His bundle parasystole: A form of A-V junctional parasystole.
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Few studies have dealt with the effects of isoproterenol on ventricular parasystole. Intravenous isoproterenol (2 to 4 micrograms/min) was administered to 11 nonmedicated patients with ventricular parasystole. At the onset of the drip infusion, 8 patients had continuous parasystole, 2 had intermittent parasystole, and 1 patient (in whom intermittent parasystole was documented 2 to 5 days earlier) showed no manifest parasystolic activity. In all patients, whose control parasystolic cycle length varied between 960 and 2,530 ms, isoproterenol caused a decrease of the parasystolic cycle lengths ranging from 12 to 36%. Therefore, isoproterenol produced a consistent increase of the parasystolic rate. In 4 patients, parasystolic activity ceased to be manifest when the concomitantly enhanced (by isoproterenol) sinus cycle lengths became shorter than 430 ms. This phenomenon reflected a tachycardia-dependent parasystolic concealment, presumably as a result of interference in the parasystolic-ventricular junction. In every case, the arrhythmia reappeared at its initial rate upon stopping the drip infusion. In no patient did parasystolic ventricular tachycardia develop. In the patient without manifest parasystolic beats, isoproterenol unmasked the intermittent parasystole that previously had been intrinsically manifest. The latter effect reflected a true exposure, or unmasking of a latent, rate-independent concealed, parasystolic focus.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Parasystole is the expression of a pacemaker that is protected from, and thus independent of, the dominant rhythm. The arrhythmia is not always associated with the 3 classic signs: variable coupling, mathematically related interectopic intervals, and fusion beats. A large amount of experimental and clinical data have pointed out several atypical phenomena that make the recognition of parasystole difficult. This especially occurs in the presence of influence exerted from sinus impulses upon the parasystolic rhythm. METHODS: A pattern of ventricular parasystole was evident throughout a 24-hour Holter recording obtained from a 55-year-old female. The following data were analyzed: a) distribution of ectopic complexes; b) parasystolic cycle duration; c) regularity of parasystole, as assessed by means of the variation index. In some sections of the tracing in which an electrotonic influence (modulation) exerted by the sinus rhythm on the parasystolic rhythm appeared as very likely, phase-response curves were constructed in order to express the time-dependent modulation effected by sinus impulses. RESULTS: Parasystole occurred in two separate periods, lasting 4 hours and 90 minutes, respectively. On both occasions, the arrhythmia was apparently precipitated by a brief episode of atrial tachycardia. Phases of regular parasystole, as well as periods of irregular modulated parasystole, were observed. The distribution of ectopic complexes was at times typical for concealed bigeminy (intervening beats always in odd numbers), but on other occasions reflected the even variant of concealed bigeminy where the intervening beats conform to the formula 1 + n (n being zero or an odd number). Some couplets of identical ectopic complexes were also observed. CONCLUSIONS: The study shows that several different expressions of parasystolic rhythm may be present within the same tracing. A minimal or absent modulation results in the classical picture of parasystole; when a mild modulating influence is present, the typical pattern of modulated parasystole ensues, whereas a strong modulation leads to disappearance of the typical features of parasystole and manifestation of concealed bigeminy. Finally, supernormal modulation is responsible for the occurrence of couplets.
As shown by Jalife and Moe, brief subliminar depolarizations induced upstreams of the protection zone may predictably modify the discharge from a parasystolic focus. In the biological and mathematical models of parasystole, numerous arrhythmias which do not fulfil the classical criteria of parasystole have been identified, some of them even mimicking a re-entry mechanism. In this paper we report the electrocardiograms of three patients in whom an electrotonic modulation mechanism may be involved. In the first patient the classical pattern of continuous parasystole without exit block was observed throughout daytime. However, between 1 and 5 a.m. non parasystolic beats lengthened or shortened the parasystolic rhythm, depending on their time-related position in the cycle. Later, the usual continuous parasystole pattern reappeared. In the second patient the patent 1:1 entrainment of parasystole by sinus beats resulted in long episodes of ventricular bigeminy with fixed coupling. A sudden slowing down of the cardiac rate disrupting the harmony of the two rhythms and, consequently, the regular entrainment of the ectopic focus, shortened the parasystolic cycle and suppressed bigeminy. In the third patient ventricular stimulation produced a hisian parasystolic rhythm resembling intermittent parasystole on surface ECG. It is concluded that, as suggested by experimental models, many disorders of cardiac rhythm which do not fulfil the criteria of parasystole can be explained in terms of modulated parasystole.
Critical analysis of a case of double ventricular parasystole revealed that one parasystolic focus manifested complete protection, whereas the second focus appeared to be intermittent, protected from sinus and other impulse formation both early, as well as late, in the parasystolic cycle. The zone of protection failure, during which extrinsic impulses could penetrate into the parasystolic focus and discharge it, is observed between these early and late phases of protection. When the intermittent parasystolic focus is challenged by the other parasystolic beat, this zone is much wider and is located later in the cycle than the sinus beat. According to this observation, it is supposed that the intermittent parasystolic focus, in this case, is anatomically surrounded by two types of fibers, each showing different degrees of phase 3 and phase 4 block. The fibers located between the major fascicles and the intermittent parasystolic focus may have a shorter phase 3 and a less steep phase 4 depolarization than those located between two parasystolic foci. It is also demonstrated that during the phase 4 depolarization in these fibers around the focus, concealed conduction into this area by the sinus beat evoked exit delay of the parasystolic impulse, resulting in prolongation of the next parasystolic cycle. In this situation, a re-entry movement around the focus was predicted and, as expected, a re-entrant bigeminy coupled with the parasystolic rhythm was observed.
As recently described by Moe et al., parasystolic modulation implies that the ectopic cycle length of a parasystolic focus can be increased or decreased by electrical influences transmitted across the zone of protection. A search for this phenomenon was made in nine patients with intermittent ventricular parasystole resulting from protection only during specific portions of the cycle. All nine patients had a period of relatively early protection affecting the initial 55-67% of the cycle preceding a period of resetting during which the parasystolic focus was discharged and fully recycled. In addition, two patients had a period of relatively late parasystolic protection. Pseudo-resetting (apparent resetting in the surface leads without interruption of activity within the parasystolic focus itself), seen throughout the entire period of late protection in these two patients, and during the relatively refractory period in one patient, was identified because the R waves causing apparent resetting were encompassed by parasystolic-to-parasystolic intervals equalling twice the ectopic cycle length. Our findings indicate that parasystolic modulation did not occur in the type of intermittent ventricular parasystole included in this study. That is, the parasystolic focus was either not affected (not modulated) during specific (early or late) portions of the cycle, or normally reset (discharged and fully recycled, but neither depressed, nor enhanced) in other portions of the cycle. This study does not exclude the occurrence of modulation in other types of parasystole, nor in some automatic nonparasystolic rhythms.
To analyze the phase-dependent sensitivity of the parasystolic pacemaker to nonparasystolic beats, 11 patients with modulated ventricular parasystole were studied using the ventricular extrastimulus method. The intrinsic parasystolic cycle lengths ranged from 1,100 to 1,800 ms. Premature stimuli altered the duration of the parasystolic cycle lengths by amounts that depended on timing of the test impulses within the parasystolic cycles. Premature impulses delivered during the first part of the parasystolic cycles prolonged the parasystolic cycle lengths to 107 to 151% of the intrinsic parasystolic cycle lengths and impulses applied during the second part abbreviated them to 70 to 81% of the intrinsic parasystolic cycle lengths. In 10 patients the accelerating effects were of greater magnitude than the decelerating effects. Transition from the accelerating to slowing phases was progressive or unstable in 9 patients and abrupt in 2. Changes induced by individual stimuli were short-lived and the parasystolic pacemakers returned immediately to their original rates. In 1 patient the biphasic sensitivity of parasystole to premature stimuli was shown to sustain for 21 days.
Sinus parasystole is the expression of a protected nondominant sinus pacemaker, which is totally independent of the dominant rhythm. Two forms of sinus parasystole are described: (1) an active form, where both the dominant and the parasystolic pacemakers are located within the sinus node and (2) a passive form, where the basic rhythm is ectopic and the sinus pacemaker is protected as a result of complete retrograde SA block. Three cases of sinus parasystole are analyzed. In the active form of the arrhythmia the parasystolic sinus P waves are identical to those of the basic sinus rhythm. The diagnosis is suggested by variably coupled premature sinus P waves occurring with mathematically related intervals. This relationship between the parasystolic intervals can not be precise whenever complicating factors such as modulation occur. The recognition of active sinus parasystole is difficult, since the parasystolic P waves do not differ from basic P waves, so that the pattern resembles that of sinus arrhythmia or sinus extrasystoles. The passive form of sinus parasystole is more easily recognized due to the clear-cut difference between the dominant ectopic atrial waves and the "parasystolic" sinus P waves, which manifest with variable coupling intervals and reflect mathematically related intervals in between.
Recently, it has been shown that in most clinical cases of parasystole, the parasystolic rhythm is not completely independent of the sinus rhythm. In this study, to disclose the mechanism of such "irregular" parasystole, parasystolic cycles with an intervening sinus QRS complex (XSX) were compared with their immediately adjacent pure parasystolic cycles without any intervening nonparasystolic QRS complexes (XX) in 10 cases of ventricular parasystole. In eight cases, the XSX interval was equal to or nearly equal to the adjacent pure XX interval; in one, the XSX interval was shorter than the XX interval; and in only one, the XSX interval was longer than the XX interval. In six cases in which the XSX interval was almost equal to the XX interval, calculated XSX intervals with a later intervening sinus QRS complex were obtained from the differences between the XSSX interval (ie, interectopic interval with two intervening sinus QRS complexes) and its adjacent XX interval. In five of the six cases, the calculated XSX interval was shorter than the XX interval. These observations suggest that in most cases of parasystole, early intervening sinus impulses do not change the parasystolic cycle, whereas late intervening sinus impulses shorten the parasystolic cycle. This suggests the presence of type I second-degree entrance block as the mechanism of "irregular" parasystole.
At the time of the first visit to our clinic, an electrocardiographic examination of a 73-year-old female patient revealed ventricular premature contractions (VPCs) with variable coupling intervals that were diagnosed as parasystole. Characteristically many of the parasystoles had no sinus contractions between two consecutive VPCs, which we referred to as pure parasystole. We first repeatedly examined variations in the length of the parasystolic cycles between January 6, 1997 and March 2, 2003 using electrocardiography. The time courses recorded over this period showed that the length of the parasystolic cycle did not remain constant, but varied irregularly within a relatively narrow range. We also recorded the length of the parasystolic cycles over 3 hours using Holter monitoring. The interectopic intervals plotted against mean sinus cycle length showed that the cycle length of pure parasystoles remained almost constant at about 1,300 ms over the 3 hours. We also examined the cycle length during exercise and found that it was slightly prolonged thereafter, while the sinus cycle length was clearly shortened after exercise. The average of six deep breathing tests showed that parasystolic cycle length did not significantly differ between deep inspiration and deep expiration, whereas the sinus cycle length during expiration was significantly longer than that during inspiration. These results indicate that the responses to both exercise and deep breathing obviously differed between the parasystolic and sinus cycle lengths.
An extremely rare instance of atrial parasystole arising from two different ectopic atrial foci, i.e. double atrial parasystole, is presented, in which both parasystolic intrinsic cycles were found to be around 0.80-0.89 sec. Atrial parasystolic trigeminy with a positive P wave in leads II and III and interectopic intervals (IEIs) of 2.40-2.68 sec continued, then intermittent atrial parasystole with a negative P wave in leads II and III and IEIs of 2.45-2.69 sec took over. A wandering pacemaker between the sinus node and the upper atrio-ventricular (A-V) junction due to autonomic imbalance, i.e. increased vagal tone, in an elderly patient with bronchial asthma was supposed to be the underlying mechanism. Resetting of the parasystolic pacemaker by the third preceding atrial impulse or mutual entrainment and the subsequent 3:1 exit block may play a role in the development of intermittent atrial parasystole with a negative P wave in this case on account of the intrinsic ectopic cycle of 0.84 sec. Alternative explanation of IEIs 2.40-2.69 sec was a 2:1 exit block with the altered basic cycle of mainly 1.24-1.29 sec in consideration of the IEI of 1.24 sec. An explanation of manifest parasystolic cycles on the basis of the theory or cardiac resonant oscillation was put forward for the first time in this report. The IEIs take certain discrete values, which may represent a quantitized property of atrial parasystolic pacemakers as oscillating systems.
The observation was conducted in 24 patients with parasystolic arrhythmias, 13 of them having parasystolic extrasystoles, and 11--paroxysmal and non-paroxysmal parasystolic tachycardia. Ventricular parasystole was found in 21 patients, atrial--in 3, atrioventricular--in 2; three patients had double parasystole with two ectopic centers. In the majority of patients their parasystole took a persistent, but relatively benign course, however one patient with ventricular parasystolic tachycardia persisting for many years had repeated ventricular fibrillations. For the treatment of supraventricular parasystolic arrhythmias beta-adrenergic receptors blocking agents, Isoptine, cardiac glycosides were used; in ventricular parasystole the more effective drugs are Lidocain, Novocainamid, Ajmalin.