Echocardiographic features of atrioventricular and ventriculoatrial conduction

Echocardiographic Features of Atrioventricular and Ventriculoatrial Conduction

MASAHITO LEONARD

NAITO,

T. JOSEPH CHIN

VAL JOEL

MARDELLI,

C. CHEN,

DANIEL ERIC

MD

S. DREIFUS,

DAVID,

MD,

FACC

MiD

MD MD

L. MICHELSON,

MD

MARCY MORGANROTH,

Philadelphia,

MD,

FACC

Pennsylvania

From the Departments of Melzficineand Physiol-

ogy, Jefferson Medical College of the Thomas Jefferson University and the Departments of Research and Medicine, The L.ankenau Hospital, Philadelohia, Pennsvlvania. Manuscriot received February 12, 1980,iccepted March il, 1980. Address for reprints: Leonard S. Dreifus, MD, Lankenau Hospital, Lancaster and City Line Avenues, Philadelphia. Pennsylvania 19151.

The potential application of diagnostic ultrasound to understanding of the hemodynamic effects of various rhythm and conduction disturbances has not been fully explored. To investigate the changes in cardiac function associated with various atrioventricular (A-V) sequencing intervals during cardiac pacing, simultaneous M mode and two dimensional echocardiographic and hemodynamic studies were performed in 23 dogs. One to one A-V and ventriculoatrial (V-A) sequential pacing at cycle lengths of 400 and 300 ms revealed a stepwise reduction in left ventricular pressure and cardiac output as the A-V interval was changed from i- 100 to -100 ms. These reductions in cardiac hemodynamics were associated with decreases in left ventricular and increases in left atrial dimensions determined with echocardiography. Mitral valve excursion and the duration of valve opening remained constant over the entire range of A-V intervals. There was angiographic evidence of retrograde blood flow from the left atrium into the pulmonary venous system at an A-V interval of -50 and -100 ms, but no evidence of mitral regurgitation. Thus, correlative echocardiographic and hemodynamic studies can suggest multiple pathophysiologic mechanisms contributing to the decrements in cardiac function observed during tachyarrhythmias with intact A-V conduction as well as those occurring consequent to A-V nodal Wenckebach cycles.

Echocardiography has revealed abnormal and occasionally characteristic ventricular wall motion patterns in association with a variety of electrocardiographic abnormalities. These electrocardiographic changes include the alterations in conduction associated with left bundle branch block,le3 accelerated idioventricular rhythms,4 preexcitation syndrome&g and, most consistently, with ventricular ectopic beats.lO Furthermore, patients with various forms of preexcitation may have such well defined wall motion abnormalities that these are virtually diagnostic for the ventricular site of insertion of the bypass tract.4,5T9 Typically, left ventricular posterior wall bypass tracts are detected more consistently than are those coursing through the interventricular septum.s,g Previous investigatorslOJ1 have also demonstrated the potential applications of echocardiography to understanding of the effects of various rhythm and conduction disturbances on cardiac performance. DeMaria et a1.12 assessed the contribution of atria1 transport to ventricular function after electroconversion of supraventricuiar arrhythmias by evaluating motion of the mitral valve with echocardiography. Similarly, other investigators13J4 described the echocardiographic manifestations of mitral valve and left atria1 wall motion in the presence of atria1 fl11tt0r

From previous work we have had a particular interest in the hemodynamic sequelae of both supraventricular and ventricular tachycardias, and in the hemodynamic consequences of various cardiac pacing

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TABLE I Effects of Various Atrioventricular (A-V) Sequential Intervals on Cardiac Hemodynamics in 15 Dogs A-V=

CL LVP LAP co

IOOms CL

A-V = 50 ms

CL

A-V = 0

CL

CL

A-V = -50

CL

CL

ms CL

A-V = -100

CL

ms CL

400

300

400

300

400

300

400

300

400

300

129 2.6 2.83

121 3.2 2.63

125” 3.2 2.26’

106 3.7 2.21”

120’ 4.5’ 1.95”

101’ 4.8’ 1.87’

116’ 5.9” 1.91”

93’ 6.6’ 1.82’

112’ 6.8” 1.83.

aa* 7.8’ 1.78’

p <0.05 (compared with value at an A-V interval of 100 ms). CL = cycle length (ms); CO = cardiac output (liters/min); LAP = left atrial pressure (mm Hg); LVP = left ventricular systolic pressure (mm Hg). l

methods.15 Thus, the present studies were designed specifically to determine the echocardiographic correlates of changes in cardiac performance secondary to changes in atrioventricular (A-V) conduction pat-

Echocardiography: M mode echocardiographic studies were obtained using a Smith-Kline Ekoline 20 interfaced with an Irex 101 Continutrace recorder. A 2.25 megahertz transducer was placed on a rigid bar that was attached to both sides of the surgical table. The methods of recording echocardiograms from the various cardiac structures were similar to those described by Kerber et al. ls In four animals, two dimensional echocardiographic recordings were also obtained using a wide angle (90”) mechanical sector scan (Advanced Technology Laboratories, Mark III). The transducer was attached to the same bar assembly used for the M mode echocardiographic transducer. In seven animals, an 8F catheter with multiple side holes at its tip was introduced into the left side of the heart through the left atria1 appendage or retrograde through the femoral artery in order to obtain left atria1 or left ventricular cineangiograms, or both, using hand injections of 5 ml of Renografin@. Contrast echocardiograms were obtained by bolus injection of saline solution directly into the left ventricle in order to determine the degree of mitral valve regurgitation.

terns. Methods Experimental preparation: Twenty-three mongrel dogs weighing 13 to 20 kg were anesthetized with intravenous administration of 20 to 30 mg/kg of sodium pentobarbital (Nembutale) and intubated. Ventilation was maintained by a Harvard respirator with use of room air. The chest was opened using a mid line incision and the pericardium was left intact. Left ventricular and aortic pressures were measured using a 7F Millar dual Mikro-Tip catheter pressure transducer (PC 771) inserted through the right femoral artery. Left atria1 pressures were obtained using a 5F Millar Mikro-Tip catheter pressure transducer (PC 350) introduced through a pulmonary vein. Cardiac output measurements were made utilizing a Swan-Ganz thermodilution catheter and an Edwards 9510A cardiac output computer. With use of 23 gauge needles, Teflon@-coated stainless steel unipolar plunge wire electrodes (0.1 mm diameter) were placed in the left atria1 appendage and the myocardium of the left ventricular apex to pace the heart. The pacing stimuli were 1 ms in duration. Both atria1 and ventricular pacing were applied using constant current pulses of twice diastolic threshhold. In addition, Teflon-coated, thin silver wire bipolar plunge electrodes were placed in the left atrial appendage and the left ventricular free wall in order to record the electrograms from each of these sites.

C L=400

ms

Echocardiographic recordings of the left atrium, left uentricle, mitral and aortic valve opening were obtained during ventricular pacing at cycle lengths of 400 and 300 ms

at multiple atrioventricular (A-V) intervals (+lOO, +50,0, -50 and -100 ms). The echocardiographic correlate of A-V nodal Wenckebach periodicity was also evaluated in seven dogs during rapid atria1 pacing at cycle lengths varying from 320 to 200 ms. Three dogs with stable, surgically induced A-V nodal heart block were studied during sequential pacing of the atria and ventricle at cycle lengths of 400 and 300 ms. The studies were repeated after the induction of atria1 fibrillation

C L=400ms’

c L=:300ms

C L=300 ms 39-

4.0

2.0

I

Lvd

A

I B

A = A-b

1OOms

B = V-A

1.0 L

LAd

A

100 ms

I B

2.0

1 A

LVd

1 l,OL B

A

LAd

J B

(n-8)

FIGURE1. Lefl panels,changesin left ventricular (LVd) and left atrial dimensions (LAd) at enddiastole in centimeters are shown as the atrioventricular (A-V) pacing interval is changed from + 100 ms (A) to -100 ms (B) at a cycle length (CL) of 400 ms. Note the reduction in left ventricular and increase in left atrial dimensions. Right panels, the same findings shown at a cycle length of 300 ms. V-A = ventriculoatrial.

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alterations occurring during pacing at a constant cycle length of 400 ms when the A-V interval was changed from +lOO ms (A) to -100 ms (B) (that is, ventriculoatrial (V-A) interval of 100 ms). In this representative case, left atria1 dimension increased from 2.3 to 2.5 cm with a concomitant decrease in left ventricular diastolic diameter from 3.9 to 3.0 cm. At an A-V interval of -100 ms left atria1 contraction occurred during the latter portion of the ventricular ejection period at a time when the A-V valves were still closed (Fig. 2B). At the shorter cycle length of 300 ms there was a similar increase in left atria1 pressure and dimension and a decrease in left ventricular pressure and dimension as the A-V interval was decreased from +lOO to -100 ms (Table I, Fig. 1). Several other notable observations were made during these studies. Mitral valve excursion and the duration of valve opening remained constant over the entire range of A-V intervals studied and were independent of alterations in cardiac hemodynamics and chamber size (Fig. 3). Left atria1 angiography was performed during each of these A-V sequencing intervals. Consistently, at A-V intervals of -50 and -100 ms, there was angiographic evidence of retrograde flow from the left atrium into the pulmonary venous system (Fig. 4) (that is, pulmonary venous regurgitation). Remarkably, there was no evidence of mitral regurgitation on left ventricular angiography or contrast echocardiography at any A-V interval

and ventricular

pacing at these same cycle lengths. One scalar electrocardiographic lead, left atrial, left ventricular and aortic pressures and the M mode echocardiograms were recorded simultaneously on an Irer: 101 Continutrace recorder. Simultaneous electrocardiographic and pressure recordings were also obtained on a Hewlett-Packard eight channel photographic recorder (model 4578A). Left ventricular and atria1 dimensions were measured at maximal diameter. At leasi, 10 beats were used in each record and all measurements were confirmed by two observers. Interobserver differences were within fO.l cm.

Results 1:l Atrioventricular and Ventriculoatrial Pacing The effects of different atrioventricular (A-V) intervals on cardiac hemodynamics during A-V sequential cardiac pacing at cycle lengths of 400 and 300 ms in 15 dogs are shown in Table I. At both pacing cycle lengths there was a stepwise reduction in left ventricul,sr pressure and cardiac output as the A-V interval was changed from +lOO to +50,0, -50 and -100 ms. These alterations in cardiac hemodynamics were associated with decreases in left ventricular and increases in left atria1 dimensions determined with M mode echocardiography (Fig. 1). Figure 2 illustrates the echocardiographic

(A) A-V=

(6) V-A=

looms

100ms ,

40 mmHg

-

FIGURE 2. Representative study showing a marked decrease in left ventricular (LV) cavity size with a concomitant increase in left atrial (LA) dimension during abnormal atrioventricular (A-V) sequencing. Top panel shows the effects of an A-V interval of 100 ms at a cycle length (CL) of 400 ms in (A) and the effects of an A-V interval of - 100 ms (V-A) in (6). Note the decrdase in left ventricular (LV) dimension from 3.9 cm (A) to 3.0 cm (B) and an increase in left atrial (LA) dimension from 2.3 cm (A) to 2.5 cm (B). Also note the elevated left atrial pressure (LAP) during the left ventricular ejection period. A = atrial pacing spike; A0 = aortic root; EKG = electrocardiogram; IVS = interventricular septum; LVP = left ventricular pressure; LVPW =: left ventricular posterior wall; V = ventricular pacing spike.

V

A

3.?cm

A0 _ 2.pzm

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during 1:l A-V or V-A pacing at cycle lengths of 400 or 300 ms (Fig. 5, A and B). In addition, in three animals with surgically induced A-V heart block atria1 fibrillation was induced by high frequency atria1 pacing. Notably, in the presence of atria1 fibrillation and A-V block there was also no evidence of mitral regurgitation during ventricular pacing at a fixed cycle length of 400 or 300 ms (Fig. 5C).

Rapid Atrial Pacing Rapid atria1 pacing at cycle lengths of less than 280 ms with 1:l A-V sequencing usually resulted in both electrical and mechanical left ventricular alternans. In Figure 6 the mechanical systole after mitral valve opening and left ventricular filling was forceful and prolonged and resulted in aortic valve opening with a normal ejection period. This prolonged systole encroached on the next atria1 contraction (arrow), resulting

CL = 400msec

A-V=

Oms

A-V=_lOOms

in an abortive attempt to open the mitral valve (asterisk). The next ventricular systole failed to open the aortic valve. However, this shorter systolic period engendered a more favorable A-V sequence that again enabled the mitral valve to open and facilitated left ventricular filling. Rapid atria1 pacing resulted in a Wenckebach pattern of A-V conduction (Fig. 7). During the prolonged pause that preceded the first conducted beat of each sequence, the lack of ventricular systole permitted an extended period of mitral valve opening and left ventricular filling. The next atria1 contraction (single arrow) reopened the mitral valve and, further, actively filled the ventricle. All of these factors contributed to the subsequent enhanced and prolonged systole (360 ms) of the first conducted beat after the pause. The hemodynamic conditions preceding the second ventricular systole in the sequence (2) were much less favorable. The next

A-V=

V-A=50ms

50ms

V-A=

looms,

FIGURE 3. Representative M mode echocardiograms of the anterior mitral leaflet (AML) during various atrioventricular (A-V) and ventriculoatrial (V-A) intervals at a cycle length (CL) of 400 ms recorded with simultaneous pressure curves. The duration of mitral valve opening and the amplitude of excursion remain essentially constant. The numbers between two transverse arrows (- +) indicate the duration of diastolic opening of the anterior mitral leaflet in milliseconds and those under a single vertical arrow (t) show the excursion of this leaflet in millimeters. Note the decrease in left ventricular (LVP) and aortic (AoP) pressures as the A-V interval was changed from +I00 to -100 ms. A = atrial pacing spike; EKG = electrocardiogram; LAP = left atrial pressure; V = ventricular pacing spike.

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CONTROL

A-V

= IOOms

V-A=

IOOms

FIGURE 4. Left atrial angiograms. Left panel (CONTROL) demonstrates the tip of a catheter located in the left atrial appendage and introduced by way of the pulmonary vein. Right panel demonstrates marked regurgitation (white arrows) of contrast medium from the left atrium (LA) into the pulmonary vein (PV) during a ventriculoatrial (V-A) pacing interval of 100 ms at a cycle length of 400 ms. No such regurgitation is observed during an atrioventricular (A-V) interval of 100 ms at a cycle length of 400 ms (middle panel).

FIGURE 5. Still frames’of a two dimensional echocardiographic left ventricular long axis view of a dog’s heart. The control state (CONT.) is shown in the upper row (A, B, C) and’ systolic frames during saline injection (INJ) in the lower row (A’, B’, C’). Whlte arrow in A indicates the anterior mitral leaflet. Changing the pacing sequence from an atrioventricular (A-V) interval of 100 ms (A, A’) to a ventriculoatrial (V-A) interval of 100 ms (B, B’) does not result in mitral regurgitation (that is, there are no saline microbubbles present in the left atrium in systole). Similarly, there is no evidence of mitral regurgitation in the presence of atrial fibrillation (A F) and A-V block with a constant ventricular rate (C and C’). LA = left atrium; LV = left ventricle; msec = milliseconds; pw = left ventricular posterior wall: RA = right atrium; RV = right ventricle; vs = interventricular septum.

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CL = 280ms

FIGURE 6. Rapid atrial pacing at a cycle length (CL) of 280 ms in this representative study shows the induction of left ventricular mechanical and electrical alternans. Pressure relations among the aorta (AoP), left ventricle (LVP) and left atrium (LAP) are shown in the upper panel and the echogram of the anterior mitral leaflet (AML) is shown in the lower panel. Note that the encroachment of the prolonged mechanical systole after the anterior mitral leaflet opening on the next atrial contraction (black arrow on the left atrial pressure curve) resulted in an abortive opening of the anterior mitral leaflet (circled asterisk). A = atrial pacing spike; EKG = electrocardiogram; P = P wave; R = QRS complex.

atria1 contraction (double arrows) could not contribute to left ventricular filling because it occurred during ventricular systole. In addition, passive left ventricular filling as evidenced by mitral valve opening was shortened by encroachment of the next ventricular systole on the previous one, as dictated by the progressive shortening of the R-R intervals during typical Wenckebach sequences. The combination of these hemodynamic events resulted in a less powerful ventricular systole that failed to open the aortic valve.

The hemodynamic conditions became even more complex when rapid atria1 pacing caused a combination of a 3:2 Wenckebach periodicity and an absolute 2:l left ventricular and atria1 alternans (Fig. 8). Because only every other elec-

trical systole (RI, Rq, R7) resulted in a mechanical response, the passive mitral valve opening time was unusually prolonged. Atria1 contraction after & enhanced opening of the mitral valve (asterisk). Of note, because of the superimposed ‘atria1 alternans, effective atria1 cont,ractions occurred only

CL= 320ms A

I

AV v

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FIGURE 7. Rapid atrial pacing at a cycle length (CL) of 320 ms in a representative dog resulted in 3:2 Wenckebach periodicity. The ladder diagram depicts the conduction pattern. Note that the prolonged period of the mitral valve opening (single arrow on the echogram of the anterior mitral leaflet [AML]) after a dropped beat results in a forceful and prolonged (360 ms) mechanical systole (I), and that the passive left ventricular filling of this cycle is shortened because of the encroachment of the next ventricular systole (2) on the previous one (1). Also note that the atrial contraction varies depending on whether it occurs during the ventricular ejection period (single and double arrows on the left atrial pressure [LAP] tracer). A = atrial pacing spike; AoP = aortic pressure; EKG = electrocardiogram; LAP = left atrial pressure; P = P wave; PML = posterior mitral leaflet: R = QRS complex.

ECHOCARDIOGRAPHYIN ABNORMAL A-V CONDUCTION-NAITO ET AL.

after each effective second ventricular systole (asterisk). Note the absence of the expected increase in atrial pressure (double arrows) during the ventricular ejection period and the closed mitral valve caused by the atria1 alternans. Thus, although atria1contractions occurred at the same position in diastole during different cycles (arrow) they failed to open the mitral valve consistently. Discussion Alterations in cardiac function associated with various cardiac arrhythmias have previously been studied but have routinely bee:n limited to measurements of traditional hemodynannic variables.15J7 Using conventional methods, several investigators15J7Js have suggested that the hemodynamic consequences of various changes in the sequence of A-V activation and in the degree of irregularity of successive cardiac cycles may also result from secondary vasomotor and neurohumoral mechanisms. It has long been recognizedlg that the so-called atria1 booster pump action present during normal A-V sequencing results in an increase in ventricular volume at end-diastole so that an approximately 10 to 20 percent larger cardiac output occurs than in the presence of A-V block. Furthermore, P wave synchronous pacing in complete A-V heart block results in a cardiac output approximately 10 to 15 percent greater than that with ventricular pacing at the same ventricular rates.20 Hemodynamic and1 chamber size alterations during A-V and V-A pacing: In a previous study,2l we demonstrated that M mode echocardiography was useful in identifying the changes in cardiac function that occur in the presence of ,various patterns of A-V and V-A

conduction. In this study, changes in cardiac hemodynamics and cardiac chamber sizes were evaluated by scanning the A-V interval from +lOO to -100 ms in the presence of A-V and V-A sequential pacing. We observed progressive decreases in systolic blood pressure, cardiac output and left ventricular size concomitant with increases in left atria1 size. As atria1 systole moved into the period of mechanical ventricular systole, the contraction of the left atrium against the closed mitral valve resulted in marked regurgitation of blood into the pulmonary venous system (Fig. 4). Hence, it would appear that, in addition to the direct loss of the atria1 contribution to ventricular filling, there was also a secondary and significant loss resulting from retrograde propulsion of blood during V-A conduction. Thus, even “stable” sustained ventricular rhythms with intact V-A conduction can result in serious hemodynamic consequences. In contrast, ventricular pacing or tachycardia in the presence of A-V block appeared hemodynamitally relatively less deleterious because there was only a random rather than regular and inadvertent association of atria1 and ventricular systole.15 Similarly, the occurrence of atrial fibrillation in association with rapid ventricular rhythms was also apparently less deleterious hemodynamically than the presence of intact 1:l rapid retrograde V-A conduction.15 Mitral valve function: Remarkably, the alterations in cardiac hemodynamics and changes in chamber dimensions during rapid 1:l A-V pacing at various sequencing intervals were not reflected in the echocardiographic features of mitral valve function (Fig. 3). However, the variations in ventricular cycle lengths that

CL=PPOmsec

FIGURE 8. Wenckebach periodicity (3:2) with left ventricular and atrial alternans observed in a representative dog at a cycle length (CL) of 220 ms. The ladder diagram relates atrial pacing stimuli (A) to atrial activation (P) and ventricular activation (R). Aortic (AoP), left ventricular (LVP) and left atrial (LAP) pressures show complex patterns of left atrial and left ventricular alternans. Note the difference between the high (asterisk) and low (arrows) left atrial pressures. AML = anterior mitral leaflet: EKG = electrocardiogram: PML = posterior mitral leaflet.

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occurred in association with progressive P-R interval prolongation during A-V nodal Wenckebach periods did affect mitral valve motion, and often obliterated the usual presystolic reversal of the A-V pressure gradient that normally places the A-V valve leaflets in a position to close early at the onset of ventricular systole. Hence, A-V valve regurgitation was observed during rapid atrial pacing causing Wenckebach periodicity and irregular R-R intervals (Fig. 9). Mitral regurgitation was never observed during sustained periods of V-A activation with constant P-R or R-P intervals as long as the R-R intervals remained constant (Fig. 5, A and B).22 This was true even in the presence of atria1 fibrillation in the dogs with heart block when the R-R intervals were kept constant (Fig. 5C). Echocardiographic changes during Wenckebach conduction: D’Cruz et a1.23 observed that during 3:2 A-V Wenckebach conduction patterns, ventricular beats exhibited alternating long and short periods of systolic opening of the pulmonary and aortic valves and alternately large and small left ventricular stroke volumes. Left ventricular stroke volume in these cases appeared to be directly proportional to the preceding end-diastolic volume. Other investigators24 observed alternating failure of mechanical responses to electrical

depolarizations during A-V Wenckebach periods in addition to those ventricular contractions lost secondary to periodic A-V block, but the precise mechanism of this phenomenon has eluded clear definition. The echocardiographic observations made in our study have revealed an important mechanism contributing to the compromised hemodynamics during typical A-V Wenckebach periods in which R-R intervals shorten successively. At critical P-R and R-R intervals there is increasing encroachment of a subsequent atrial systole into the left ventricular ejection period of the previous systole. This successively shortens the duration of the opening of the mitral valve, abolishes active atria1 transport and thereby reduces left ventricular filling. Other Wenckebach patterns might further compromise cardiac hemodynamics. However, the longer pause that follows the dropped beat does enable adequate mitral valve opening and left ventricular filling and thereby facilitates an effective subsequent beat (Fig. 7). Clinical implications: As shown in the present study, echocardiography can provide considerable insight into the mechanisms responsible for the marked hemodynamic derangements that result from various patterns of A-V conduction. Such deleterious hemodynamic consequences could not be anticipated from

FIGURE 0. Atrioventricular regurgitation during rapid atria1 pacing. A, left ventricular long axis two dlmensionai echocardiographic view of a representative dog heart during rapid atriai pacing causing Wenckebach periodicity. Ao = aorta; LA = left atrium; LV = left ventricle. The anterior mitral leaflet is marked by a whife arrow. B, a still frame during systoie of the same dog during saline injection into the left ventricle. Regurgitation of contrast medium into the left atrium is indicated by the Mach arrows. The arrowto the right of the electrocardiogram indicates the precise timing of the stop-frame echocardiogram. The lower part of the figure shows the electrocardiogram and corresponding ladder diagram (A = atrial: A-V = atrioventricuiar; V = ventricular conduction). At top of figure, A = anterior; I = inferior; P = posterior: S = superior.

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analyses limited to the electrocardiogram. Echocardiography can be especially useful in understanding the effects of comnlex abnormalities such as those resulting from the superimposition of mechanical (for example, alternans) and electrical (for example, Wenckebach periodicity) phenomena during sutiraventricular arrhythmias. In addition, these studies provide further experimental evidence emphasizing the potential clin-

ical benefits of those cardiac pacing methods that provide optimal A-V sequencing intervals. Acknowledgment We acknowledge the technical assistance of James J. Kmetzo, Mark Schaffenhurg and the assistance of Marie Sciocchetti in the preparation of the manuscript.

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