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Dynamic characterization of premature ventricular beats and ventricular tachycardias
Dynamic Characterization
of Premature
Ventricular Beats and Ventricular Tachycardias
LESLIE M. EBER, MD BAROUH V. BERKOVITS, Ing EE, FACC JACK M. MATLOFF, MD, FACC RICHARD GORLIN, MD, FACC with the technical assistance of JOHN M. COOKE Boston, Massachusetts
The contraction patterns induced by ectopic ventricular premature beats and ventricular tachycardias occurring in man during left ventriculography were analyzed. These were compared with contraction patterns induced by ventricular premature beats and tachycardias produced in five dogs by epicardial left ventricular apical or basilar stimulation. Two patterns of contraction observed in the animals corresponded to two patterns observed in man. Apically stimulated left ventricular beats produced an “hourglass” type of contraction pattern and were hemodynamically more effective than beats arising from basilar stimulation, which produced an inverse “teardrop” pattern. The same patterns were reproduced by experimental ventricular tachycardias. These observations stress the importance of a normal sequence of ventricular contraction to optimal cardiac function in man and warn against the hazards of misinterpretation of the left ventricular contraction pattern if the beat originates ectopically during ventriculography.
The hemodynamic consequences of ectopic cardiac stimulation were first described by Wiggers’ in 1925. He believed that “a certain orderliness in the mode of contraction may be necessary in order to produce a maximal effect on intraventricular pressure.” Further clinical interest in this subject was engendered by t,he advent of the permanent epicardial pacemaker lead for treating complete heart block. Complete agreement still does not exist as to the optimal site for epicardial pacing. Corday et al.2 described both a “benign” and “malignant” ventricular tachycardia based upon the hemodynamic response to apical versus basilar stimulation of the left ventricle, respectively. Clinical left cineventriculography has confirmed that ventricular premature beats are associated with asynchronous patterns of contraction.:j The purpose of this report is to describe the various patterns of left ventricular contraction in catheter-induced ectopic beats during cardiac catheterization in man and to correlate these with the contraction patterns of ectopically stimulated intact dog hearts.
Material and Methods Studies in Man
From the Cardiovascular Division, Department of Medicine, Division of Cardiothoracic Surgery, Department of Surgery, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Mass. This study was supported by U. S. Public Heatth Service Grants 2POl-11306 and 5T015679. Manuscript accepted July 11. 1973. Address for reprints: Richard Gorlin, MD, Cardiovascular Division, Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, Mass. 02115.
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Left cineventriculograms with normal contraction patterns were selected from patients undergoing diagnostic cardiac catheterization. Ventriculograms were obtained in the 30’ right anterior oblique position and recorded on 16 mm film at 60 frames/set utilizing a 9 inch X-ray image intensifier system; 35 to 45 ml of 75 percent sodium and meglumine diatrizoate was injected over 2 seconds by a power injector through a catheter in the left ventricle.4 The electrocardiogram and brachial arterial blood pressure were recorded simultaneously with the ventriculogram. An event marker system permitted exact matching of this graphic information with each tine frame, thus permitting accurate identification of ventricular premature beats. The ventriculograms included in this study had to meet the following criteria:
The American Journal of CARDIOLOGY
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ET AL.
1. A premature beat was studied if it followed a normally conducted beat, with which it was then compared. 2. If the premature beat occurred first, it was compared with a beat at least once removed from the immediate postextrasystolic beat. The ventriculograms were projected to life-size dimensions based upon known catheter diameter. A normally conducted beat and a premature beat occurring during the same injection were traced frame by frame. Motion analysis was carried out by a method previously described” but, to minimize error, the minor axes drawn perpendicular to the long axis were considered as total segments rather than as hemisegments representing anterior and inferior wall contractions. This procedure will be further illustrated in the text. Ten ventriculograms in 10 patients with minimal or no coronary artery disease satisfied the criteria cited and were of sufficient radiographic quality to be included in the study. Animal Experiments The response of the left ventricle to ectopic stimulation was observed during multiple ventriculographic studies conducted in five dogs. Observations were made with both single ectopic beats and ventricular tachycardia. With the animals under general anesthesia, a thoracotomy was performed and pacemaker wires were sutured epicardially to the left ventricular apex, left ventricular outflow tract, right atrium and mid-right ventricle. A metal clip was placed on the myocardium at the site of each pacemaker wire. These wires were passed to the exterior through a stab wound in the chest and labeled as to site. A cannula inserted and fixed in the left atrium was also passed t,o the exterior and capped for future use. The dogs were permitted to recover and maintained in their quarters. They were studied 4 days to 2 weeks after operation according to the following protocol: Anesthesia was provided with use of morphine-Nembutale or morphine-chloralose and urethane. Each dog was intubated and put on a mechanical respirator and then secured to a rotating table top. The left ventricle was entered retrograde across the aortic valve with either a Statham SF1 catheter or a metal cannula fashioned from a large standard transseptal needle introduced by way of the carotid artery and connected directly to a pressure transducer. A standard catheter was placed in the aortic arch by way of the femoral artery. The dogs were permitted to maintain their own sinus rhythm. An experimental triggered pacemaker was connected to each lead and programmed so as to deliver a premature stimulus after every third or fourth sinus beat. This instrument had a coupling interval adjustable from 0 to 1 second, a refractory interval adjustable from 0.1 to 10 seconds and a 2 msec pacemaker impulse adjustable from 0 to 25 volts. The degree of prematurity was regulated in successive studies so as to produce early and late premature ventricular beats. The intensity of the stimulus was adjusted to the lowest level that would produce a mechanical response. In the same animal, sustained ventricular tachycardia was produced from the same pacemaker sites and studied ventriculographically. The animal was placed in the right anterior oblique position. Hand injections of 20 to 30 cc of 75 percent sodium and meglumine diatrizoate were made through the left atria1 cannula. The ventriculograms were recorded at 60 frameslsec. An average of six ventriculograms were obtained in each animal. A 20 minute interval between successive ventriculograms allowed subsidence of ventricular depression induced by the contrast agent. As in
FIGURE 1. Comparison of the motion analysis of a sinus beat (left) with that of a premature ventricular beat (right) occurring in the same ventriculogram in a normal patient. The code for the segments involved is illustrated in the figure. L represents the long axis of the ventricle drawn from apex to the midportion of the aortic valve. Dj, D2 and Ds represent three minor axes constructed perpendicular to L quadrisecting the long axis. The percent change of each segment from its end-diastolic length is plotted against time. Expansion of a segment is plotted as a positive change from zero, and contraction or shortening as a negative change. In comparison with the sinus beat, the premature beat resulted in slight movement of the major axis and periapical asynchrony. This pattern is similar to that observed in experimental animals during epicardial stimulation of the apex.
the human studies, each tine frame could be matched with pressure and electrocardiographic events through the use of an event marker. Results Studies in Man Each premature beat that could be identified electrocardiographically as ventricular in origin produced an abnormal contraction pattern in comparison with its control beat. Figure 1 illustrates motion analyses of two beats from the same ventriculogram. The premature beat produced long axis akinesis and periapical asynchrony. Figure 2, A and B, illustrates the left ventricular silhouette during control and ventricular premature beats in a patient with normal coronary arteries and hemodynamic status. The left ventricle has a “crenated” appearance during the ventricular premature beat and a symmetrical pattern of reduction in size during the normal beat. Even ventricular premature beats occurring with long sinus beat to premature beat intervals produce abnormal contraction patterns. Figure 3 graphically analyzes the motion of the beats drawn in Figure 2. In comparison to the control beat, the premature beat produces dyskinesis of all the minor axes with the only progressive shortening occurring in the major ventricular axis.
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ET AL.
Two runs of ventricular tachycardia were analyzed, but, unfortunately, the ventriculograms in these cases did not contain sinus beats for comparison. The ventricular contraction patterns induced by ventricular tachycardia did not differ appreciably from those observed during isolated ventricular premature beats. Beats occurring serially during ventricular tachycardia tended to produce a similar but not necessarily identical contraction pattern.
END DIASTOLE
MID SYSTOLE
Studies in Animals
END SYSTOLE
.-
A
8
FIGURE 2. Selected left ventricular silhouettes from enddiastole, mid-systole and end-systole with a normal sinus beat (A) and a premature beat (B) in the same ventriculogram. Note the highly irregular and almost “crenated” appearance of the ectopically stimulated ventricle during contraction.
In general, ventricular premature beats tended to produce several distinctive contraction patterns. The two most often seen have already been illustrated. In Figure 1, contraction occurred mostly in the peribasilar and midportion minor axes. The periapical segment displayed asynchrony or dyskinesis, or both. The long axis exhibited minimal shortening. The net effect of this pattern would be to “propel” blood toward the apex. Another common contraction pattern of ventricular premature beats is illustrated in Figure 3 and has as its net effect the formation roughly of a globular shaped left ventricle with the long axis shortening at the “expense” of the minor axes.
FIGURE 3. Motion analyses of the two beats drawn in Figure 2. There is paradoxical systolic expansion of all segments except the long axis.
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The American Journal of CARDIOLOGY
Ventricular premature beats: Adequate comparison between apically and basally stimulated left ventricular ectopic beats was made in two ventriculograms from each of three dogs. Stimuli applied to the left ventricle produced two distinct patterns of contraction depending on whether the apex or base was stimulated. In either instance, the initial salient feature was an expansion of the segment adjacent to the site of the stimulus. This pattern was observed regardless of the timing of the premature beat. Figure 4A illustrates selected silhouettes and a motion analysis of an apically stimulated ventricular premature beat. There was paradoxical systolic expansion of the periapical segments with vigorous contraction of the base and midportion of the ventricle. These findings should be contrasted with results of the premature beat illustrated in Figure 4B, taken from a subsequent ventriculogram in the same animal. In this case, the ventricle was stimulated by means of the wire attached to the left ventricular outflow tract. Here, the basilar portion of the left ventricle expanded paradoxically whereas the periapical portion contracted. From these two distinct contraction patterns simplified conceptual models may be constructed. Apical stimulation results in trapping of blood in the apical regions, whereas basilar stimulation results in a more globular left ventricular configuration with blood being sequestered in an expanded outflow tract region. The hemodynamic correlates of apical versus basilar stimulation can be illustrated by comparison of the two beats cited. Table I shows the R-R interval for the normal control beat and the ventricular premature beat, left ventricular volumes and peak pressures for control and ventricular premature beats originating with apical and basilar stimuli. The data were derived from two sequential ventriculograms in one experimental preparation. Apical stimulation was more effective hemodynamically than outflow tract stimulation when beats with the same diastolic filling period were compared. Stimulation of the apex produced a greater percent of control aortic pressure and a larger ejection fraction than did stimulation of the base. This was true in all ventricular premature beats which appeared late enough to open the aortic valve. When the beats appeared too early to produce a rise in aortic pressure, the patterns of contractions were the same as those just described. When ejection of blood did not occur, early ventricular stimulation gave rise to an internal rearrangement of the ventric-
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ET AL.
FIGURE 4. Selected silhouettes and motion analysis after apically stimulated (A) and basally stimulated (B) ventricular premature beats in a dog. Note the paradoxical systolic exoansion of the oeriaoical seament DR in A and the marked’ paradoxical expansion of the peribasilar segment D, in B.
ular contents. It is also possible that mitral regurgitation occurred with these beats. Ventricular tachycardia: Experimental ventricular tachycardia was produced by stimulating the left ventricular apex or base at a rate sufficient to drive the ventricle (190 to 210 beats/min). The ventriculograms obtained during the arrhythmia showed patterns similar to those produced by single ventricular premature beats in each area. However, when the ventricle was apically stimulated, there tended to be more paradoxical expansion in the long axis than with the single ventricular premature beat. Figure 5A shows a sequence of four silhouettes during a typical beat of apical ventricular tachycardia. In mid to late systole, the lengthening of the major axis and the circumferential contraction of the midportion of the left ventricle about the minor axis gave an “hourglass” appearance to the left ventricular cavity. This was
most notable when the ventriculogram was projected at normal film speed. Ventricular tachycardia produced by stimulation of the base showed expansion of the basilar area with normal shortening of the major axis. The ventricle became more globular in appearance, resembling an inverse teardrop with the point toward the apex. Selected silhouettes drawn from the ventriculogram obtained during a basally stimulated ventricular tachycardia beat are shown in Figure 5B.
TABLE
‘:-:i
I
Effect of Site of Pacemaker Interval (msec)
Site Control LV apex Control LV base
Normal R-R
R-R (VPB)
376 ... 380 ...
... 288 ... 288
on Left Ventricular
Performance
LV Pressure Peak % of (mm Hg) Control 96 80 116 86
... 83 ... 74
LV Volumes (ml) EDV
ESV
SV
EF
49 50 52 46
18 27 18 33
31 23 34 13
0.63 0.46 0.65 0.28
EDV = end-diastolic volume; EF = ejection fraction; ESV = end-systolic volume; LV = left ventricular; SV = stroke volume; VPB = ventricular premature beat.
Discussion
The apparent regional expansion of the stimulated portion of the left ventricle has been noted by others.5.6 Our study confirms these observations for left ventricular apical and basilar ventricular premature beats and tachycardias. The general patterns of contraction observed are unrelated to preload, diastolic filling periods, or even the presence or absence of aor-
END
DIASTOLE
END
DIASTOLE
EARLY
SYSTOLE
MID
LATE
SYSTOLE
SYSTOLE
\
END
END
SYSTOLE
SYSTOLE 1
FIGURE 5. Left ventricular silhouettes during experimental tachycardia. See text for details.
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tic ejection, but are determined solely by the point of stimulus application. The relative importance of ventricular asynchrony and the temporal relation between atria1 and ventricular activation in producing a hemodynamic deficit with epicardial pacing has been studied in the dog heart. Daggett and co-workers7 compared atrial, atrioventricular and right ventricular epicardial pacing in a dog preparation. They demonstrated that atrioventricular pacing at properly adjusted intervals tended to override hemodynamically the adverse effect of having the ventricular impulse applied ectopitally. From this observation they concluded that the interval between atria1 and ventricular systole was a more important determinant of ventricular function during cardiac pacing than the site of entry of the impulse to the ventricle. In another series of experiments, Daggett et al. utilized the isovolumic left ventricle to study the hemodynamic effects of pacing from various epicardial sites. They showed that better performance was obtained with stimulation of the left ventricular apex than with stimulation of the right ventricle. However, their study did not mention the influence of atrioventricular sequential pacing in the intact heart when the pacing site was varied on the left ventricle itself. In our study, the production of single ventricular premature beats showed a hemodynamic and morphologic difference depending upon stimulus site when diastolic filling time was constant. This mechanism should be independent of atria1 systolic-ventricular systolic interval (As-Vs) in experiments of the type illustrated in Table I. It is conceivable that basilar stimulation may produce more mitral regurgitation than apical stimulation even at fixed As-Vs intervals, since these patterns of contraction are so different. In our animal experiments, quantification of mitral regurgitation was not possible since the injections were made by way of the left atrium to avoid unwanted stimulation of the ventricle during injection of dye. In the dog experiments, there was a constant directional hemodynamic difference between apical and basilar stimulation of the left ventricle. Stimulation of the apex resulted in a greater percentage of aortic pressure even when R-R intervals and end-diastolic volumes were constant. This finding is in contradistinction to some earlier observations.ssg Our data emphasize the hemodynamic importance of synchronous ventricular contraction patterns that operate independently of atria1 transport function. Experimentally produced asynchrony with its attendant shortened ejection time vitiates the Starling effect. In the one example listed in Table I, the end-diastolic volumes of the control and apically stimulated beat were prac-
tically the same, but the ejection fraction of the latter beat was considerably reduced. Our study encompassed observations on similar phenomena in man and dogs. During clinical diagnostic ventriculography, the occurrence of ventricular premature beats is commonplace. Careful examination of a number of these beats revealed two major contraction patterns that were similar to those evoked with epicardial stimulation in dogs. It is difficult to make a direct comparison of these patterns in man to those in experimental animals since the exact stimulus site in each clinical case is unknown. A catheter passed retrograde across the aortic valve may stimulate the outflow tract by direct contact or stimulate the apical region by a jet stream of contrast material during the injection. To relate the two aspects of this study, two assumptions must be made: (1) that endocardial stimuli induce the same contraction pattern as epicardial stimuli, and (2) that in the human observations, the stimulus sites were indeed similar to those applied in the experimental animals. The minimal conclusion to be drawn from the human observations is that ventricular premature beats in man vary in their associated patterns of left ventricular contraction and that these may be categorized. Clinical implications: Our study showed that ventricular stimulation either of the single ventricular premature beat type or of the repetitive tachycardia type results in a similar pattern of contraction. The .observation that apically induced ventricular premature beats are more hemodynamically effective than basilar ventricular premature beats supports the concept of Corday et al2 that ventricular tachycardias may be benign or malignant depending upon their site of origin within the ventricle. Some of the contraction patterns observed in our study bore great similarity to those seen during sinus rhythm in patients with segmentally diseased or ischemit ventricles.lO The slower ventricular tachycardias occurring during ventriculography in the normal patient might lead to an erroneous diagnosis of asynergy. Our results emphasize the importance of maintaining and documenting normal sinus rhythm before assessing a left ventricular contraction pattern from the ventriculogram. If ectopic beats occur, it is essential to .recognize them as such. In our study, it was possible to identify the site of application of a stimulus to the dog’s left ventricle by the type of,contraction pattern produced. Interpretation of ventriculograms in which ectopic beats occur can be subject to serious error. Acknowledgment We acknowledge the help of Drs. C. W. Urschel and E. H. Sonnenblick for their criticism of this work.
References 1. Wiggers CJ: The muscular reactions of the mammalian ventricles to artificial surface stimuli. Am J Physiol 73:346-378. 1925 2. Corday E, Gold H, cleVera LB, et al: Effect of the cardiac ar-
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rhythm& on the coronary circulation. Ann Intern Med 50535~ 553, 1959 3. Herman MV, Heinle RA, Klein MD, et al: Localized disorders in
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VENTRiCiJLAR mEMATURE
4. 5.
6.
7.
myocardiil contraction--asynergy and its role in congestive heart faiiure. N Engl J bled 277:222-232, 1967 Kkln MD, Herman MV, Gorfin R: A hemodynamic study of left ventricular aneurysm. Circulation 35614-630, 1967 Hood WB Jr, Covelli VH, Normal JC. et al: Systolic bulging at sites of left ventricular stimulation. Circulation 38:suppi Vi:Vi102, 1968 Ueda H, Hand K. Ueda K: Cineangiocardiqraphic observations on the asynchronism of cardiac contraction during ventricular pacing. Jap Heart J 9:295-302.1968 Deggett WM, Bienco JA, Powell WJ, et al: Retative contribu-
BEATS AND TACHYCARDIAS-EBER
ET AL.
tions of the atrial systole-ventricular systoie interval and of patterns of ventricular activation to ventricular function during electrical pacing of the dog heart. Circ Res 27:69-79, 1970 8. Abffdskov JA, Eich RH, Haruml K, et al: Observations on the reiatiin between ventricuiar activation sequence and the hemodynamic state. Circ Res 17:236-247. 1965 9. Trembley GM, Nahas M: Location of epicardial pacemaker electrodes and myocardiii contractility. Can J Physiol Pharmacoi 47:267-271, 1969 10. Herman MV, Gorlln R: implications of left ventricular asynergy. Am J Cardiii 23536-547, 1969
March 1974
The American Journal of CARDIOLOGY
Volume 33
383
of Premature
Ventricular Beats and Ventricular Tachycardias
LESLIE M. EBER, MD BAROUH V. BERKOVITS, Ing EE, FACC JACK M. MATLOFF, MD, FACC RICHARD GORLIN, MD, FACC with the technical assistance of JOHN M. COOKE Boston, Massachusetts
The contraction patterns induced by ectopic ventricular premature beats and ventricular tachycardias occurring in man during left ventriculography were analyzed. These were compared with contraction patterns induced by ventricular premature beats and tachycardias produced in five dogs by epicardial left ventricular apical or basilar stimulation. Two patterns of contraction observed in the animals corresponded to two patterns observed in man. Apically stimulated left ventricular beats produced an “hourglass” type of contraction pattern and were hemodynamically more effective than beats arising from basilar stimulation, which produced an inverse “teardrop” pattern. The same patterns were reproduced by experimental ventricular tachycardias. These observations stress the importance of a normal sequence of ventricular contraction to optimal cardiac function in man and warn against the hazards of misinterpretation of the left ventricular contraction pattern if the beat originates ectopically during ventriculography.
The hemodynamic consequences of ectopic cardiac stimulation were first described by Wiggers’ in 1925. He believed that “a certain orderliness in the mode of contraction may be necessary in order to produce a maximal effect on intraventricular pressure.” Further clinical interest in this subject was engendered by t,he advent of the permanent epicardial pacemaker lead for treating complete heart block. Complete agreement still does not exist as to the optimal site for epicardial pacing. Corday et al.2 described both a “benign” and “malignant” ventricular tachycardia based upon the hemodynamic response to apical versus basilar stimulation of the left ventricle, respectively. Clinical left cineventriculography has confirmed that ventricular premature beats are associated with asynchronous patterns of contraction.:j The purpose of this report is to describe the various patterns of left ventricular contraction in catheter-induced ectopic beats during cardiac catheterization in man and to correlate these with the contraction patterns of ectopically stimulated intact dog hearts.
Material and Methods Studies in Man
From the Cardiovascular Division, Department of Medicine, Division of Cardiothoracic Surgery, Department of Surgery, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Mass. This study was supported by U. S. Public Heatth Service Grants 2POl-11306 and 5T015679. Manuscript accepted July 11. 1973. Address for reprints: Richard Gorlin, MD, Cardiovascular Division, Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, Mass. 02115.
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March 1974
Left cineventriculograms with normal contraction patterns were selected from patients undergoing diagnostic cardiac catheterization. Ventriculograms were obtained in the 30’ right anterior oblique position and recorded on 16 mm film at 60 frames/set utilizing a 9 inch X-ray image intensifier system; 35 to 45 ml of 75 percent sodium and meglumine diatrizoate was injected over 2 seconds by a power injector through a catheter in the left ventricle.4 The electrocardiogram and brachial arterial blood pressure were recorded simultaneously with the ventriculogram. An event marker system permitted exact matching of this graphic information with each tine frame, thus permitting accurate identification of ventricular premature beats. The ventriculograms included in this study had to meet the following criteria:
The American Journal of CARDIOLOGY
Volume 33
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ET AL.
1. A premature beat was studied if it followed a normally conducted beat, with which it was then compared. 2. If the premature beat occurred first, it was compared with a beat at least once removed from the immediate postextrasystolic beat. The ventriculograms were projected to life-size dimensions based upon known catheter diameter. A normally conducted beat and a premature beat occurring during the same injection were traced frame by frame. Motion analysis was carried out by a method previously described” but, to minimize error, the minor axes drawn perpendicular to the long axis were considered as total segments rather than as hemisegments representing anterior and inferior wall contractions. This procedure will be further illustrated in the text. Ten ventriculograms in 10 patients with minimal or no coronary artery disease satisfied the criteria cited and were of sufficient radiographic quality to be included in the study. Animal Experiments The response of the left ventricle to ectopic stimulation was observed during multiple ventriculographic studies conducted in five dogs. Observations were made with both single ectopic beats and ventricular tachycardia. With the animals under general anesthesia, a thoracotomy was performed and pacemaker wires were sutured epicardially to the left ventricular apex, left ventricular outflow tract, right atrium and mid-right ventricle. A metal clip was placed on the myocardium at the site of each pacemaker wire. These wires were passed to the exterior through a stab wound in the chest and labeled as to site. A cannula inserted and fixed in the left atrium was also passed t,o the exterior and capped for future use. The dogs were permitted to recover and maintained in their quarters. They were studied 4 days to 2 weeks after operation according to the following protocol: Anesthesia was provided with use of morphine-Nembutale or morphine-chloralose and urethane. Each dog was intubated and put on a mechanical respirator and then secured to a rotating table top. The left ventricle was entered retrograde across the aortic valve with either a Statham SF1 catheter or a metal cannula fashioned from a large standard transseptal needle introduced by way of the carotid artery and connected directly to a pressure transducer. A standard catheter was placed in the aortic arch by way of the femoral artery. The dogs were permitted to maintain their own sinus rhythm. An experimental triggered pacemaker was connected to each lead and programmed so as to deliver a premature stimulus after every third or fourth sinus beat. This instrument had a coupling interval adjustable from 0 to 1 second, a refractory interval adjustable from 0.1 to 10 seconds and a 2 msec pacemaker impulse adjustable from 0 to 25 volts. The degree of prematurity was regulated in successive studies so as to produce early and late premature ventricular beats. The intensity of the stimulus was adjusted to the lowest level that would produce a mechanical response. In the same animal, sustained ventricular tachycardia was produced from the same pacemaker sites and studied ventriculographically. The animal was placed in the right anterior oblique position. Hand injections of 20 to 30 cc of 75 percent sodium and meglumine diatrizoate were made through the left atria1 cannula. The ventriculograms were recorded at 60 frameslsec. An average of six ventriculograms were obtained in each animal. A 20 minute interval between successive ventriculograms allowed subsidence of ventricular depression induced by the contrast agent. As in
FIGURE 1. Comparison of the motion analysis of a sinus beat (left) with that of a premature ventricular beat (right) occurring in the same ventriculogram in a normal patient. The code for the segments involved is illustrated in the figure. L represents the long axis of the ventricle drawn from apex to the midportion of the aortic valve. Dj, D2 and Ds represent three minor axes constructed perpendicular to L quadrisecting the long axis. The percent change of each segment from its end-diastolic length is plotted against time. Expansion of a segment is plotted as a positive change from zero, and contraction or shortening as a negative change. In comparison with the sinus beat, the premature beat resulted in slight movement of the major axis and periapical asynchrony. This pattern is similar to that observed in experimental animals during epicardial stimulation of the apex.
the human studies, each tine frame could be matched with pressure and electrocardiographic events through the use of an event marker. Results Studies in Man Each premature beat that could be identified electrocardiographically as ventricular in origin produced an abnormal contraction pattern in comparison with its control beat. Figure 1 illustrates motion analyses of two beats from the same ventriculogram. The premature beat produced long axis akinesis and periapical asynchrony. Figure 2, A and B, illustrates the left ventricular silhouette during control and ventricular premature beats in a patient with normal coronary arteries and hemodynamic status. The left ventricle has a “crenated” appearance during the ventricular premature beat and a symmetrical pattern of reduction in size during the normal beat. Even ventricular premature beats occurring with long sinus beat to premature beat intervals produce abnormal contraction patterns. Figure 3 graphically analyzes the motion of the beats drawn in Figure 2. In comparison to the control beat, the premature beat produces dyskinesis of all the minor axes with the only progressive shortening occurring in the major ventricular axis.
March 1974
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ET AL.
Two runs of ventricular tachycardia were analyzed, but, unfortunately, the ventriculograms in these cases did not contain sinus beats for comparison. The ventricular contraction patterns induced by ventricular tachycardia did not differ appreciably from those observed during isolated ventricular premature beats. Beats occurring serially during ventricular tachycardia tended to produce a similar but not necessarily identical contraction pattern.
END DIASTOLE
MID SYSTOLE
Studies in Animals
END SYSTOLE
.-
A
8
FIGURE 2. Selected left ventricular silhouettes from enddiastole, mid-systole and end-systole with a normal sinus beat (A) and a premature beat (B) in the same ventriculogram. Note the highly irregular and almost “crenated” appearance of the ectopically stimulated ventricle during contraction.
In general, ventricular premature beats tended to produce several distinctive contraction patterns. The two most often seen have already been illustrated. In Figure 1, contraction occurred mostly in the peribasilar and midportion minor axes. The periapical segment displayed asynchrony or dyskinesis, or both. The long axis exhibited minimal shortening. The net effect of this pattern would be to “propel” blood toward the apex. Another common contraction pattern of ventricular premature beats is illustrated in Figure 3 and has as its net effect the formation roughly of a globular shaped left ventricle with the long axis shortening at the “expense” of the minor axes.
FIGURE 3. Motion analyses of the two beats drawn in Figure 2. There is paradoxical systolic expansion of all segments except the long axis.
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March 1974
The American Journal of CARDIOLOGY
Ventricular premature beats: Adequate comparison between apically and basally stimulated left ventricular ectopic beats was made in two ventriculograms from each of three dogs. Stimuli applied to the left ventricle produced two distinct patterns of contraction depending on whether the apex or base was stimulated. In either instance, the initial salient feature was an expansion of the segment adjacent to the site of the stimulus. This pattern was observed regardless of the timing of the premature beat. Figure 4A illustrates selected silhouettes and a motion analysis of an apically stimulated ventricular premature beat. There was paradoxical systolic expansion of the periapical segments with vigorous contraction of the base and midportion of the ventricle. These findings should be contrasted with results of the premature beat illustrated in Figure 4B, taken from a subsequent ventriculogram in the same animal. In this case, the ventricle was stimulated by means of the wire attached to the left ventricular outflow tract. Here, the basilar portion of the left ventricle expanded paradoxically whereas the periapical portion contracted. From these two distinct contraction patterns simplified conceptual models may be constructed. Apical stimulation results in trapping of blood in the apical regions, whereas basilar stimulation results in a more globular left ventricular configuration with blood being sequestered in an expanded outflow tract region. The hemodynamic correlates of apical versus basilar stimulation can be illustrated by comparison of the two beats cited. Table I shows the R-R interval for the normal control beat and the ventricular premature beat, left ventricular volumes and peak pressures for control and ventricular premature beats originating with apical and basilar stimuli. The data were derived from two sequential ventriculograms in one experimental preparation. Apical stimulation was more effective hemodynamically than outflow tract stimulation when beats with the same diastolic filling period were compared. Stimulation of the apex produced a greater percent of control aortic pressure and a larger ejection fraction than did stimulation of the base. This was true in all ventricular premature beats which appeared late enough to open the aortic valve. When the beats appeared too early to produce a rise in aortic pressure, the patterns of contractions were the same as those just described. When ejection of blood did not occur, early ventricular stimulation gave rise to an internal rearrangement of the ventric-
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VENTBlCtJLAR PBEMATlJBE BEATS AND TACHYCARDIAS-EBER
ET AL.
FIGURE 4. Selected silhouettes and motion analysis after apically stimulated (A) and basally stimulated (B) ventricular premature beats in a dog. Note the paradoxical systolic exoansion of the oeriaoical seament DR in A and the marked’ paradoxical expansion of the peribasilar segment D, in B.
ular contents. It is also possible that mitral regurgitation occurred with these beats. Ventricular tachycardia: Experimental ventricular tachycardia was produced by stimulating the left ventricular apex or base at a rate sufficient to drive the ventricle (190 to 210 beats/min). The ventriculograms obtained during the arrhythmia showed patterns similar to those produced by single ventricular premature beats in each area. However, when the ventricle was apically stimulated, there tended to be more paradoxical expansion in the long axis than with the single ventricular premature beat. Figure 5A shows a sequence of four silhouettes during a typical beat of apical ventricular tachycardia. In mid to late systole, the lengthening of the major axis and the circumferential contraction of the midportion of the left ventricle about the minor axis gave an “hourglass” appearance to the left ventricular cavity. This was
most notable when the ventriculogram was projected at normal film speed. Ventricular tachycardia produced by stimulation of the base showed expansion of the basilar area with normal shortening of the major axis. The ventricle became more globular in appearance, resembling an inverse teardrop with the point toward the apex. Selected silhouettes drawn from the ventriculogram obtained during a basally stimulated ventricular tachycardia beat are shown in Figure 5B.
TABLE
‘:-:i
I
Effect of Site of Pacemaker Interval (msec)
Site Control LV apex Control LV base
Normal R-R
R-R (VPB)
376 ... 380 ...
... 288 ... 288
on Left Ventricular
Performance
LV Pressure Peak % of (mm Hg) Control 96 80 116 86
... 83 ... 74
LV Volumes (ml) EDV
ESV
SV
EF
49 50 52 46
18 27 18 33
31 23 34 13
0.63 0.46 0.65 0.28
EDV = end-diastolic volume; EF = ejection fraction; ESV = end-systolic volume; LV = left ventricular; SV = stroke volume; VPB = ventricular premature beat.
Discussion
The apparent regional expansion of the stimulated portion of the left ventricle has been noted by others.5.6 Our study confirms these observations for left ventricular apical and basilar ventricular premature beats and tachycardias. The general patterns of contraction observed are unrelated to preload, diastolic filling periods, or even the presence or absence of aor-
END
DIASTOLE
END
DIASTOLE
EARLY
SYSTOLE
MID
LATE
SYSTOLE
SYSTOLE
\
END
END
SYSTOLE
SYSTOLE 1
FIGURE 5. Left ventricular silhouettes during experimental tachycardia. See text for details.
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PREMATURE SEATS AND TACHYCARMAS-EBER
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tic ejection, but are determined solely by the point of stimulus application. The relative importance of ventricular asynchrony and the temporal relation between atria1 and ventricular activation in producing a hemodynamic deficit with epicardial pacing has been studied in the dog heart. Daggett and co-workers7 compared atrial, atrioventricular and right ventricular epicardial pacing in a dog preparation. They demonstrated that atrioventricular pacing at properly adjusted intervals tended to override hemodynamically the adverse effect of having the ventricular impulse applied ectopitally. From this observation they concluded that the interval between atria1 and ventricular systole was a more important determinant of ventricular function during cardiac pacing than the site of entry of the impulse to the ventricle. In another series of experiments, Daggett et al. utilized the isovolumic left ventricle to study the hemodynamic effects of pacing from various epicardial sites. They showed that better performance was obtained with stimulation of the left ventricular apex than with stimulation of the right ventricle. However, their study did not mention the influence of atrioventricular sequential pacing in the intact heart when the pacing site was varied on the left ventricle itself. In our study, the production of single ventricular premature beats showed a hemodynamic and morphologic difference depending upon stimulus site when diastolic filling time was constant. This mechanism should be independent of atria1 systolic-ventricular systolic interval (As-Vs) in experiments of the type illustrated in Table I. It is conceivable that basilar stimulation may produce more mitral regurgitation than apical stimulation even at fixed As-Vs intervals, since these patterns of contraction are so different. In our animal experiments, quantification of mitral regurgitation was not possible since the injections were made by way of the left atrium to avoid unwanted stimulation of the ventricle during injection of dye. In the dog experiments, there was a constant directional hemodynamic difference between apical and basilar stimulation of the left ventricle. Stimulation of the apex resulted in a greater percentage of aortic pressure even when R-R intervals and end-diastolic volumes were constant. This finding is in contradistinction to some earlier observations.ssg Our data emphasize the hemodynamic importance of synchronous ventricular contraction patterns that operate independently of atria1 transport function. Experimentally produced asynchrony with its attendant shortened ejection time vitiates the Starling effect. In the one example listed in Table I, the end-diastolic volumes of the control and apically stimulated beat were prac-
tically the same, but the ejection fraction of the latter beat was considerably reduced. Our study encompassed observations on similar phenomena in man and dogs. During clinical diagnostic ventriculography, the occurrence of ventricular premature beats is commonplace. Careful examination of a number of these beats revealed two major contraction patterns that were similar to those evoked with epicardial stimulation in dogs. It is difficult to make a direct comparison of these patterns in man to those in experimental animals since the exact stimulus site in each clinical case is unknown. A catheter passed retrograde across the aortic valve may stimulate the outflow tract by direct contact or stimulate the apical region by a jet stream of contrast material during the injection. To relate the two aspects of this study, two assumptions must be made: (1) that endocardial stimuli induce the same contraction pattern as epicardial stimuli, and (2) that in the human observations, the stimulus sites were indeed similar to those applied in the experimental animals. The minimal conclusion to be drawn from the human observations is that ventricular premature beats in man vary in their associated patterns of left ventricular contraction and that these may be categorized. Clinical implications: Our study showed that ventricular stimulation either of the single ventricular premature beat type or of the repetitive tachycardia type results in a similar pattern of contraction. The .observation that apically induced ventricular premature beats are more hemodynamically effective than basilar ventricular premature beats supports the concept of Corday et al2 that ventricular tachycardias may be benign or malignant depending upon their site of origin within the ventricle. Some of the contraction patterns observed in our study bore great similarity to those seen during sinus rhythm in patients with segmentally diseased or ischemit ventricles.lO The slower ventricular tachycardias occurring during ventriculography in the normal patient might lead to an erroneous diagnosis of asynergy. Our results emphasize the importance of maintaining and documenting normal sinus rhythm before assessing a left ventricular contraction pattern from the ventriculogram. If ectopic beats occur, it is essential to .recognize them as such. In our study, it was possible to identify the site of application of a stimulus to the dog’s left ventricle by the type of,contraction pattern produced. Interpretation of ventriculograms in which ectopic beats occur can be subject to serious error. Acknowledgment We acknowledge the help of Drs. C. W. Urschel and E. H. Sonnenblick for their criticism of this work.
References 1. Wiggers CJ: The muscular reactions of the mammalian ventricles to artificial surface stimuli. Am J Physiol 73:346-378. 1925 2. Corday E, Gold H, cleVera LB, et al: Effect of the cardiac ar-
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rhythm& on the coronary circulation. Ann Intern Med 50535~ 553, 1959 3. Herman MV, Heinle RA, Klein MD, et al: Localized disorders in
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4. 5.
6.
7.
myocardiil contraction--asynergy and its role in congestive heart faiiure. N Engl J bled 277:222-232, 1967 Kkln MD, Herman MV, Gorfin R: A hemodynamic study of left ventricular aneurysm. Circulation 35614-630, 1967 Hood WB Jr, Covelli VH, Normal JC. et al: Systolic bulging at sites of left ventricular stimulation. Circulation 38:suppi Vi:Vi102, 1968 Ueda H, Hand K. Ueda K: Cineangiocardiqraphic observations on the asynchronism of cardiac contraction during ventricular pacing. Jap Heart J 9:295-302.1968 Deggett WM, Bienco JA, Powell WJ, et al: Retative contribu-
BEATS AND TACHYCARDIAS-EBER
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tions of the atrial systole-ventricular systoie interval and of patterns of ventricular activation to ventricular function during electrical pacing of the dog heart. Circ Res 27:69-79, 1970 8. Abffdskov JA, Eich RH, Haruml K, et al: Observations on the reiatiin between ventricuiar activation sequence and the hemodynamic state. Circ Res 17:236-247. 1965 9. Trembley GM, Nahas M: Location of epicardial pacemaker electrodes and myocardiii contractility. Can J Physiol Pharmacoi 47:267-271, 1969 10. Herman MV, Gorlln R: implications of left ventricular asynergy. Am J Cardiii 23536-547, 1969
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