Left fascicular blocks during right-heart catheterization using the Swan-Ganz catheter.

During insertion of Swan-Ganz catheters, mechanical right bundle branch block occurred in association with left posterior fascicular block in two patients and with left anterior fascicular block in two. None of the four patients had acute myocardial infarction or acute (spontaneous or iatrogenic) pulmonary disease. In two cases, electrophysiologic studies demonstrated the coexistence of intra- and infra-Hisian conduction delays and blocks. Although the right bundle branch block may have resulted from injury to the central or peripheral right branch, the left fascicular blocks could not be explained by direct trauma to these left-sided structures. Our findings support the recent clinical and experimental reports that show that left fascicular block (as well as right bundle branch block) may be due to lesions involving the His bundle; presumably because of longitudinal dissociation of this structure affecting the transverse interconnections. In one patient, 2:1 intra-Hisian block may have coexisted with bradycardia-dependent (phase 4) right bundle branch block. More studies are required to determine the implications of catheter-induced conduction disturbances in other clinical settings, such as acute myocardial infarction.

Right ventricular apical activation times in patients with conduction disturbances occurring during acute transmural myocardial infarction.

His bundle and right ventricular apical electrograms were recorded in 18 patients with acute transmural myocardial infarction in whom catheter insertion was considered necessary for clinical reasons. The V-RVA and H-V intervals were of normal duration (5 to 30 and 35 to 55 msec, respectively) in five patients (Group 1) with persistently narrow (less than 100 msec) QRS complexes. In contrast, 13 patients (Group 2) who manifested a "complete" right bundle branch block pattern within 96 hours after admission had prolonged V-RVA intervals (range 50 to 80 msec, mean 59.2 msec) and H-V intervals that were at the upper limits of normal or prolonged (range 55 to 90 msec, mean 63 msec). In 6 of these 13 patients, the duration of the V-RVA interval became normal when the "complete" right bundle branch block pattern disappeared and was replaced by a "complete" left bundle branch block pattern in three patients and by narrow QRS complexes in the three other patients. This study showed that transmural myocardial infarction in itself did not increase the duration of the V-RVA interval even when "complete" left bundle branch block was present. Moreover, a prolonged V-RVA interval coexsting with a "complete" right bundle branch block pattern was not due to distal right bundle branch block but resulted from a conduction disturbance located in the proximal portions of the right bundle, or perhaps, even within the His bundle itself.

Primary ventricular fibrillation. Some unusual features.

A 47-year-old man experienced ventricular fibrillation three times during a 3 1/2-year period. Each episode was preceded by an auditory aura, and no ventricular irritability was identified between episodes. The results of coronary arteriographic, hemodynamic, and intracardiac electrophysiologic studies were all normal. Hypokalemia and abnormal oxyhemoglobin dissociation were present. The possible relationships of these unusual features to the patient's disturbances in rhythm are discussed.

Intermittent AV conduction disturbances in patients with AV nodal bypass tracts. Possible mechanisms of unusual variant of tachycardia-bradycardia syndrome.

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.

Intermittent pseudocomplete A-V block due to A-V dissociation in presence of 2:1 A-V block.

A false pattern of intermittent complete A-V block was seen in two asymptomatic patients when A-V dissociation was superimposed on a basic 2:1 A-V block. Although the conduction disturbance occurred at the A-V nodal level in both cases, in Case 2 it resembled A-V block due to bilateral or trifascicular disease. This arrhythmia was the end result of Type I (Wenckebach) block and apparently has a better prognosis than those emerging from a Type II (Mobitz) block.

Double ectopic accelerated ventricular and nonaccelerated ventricular or supraventricular rhythms.

Three patients with acute inferior wall myocardial infarction has accelerated idioventricular rhythms alternating and (or) coexisting with: (a) AV junctional (or low atrial) rhythm (Case 2); (b) paroxysmal ventricular tachycardia and another accelerated idioventricular rhythm (Case 3); and (c) AV junctional rhythm, paroxysmal ventricular tachycardia and accelerated idioventricular rhythm from another center (Case 4). The tracings from a fourth patient (Case 1) served to focus attention on one of the most pertinent features of accelerated idioventricular rhythms, namely the gradual decrease in rate to values below that of the preexisting basic rhythm. Cardioacceleration with atropine and cardiosuppression with lidocaine failed to abolish the arrhythmias or relieve the symptoms in cases 3 and 4. Atrial stimulation proved the most effective mode of therapy in these two patients.