Retrograde properties of the fast pathway in patients with paroxysmal atrioventricular nodal reentrant tachycardia.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to C R Wyndham.
Explore the source record for details and available documents.
Four patients with coronary artery disease and chronic marked left axis deviation, defined as a frontal QRS axis more negative than -45 degrees, were studied with epicardial mapping during coronary bypass surgery. All patients had normal right ventricular and inferior left ventricular epicardial breakthrough sites and activation sequence. Normal breakthrough in the basal anterolateral left ventricular epicardium was absent in all four patients. Two patients had breakthrough in the apical region of the anterolateral left ventricle. In the other two this region was activated from wave fronts emerging in the right ventricle and inferior left ventricle. The latest site of left ventricular activation was the basal segment of the anterolateral wall, a site never found to be the latest activated in our previously studied patients without conduction defects. This site was activated during or slightly after the terminal portion of the QRS complex. It is concluded that marked left axis deviation in patients with coronary artery disease reflects delayed activation of the basal anterolateral left ventricle, and is consistent with the presence of block or delay in the anterior "fascicle" of the left bundle branch.
To describe the epicardial ventricular activation sequence in the intact human heart, we obtained epicardial maps from 11 patients with normal QRS undergoing open heart surgery. Epicardial breakthrough (EBT), defined as the emergence of a radially propagating epicardial wavefront, occurred in three to five sites in each patient, and was earliest in the anterior right ventricle, 7--25 msec (mean 17 msec) after the onset of the QRS in all patients. Subsequent EBT occurred in the inferior right ventricle (10 sites in 10 patients), in the anterolateral left ventricle (13 sites in 10 patients), and the inferior left ventricle (eight sites in seven patients). Latest epicardial activation (LEA), defined as the latest site of recordable epicardial activity, occurred in the basal segments in all patients, anteriorly in the right ventricle in five patients, and inferiorly in six patients, four on the right and two on the left. LEA occurred 63--96 msec (mean 77 msec) after the onset of the QRS, and was recorded within 20 msec of the end of the QRS in all patients. Sequence of epicardial activation reflected a fusion process among the wavefronts. This descriptive and quantitative data should provide a suitable basis for comparison of abnormal ventricular activation sequences in patients undergoing surgery for preexcitation or ventricular tachycardia.
Electrophysiologic studies were performed in a patient who had an apparently uncomplicated complete trifascicular block. His bundle recordings revealed atrioventricular dissociation with: 1) an atrial rate of 58 beats/min, 2) an idioventricular escape rate of 45 beats/min, and 3) nonparoxysmal junctional tachycardia (His bundle rhythm) at a rate of 65--85 beats/min. The latter arrhythmia was electrocardiographically silent, influencing neither atrial nor ventricular events. The arrhythmia probably reflected digitalis intoxication (digoxin level of 3.3 ng/ml). A repeat electrophysiologic study 4 days after digoxin was discontinued revealed complete trifascicular block (distal to H) with intact conduction between the atrium and the His bundle (AH of 150 msec). Thus, electrophysiologic study demonstrated an electrocardiographically silent but clinically relevant arrhythmia, suggesting that His bundle recording should be part of diagnostic study during temporary pacemaker implantation in patients with atrioventricular block.
Seventy-nine patients without ventricular preexcitation but with documented paroxysmal supraventricular tachycardia were analyzed. Electrophysiologic studies suggested atrioventricular (A-V) nodal reentrance in 50 patients, reentrance utilizing a concealed extranodal pathway in 9, sinus or atrial reentrance in 7 and ectopic automatic tachycardia in 3. A definite mechanism of tachycardia could not be defined in 10 patients (including 7 whose tachycardia was not inducible). The three largest groups with inducible tachycardias were compared in regard to age, presence of organic heart disease, rate of tachycardia, functional bundle branch block during tachycardia and relation of the P wave and QRS complex during tachycardia. A-V nodal reentrance was characterized by a narrow QRS complex and a P wave occurring simultaneously with the QRS complex during tachycardia. Reentrance utilizing a concealed extranodal pathway was characterized by young age, absence of organic heart disease, fast heart rate, presence of bundle branch block during tachycardia and a P wave following the QRS complex during tachycardia. Sinoatrial reentrance was characterized by frequent organic heart disease, a narrow QRS complex and a P wave in front of the QRS complex during tachycardia. In conclusion, a mechanism of paroxysmal supraventricular tachycardia could be defined in most patients. Observations of clinical and electrocardiographic features in these patients should allow prediction of the mechanism of the tachycardia.
A patient is described with drug-resistant recurrent paroxysmal atrial flutter. Electrophysiologic studies demonstrated that flutter was inducible with rapid atrial stimulation (stimulation rates of 375 to 400/min) and convertible with rapid atrial stimulation (rates of 400 to 460/min). Because of the latter response, a radio-frequency atrial pacemaker was implanted, which allowed self-initiated conversion of flutter episodes with rapid stimulation.
Explore the source record for details and available documents.
Paroxysmal supraventricular tachycardia may result from re-entrance in the AV node, the normal A-V pathway with an accessory AV connection, in the sino-atrial node, in the atria, or else reflect ectopic impulse formation in a spontaneously automatic supraventricular focus. Electrocardiographic criteria which are helpful in differentiating these mechanisms involve an analysis of cycle length, changes in cycle length with intermittent bundle branch block, P wave morphology and the relationship of P wave to QRS complex, P-R interval, the presence of A-V block during tachycardia and the influence of autonomic tone on the tachycardia. Electrophysiologic studies further elucidate mechanism by demonstrating the mode of induction and termination of the tachycardia, the characteristics of antegrade and retrograde A-V conduction curves and refractory periods, atrial activation sequence of echo beats and the influence of premature beats introduced during tachycardia. These features are summarised in Table 1. Therapy can be accurately planned according to the results of experimental administration of antiarrhythmic agents and of pacing sequences upon induction and termination of tachycardia in the catheterisation laboratory.
Atrial pacing at multiple sites was used in an attempt to predict the site of pre-excitation in 5 patients with Wolff-Parkinson-White syndrome with 5 different anomalous pathway locations (right anterior, right posterior, septal, left posterior, and left lateral). At least 3 atrial pacing sites were tested in each patient. Pacing sites tested included high right atrium, low lateral right atrium, low septal right atrium, proximal coronary sinus, and distal coronary sinus. Atrial stimulation sites with shortest and longest stimulus-delta intervals could be identified in each patient, the shortest stimulus-delta interval in each case ranging from 60 to 80 ms. The difference between the shortest and longest stimulus-delta interval in each case ranged from 60 to 110 ms. It was suggested that the site with the shortest stimulus-delta interval corresponded to a site close to the atrial insertion of the anomalous pathway. This hypothesis was confirmed in all cases (3 with epicardial mapping and 2 with retrograde atrial activation data). In conclusion, atrial pacing at multiple sites is helpful in predicting the site of anterogradely conducting anomalous pathways, and appears particularly useful for differentiation of right posterior, left posterior, and septal pre-excitation.
The effect of cycle length on atrial vulnerability was studied in 14 patients manifesting reproducible repetitive atrial firing during atrial extra-stimulus (A2) testing. Repetitive atrial firing was defined as the occurrence of two or more premature atrial responses with return cycle (A2-A3) of 250 msec or less and subsequent mean cycle length of 300 msec or less, following A2. The zone of repetitive atrial firing could be defined in terms of its longest and shortest A1-A2 coupling intervals. Each patient was tested at a long cycle length (CL1) (mean 884 msec) and a short cycle length (CL2) (mean 557 msec). CL1 was sinus rhythm and CL2, an atrial paced rhythm. Repetitive atrial firing occurred in two patients at CL1 and in all patients at CL2. Of the former two patients (group 2), the zone of repetitive atrial firing was markedly widened in one at CL2 due to a shortening of atrial functional refractory period (FRP) at CL2. In the other, zone of repetitive atrial firing could not be totally defined due to induction of sustained atrial flutter preventing definition of atrial FRP. The occurrence of repetitive atrial firing at only CL2 in 12 patients (group 1) reflected: 1) a shortening of atrial FRP from 294 +/- 11 msec at CL1 to 242 +/- 10 msec at CL2 (mean +/- SEM; P less than 0.01), allowing delivery of A2 at shorter coupling intervals (9); 2) the new occurrence of repetitive atrial firing at A1-A2 coupling intervals achievable at both cycle lengths (1); or 3) both effects (2). In conclusion, decrease of cycle length potentiated atrial vulnerability. This demonstration implies that atrial pacing could potentiate occurrence of paroxysmal atrial fibrillation or flutter.
Explore the source record for details and available documents.
Three patients with paroxysmal supraventricular tachycardia (PSVT) had discontinuous ventriculo-artrial conduction curves (V1-V2, A1-A2), suggesting dual A-V nodal pathways. Ventricular echoes occurred simultaneously with sudden increase of V-A interval. These echoes were characterized by retrograde P waves occurring in front of QRS, suggesting utilization of a slow pathway for retrograde conduction and a fast pathway for antegrade conduction. In case one, atropine improved retrograde slow pathway and antegrade fast pathway conduction and made A-V nodal re-entry sustained, resulting in PSVT (with retrograde P in front of the QRS). In cases 2 and 3, atropine markedly shortened retrograde fast pathway refractory period and slightly improved antegrade slow pathway conduction. The discontinuous V1-V2, A1-A2 curves and echoes were no longer demonstrable. However, with improvement of retrograde fast pathway and antegrade slow pathway conduction, A-V nodal re-entrant echoes and PSVT were observed, utilizing the slow pathway for antegrade conduction and the fast pathway for retrograde conduction (P simultaneous with QRS).
In patients with dual atrioventricular (A-V) nodal pathways, atrial extrastimulus testing induces either no echoes, single atrial echoes (Ae), or repetitive re-entrance (repetitive atrial and ventricular beating). We examined the fast and slow pathways properties in 38 patients with dual pathways in order to delineate the determinants of re-entrance. Seventeen patients had no Ae. Of these, six had no V-A conduction and 11, intact V-A conduction. The mean paced ventricular cycle length producing retrograde V-A block (VABCL) in this group (a measure of retrograde fast pathway refractoriness) was 552 +/- 32 msec (mean +/- SEM; 10 pts). In contrast, all 21 patients with Ae had intact V-A conduction with mean VABCL of 382 +/- 21 msec (14 pts) (P less than 0.05). Repetitive re-entrance occurred only when Ae conducted to the ventricles. Seven patients had only single Ae. The mean paced atrial cycle length producing Wenckebach periodicity (CLAWP) in this group (a measure of antegrade slow pathway refractoriness) was 490 +/- 31 msec (5 pts). Fourteen patients had repetitive re-entrance. The mean CLAWP in this group was 399 +/- 18 msec (8 pts) (P less than 0.05). In conclusion, our results suggest that in patients with dual pathway, the occurrence of single or repetitive re-entry is dependent upon measurable slow and fast pathway properties.
Explore the source record for details and available documents.
Prospective follow-up studies of 277 patients with chronic bifascicular block showed that 30 patients developed sudden cardiac death (SCD). Cumulative one-, two-, and three-year SCD mortality was computed. The patients that developed SCD were compared with the remaining patients (209 alive and 38 dead). The groups were similar in regard to age, sex, AH, and HV intervals. The following were more frequent in the SCD group (P less than .05): angina, previous myocardial infarction, heart failure, cardiomegaly, left bundle-branch block, premature ventricular beats, and ventricular tachycardia. Ventricular fibrillation was the cause of death in four cases of SCD where terminal ECG documentation was available. We concluded that SCD is a major cause of mortality in patients with chronic bifascicular block. The association of SCD with coronary disease and ventricular dysrhythmia suggested ventricular fibrillation as a frequent mechanism.
An experiment was designed to determine optimal methods of myocardial reperfusion after normothermic ischemic arrest in the in vivo pig heart. Four variables were studied: 1) ischemic arrest for 15 minutes repeated six times vs 30 minutes repeated three times: 2) coronary reperfusion between each arrest period lasting 5 or greater than or equal to 15 minutes (the latter duration dependent upon electrocardiographic reversal of ischemic); 3) perfusion pressure of 50, 75, or 100 mm Hg; and 4) a beating or fibrillating heart during reperfusion. The effects of perfusion were monitored by measuring the endocardial/epicardial perfusion ratio (with ratioactive microspheres), coronary blood flow, and coronary reactive hyperemia by measuring coronary vascular resistance during reperfusion. Electron micrographs were examined to determine if subtle distinctions between groups could be measured. A total of 78 pigs (60 experimental and 18 control) were evaluated. The experimental animals were divided into 10 groups of six pigs each. In each group only one of the four variables (beating or fibrillating ventricle, perfusion pressure, duration of ischemia, and duration of reperfusion) was altered to provide comparative data. Results are based on improved endocardial perfusion and a greater coronary reactive hyperemic response when comparing each experimental group to one another and to control animals. Reperfusion of a contracting rather than fibrillating ventricle resulted in improved endocardial flow as did reperfusion at a low (50 or 75 mm Hg) rather than a high (100 mm Hg) perfusion pressure. A short ischemic interval repeated six times rather than a longer ischemic interval repeated three times also allowed for improved subendocardial perfusion and a greater reactive hypermic response as did a longer reperfusion period between equal ischemic intervals. Electron microscopic studies showed a gradation of abnormalities ranging from little deviation from control in beating hearts and short ischemia and long duration, low pressure reperfusion to marked mitochondrial vacuolization in fibrillating hearts subjected to long ischemia, short reperfusion at high perfusion pressures. The best technique for myocardial reperfusion based on available data is to provide reperfusion of adequate duration in order to reverse the ischemic electrocardiogram in a beating heart, avoiding an excessively high perfusion pressure.
Electrophysiological and epicardial mapping studies are described in a patient without pre-excitation who had intractable recurrent paroxysmal supraventricular tachycardia. Electrophysiological studies revealed fixed VA conduction times during both rapid ventricular pacing and coupled ventricular stimulation. Catheter mapping of atrial activation during retrograde conduction and during induced paroxysmal supraventricular tachycardia revealed early distal coronary sinus activation (posterior left atrium) relative to the low septal, low lateral, and high lateral right atrium. These studies suggested the presence of a concealed left-sided bypass tract. The patient underwent surgical interruption of the His bundle for control of paroxysmal supraventricular tachycardia. Epicardial mapping of the atria (during ventricular pacing) confirmed the presence of a concealed left-sided bypass tract. Surgery produced antegrade av block (while retrograde conduction was maintained) and total cure of paroxysmal supraventricular tachycardia. This is the first reported case of a concealed retrograde extranodal pathway documented by epicardial mapping.
Electrophysiological studies (His bundle recordings and atrial stimulation) were performed in nine patients who manifested periods of both right and left bundle branch block (RBBB and LBBB). In seven of the patients, alternating bundle branch block appeared to reflect intermittent or chronic bundle branch block superimposed on incomplete (but electrocardiographically complete) block of the contralateral bundle branch. In three of these seven, shift from one bundle branch block pattern to the other was associated with reproducible change in H-V (mean change 30 msec), and could be induced by alteration of cardiac rate with carotid massage, coupled atrial stimulation, and rapid atrial pacing. In one of the seven, RBBB with a P-R of 0.20 seconds preceded chronic LBBB with a P-R of 0.24 seconds, implying that RBBB had been incomplete. In three of the seven, although a definite mechanism of alternation could not be demonstrated, transient contralateral bundle branch block occurred superimposed on chronic ipsilateral bundle branch block, implying that the ipsilateral block was incomplete. Two patients manifested periods of narrow QRS, LBBB, RBBB, and paroxysmal A-V block. Based upon pathological data (one case), this pattern appeared to reflect a lesion involving the distal His bundle and proximal bundle branches. In the total group of patients, clinical course was primarily determined by the severity of heart disease and not by occurrence of A-V block. The conduction defect in the majority of patients was surprisingly benign.