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Two cases of sinus rhythm with ventricular extrasystoles are reported in which extrasystoles arising from the same focus obey the rule of "comcealed bigeminy" and the "rule of bigeminy". In a comparatively rapid sinus rhythm, shortening of the sinus cycle favors the appearance of extrasystoles, and the extrasystoles obey the fule of "concealed bigeminy"; namely, sinus impulses intervene between extrasystoles in even numbers. The sinus impulses here include those both conducted and not conducted to the ventricles. Conversely, in a comparatively slow sinus rhythm, interectopic sinus impulses appear in odd numbers only, and the extrasystoles obey the "rule of bigeminy"; namely, lengthening of the sinus cycle favors the appearance of extrasystoles. From these observations, a new mechanism governing both of the rules is suggested as follows. Ectopic impulses arise following all the interctopic sinus beats, but they become concealed extrasystoles of two types. One of them is the "concealed extrasystole due to interference at the external end of the ventricular-ectopic (V-E) junction."The other is the "concealed extrasystole due to exit block within the V-E junction" because of refractoriness following stimulation. They alternate with each other. In the of "concealed begeminy", the last concealed extrasystole intervening between manifest extrasystoles is due to exit block, whereas in the "rule of bigeminy", it is due to interference.
The concept of two different types of extrasystoles, parasystolic and coupled, depends upon two distinguishing characteristics of these beats. The characteristics of the parasystolic extrasystoles are the invariability of the ectopic cycle together with their independence from the basic rhythm. Coupled extrasystoles demonstrate a dependence upon the basic rhythm although they may express some degree of ectopic variability. The degree of variation of the interectopic interval or its common denominator measures the irregularity of the ectopic parasystolic rhythm. The variation of coupling intervals describes the dependence of the ectopic beat upon the basic rhythm. In a study of 719 electrocardiograms with ventricular extrasystoles, about one-third of the extrasystoles appeared intermediate between these types since they had both variable coupling intervals and variable interectopic intervals. Some of these had total variability of coupling intervals and of the interectopic intervals (random non-parasystolic coupling), and others had limited variation of coupling intervals when expressed in relationship to the total duration of electrical diastole (approximate non-parasystolic coupling). Both these ectopic types appeared to be associated with cardiac disease, and repetitive ventricular extrasystoles. Left bundle branch type extra-with fixed coupling. There were no obvious relationships between the contour and the type of coupling of ventricular extrasystoles. Left bundle branch type extrasystoles with vertical or right axis were the most frequent, particularly in normal subjects, but in the presence of cardiac disease there were more electrocardiograms with right bundle branch type extrasystoles. Extrasystoles in the presence of underlying conduction defects were usually of opposite configuration to this defect. The contour of uniform extrasystoles did not appear to predispose to serious ventricular arrhythmias but multiformity of extrasystoles was an important prognostic indicator. It is suggested that variability of contour and coupling are important signs of inhomogenous conduction and may precede the onset of severe ventricular arrhythmias. Random nonparasystolic coupling and marked multiformity indicate a more sinister arrhythmic state.
Eight patients with ventricular extrasystoles are reported in whom coupling intervals of the extrasystoles to the proceding sinus beats were variable and in whom paired ventricular extrasystoles were occasionally seen. In all patients, paired ventricular extrasystoles were initiated only by comparatively late coupled ventricular extrasystoles. However, the interval between the first and the second of these paired extrasystoles was always much shorter than the coupling interval of this first extrasystole to the preceding sinus beat, so that the latter extrasystole often interrupted the T wave of the first one, indicating the R-on-T phenomenon. In two patients there was a gap between the ranges of coupling intervals for single extrasystoles and for the first ones of paired extrasystoles. These observations suggest the presence of longitudinal dissociation in the reentrant pathway as one of the causes of paired ventricular extrasystoles.
Changes of contractility resulting from changes in stimulation pattern (post-extrasystolic potentiation - PESP) were investigated in right ventricular papillary muscles from female albino rats (EPM strain, 160-200 g). The preparations were superfused with bicarbonate buffered solution at 24 +/- 0.5 degrees C, and stimulated at 0.5 Hz. Maintained paired stimulation was performed at several coupling intervals (360, 500, 660, 770 and 920 ms) with normal Krebs for 30 s. After treatment with ryanodine (1 microM), used as an inhibitor of the release of sarcoplasmic reticulum Ca2+ activity, the same protocol was repeated in the presence of normal Krebs, low Na+ (80 mM, LiCl used as substitute) and low K+ concentrations to change the level of activity of the Na+/Ca2+ exchange mechanism. With normal Krebs, paired pulse stimulation produced a maintained potentiation of the post-extrasystolic beat and an extrasystole with a reduced force generation when compared to the control steady-state contraction. As the interval between the extrasystole and the normal beat was increased the potentiation of the post-extrasystolic beat was reduced and the force of the extrasystole was increased. Ryanodine treatment reduced the force of contraction and increased its duration, and the pattern of the PESP phenomenon was altered. Both the post-extrasystolic and the extrasystolic beats were potentiated compared to the steady-state contraction obtained under ryanodine treatment. The extrasystole displayed a greater potentiation than the post-extrasystolic beat. As the interval between them increased the amplitude of the extrasystolic beat was enhanced.(ABSTRACT TRUNCATED AT 250 WORDS)
Unidirectional conduction block of premature extrasystoles can lead to initiation of cardiac reentry, causing lethal arrhythmias including ventricular fibrillation. Multiple extrasystoles are often more effective at inducing unidirectional conduction block and reentry than a single extrasystole. Since the substrate for conduction block is spatial dispersion of refractoriness, in this study we investigate how the first extrasystole modulates this dispersion to influence the "vulnerable window" for conduction block by subsequent extrasystoles, particularly in relation to action potential duration restitution and conduction velocity restitution properties. Using a kinematic model to represent wavefront-waveback interactions and simulations with the Luo-Rudy model in a one-dimensional cable of cardiac cells, we show that in homogeneous tissue, a premature extrasystole can create a large dispersion of refractoriness leading to conduction block of a subsequent extrasystole. In heterogeneous tissue, however, a premature extrasystole can either reduce or enhance the dispersion of refractoriness depending on its propagation direction with respect to the previous beat. With multiple extrasystoles at random coupling intervals, vulnerability to conduction block is proportional to their number. In general, steep action potential duration restitution and broad conduction velocity restitution promote dispersion of refractoriness in response to multiple extrasystoles, and thus enhance vulnerability to conduction block. These restitution properties also promote spatially discordant alternans, a setting which is particularly prone to conduction block. The equivalent dispersion of refractoriness created dynamically in homogeneous tissue by spatially discordant alternans is more likely to cause conduction block than a comparable degree of preexisting dispersion in heterogeneous tissue.
Ventricular extrasystoles were analysed by a computerised monitor in 144 patients during the first three days of myocardial infarction. The patients had been hospitalised within 6 hours (77% of cases) and within 12 hours (92% of cases) of onset of symptoms. The patients were divided into 4 groups: Group A (46 cases) without repetitive ventricular extrasystoles; Group B (37 cases) with repetitive ventricular extrasystoles but without frequent isolated extrasystoles; Group C (25 patients) with repetitive ventricular extrasystoles and frequent isolated extrasystoles but without polymorphism or R on T phenomenon; and Group D (36 patients) with repetitive extrasystoles, frequent isolated polymorphic extrasystoles and/or R on T phenomenon. The size of infarction, as judged by peak CPK values, was smaller in Group A than in the other groups but was not significantly different in Groups B, C and D. The incidence of cardiac failure was comparable in Groups A and B and in Groups C and D, and was higher in the latter two groups than in A and B. The cardiothoracic ratio on admission was increased more often in Group D than in the other groups. Therefore, repetitive ventricular extrasystoles are the result of large infarcts. Their association with frequent isolated ventricular extrasystoles is a sign of insufficiency of the remaining myocardium. Patients with pre-existing poor myocardial function develop polymorphism and R on T phenomenon, signs which are associated with a particularly poor prognosis (hospital mortality: 42%). On the other hand, patients in Group B appeared to have satisfactory myocardial function despite the size of their infarcts, and the mortality, nil in this group, was less than in patients without arrhythmias.
Maximum flow velocity waveforms at atrioventricular and outflow tract level were studied cross-sectionally in 19 human fetuses with conducted and/or blocked supraventricular extrasystoles ranging from 25 to 38 weeks of gestation. At outflow tract level, peak systolic velocity and acceleration time for extrasystolic and post-extrasystolic beats were compared with those for the immediately preceding normal beat. Regression lines were calculated for peak systolic velocities with filling time. At atrioventricular level, peak-E wave and peak-A wave velocities and E/A ratio for the extrasystolic and post-extrasystolic beats were compared with those for the normal beat. At all levels, time-averaged velocities were compared with reference charts standardized for gestational age.Peak systolic velocity and acceleration time during the post-extrasystolic beat were higher than during the normal beat; the Frank-Starling mechanism, post-extrasystolic potentiation as well as reduced ventricular afterload may all play a role in this. At all measuring levels, time-averaged velocity during the extrasystolic beat was strikingly lower than the reference velocities. It is postulated that the increased blood volume and contraction force during the post-extrasystolic beat cause the valve area to become larger, resulting in a relative decrease in velocities measured by Doppler ultrasound.
Mechanisms involved in the development of parasystole and extrasystole are substantiated on the basis of vast clinical material (261 patients with parasystole and 45 with extrasystole). The use of functional tests employing exercise and atropine contributed to both the correct diagnosis of parasystole and extrasystole and a logical explanation of the mechanisms governing their development. Prolonged ECG recording identified, for the first time ever, the limits of the maximum admissible coupling interval for normotopic extrasystole, as the preliminary diagnosis of the nature of the arrhythmia was only made after the said tests. Parasystole was shown to be rooted in a pathologic automatism, and extrasystole, in the summation of extrasystolic focus potentials and the principal pacemaker potential during movement as well as the principal pacemaker impulse along the route of the minor circular wave on Purkinje' level. The localization of ectopic foci in parasystole and extrasystole confirms the hypothesis of the mechanisms involved in these arrhythmias. A parallel study of parasystole and extrasystole defined parasystole as active heterotopia, and extrasystole, as passive heterotopia incapable of generating a rhythm.
Electrocardiography was performed in a newborn boy without organic heart disease, in whom supraventricular extrasystoles with varying coupling were seen. The supraventricular extrasystoles were occasionally followed by ventricular extrasystoles. The coupling intervals of ventricular extrasystoles to the preceding supraventricular extrasystoles were also considerably variable. Ventricular tachycardia occurred following comparatively late coupled ventricular extrasystoles. This is the first known report on ventricular tachycardia following comparatively late coupled ventricular extrasystoles in a newborn infant. This strengthens our previous suggestion that such ventricular tachycardia can be caused by longitudinal dissociation in the reentrant pathway of extrasystoles.
Measurement of the pre-ejection period (PEP), a non-invasive index of cardiac function, was made in a human fetus with a disturbance of cardiac rhythm manifested by: (i) intermittent mechanically ineffective extrasystoles (ventricular premature beats) and (ii) pauses. The mean interval between the sinus beats before and following extrasystoles was virtually the same as that before and following pauses. The PEP was shortened at the first sinus beat following both extrasystoles and pauses, but to a greater extent following extrasystoles. The PEP was still shortened at the second sinus beat following extrasystoles, but prolonged at the same cardiac cycle following pauses. These data demonstrate that fetal cardiac post-extrasystolic potentiation was taking place and that this was due in part to inotropic potentiation of the post-extrasystolic beats. Inotropic potentiation of post-extrasystolic beats is due to a fundamental property of cardiac muscle relating frequency of stimulation to strength of contraction (the so-called 'force-interval' relationship). Our data present the first evidence, to our knowledge, that the inotropic state of the human fetal heart in vivo is modulated by this mechanism.
Horizontal and frontal plane QRS loops of patients in sinus rhythm with uniform ventricular extrasystoles were constructed from digitised Frank orthogonal electrocardiograms. In 4 patients ventricular extrasystoles were indistinguishable from right bundle-branch complexes, and in another they were indistinguishable from left bundle-branch complexes. In 25 patients ventricular extrasystoles showed an initial delay (greater than or equal to 20 ms) of the QRS, followed by an R loop, which in 13 patients resembled left bundle-branch block complexes, and in 12 patients resembled right bundle-branch block complexes, with an anterior clockwise loop in the horizontal plane. However, the frontal plane loop often did not resemble that of either right or left bundle-branch block. In 51 patients ventricular extrasystoles had an initial delay which was prolonged into the efferent limb of the QRS loop with acceleration of the afferent limb, and/or the QRS loop was directed anteriorly, inferiorly, and to the left. Conventional recordings of these extrasystoles usually showed an initial slow upstroke (or downstroke) of the QRS resembling a delta wave. Apparently uniform ventricular extrasystoles on scalar recordings were shown to be multiform vectorcardiographically though in all such cases the direction of the initial 40 ms forces was constant. It is suggested that the slow initial inscription of ventricular extrasystoles is the result of excitation of ventricular muscle directly and not through specialised His-Purkinje fibres, and that the direction of such initial forces may indicate the ventricular origin of ventricular extrasystoles.