- Email: [email protected]
Abnormal Systemic Venous Doppler Flow Patterns in Atrial Tachycardia in Infants
resolution in the lower range was available. Nonetheless, our findings do suggest a need for further work to investigate the contribution of elevated serum endothelin levels to abnormalities of both somatic and visceral nociception in syndrome X patients. Such investigations might be performed in a blinded fashion using specific endothelin antagonists. The relative contribution of the vasoconstrictive and algogenic properties of endothelin to such nociceptive abnormalities also remains speculative, but it is a hypothetical possibility that a combined mechanism exists in which endothelin’s vasoactive effects may contribute to the evolution of an ischemic stimulus that is ‘‘amplified’’ by reduced nociceptive thresholds.5,6 In conclusion, the results of this study suggest that elevated serum endothelin levels may contrib-
ute to abnormalities of somatic pain perception in patients with cardiac syndrome X. 1. Rosen SD, Uren NG, Kaski JC, Tousoulis D, Davies GJ, Camici PG. Coronary
vasodilator reserve, pain perception, and sex in patients with syndrome X. Circulation 1994;90:50 – 60. 2. Lagerqvist B, Sylven C, Wa¨ldenstrom A. Lower threshold for adenosineinduced chest pain in patients with angina and normal coronary angiograms. Br Heart J 1992;68:282–285. 3. Turiel M, Galassi AR, Glazier JJ, Kaski JC, Maseri A. Pain threshold and tolerance in women with syndrome X and women with stable angina pectoris. Am J Cardiol 1987;60:503–507. 4. Kaski JC, Elliott PM, Salomone O, Dickinson K, Gordon D, Hann C, Holt DW. Concentration of circulating plasma endothelin in patients with angina and normal coronary angiograms. Br Heart J 1995;74:620 – 624. 5. Yanagisawa M, Kurihara H, Kimura S, Tomobe Y, Kobayashi M, Mitsui Y, Yazaki Y, Goto K, Masaki T. A novel potent vasoconstrictor peptide produced by vascular endothelial cells. Nature 1988;332:411– 415. 6. Raffa RB, Shupsky JJ, Martı´nez RP, Jacoby HI. Endothelin-1-induced nociception. Life Sci 1991;49:61– 65.
Abnormal Systemic Venous Doppler Flow Patterns in Atrial Tachycardia in Infants Janette F. Strasburger,
MD,
C. Elise Duffy,
uring supraventricular tachycardia and intraatrial D reentrant tachycardia (atrial flutter) in the infant and fetus, hemodynamic alterations result in rapid development of congestive heart failure and hydrops fetalis.1– 4 Altered preload, diastolic function, myocardial perfusion, or a combination of these factors have been postulated as the etiology of diminished cardiac output.5–7 However, human studies have not specifically assessed diastolic function parameters and tachycardia mechanism. We hypothesized that diastolic dysfunction due to atrial tachycardia would be demonstrable during supraventricular tachycardia in infants. In particular, Doppler venous and intracardiac flow patterns could be altered by atrioventricular contraction sequence, abnormal atrial activation, and excess rate. This study defines Doppler flow characteristics during sinus rhythm, atrial paced rhythm, and during atrial tachycardia in infants presenting with tachycardia-induced congestive heart failure or hydrops fetalis. •••
The cohort for this study comprised 17 infants with supraventricular tachycardia-related congestive heart failure or hydrops fetalis, presenting in utero or during the first 6 months of life. None had structural cardiac defects. All underwent transesophageal electrophysiologic procedures either emergently (6 patients) or electively within 2 weeks of birth or clinical presentation (11 patients). The methods for transesophageal pacing procedure and its use for defining supraventricular From the Division of Cardiology, The Children’s Memorial Hospital, Chicago, Illinois. Dr. Strasburger’s address is: Division of Cardiology, Children’s Memorial Hospital, 2300 Children’s Plaza, Box 21, Chicago, Illinois 60614. Manuscript received January 16, 1997; revised manuscript received and accepted April 14, 1997.
640
©1997 by Excerpta Medica, Inc. All rights reserved.
MD,
and Samuel S. Gidding,
MD
tachycardia mechanisms and localization of accessory connection have been previously described.8,9 All pulsed Doppler measurements were obtained with parental consent during transesophageal pacing procedure in the sedated infant using commercially available cardiac ultrasound equipment (HewlettPackard model 77020A, 5.0 MHZ medium-focus, phased-array transducer, Andover, Massachusetts). The phase delay constant for video display of electrocardiographic and Doppler signals was predetermined by Hewlett-Packard, and based on pulse repetition rates, maximum delay was not more than 30 ms. Pulsed Doppler was obtained during sinus rhythm, during atrial paced rhythm at varying cycle lengths (8 extrastimuli at 300- to 200-ms intervals), and during sustained tachycardia induced as part of the procedure. Lead I electrocardiographic recording (with or without esophageal atrial electrogram) was acquired simultaneously. The pulsed Doppler sample volume was positioned in the superior vena cava just below the origin of the innominate vein from the suprasternal notch or right parasternal projection, and in the inflow region of the tricuspid valve at the valve leaflet tips from an apical 4-chamber projection. This allowed an angle of incidence of ,30° and angle correction was not performed. At least 10 representative cardiac cycles were recorded (Honeywell strip-chart recorder, 100 mm/s) during sinus rhythm and each tachycardia, then analyzed off-line using a graphics tablet, microcomputer, and custom-written software (Freeland Medical System Cardiac Workstation GTI, Denver, Colorado) using modifications of Doppler analysis techniques previously described.10 –16 In the superior vena cava, both the onset and duration of reversed flow velocities were assessed. The onset of reversed flow was measured from QRS onset 0002-9149/97/$17.00 PII S0002-9149(97)00440-2
lated to an accessory atrioventricular connection, 5 had intraatrial reentrant tachycardia, and 1 patient had both. Orthodromic reciprocating tachycardia was induced in 12 of 14 episodes and antidromic reciprocating tachycardia in 2. Five of 17 patients had ventricular preexcitation (Wolff-Parkinson-White syndrome) during sinus rhythm. One patient had 2 distinct intraatrial reentrant tachycardias. Mean ventricular cycle lengths for atrioventricular reentrant tachycardia were 234 6 25 ms and for intraatrial reentrant tachycardia 246 6 22 ms (p 5 NS). During intraatrial reentrant tachycardia, predominantly 2:1 atrioventricular conduction was present in 6 patients and FIGURE 1. A schematic of the electrocardiogram (ECG) (lead I) during tachycardia and variable 1:1 and 2:1 conduction in 1. Doppler inflow pattern obtained from the superior vena cava (SVC). Reversed flow Retrograde flow in the superior velocities are represented above the baseline. The onset of reversal of flow (Q-ORF), vena cava during sinus rhythm was duration of reversed flow (DRF), and RR interval were measured as shown in the superior vena cava during atrial tachycardia. Similar measurements were obtained durpresent in 7; the amount of reversal ing sinus rhythm. was ,18% of total flow (mean 11 6 1%). In 5 infants with spontaneous sinus tachycardia at cycle lengths of to onset of flow reversal at baseline. Duration of 320 to 300 ms, flow reversal also was not noted. reversed flow was measured from the baseline at the During esophageal atrial pacing (eccentric atrial actibeginning and the end of the flow envelope. Second, vation) at cycle lengths ,280 ms, reversal of flow in the ratio of reversed flow (time velocity integral ret- the superior vena cava was present. During atrial rograde) to total flow (time velocity integrals prograde tachycardia, retrograde flow was present in all 14 and retrograde) was determined in order to predict atrioventricular reentrant tachycardias, and in all epipercent reversed flow (Figure 1).11–16 For this study sodes of intraatrial reentrant tachycardia during 1:1 we compared reversed velocities to ‘‘total’’ forward atrioventricular association. Reversed flow velocities and reversed velocities, using the formula: reversed represented a mean of 38 6 1% of total superior vena time velocity integral/reversed time velocity inte- cava flow and were present for 33 6 1% of the cardiac gral 1 forward time velocity integral 3 100 5 percent cycle. Reversal began at initiation of spontaneous or reversal of total flow velocities. Cycle lengths were induced tachycardia, and no significant change in different during sinus rhythm and tachycardia; there- amount of reversed flow occurred over minutes of fore, values were analyzed as a percentage of the RR observation in these infants. interval (measured onset or duration [ms]/RR interval The onset of retrograde flow in the superior vena [ms] 3 100). cava during atrial tachycardia correlated with the venWith use of techniques previously described13,17 triculoatrial interval (r 5 0.72, p ,0.01) in patients for the tricuspid valve, the mean velocity in centime- with 1:1 ventriculoatrial conduction (Figure 3). This ters per second and time velocity integral in centime- suggested that retrograde flow was caused by atrial ters were evaluated. The product of the time velocity contraction against a closed tricuspid valve after reintegral times heart rate was examined as a crude entry. Duration and amount of venous flow reversal indicator of cardiac output at the tricuspid valve.14,15 did not appear to correlate with ventriculoatrial interThe time to onset of diastolic filling, and diastolic val or cycle length of atrial tachycardia. filling period at the tricuspid valve were also measured Tricuspid valve mean velocities and time velocity (Figure 2). integrals were different from sinus rhythm. Mean veData are presented as mean 6 SEM. Paired t tests locity decreased (34 6 0.08 to 28 6 0.06 cm/s [p were performed for comparisons between sinus ,0.01]), as did time velocity integral (6.8 6 2.3 to rhythm and induced tachycardia. Unpaired t tests were 2.9 6 1.0 cm [p ,0.001]). The time velocity integral used for subgroup comparisons. Linear regression was times heart rate product was 8,875 6 2,573 cm beats/ performed to correlate superior vena cava and tricus- min for sinus rhythm and 7,370 6 2,889 for tachypid valve Doppler measures with ventriculoatrial in- cardia (p ,0.01). A positive correlation existed beterval. tween normalized ventriculoatrial interval and In the 17 infants, 21 distinct tachycardias were tricuspid valve mean velocity (r 5 0.53, p ,0.05), induced (14 orthodromic or antidromic reciprocating suggesting that longer ventriculoatrial intervals were tachycardias and 7 intraatrial reentrant tachycardias). associated with greater tricuspid inflow. No differEleven patients had supraventricular tachycardia re- ences in inflow mean velocities and time velocity BRIEF REPORTS
641
FIGURE 2. A schematic of tricuspid valve inflow Doppler velocities during supraventricular tachycardia. Onset of diastolic filling (Q-ODF), diastolic filling period (DFP), and RR interval were measured as shown. Time velocity integral and mean velocity were obtained by tracing the envelope during sinus rhythm and tachycardia. Duration of diastolic filling included both early passive (E wave) and late (A wave) diastolic phases. These phases were superimposed during tachycardia. ECG 5 electrocardiogram; RA 5 right atrium; RV 5 right ventricle.
ure have speculated that congestive heart failure is caused by alterations in systemic venous and intracardiac diastolic flow.18 This study has demonstrated that supraventricular tachycardia causes reversal of systemic venous Doppler flow, decreased diastolic duration, delayed diastolic onset, and decreased right heart filling velocities. A critical observation in this study is the relation of ventriculoatrial interval during tachycardia with onset of superior vena cava flow reversal. In addition, a longer ventriculoatrial interval was associated with greater diastolic filling velocities at the tricuspid valve. This combination of findings suggests the importance of electrophysiologic features of tachycardia as a factor in the onset of congestive heart failure. We speculate that the neonate or fetus with 1:1 ventriculoatrial association and ventriculoatrial interval ,50% of the RR interval would be most likely to develop rapid onset of supraventricular tachycardiarelated congestive heart failure. Systemic and intracardiac venous flow abnormalities did not appear to correlate with shorter tachycardia cycle lengths. Flow reversal is related to ventricular compliance and right ventricular end-diastolic pressure, neither of which is directly linked to cycle length.10 –12,19 –21 Zales et al20 reported that supraventricular tachycardia–induced hydrops fetalis develops at cycle lengths longer than commonly observed in the neonate. We have found in 30 patients with fetal tachycardia that duration of tachycardia and gestational age were the most important factors associated with hydrops.21 Thus, we speculate that the development of congestive heart failure may be linked to specific electrophysiologic activation patterns affecting the sequence of cardiac contraction.
In summary, abnormal retrograde venous flow patterns in the superior vena cava were uniformly present in atrioventricular reenFIGURE 3. Relation of ventriculoatrial interval (VA/RR) to onset of superior vena cava trant tachycardia with a 1:1 atrioflow reversal (ORF/RR). R 5 0.72, p <0.01. ventricular relation. The onset of retrograde venous flow in the superior vena cava correlated with integrals were observed when intraatrial reentrant the ventriculoatrial interval. Tricuspid inflow tachycardia was compared with atrioventricular reen- Doppler characteristics were also altered during supraventricular tachycardia, including a later ontrant tachycardia. During supraventricular tachycardia, onset of dia- set of diastolic flow, decreased flow duration, and stolic flow was displaced late into the cardiac cycle, decreased mean flow velocity. with the onset of diastolic filling occurring 91 6 9% Acknowledgment: We wish to thank Kay Berdusis through the cardiac cycle versus 73 6 8% in sinus and members of the Echocardiography Laboratory rhythm. The filling duration in diastole (normalized to Children’s Memorial Hospital for their technical asRR) was shorter during supraventricular tachycardia sistance, and Laura Hovis and Kristen Carr for assisthan during sinus rhythm (33 6 6% vs 39 6 8%, p tance in manuscript preparation. ,0.01). •••
Animal studies and reviews of infants with both supraventricular tachycardia and congestive heart fail642
THE AMERICAN JOURNAL OF CARDIOLOGYT
VOL. 80
1. van Engelen AD, Weijtens O, Brenner JI, Kleinman CS, Copel JA, Stoutin-
beck P, Meijboom EJ. Management outcome and follow-up of fetal tachycardia. J Am Coll Cardiol 1994;24:1371–1375.
SEPTEMBER 1, 1997
2. Newburger JW, Keane JF. Intrauterine supraventricular tachycardia. J Pediatr 1979;95:780 –786. 3. Naito M, David D, Michelson EL, Schaffenburg M, Dreifus LS. The hemodynamic consequences of cardiac arrhythmias: evaluation of relative roles of abnormal atrioventricular sequencing, irregularity of ventricular rhythm and atrial fibrillation in a canine model. Am Heart J 1983;106:284 –291. 4. Gembruch U, Redel DA, Bald R, Hansman M. Longitudinal study in 18 cases of fetal supraventricular tachycardia: Doppler echocardiographic findings and pathophysiologic implications. Am Heart J 1993;125:1290 –1301. 5. Brutsaert DL, Sys SU, Gillebert TC. Diastolic failure: pathophysiology and therapeutic implications. J Am Coll Cardiol 1993;22:318 –235. 6. Hoffman JI. Transmural myocardial perfusion. Prog Cardiovasc Dis 1987; 29:429 – 64. 7. Paridon SM, Fisher DJ. Regulation of myocardial blood flow and oxygen consumption. In: Garson A Jr, Bricker JT, and McNamara DG, eds. Science and Practice of Pediatric Cardiology, vol III. Philadelphia: Lea & Febiger Co, 1990: 250 –266. 8. Ko JK, Deal BJ, Strasburger JF, Benson DW Jr. Supraventricular tachycardia mechanisms and their age distribution in pediatric patients. Am J Cardiol 1992; 69:1028 –1032. 9. Benson DW, Dunnigan A, Benditt DG. Follow-up evaluation of paroxysmal atrial tachycardia: transesophageal study. Circulation 1987;75:542–549. 10. Meijboom EJ, Horowitz S, Valdez-Cruz LM, Sahn DJ, Larson DF, Lima CO. A Doppler echocardiographic method for calculating volume flow across the tricuspid valve: correlative laboratory and clinical studies. Circulation 1985;71:551–556. 11. Hecher K, Campbell S, Doyle P, Harrington K, Nicolaides K. Assessment of fetal compromise by Doppler ultrasound investigation of the fetal circulation: arterial, intracardiac, and venous blood flow velocity studies. Circulation 1995; 91:129 –138. 12. Gest AL, Martin CG, Moise AA, Hansen TN. Reversal of venous blood flow with atrial tachycardia and hydrops in fetal sheep. Pediatr Res 1990;28:223–226.
13. Riggs TW, Rodriguez R, Snider AR, Batton D. Doppler echocardiographic evaluation of right and left ventricular diastolic function in normal neonates. J Am Coll Cardiol 1989;13:700 –705. 14. Tulzer G, Khowsathit P, Gudmundsson S, Wood DC, Tian ZY, Schmitt K, Huhta JC. Diastolic function of the fetal heart during second and third trimester: a prospective longitudinal Doppler-echocardiographic study. Eur J Pediatr 1994; 153:151–154. 15. Sharif DS, Huhta JC, Moise KJ, Morrow RW, Yoon GY. Changes in fetal hemodynamics with terbutaline treatment and premature labor. J Clin Ultrasound 1990;18:85– 89. 16. Gudmundsson S, Huhta JC, Wood DC, Tulzer G, Cohen AW, Weiner S. Venous Doppler ultrasonography in the fetus with nonimmune hydrops. Am J Obstet Gynecol 1991;164:33–37. 17. Snider AR, Serwer GA. Methods for obtaining quantitative information from the echocardiographic examination. In: Snider AR, Serwer GA, Ritter SB, eds. Echocardiography in Pediatric Heart Disease. St. Louis, MO: Mosby Yearbook, 1990:78 –133. 18. Tomita M, Spinale FG, Crawford FA, Zile MR. Changes in left ventricular volume, mass, and function during the development and regression of supraventricular tachycardia-induced cardiomyopathy. Circulation 1991;83: 635– 644. 19. Rudolph AM, Heymann MA. Cardiac output in the fetal lamb: the effects of spontaneous and induced changes of heart rate on right and left ventricular output. Am J Obstet Gynecol 1976;124:183–192. 20. Zales VR, Dunnigan A, Benson DW Jr. Clinical and electrophysiologic features of fetal and neonatal paroxysmal atrial tachycardia resulting in congestive heart failure. Am J of Cardiol 1988;62:225–228. 21. Naheed Z, Strasburger JF, Deal BJ, Gidding SS, Benson DW. Fetal tachycardia: mechanisms and predictors of hydrops fetalis. J Am Coll Cardiol 1996; 27:1736 –1740.
A New Approach for DDD(R) Pacing Using a Single-Pass DDD Lead Barbara Naegeli, MD, Edwin Straumann, MD, Andreas Gerber, Urs Niederha ¨ user, MD, and Osmund Bertel, MD ecent studies have shown that a single lead VDD R pacing system in properly selected patients is an interesting alternative to physiologic DDD pacing, espe1– 4
cially in view of lower costs, ease of single-lead implantation, and the high reliability of stable atrioventricular synchronization.5 The major clinical limitation of singlelead VDD pacing is the inability to pace the atrium. This means that this pacing mode is limited to patients with a higher degree of heart block and normal sinus node function. Therefore, the possibility of reliably performing DDD pacing with a single lead would be significant progress in cardiac pacing. Preliminary data from several single lead VDD studies6 – 8 have shown successful attempts to pace the atrium and ventricle by a single-pass electrode at the time of implantation only. This study evaluates the possibility as well as short- and long-term stability of atrioventricular sequential pacing, using a new quadripolar single-pass DDD lead which has closely spaced polished cylindrical dipoles for atrial sensing and pacing, in conjunction with a DDD(R) pacemaker (PM) (TheraTM DR, models 7940/7941/7942, Medtronic, Inc., Minneapolis, Minnesota). ••• From the Cardiac Unit, Department of Internal Medicine, and Department of Cardiac Surgery, Stadtspital Triemli, Zu¨rich, Switzerland. Dr. Naegeli’s address is: Cardiac Unit, Department of Internal Medicine, Stadtspital Triemli, CH-8063 Zu¨rich, Switzerland. Manuscript received January 15, 1997; revised manuscript received and accepted April 21, 1997. ©1997 by Excerpta Medica, Inc. All rights reserved.
MD,
The protocol was approved by the local ethical committee. Between March and May 1995, 3 consecutive patients (2 men, 1 woman) with a mean age of 72 6 5 years and symptomatic second (n 5 1) or third degree (n 5 2) atrioventricular block and intact sinus node function received a single-pass DDD lead in combination with a DDD(R) PM at the Stadtspital Triemli in Zu¨rich. Patients with chronotropic incompetence or a history of atrial fibrillation were excluded from the study. The mean follow-up was 10.7 6 1.2 months (range 10 to 12). The study was performed using the new singlepass DDD lead (model 2975, Medtronic, Inc.), a single lead with 2 additional atrial ring electrodes on a preshaped lead body, fixed alongside the distal atrial ring (Figure 1). This tined, steroid eluting pacing lead is 58 cm in length and incorporates 4 multilumen conduction coils of nickel alloy. The lead insulation is made of silicone rubber and its maximum diameter is 3.25 mm. The distance between the ventricular tip and the center of the atrial ring pair is 13.2 cm and the atrial ring electrodes are spaced 10 mm apart. At the proximal end, the lead bifurcates into 2 IS-1 connectors (both bipolar). The main physical and electrical characteristics of the lead are shown in Table I. All leads were inserted via right subclavian puncture. Under fluoroscopy, the lead was placed in the right ventricular apex as a standard ventricular lead. Ventricular parameters were measured routinely. Af0002-9149/97/$17.00 PII S0002-9149(97)00441-4
643
ute to abnormalities of somatic pain perception in patients with cardiac syndrome X. 1. Rosen SD, Uren NG, Kaski JC, Tousoulis D, Davies GJ, Camici PG. Coronary
vasodilator reserve, pain perception, and sex in patients with syndrome X. Circulation 1994;90:50 – 60. 2. Lagerqvist B, Sylven C, Wa¨ldenstrom A. Lower threshold for adenosineinduced chest pain in patients with angina and normal coronary angiograms. Br Heart J 1992;68:282–285. 3. Turiel M, Galassi AR, Glazier JJ, Kaski JC, Maseri A. Pain threshold and tolerance in women with syndrome X and women with stable angina pectoris. Am J Cardiol 1987;60:503–507. 4. Kaski JC, Elliott PM, Salomone O, Dickinson K, Gordon D, Hann C, Holt DW. Concentration of circulating plasma endothelin in patients with angina and normal coronary angiograms. Br Heart J 1995;74:620 – 624. 5. Yanagisawa M, Kurihara H, Kimura S, Tomobe Y, Kobayashi M, Mitsui Y, Yazaki Y, Goto K, Masaki T. A novel potent vasoconstrictor peptide produced by vascular endothelial cells. Nature 1988;332:411– 415. 6. Raffa RB, Shupsky JJ, Martı´nez RP, Jacoby HI. Endothelin-1-induced nociception. Life Sci 1991;49:61– 65.
Abnormal Systemic Venous Doppler Flow Patterns in Atrial Tachycardia in Infants Janette F. Strasburger,
MD,
C. Elise Duffy,
uring supraventricular tachycardia and intraatrial D reentrant tachycardia (atrial flutter) in the infant and fetus, hemodynamic alterations result in rapid development of congestive heart failure and hydrops fetalis.1– 4 Altered preload, diastolic function, myocardial perfusion, or a combination of these factors have been postulated as the etiology of diminished cardiac output.5–7 However, human studies have not specifically assessed diastolic function parameters and tachycardia mechanism. We hypothesized that diastolic dysfunction due to atrial tachycardia would be demonstrable during supraventricular tachycardia in infants. In particular, Doppler venous and intracardiac flow patterns could be altered by atrioventricular contraction sequence, abnormal atrial activation, and excess rate. This study defines Doppler flow characteristics during sinus rhythm, atrial paced rhythm, and during atrial tachycardia in infants presenting with tachycardia-induced congestive heart failure or hydrops fetalis. •••
The cohort for this study comprised 17 infants with supraventricular tachycardia-related congestive heart failure or hydrops fetalis, presenting in utero or during the first 6 months of life. None had structural cardiac defects. All underwent transesophageal electrophysiologic procedures either emergently (6 patients) or electively within 2 weeks of birth or clinical presentation (11 patients). The methods for transesophageal pacing procedure and its use for defining supraventricular From the Division of Cardiology, The Children’s Memorial Hospital, Chicago, Illinois. Dr. Strasburger’s address is: Division of Cardiology, Children’s Memorial Hospital, 2300 Children’s Plaza, Box 21, Chicago, Illinois 60614. Manuscript received January 16, 1997; revised manuscript received and accepted April 14, 1997.
640
©1997 by Excerpta Medica, Inc. All rights reserved.
MD,
and Samuel S. Gidding,
MD
tachycardia mechanisms and localization of accessory connection have been previously described.8,9 All pulsed Doppler measurements were obtained with parental consent during transesophageal pacing procedure in the sedated infant using commercially available cardiac ultrasound equipment (HewlettPackard model 77020A, 5.0 MHZ medium-focus, phased-array transducer, Andover, Massachusetts). The phase delay constant for video display of electrocardiographic and Doppler signals was predetermined by Hewlett-Packard, and based on pulse repetition rates, maximum delay was not more than 30 ms. Pulsed Doppler was obtained during sinus rhythm, during atrial paced rhythm at varying cycle lengths (8 extrastimuli at 300- to 200-ms intervals), and during sustained tachycardia induced as part of the procedure. Lead I electrocardiographic recording (with or without esophageal atrial electrogram) was acquired simultaneously. The pulsed Doppler sample volume was positioned in the superior vena cava just below the origin of the innominate vein from the suprasternal notch or right parasternal projection, and in the inflow region of the tricuspid valve at the valve leaflet tips from an apical 4-chamber projection. This allowed an angle of incidence of ,30° and angle correction was not performed. At least 10 representative cardiac cycles were recorded (Honeywell strip-chart recorder, 100 mm/s) during sinus rhythm and each tachycardia, then analyzed off-line using a graphics tablet, microcomputer, and custom-written software (Freeland Medical System Cardiac Workstation GTI, Denver, Colorado) using modifications of Doppler analysis techniques previously described.10 –16 In the superior vena cava, both the onset and duration of reversed flow velocities were assessed. The onset of reversed flow was measured from QRS onset 0002-9149/97/$17.00 PII S0002-9149(97)00440-2
lated to an accessory atrioventricular connection, 5 had intraatrial reentrant tachycardia, and 1 patient had both. Orthodromic reciprocating tachycardia was induced in 12 of 14 episodes and antidromic reciprocating tachycardia in 2. Five of 17 patients had ventricular preexcitation (Wolff-Parkinson-White syndrome) during sinus rhythm. One patient had 2 distinct intraatrial reentrant tachycardias. Mean ventricular cycle lengths for atrioventricular reentrant tachycardia were 234 6 25 ms and for intraatrial reentrant tachycardia 246 6 22 ms (p 5 NS). During intraatrial reentrant tachycardia, predominantly 2:1 atrioventricular conduction was present in 6 patients and FIGURE 1. A schematic of the electrocardiogram (ECG) (lead I) during tachycardia and variable 1:1 and 2:1 conduction in 1. Doppler inflow pattern obtained from the superior vena cava (SVC). Reversed flow Retrograde flow in the superior velocities are represented above the baseline. The onset of reversal of flow (Q-ORF), vena cava during sinus rhythm was duration of reversed flow (DRF), and RR interval were measured as shown in the superior vena cava during atrial tachycardia. Similar measurements were obtained durpresent in 7; the amount of reversal ing sinus rhythm. was ,18% of total flow (mean 11 6 1%). In 5 infants with spontaneous sinus tachycardia at cycle lengths of to onset of flow reversal at baseline. Duration of 320 to 300 ms, flow reversal also was not noted. reversed flow was measured from the baseline at the During esophageal atrial pacing (eccentric atrial actibeginning and the end of the flow envelope. Second, vation) at cycle lengths ,280 ms, reversal of flow in the ratio of reversed flow (time velocity integral ret- the superior vena cava was present. During atrial rograde) to total flow (time velocity integrals prograde tachycardia, retrograde flow was present in all 14 and retrograde) was determined in order to predict atrioventricular reentrant tachycardias, and in all epipercent reversed flow (Figure 1).11–16 For this study sodes of intraatrial reentrant tachycardia during 1:1 we compared reversed velocities to ‘‘total’’ forward atrioventricular association. Reversed flow velocities and reversed velocities, using the formula: reversed represented a mean of 38 6 1% of total superior vena time velocity integral/reversed time velocity inte- cava flow and were present for 33 6 1% of the cardiac gral 1 forward time velocity integral 3 100 5 percent cycle. Reversal began at initiation of spontaneous or reversal of total flow velocities. Cycle lengths were induced tachycardia, and no significant change in different during sinus rhythm and tachycardia; there- amount of reversed flow occurred over minutes of fore, values were analyzed as a percentage of the RR observation in these infants. interval (measured onset or duration [ms]/RR interval The onset of retrograde flow in the superior vena [ms] 3 100). cava during atrial tachycardia correlated with the venWith use of techniques previously described13,17 triculoatrial interval (r 5 0.72, p ,0.01) in patients for the tricuspid valve, the mean velocity in centime- with 1:1 ventriculoatrial conduction (Figure 3). This ters per second and time velocity integral in centime- suggested that retrograde flow was caused by atrial ters were evaluated. The product of the time velocity contraction against a closed tricuspid valve after reintegral times heart rate was examined as a crude entry. Duration and amount of venous flow reversal indicator of cardiac output at the tricuspid valve.14,15 did not appear to correlate with ventriculoatrial interThe time to onset of diastolic filling, and diastolic val or cycle length of atrial tachycardia. filling period at the tricuspid valve were also measured Tricuspid valve mean velocities and time velocity (Figure 2). integrals were different from sinus rhythm. Mean veData are presented as mean 6 SEM. Paired t tests locity decreased (34 6 0.08 to 28 6 0.06 cm/s [p were performed for comparisons between sinus ,0.01]), as did time velocity integral (6.8 6 2.3 to rhythm and induced tachycardia. Unpaired t tests were 2.9 6 1.0 cm [p ,0.001]). The time velocity integral used for subgroup comparisons. Linear regression was times heart rate product was 8,875 6 2,573 cm beats/ performed to correlate superior vena cava and tricus- min for sinus rhythm and 7,370 6 2,889 for tachypid valve Doppler measures with ventriculoatrial in- cardia (p ,0.01). A positive correlation existed beterval. tween normalized ventriculoatrial interval and In the 17 infants, 21 distinct tachycardias were tricuspid valve mean velocity (r 5 0.53, p ,0.05), induced (14 orthodromic or antidromic reciprocating suggesting that longer ventriculoatrial intervals were tachycardias and 7 intraatrial reentrant tachycardias). associated with greater tricuspid inflow. No differEleven patients had supraventricular tachycardia re- ences in inflow mean velocities and time velocity BRIEF REPORTS
641
FIGURE 2. A schematic of tricuspid valve inflow Doppler velocities during supraventricular tachycardia. Onset of diastolic filling (Q-ODF), diastolic filling period (DFP), and RR interval were measured as shown. Time velocity integral and mean velocity were obtained by tracing the envelope during sinus rhythm and tachycardia. Duration of diastolic filling included both early passive (E wave) and late (A wave) diastolic phases. These phases were superimposed during tachycardia. ECG 5 electrocardiogram; RA 5 right atrium; RV 5 right ventricle.
ure have speculated that congestive heart failure is caused by alterations in systemic venous and intracardiac diastolic flow.18 This study has demonstrated that supraventricular tachycardia causes reversal of systemic venous Doppler flow, decreased diastolic duration, delayed diastolic onset, and decreased right heart filling velocities. A critical observation in this study is the relation of ventriculoatrial interval during tachycardia with onset of superior vena cava flow reversal. In addition, a longer ventriculoatrial interval was associated with greater diastolic filling velocities at the tricuspid valve. This combination of findings suggests the importance of electrophysiologic features of tachycardia as a factor in the onset of congestive heart failure. We speculate that the neonate or fetus with 1:1 ventriculoatrial association and ventriculoatrial interval ,50% of the RR interval would be most likely to develop rapid onset of supraventricular tachycardiarelated congestive heart failure. Systemic and intracardiac venous flow abnormalities did not appear to correlate with shorter tachycardia cycle lengths. Flow reversal is related to ventricular compliance and right ventricular end-diastolic pressure, neither of which is directly linked to cycle length.10 –12,19 –21 Zales et al20 reported that supraventricular tachycardia–induced hydrops fetalis develops at cycle lengths longer than commonly observed in the neonate. We have found in 30 patients with fetal tachycardia that duration of tachycardia and gestational age were the most important factors associated with hydrops.21 Thus, we speculate that the development of congestive heart failure may be linked to specific electrophysiologic activation patterns affecting the sequence of cardiac contraction.
In summary, abnormal retrograde venous flow patterns in the superior vena cava were uniformly present in atrioventricular reenFIGURE 3. Relation of ventriculoatrial interval (VA/RR) to onset of superior vena cava trant tachycardia with a 1:1 atrioflow reversal (ORF/RR). R 5 0.72, p <0.01. ventricular relation. The onset of retrograde venous flow in the superior vena cava correlated with integrals were observed when intraatrial reentrant the ventriculoatrial interval. Tricuspid inflow tachycardia was compared with atrioventricular reen- Doppler characteristics were also altered during supraventricular tachycardia, including a later ontrant tachycardia. During supraventricular tachycardia, onset of dia- set of diastolic flow, decreased flow duration, and stolic flow was displaced late into the cardiac cycle, decreased mean flow velocity. with the onset of diastolic filling occurring 91 6 9% Acknowledgment: We wish to thank Kay Berdusis through the cardiac cycle versus 73 6 8% in sinus and members of the Echocardiography Laboratory rhythm. The filling duration in diastole (normalized to Children’s Memorial Hospital for their technical asRR) was shorter during supraventricular tachycardia sistance, and Laura Hovis and Kristen Carr for assisthan during sinus rhythm (33 6 6% vs 39 6 8%, p tance in manuscript preparation. ,0.01). •••
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1. van Engelen AD, Weijtens O, Brenner JI, Kleinman CS, Copel JA, Stoutin-
beck P, Meijboom EJ. Management outcome and follow-up of fetal tachycardia. J Am Coll Cardiol 1994;24:1371–1375.
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2. Newburger JW, Keane JF. Intrauterine supraventricular tachycardia. J Pediatr 1979;95:780 –786. 3. Naito M, David D, Michelson EL, Schaffenburg M, Dreifus LS. The hemodynamic consequences of cardiac arrhythmias: evaluation of relative roles of abnormal atrioventricular sequencing, irregularity of ventricular rhythm and atrial fibrillation in a canine model. Am Heart J 1983;106:284 –291. 4. Gembruch U, Redel DA, Bald R, Hansman M. Longitudinal study in 18 cases of fetal supraventricular tachycardia: Doppler echocardiographic findings and pathophysiologic implications. Am Heart J 1993;125:1290 –1301. 5. Brutsaert DL, Sys SU, Gillebert TC. Diastolic failure: pathophysiology and therapeutic implications. J Am Coll Cardiol 1993;22:318 –235. 6. Hoffman JI. Transmural myocardial perfusion. Prog Cardiovasc Dis 1987; 29:429 – 64. 7. Paridon SM, Fisher DJ. Regulation of myocardial blood flow and oxygen consumption. In: Garson A Jr, Bricker JT, and McNamara DG, eds. Science and Practice of Pediatric Cardiology, vol III. Philadelphia: Lea & Febiger Co, 1990: 250 –266. 8. Ko JK, Deal BJ, Strasburger JF, Benson DW Jr. Supraventricular tachycardia mechanisms and their age distribution in pediatric patients. Am J Cardiol 1992; 69:1028 –1032. 9. Benson DW, Dunnigan A, Benditt DG. Follow-up evaluation of paroxysmal atrial tachycardia: transesophageal study. Circulation 1987;75:542–549. 10. Meijboom EJ, Horowitz S, Valdez-Cruz LM, Sahn DJ, Larson DF, Lima CO. A Doppler echocardiographic method for calculating volume flow across the tricuspid valve: correlative laboratory and clinical studies. Circulation 1985;71:551–556. 11. Hecher K, Campbell S, Doyle P, Harrington K, Nicolaides K. Assessment of fetal compromise by Doppler ultrasound investigation of the fetal circulation: arterial, intracardiac, and venous blood flow velocity studies. Circulation 1995; 91:129 –138. 12. Gest AL, Martin CG, Moise AA, Hansen TN. Reversal of venous blood flow with atrial tachycardia and hydrops in fetal sheep. Pediatr Res 1990;28:223–226.
13. Riggs TW, Rodriguez R, Snider AR, Batton D. Doppler echocardiographic evaluation of right and left ventricular diastolic function in normal neonates. J Am Coll Cardiol 1989;13:700 –705. 14. Tulzer G, Khowsathit P, Gudmundsson S, Wood DC, Tian ZY, Schmitt K, Huhta JC. Diastolic function of the fetal heart during second and third trimester: a prospective longitudinal Doppler-echocardiographic study. Eur J Pediatr 1994; 153:151–154. 15. Sharif DS, Huhta JC, Moise KJ, Morrow RW, Yoon GY. Changes in fetal hemodynamics with terbutaline treatment and premature labor. J Clin Ultrasound 1990;18:85– 89. 16. Gudmundsson S, Huhta JC, Wood DC, Tulzer G, Cohen AW, Weiner S. Venous Doppler ultrasonography in the fetus with nonimmune hydrops. Am J Obstet Gynecol 1991;164:33–37. 17. Snider AR, Serwer GA. Methods for obtaining quantitative information from the echocardiographic examination. In: Snider AR, Serwer GA, Ritter SB, eds. Echocardiography in Pediatric Heart Disease. St. Louis, MO: Mosby Yearbook, 1990:78 –133. 18. Tomita M, Spinale FG, Crawford FA, Zile MR. Changes in left ventricular volume, mass, and function during the development and regression of supraventricular tachycardia-induced cardiomyopathy. Circulation 1991;83: 635– 644. 19. Rudolph AM, Heymann MA. Cardiac output in the fetal lamb: the effects of spontaneous and induced changes of heart rate on right and left ventricular output. Am J Obstet Gynecol 1976;124:183–192. 20. Zales VR, Dunnigan A, Benson DW Jr. Clinical and electrophysiologic features of fetal and neonatal paroxysmal atrial tachycardia resulting in congestive heart failure. Am J of Cardiol 1988;62:225–228. 21. Naheed Z, Strasburger JF, Deal BJ, Gidding SS, Benson DW. Fetal tachycardia: mechanisms and predictors of hydrops fetalis. J Am Coll Cardiol 1996; 27:1736 –1740.
A New Approach for DDD(R) Pacing Using a Single-Pass DDD Lead Barbara Naegeli, MD, Edwin Straumann, MD, Andreas Gerber, Urs Niederha ¨ user, MD, and Osmund Bertel, MD ecent studies have shown that a single lead VDD R pacing system in properly selected patients is an interesting alternative to physiologic DDD pacing, espe1– 4
cially in view of lower costs, ease of single-lead implantation, and the high reliability of stable atrioventricular synchronization.5 The major clinical limitation of singlelead VDD pacing is the inability to pace the atrium. This means that this pacing mode is limited to patients with a higher degree of heart block and normal sinus node function. Therefore, the possibility of reliably performing DDD pacing with a single lead would be significant progress in cardiac pacing. Preliminary data from several single lead VDD studies6 – 8 have shown successful attempts to pace the atrium and ventricle by a single-pass electrode at the time of implantation only. This study evaluates the possibility as well as short- and long-term stability of atrioventricular sequential pacing, using a new quadripolar single-pass DDD lead which has closely spaced polished cylindrical dipoles for atrial sensing and pacing, in conjunction with a DDD(R) pacemaker (PM) (TheraTM DR, models 7940/7941/7942, Medtronic, Inc., Minneapolis, Minnesota). ••• From the Cardiac Unit, Department of Internal Medicine, and Department of Cardiac Surgery, Stadtspital Triemli, Zu¨rich, Switzerland. Dr. Naegeli’s address is: Cardiac Unit, Department of Internal Medicine, Stadtspital Triemli, CH-8063 Zu¨rich, Switzerland. Manuscript received January 15, 1997; revised manuscript received and accepted April 21, 1997. ©1997 by Excerpta Medica, Inc. All rights reserved.
MD,
The protocol was approved by the local ethical committee. Between March and May 1995, 3 consecutive patients (2 men, 1 woman) with a mean age of 72 6 5 years and symptomatic second (n 5 1) or third degree (n 5 2) atrioventricular block and intact sinus node function received a single-pass DDD lead in combination with a DDD(R) PM at the Stadtspital Triemli in Zu¨rich. Patients with chronotropic incompetence or a history of atrial fibrillation were excluded from the study. The mean follow-up was 10.7 6 1.2 months (range 10 to 12). The study was performed using the new singlepass DDD lead (model 2975, Medtronic, Inc.), a single lead with 2 additional atrial ring electrodes on a preshaped lead body, fixed alongside the distal atrial ring (Figure 1). This tined, steroid eluting pacing lead is 58 cm in length and incorporates 4 multilumen conduction coils of nickel alloy. The lead insulation is made of silicone rubber and its maximum diameter is 3.25 mm. The distance between the ventricular tip and the center of the atrial ring pair is 13.2 cm and the atrial ring electrodes are spaced 10 mm apart. At the proximal end, the lead bifurcates into 2 IS-1 connectors (both bipolar). The main physical and electrical characteristics of the lead are shown in Table I. All leads were inserted via right subclavian puncture. Under fluoroscopy, the lead was placed in the right ventricular apex as a standard ventricular lead. Ventricular parameters were measured routinely. Af0002-9149/97/$17.00 PII S0002-9149(97)00441-4
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