Marcelo V. Elizari

Frontiers of cardiac electrophysiology

The clinical significance of the negative U wave was examined in 488 consecutive patients. A negative U wave was highly specific for the presence of heart disease and was associated with other ECG abnormalities in 94.9% of patients. The three most common conditions associated with negative U wave were: systemic hypertension, aortic and mitral regurgitation, and ischemic heart disease. The U wave vector was directed opposite to the QRS axis in the horizontal plane in patients with both left and right ventricular hypertrophy. In patients with ischemic heart disease, the U wave vector was directed away from the site of akinetic or dyskinetic region. The change from negative to upright U wave after lowering blood pressure, renal transplantation, insertion of valve prosthesis, or coronary artery-aorta bypass graft procedure was associated with decrease in the QRS amplitude, but no consistent changes in T wave polarity. The timing of U wave apex was dependent on the duration of ventricular repolarization but not on the duration of the QRS complex. Several observations in this study are explained better by the ventricular relaxation rather than the Purkinje fiber repolarization theory of U wave genesis.

A Reappraisal of Supernormal Conduction

According to some authors [1] “supernormal conduction is said to occur when impulse conduction is better than expected”. According to others [2] “conduction may be called supernormal when it is better than anticipated under the circumstances, or where propagation succeeds early in diastole and fails at all other times”. Still others [3] are of opinion that “the term supernormal phase designates a short, early, and limited period of the cardiac cycle during which a stimulus elicits either a totally unexpected response or one that is less abnormal than expected considering the state of recovery from the preceding impulse”.

Electrotonic Modulation of Ventricular Repolarization and Cardiac Memory

It is a well-known and widely accepted fact that T wave changes are either primary or secondary in nature [1,2] and that this simple classification covers all T wave abnormalities occurring in the human ECG[3]. Secondary T wave changes are those provoked by variations of the QRS, whereas primary T wave changes occur as independent phenomena. The latter are considered to imply a change of the ventricular gradient (VG), while the former are not [2–4].

The Role of Phase 3 and Phase 4 Block in Clinical Electrocardiography

In the past, automaticity and conduction were thought to be independent and totally unrelated physiologic properties of the specific tissues of the heart. It was then only natural that, abnormalities of conduction and alterations of automaticity (the latter still poorly known and almost unexplored) were discussed in separate and disconnected chapters in books of arrhythmias and electrocardiography. However, in the last few years, the development of the concept of phase 4 block (144, 237, 240, 241, 691–694, 696) brought into focus the existence of a relationship between automaticity and conduction, which may prove to have significant physiologic as well as clinical and electrocardiographic and even therapeutic consequences. This relationship may perhaps open a new chapter in contemporary electrocardiography; and although this statement may at first glance appear as too provocative or overhasty, it is greatly supported by Alfred Pick (632), teacher, friend and deep thinker of the electrocardiography of all times, when he says that ‘hemiblocks and phase 4 block are the two most important advances of electrocardiography in the last ten years’. However, whether or not a new chapter will open its way, this is less important than the fact that the concept of phase 4 block (together with its closely associated phase 3 block) may be dealt with as a multipurpose concept which may serve to explain a series of old and still puzzling problems of clinical electrocardiography. Among these, I have selected for this chapter the following five: intermittent bundle branch block (BBB), paroxysmal AV block, parasystole, Wolff-Parkinson-White syndrome and the effects of certain drugs upon conduction. Essentially, I will try to show how these five problems, apparently so dissimilar and heterogeneous, can be aligned together on behalf of the newly established relationship between automaticity and conduction.

Right Bundle-Branch Block and Left Anterior Fascicular Block (Left Anterior Hemiblock) Following Tricuspid Valve Replacement

Right bundle-branch block occurred in 42.8% and left anterior hemiblock in 35% of 14 patients after surgical replacement of the tricuspid valve. The combination of RBBB with left anterior hemiblock is caused by injury to the branching portion of the bundle of His or more likely, by a lesion involving the pseudobifurcation. This study provides further proof that left anterior hemiblock may be produced by a “central” lesion of the conduction system. An attempt was made to re-define the relationships of the bundle of His and bundle branches to the membranous septum and septal leaflet of the tricuspid valve and to correlate the site of surgical injury with the type of conduction disturbances produced.

The Experimental Evidence for the Role of Phase 3 and Phase 4 Block in the Genesis of A-V Conduction Disturbances

Clinical (237, 692, 694) and experimental (240, 241) studies have demonstrated two types of rate dependent conduction disturbances. In one of these, the conduction disturbance occurs when the heart rate is accelerated (phase 3 block) and in the other, the conduction disturbance appears after long diastolic intervals or when the heart rate is slowed (phase 4 block). The term ‘phase 3 block’ has been used since it is assumed that the blocked impulse reaches the injured fibers of the involved region during phase 3 of abnormally prolonged action potentials (237, 240, 692, 694). Phase 4 block has been attributed to a loss of maximum diastolic potential (hypopolarization), enhanced spontaneous diastolic depolarization (SDD), and a shift in threshold potential towards zero (692, 694, 760).

Mechanism of Mobitz II Periodicities

In contrast to the multiple mechanisms that have been invoked to explain Wenckebach periods, relatively few attempts have been made to unravel the electrophysiological basis of Mobitz II block [1]. Hay [2] suggested that the block was due to a depression of ventricular excitability, an explanation with which Wenckebach agreed [3]. A Wedensky phenomenon was invoked by others [4]. To explain the fact that blocked beats occur without variation of the P-R interval, Katz and Pick [5] suggested a prolongation of the absolute refractory period without concomitant prolongation of the relative refractory period; and subsequently, Pick and Langendorf [1] implied that the relative refractory period could even be shorter than normal. Recently [6–8], it has been suggested that Mobitz II block does not exist as a separate entity, but merely represents a Wenckebach periodicity in which prolongation of the conduction time is so small that it is not detectable on the surface ECG. This latter hypothesis has been considered of doubtful validity by Zipes [9] and Pick and Langendorf [1]. In 1927, Wenckebach and Winterberg [10] stated that “Most of the newer authors pass over silently the problem of Type II A-V block. However, this does not achieve anything. The problem does exist and requires solution, for none of the theories of conduction disorders is entirely satisfactory as long as it does not include all the facts doing them justice”. Much more recently Pick and Langendorf [1] concluded that “the problem stated by Wenckebach is still with us and unresolved”.

Clinical Studies on the Mechanism of Ventricular Arrhythmias

Cardiac arrhythmias can result from either abnormalities of impulse generation or abnormalities of impulse propagation [1, 2]. However, the mechanism of ventricular arrhythmias is not always well understood. For example, it is difficult to assess the way in which ventricular parasystole (VP) [3–5] is affected by “exogenous” electrical or neural influences, or by “intrinsic” variations of the parasystolic system itself. The role of reentry versus automatic and triggered activity in the mechanism of ventricular extrasystoles (VE) and tachycardias (VT) is also under discussion [6–12]. The old question as to whether VP and VE are mechanistically related is still a matter of debate [7–9, 13–17]. Some of these problems will be addressed in this review. Special emphasis will be laid upon the way in which ventricular arrhythmias relate to each other, as well as the manner in which they are affected by electrical activity going on elsewhere in the heart and by changes in the autonomic tone. To that effect, 71 cases of VP, 29 cases of VE, and 3 different forms of VT will be analyzed.

Normal and Abnormal Ventricular Automaticity in the Human Heart

Studies of the factors which may affect the activity of normal idioventricular pacemakers or cause abnormal ventricular automaticity in the human heart, have been scarce [1–4]. In this article, we will discuss: 1) some basic properties of idioventricular pacemakers; 2) the ventricular escapes arising from the injured fascicle (EIF) in patients with bundle branch block (BBB); and 3) the main features of ventricular automaticity in patients with complete A-V block.

The Different Varieties of 2:1 Bundle Branch Block

Two to one bundle branch block (BBB) is a particular form of intermittent BBB in which beats showing high grade BBB alternate regularly with beats showing normal conduction [1–4]. It is physiologically equivalent to the much more common 2:1 A-V block. Both have been related to a critical increase of the heart rate in the presence of a prolonged refractory period, assuming that every other impulse falls on the refractory phase and is blocked, whereas the alternate beats fall after recovery has been completed and are normally conducted. However, we have previously suggested [5] that several varieties of 2:1 BBB may exist. Thus, when 25 cases were analyzed, the 2:1 BBB was found to occur in three different ways: 1) in relation to phase-3 block; 2) in relation to supernormal conduction; and 3) in relation to phase-4 block. In this study, we will stress the decisive role that concealed anterograde and retrograde conduction may play in the mechanism of these three varieties of 2:1 BBB.