissues of the central conduction system (e.g. atrioventricular ring and bundles). In quantitative analyses, we found that whereas the number of beta-gal+ myocyte nuclei per clone more than doubled between E14 and E18, the number of beta-gal+ Purkinje fiber nuclei remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Radiofrequency Catheter Ablation of an Accessory Pathway in a Young Man with Dextroversion

We report an observation of a radiofrequency catheter ablation of an accessory pathway (AP) in a patient with Wolff-Parkinson-White syndrome (WPW) and dextroversion. Atrioventricular rings were mapped by the ablation catheter to locate the shortest local atrioventricular conduction time in sinus rhythm and ventriculoatrial conduction time during orthodromic tachycardia or ventricular pacing. Successful ablation confirmed a right posteroseptal AP localization. Thus, the electrocardiographic modifications due to an AP in this location in the presence of dextroversion were defined.

Major coronary sinus abnormalities: Identification of occurrence and significance in radiofrequency ablation of supraventricular tachycardia

Coronary sinus catheterization is important in electrophysiologic study of patients with supraventricular tachycardia. It can provide an anatomic guide for localization of slow atrioventricular nodal pathway and accessory pathways in the posteroseptal area and left-sided atrioventricular ring. However, the morphologic features of the coronary sinus and its significance in patients with supraventricular tachycardia have not been determined. Four hundred eight patients with accessory pathway-mediated tachyarrhythmia and atrioventricular nodal reentrant tachycardia underwent coronary arteriography for a coronary sinus venogram before electrophysiologic study and radiofrequency ablation. The venous phase of left coronary arteriography that delineated the morphologic features of the coronary sinus was carefully evaluated and recorded in multiple projections. Major coronary sinus abnormalities were defined, and they were found in 12 patients (2.9%). Six patients had angulation of the coronary sinus, 4 patients had hypoplasia of the coronary sinus, 1 patient had narrowing of the proximal coronary sinus, and 1 patient had a fistula from persistent left superior vena cava to the coronary sinus. Of 175 patients with atrioventricular nodal reentrant tachycardia, only 1 patient had major coronary sinus abnormalities (proximal angulation), whereas of 233 patients with accessory pathway-mediated tachycardia, 11 patients had major coronary sinus abnormalities (0.6% vs 4.7%, p < 0.05). The accessory pathways in patients with major coronary sinus abnormalities were located exclusively in the left free wall and posteroseptal area. Proper coronary sinus catheterization could be accomplished in 396 patients with a normal coronary sinus, whereas it could be accomplished in only 1 of the 12 patients with major coronary sinus abnormalities ( 396 396 vs 1 12 , p < 0.0001 ). However, radiofrequency ablation was successful in all 12 patients with major coronary sinus abnormalities. In conclusion, major coronary sinus abnormalities are not common in patients with supraventricular tachycardia. They are more frequently found in patients with accessory pathway-mediated tachycardia and are anatomically related to the location of accessory pathways. They almost always preclude proper coronary sinus catheterization. However, radiofrequency ablation is still feasible with a high success rate in these patients.

Operation for the Wolff-Parkinson-White syndrome in the Catheter ablation era

Catheter ablation has greatly altered surgical referral patterns for the Wolff-Parkinson-White syndrome. We describe 51 patients (aged 9 to 63 years; 35 male, 16 female) referred for operation from our institution and elsewhere between August 1990 and August 1993, coincident with the inception of our ablation program. During the same period, 375 patients with problematic Wolff-Parkinson-White syndrome had ablation procedures. Operation was the initial therapy in 26 patients, due to physician preference in 23 and the need for a concomitant cardiac operation in 3. Operation was related to ablation failure in 22 patients and was urgent in 3 patients. Previous ablation was not associated with added surgical difficulties, and all pathways were ablated intraoperatively on the first attempt using the epicardial approach. Visible epicardial lesions were observed in 8 patients at the site of the accessory pathway. In 2 patients, the lesions were remote to the atrioventricular ring. There was a striking significant increase in proportion of right free wall pathways after attempted ablation (27% versus 8%) as compared with the preablation era. We conclude that previous attempted ablation does not impair efficacy and safety of operative therapy. Operation remains a useful alternative for ablation failure and as a back-up for acute complications.

Quantitative effects of myocardial edema on the left ventricular pressure-volume relation: Influence of cardioplegia osmolarity over two hours of ischemic arrest

We previously studied edema and left ventricular pressure-volume relations in a porcine heart model in which edema occurred even with hyperosmolar crystalloid cardioplegia. This susceptibility to edema was attributed to venous occlusion and an initial 20-minute period of ischemia. Results did not demonstrate reversal of edema by hyperosmolar perfusates. Accordingly, in the present study, heart weight, myocardial water content, and left ventricular pressure-volume curves were measured before and after perfusion-induced edema in eight isolated, arrested, hypothermic porcine hearts. Cardioplegic solution was infused 2.1 +/- 0.8 minutes after the onset of ischemia, and the atrioventricular ring was not clamped during the administration of cardioplegic solution. Cardioplegic solution (1 L) was infused at intervals of 33 +/- 6 minutes at 4 degrees C. Solution osmolarity was 380 (Stanford solution) or 294 mOsm/L (Plegisol solution). The perfusion sequence was 380-1, 380-2, 294-1, 380-3. Pressure-volume relations were assessed with the use of left ventricular volume at a pressure of 10 mm Hg and the ventricular chamber stiffness constant, beta, derived from P = alpha e beta V. Perfusions 380-1 and 380-2 did not affect the pressure-volume curve. Perfusion 294-1 increased heart weight and water content (p < 0.05) and decreased left ventricular volume at 10 mm Hg compared with perfusions 380-1, 380-2, and 380-3. In addition, beta increased (0.023 +/- 0.005 versus 0.029 +/- 0.006, p < 0.05) after perfusion 294-1, compared with 380-1. Correlation coefficients for linear regressions between left ventricular volume at 10 mm Hg and heart weight and water content were r = 0.84 and r = 0.70, respectively. We conclude that under conditions similar to those used clinically, the left ventricle of the pig does not develop edema with Stanford solution (380 mOsm/L). Edema does follow Plegisol solution (294 mOsm/L) cardioplegia. Edema and reduced compliance are incompletely reversed by hypertonic cardioplegia. The porcine left ventricle can usefully replicate the clinical model.

Circus movement atrial flutter in the canine sterile pericarditis model. Cryothermal termination from the epicardial site of the slow zone of the reentrant circuit.

We have shown that atrial flutter (AF) in dogs with sterile pericarditis is commonly due to a single-loop reentrant circuit in the lower right atrium comprised of a functional or functional/anatomic obstacle and a slow zone of conduction (SZ) between the central obstacle and the atrioventricular (AV) ring. The goals of the present study were 1) to establish that the epicardial SZ is the critical component of circus movement AF and 2) to identify the optimal site within the epicardial SZ at which interruption of circus movement can be accomplished by ablative techniques. We analyzed the atrial activation patterns during epicardial cooling of the SZ with as N2O-cooled probe in eight dogs (five with clockwise [CW] reentrant circuit, one with counterclockwise [CCW] reentrant circuit, and two with both CW and CCW reentrant circuits around the same pathway). In all eight dogs, cooling (-5 to +5 degrees C for 5-20 seconds) the narrow isthmus at the inferoposterior part of the SZ between the central obstacle and the AV ring reversibly terminated the reentrant circuit, whereas cooling outside this area failed to terminate the reentrant circuit. The circus movement was not observed to continue along alternate pathways when conduction in this critical zone was interrupted. Both CW and CCW reentrant circuits could be terminated from the same site within the SZ. Cooling resulted in slowing of conduction in the SZ (55 +/- 15 msec) in both CW and CCW reentrant circuits. Cooling-induced termination of CW reentrant circuits was characteristically associated with oscillations of conduction in the cooled zone of the last three cycles before termination and conduction block occurred within the cooled zone. The last "manifest" reentrant cycle was associated with the longest conduction delay in the cooled zone. However, this delay was not necessarily reflected in the length of the last reentrant cycle because of compensatory acceleration of conduction in the rest of the pathway. On the other hand, in CCW reentrant circuits, conduction block occurred abruptly at the distal border of the SZ and without significant oscillations of conduction. The present study provides convincing evidence that single-loop circus movement in this model is critically dependent on an obligatory conduction in a SZ in the inferoposterior portion of the free right atrial wall between a functional obstacle and the AV ring. Because the atrial myocardium behaves electrophysiologically as a two-dimensional surface, the results of this study may help to guide the endocardial electrode catheter ablative technique for treatment of clinical AF.

Development of the coronary arteries and cardiac veins in the dogfish (Scyliorhinus canicula).

The development of the coronary system in the Dogfish was studied using light microscopy. The sample examined consisted of 44 embryos and four newborns. The chronology of events occurring during the process was referred to the total length (TL) of the specimens. The nourishment of the developing myocardium first takes place by means of intertrabecular sinusoids. This system is later switched to a circulation through coronary vessels. The cardiac veins develop earlier than the coronary arteries. The earliest evidence of development of heart vessels in the present sample was the appearance of a diverticulum from the sinus venosus in three embryos of 31 mm TL. This diverticulum outlined the future coronary sinus. Both the atrioventricular and conoventricular venous rings were completely developed in an embryo of 36 mm TL. Coronary artery vessels appeared for the first time in embryos of 40 mm TL. In these specimens, two arteries arose from the midventral hypobranchial artery and divide to give rise to the four coronary artery conal trunks. In a 51-mm TL embryo it was already possible to follow the course of the coronary arteries, from the hypobranchial artery to the conoventricular groove. All main coronary vessels were fully developed in embryos of more than 58 mm TL. However, the arteries supplying the atrium were firstly recorded in a newborn of 77 mm TL. Birth usually occurs when the shark reaches about 72-76 mm TL.