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His bundle recordings were performed in 2 patients in whom AV nodal bypass tracts coexisted with intermittent AV conduction disturbances occurring below the site from which the His bundle deflection was recorded. Case 1 had: (a) tachycardia dependent right bundle-branch block, (b) persistent HV prolongation, and (c) bradycardia dependent AV block. Case 2 showed: (a) intra-atrial conduction delay, (b) tachcardia dependent left bundle-branch block with HV prolongation, (c) bradycardia dependent HV conduction disturbance, (d) tachycardia-bradycardia syndrome of an unusual type; the latter presumably resulted, during atrial flutter, from the alternation of rapid AH conduction through the bypass tract with intermittent (complete) distal His bundle block or bilateral bundle-branch block. [ABSTRACT FROM PUBLISHER]

His bundle electrograms were recorded in 2 patients with ectopic beats arising in accessory atrioventricular tracts. Case 1 had Wolff-Parkinson-White (WPW) type A and a left-sided Kent tract with a short effective refractory period. Though ectopic impulse formation most probably occurred within the Kent tract itself, a vulnerability-related origin in the ventricular muscle close to the distal end of the Kent tract could not be excluded. In Case 2, with a Mahaim tract extending from His bundle to ventricles, there were three types of QRS morphologies resulting from : (a) atrioventricular conduction exclusively through the normal pathways; (b) atrioventricular conduction through both, normal pathway, and Mahaim tract; and (c) ectopic impulse formation in the Mahim tract. Specialized electrophysiological studies were essential to diagnose these unusual arrhythmias. [ABSTRACT FROM PUBLISHER]

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval. [ABSTRACT FROM PUBLISHER]

In a patient with a Wolff-Parkinson-White (WPW) syndrome type A mid-right atrial stimulation at a rate of 73/min produced a lesser degree of ventricular pre-excitation than when a slower sinus rhythm was present. This paradoxical effect was not related to tachycardia-dependent block in the accessory pathway because pre-excitation again increased at faster pacing rates. It was partly the result of a (proportionally) greater prolongation of intra-atrial conduction time to the accessory pathway than to the atrioventricular node and partly of a faster atrioventricular nodal conduction time. The latter, in turn, could be attributed either to later-than-normal arrival of excitation at the atrioventricular node, at a time when this structure was more recovered, or to a change in the site or mode of entry into the atrioventricular node. A gap in the atria was present because at a St1-St2 interval shorter than that which A2 had been blocked in the accessory pathway conduction was again possible, but with longer A1-A2 intervals. Finally, at similar, short, coupling intervals the impulse penetrated the atrioventricular node from the mid-right atrium but not from the coronary sinus. The unusual findings in this case support a recent assumption that in patients with WPW type A atrial stimulation should be performed from the coronary sinus to minimize the potential sources of error which can be produced by intra-atrial delay. [ABSTRACT FROM PUBLISHER]

Intracardiac electrophysiological studies were performed in two patients with a documented history of repetitive supraventricular tachyarrhythmias. Case 1, with short PR interval and narrow QRS complexes had a short AH interval and intermittent right bundle-branch block. Thus the short PR wide QRS syndrome is not always a result of the Wolff-Parkinson-White syndrome but can also be seen in the Lown-Ganong-Levine syndrome coexisting with bundle-branch block. Case 2, with normal PR and AH at the lower limits of normal, showed the dual pathway response to atrial pacing that can occur in patients with Lown-Ganong-Levine syndrome. He also had tachycardia-dependent right bundle-branch block and left posterior hemiblock. Therefore, neither the short PR interval nor the narrow QRS complexes characterized these forms of pre-excitation. The constant features were, from the clinical viewpoint, the occurrence of repetitive supraventricular tachyarrhythmias, and electrophysiologically the abnormal response to atrial stimulation. [ABSTRACT FROM PUBLISHER]

Filtered bipolar catheter electodes, I mm apart, were used to pace and record from the high right atrium, right ventricular apex, right ventricular outflow tract, right ventricular inflow tract, middle cardiac vein, great cardiac vein, and endocardium of the left ventricular septal surface. Right ventricular apex to middle cardiac vein and the middle cardiac vein to right ventricular apex conduction intervals gave a rough estimate of anteroposterior and posteroanterior "transseptal plus free left ventricular wall" conduction times, respectively. On the other hand, the right ventricular apex to left ventricular septal surface and left ventricular septal surface to right ventricular apex intervals represented pure "transseptal" conduction times, since both sets of electrodes were in contact with the respective septal surface. During stimulation of the intermediately located right ventricular inflow tract propagation to the right ventricular apex and right ventricular outflow tract was longer than between these two sites. Moreover, conduction was almost as delayed to the right ventricular apex and right ventricular outflow tract as it was to the left ventricular septal surface. These findings were attributed to the peculiar electrophysiological behaviour of the right ventricular inflow tract muscle. Pacing from different segments of the great cardiac vein produced QRS morphologies and arrival of excitation patterns consistent with the relation between the anatomical location of this structure and the recording electrodes. However, from this study no inferences could be drawn regarding the conduction velocity or specific conduction pathways used by the stimulus in its journey from stimulating to recording areas. [ABSTRACT FROM PUBLISHER]

Eleven patients were studied and a total of 144 Wenckebach cycles in the AV node and 118 Wenckebach cycles in the His-Purkinje system were analysed to determine the incidence of typical and atypical Wenckebach periodicity, with particular emphasis on one variant of atypical Wenckebach that may simulate a Mobitz type II block. This pseudo-Mobitz II pattern was defined as a long Wenckebach cycle in which, at least, the last three beats of the cycle show relatively constant PR intervals (variation of no more than 0.02 s in surface leads and no more than 10 ms in His bundle electrograms) and in which the PR interval immediately following the blocked beat is shorter than the PR interval before the block by 0.04 s or more. Atypical Wenckebach cycles were found to be more common than the typical variety at both the AV node (67%) and His-Purkinje system (69%). The pseudo-Mobitz II pattern was seen in 19 per cent of atypical AV nodal Wenckebach periods and in 17 per cent of atypical His-Purkinje system Wenckebach cycles. The need to discern a 'classical' Mobitz II block from a pseudo-Mobitz II pattern, especially in the setting of an acute inferior myocardial infarction, is emphasised. [ABSTRACT FROM PUBLISHER]

Atrial echo beats resulting from a reciprocating mechanism involving the bundle-branches were produced by premature atrial impulses in a patient with an A-V nodal bypass tract. The mechanism of the arrhythmia was suggested by the presence of a retrograde His bundle deflection which appeared 'sandwiched' in between a QRS complex with complete right bundle-branch morphology and a negative P wave. Though at a shorter cycle length the His bundle was still activated retrogradely echo beats were not seen because the retrograde H deflection occurred too early, when both bypass tract and A-V node were still effectively refractory. At the faster driven rate concealed retrograde activation of the right branch (by the premature impulse) was responsible for the right bundle-branch block patterns shown by the post-premature driven beat. [ABSTRACT FROM PUBLISHER]

Comments on the importance of His' bundle recordings approach in patients with acute myocardial infarction complicated by incomplete bilateral bundle branch block. Mortality rate associated with incomplete bilateral bundle branch block; Prognosis for patients with persistent right bundle branch block.

This paper reports the unusual case of a 76-year-old woman who was discovered to have a hemodynamically significant patent ductus arteriosus following uneventful mitral valve replacement, utilizing cardiopulmonary bypass. The shunt was successfully eliminated using a new transcatheter device, thereby obviating the need for further surgery. The patient did not have calcification within the ductus, making diagnosis prior to surgery more difficult.

In patients with WPW syndrome the maximal ventricular rate attained during ectopic rapid supraventricular thythms depended on the type of arrhythmia as well as on the physiological properties of the AP. During reciprocating tachycardias the impulse is almost invariably conducted to the ventricles through the AV node. Therefore, the maxiaml ventricular rate is a function of the AV nodal ERP. On the other hand, when atrial flutter or atrial fibrillation were present the ventricular rate could be moderately elevated (when the ERP of the AP was longer than that of the AV node) or very rapid where the ERP of the AP was significantly short. Therefore, from the electrophysiological viewpoint, the AP appears to behave as His-Purkinje tissue in some cases and as ordinary artrial muscle in other patients. These assumptions await further documentation.

This report presents the experience obtained with the use of mechanical stimulation of the heart by external ("chest thump") and internal (stimulation via catheter) means in the treatment of tachyarrhythmias. The chest thump was used primarily for termination of ventricular tachyarrhythmias. Endocardial stimulation of the right and left ventricles and right atrium via catheters was used for both ventricular and supraventricular arrhythmias. The experience reported includes 68 patients, 19 of whom were treated successfully with mechanical stimulation and 49 of whom required other types of treatment. Of the 32 patients with 33 episodes of atrial tachycardia, eight episodes (24%) were treated successfully (three episodes by right atiral stimulation and five by right ventricular stimulation). Of the four patients with five episodes of junctional tachycardia, three episodes (60%) were treated successfully (one episode by right atrial stimulation and two by right ventricular stimulation). Of the 32 patients with ventricular tachycardia who experienced 37 episodes, 15 episodes (41%) were treated successfully (three by right ventricular stimulation, two by left ventricular stimulation, and ten by chest thump). In two of these patients, the thump was applied to an area of paradoxical pulsation.

The relationship between systemic and renal hemodynamics was studied in 20 patients with advanced cirrhosis of the liver. Cardiac output was assessed by an indicator dilution technique, and both mean renal blood flow and intrarenal blood flow distribution were determined by the 133Xe washout method. Ten patients had elevated cardiac outputs (7.14 to 13.58 L/min; HCO group), seven patients had normal cardiac ouptputs (5.16 to 6.78; NCO group), and three had low cardiac outputs (3.65 to 4.1; LCO group). Renal hemodynamics did not correlate with cardiac output (r = 0.051; N.S.), since comparable reductions in mean renal blood flow occurred in both the LCO and HCO patients. Similarly, the degree of cortical ischemia, as assessed by percentage flow to the rapid flow component (C1%), did not correlate with cardiac output (r = 0.007; N.S.). Vasomotor instability as assessed by intrapatient variability of sequential xenon washout studies occurred frequently, and its magnitude did not correlate with cardiac output (r = -0.069; N.S.). These studies demonstrate that the abnormalities of intrarenal blood flow in cirrhosis are independent of alterations in cardiac output. Furthermore, the finding of marked intrarenal hemodynamic instability in the majority of patients with cirrhosis suggests that caution should be exercised in interpreting studies assessing the efficacy of vasoactive agents on renal hemodynamics in this disease, since the changes attributed to treatment may merely reflect spontaneous change.

The R-on-T phenomenon was observed in two patients with narrow QRS complexes and repetitive supraventricular tachyarrhythmias. Case 1 had a typical Lown-Ganong-Levine syndrome in which the shortening of the P-R interval was due to a reduction of the A-H interval. In Case 2 the P-R interval (140 msec) was not short but the A-H interval was at the lower limits of normal (50 msec) and the P-A interval at the upper limits of normal (40 msec). Both patients showed the R-on-T phenomenon during periods of 1:1 A-V conduction occurring during atrial stimulation at a rate of 200/min (Case 1) and atrial flutter with a rate of 300/min (Case 2). Although total A-V conduction time was prolonged, the magnitude of this prolongation appeared to have been less than that occurring in normal subjects. This was attributed to the presence of an accessory pathway bypassing the area where the most significant delay occurred at the A-V node. The findings in Case 2 suggest, but do not prove, that a similar bypass might be operative in patients with atrial flutter with periods of 1:1 conduction, regardless as to whether the R-on-T phenomenon is, or is not, present.

The analysis of the common bundle and of the ventrical filtered electrograms has incrased our knowledge of the intraventricular conduction following the simulation of the PVS as well as the different types or reciprocating that can be produced by premature beats. 2. The positive QRS complexes in V1 produced from PVD by St2 can be explained as a greater degree of incomplete recuperation of the right ventricular wall than in the interventricular septum. In contrast with what happened in the basal beats, where the front took longer to reach the TSVD than the VI. 3. The refractarines of the transitional tissues that serve as the phisiological banier was longer than the banal myocardium. The intraventricular propagation, and therefore the morphology and direction of QRS, depended of this one; while the moment of arrival of activation retrogradly to the common bundle was conditioned by the transitional tissues. 4. Episodes of ventricular taquicardies with QRS positive complexes in V1 can be due to a re-entry throught the bundle branches or in (or around) an area that has been recently injured.