Gaetano Satullo

Supernormal Conduction in the Left Bundle Branch Unmasked by the Linking Phenomenon

This presentation reflects a case of phase‐3 left bundle branch block (LBBB). Analysis reveals that relatively early QRS complexes are wide, whereas beats occurring later than a critical time are narrow. There are, however, two unexpected phenomena: (1) an overlap occurs between the range of R‐R intervals resulting in normal intraventricular conduction and the range of R‐R intervals resulting in LBBB pattern. Complexes that follow a wide beat are often wide although they are associated with relatively long R‐R intervals, whereas complexes that follow a normal beat tend to be normal even after relatively short R‐R cycles. This is due to concealed retrograde penetration of the bundle branch that is blocked in anterograde direction (the so‐called linking phenomenon). (2) Some early supraventricular impulses, paradoxically, resulted in normal intraventricular conduction. The phenomenon is a manifestation of supernormal LBB conduction, and only occurs following a wide QRS complex associated with retrograde activation of the LBB. The linking phenomenon reveals or unmasks the supernormal phase of LBB conduction. Following a retrograde and delayed activation of the LBB, the refractory period of the bundle branch is postponed, in such a way that a supraventricular impulse is allowed to occur during the early phase of supernormal conduction.

Concealed ventricular quadrigeminy linked to atrial quadrigeminy: A manifestation of modulated parasystole

Analysis of a long electrocardiographic recording including many atrial and ventricular extrasystoles shows that when atrial extrasystoles are in a quadrigeminal distribution, the ventricular extrasystoles also manifest a quadrigeminal distribution or reflect a distributional pattern of concealed quadrigeminy. Conversely, when atrial extrasystoles are other than in a quadrigeminal distribution, the ventricular extrasystoles do not occur in a quadrigeminal or concealed quadrigeminal distribution. This pattern is explained on the basis of modulated parasystole. A biphasic phase-response curve explains the observed phenomena on the basis of variations of the parasystolic cycle length due to the modulating effect of supraventricular beats.

Longitudinal Dissociation within the Reentry Pathway of Ventricular Tachycardia

SATULLO, G., ET AL.: Longitudinal Dissociation within the Reentry Pathway of Ventricular Tachycardia. Two cases of nonsustained, repetitive ventricular tachycardia are analyzed. In both, the episodes of tachycardia do not contain random numbers of beats, but the complexes in each phase of tachycardia are either always in even numbers (case 1) or always in odd numbers (case 2). This indicates longitudinal dissociation within the reentry circuit: i.e., there are two functionally separate pathways in some part of the reentry circuit, and the reciprocating impulse runs alternatively through the two pathways. Tachycardia ends due to block of the impulse always in the same pathway, thus, the number of beats in each episode of tachycardia is always either in odd or even numbers. (PACE, Vol. 13, December, Part 1 1990)

Non-sustained ventricular tachycardia with Wenckebach exit block.

A case of non-sustained, recurrent ventricular tachycardia, manifesting with irregular R-R intervals, is described. Analysis of a long electrocardiographic recording reveals that the arrhythmia is generated by a regularly discharging ectopic ventricular focus, the R-R interval variations being due to a Wenckebach form of exit block.

Progressive prolongation of the second conduction interval throughout successive 3:2 Wenckebach sequences: The double Wenckebach phenomenon

relatively empty cavity then may cause an inappropriate stimulation of cardiac sensory receptors with nonmyelinated (C-fiber) vagal afferents.5T6 This results in arterial vasodilation and bradycardia, which is at least partially due to parasympathetic discharge. In most patients with neurally mediated syncope studied by head-up tilt testing, hypotension precedes bradycardia.5 Once bradycardia occurs, hypotension is exacerbated and the process tends to be self-perpetuating. In our patient, a decrease in blood pressure correlated with the onset of symptoms and preceded bradycardia by approximately 45 seconds. The failure of ventricular pacing to alleviate symptoms or hypotension further supports arterial vasodilation as the primary cause of syncope. Beta-adrenergic blockers may blunt the profound bradycardia and hypotension reflex to upright tilt in patients with neurally mediated syncope by preventing overstimulation of left ventricular C-fiber receptors. Since an excessive vagal reflex in response to marked beta-adrenergic stimulation is also the most likely mechanism for post-exercise vasodepressor and vasovagal reactions, beta-blocking agents may be effective by preventing the initiating excessive beta stimulation. As demonstrated by this case and by one previously reported case,4 severe life-threatening postexercise vagal reactions can be abolished by the administration of oral beta blockers. This case demonstrates the utility of head-up tilt testing in predicting which patients with post-exercise vasovagal reactions will respond to long-term beta-adrenergic therapy.

Alternating left and right bundle branch block aberration of atrial extrasystoles in bigeminal rhythm.

We report two cases of atrial extrasystolic bigeminy manifesting with alternating right and left bundle branch block aberration. The manifestation is explained on the basis of cycle‐dependent variations of the bundle branch refractory period with alternate resetting of bundle branch refractoriness.

Intermittent sinus bigeminy as an expression of sinus parasystole: a case report.

A case of sinus parasystole is reported. The diagnosis of sinus parasystole is relatively difficult because there is no difference between the basic sinus P wave and the parasystolic wave. Sinus parasystole is diagnosed according to the following electrocardiographic criteria: (1) premature P waves having contour identical to P waves of basic beats; (2) intervals between premature P waves mathematically related. In the case reported, the coupling intervals during long phases of intermittent sinus bigeminy were nearly fixed, because there was little variability in the returning cycles, making the diagnosis of sinus parasystole difficult.

Irregular Sinus Parasystole Due to Intermittency and Modulation of Parasystolic Activity

Intermittent Sinus Parasystole. A case of intermittent sinus parasystole in which the parasystolic focus is protected from the dominant sinus rhythm only during the second half of its intrinsic cycle is reported. In addition, a modulating (i.e., electrotonic) effect is often clearly exerted from the dominant rhythm upon the focus during the protected period. Coexistence of both modulation and intermittency in sinus parasystole, as well as a modulating effect limited to the second part of the parasystolic cycle, have not been previously reported.

Changes in Morphology of the Paced QRS Complex Related to Atrial Contraction

A patient with 2:1 AV block underwent temporary ventricuJar pacing. AU the paced stimuli resuited in ventricular capture, but a marked variability in morphology of the paced QRS complexes occurred. Two different types of paced QRS complex (labeled A and B) were recognized. Type B complexes were manifest only when the pacing stimulus was preceded hy a sinus P wave within a time interval ranging from 0.15 to 0.52 sec. The P wave‐induced changes in morphology of the paced QRS complexes were interpreted as due to displacement of the pacing ventricular lead caused by atrial systole.

4:2 Atrioventricular Block:

The ECG (Fig. 1, continuous tracings) recorded from a 73-year-old male patient with hyperkalemia (K+ 7.3 mEq/L) shows sinus rhythm at a rate of about 95 beats/min complicated by second-degree AV block with constant 4:2 conduction ratio. A difference between the first and the second QT interval is evident for each 4:2 succession: the second QT interval (i.e., the one following the second conducted QRS complex), is slightly—but constantly—shorter than the first one, so that the second—still conducted— P wave of each sequence can be seen on the T wave of the preceding ventricular complex, while the third P wave— nonconducted—is clearly separated from the previous T wave.