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Permanent pacing in children presents special problems fat the pediatric cardiologist and the cardiac surgeon (f-17). These include the need to provide pacing for a period that may span many decades, small patient size and the common presence of structural congenital heart dis patients who require permanent pacing. infants and children has been performed because of brady- cardia produced by sinus node dysfunction or atrioventric- ular (AV) block. As the role of pacing for treatment (18-20) or prevention (21) of tachycardia expands in this patient group, the number of pediatric patients undergoing implan- tation of a permanent pacing system will continue to grow. Over the last decade, transvenous endocardial pacing leads have gained favor for use in smaller and smaller children including infants and children weighing ~10 kg From the Division of Pediatric Cardiology and Department of Cardiac and Thoracic Surgery, Vanderbilt University School of Medicine. Nashville. Tennessee. This work was presented in part at the IXth World Symposium on Cardiac Pacing and Electrophysiology, Washington, DC.. May 29, 1991. It was funded in part by agrant from Medtronic, Minneapolis, Minnesota to the Vanderbilt Pediatric Cardiology Development Fund, Vanderbilt University Medical Center. Manuscript received October 15, 1991; revised manuscript received March 5, 1992. accepted March 25, !992. Add ess for correspondence: James A. Johns. MD, Division of Pediatric Cardioligy, D-2217 Medical Center North, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2572. 01992 by the American College of Cardiology (22~27). The pacing and sensing characteristics of thcsc leads have generally been excellen:. Although t results are quit2 favorable, there is a poten obstruction by relatively large transve us leads (281, par- ticularly in children who are likely to r ire multiple pacing ieads over their lifetime. This problem can be of particular concern because of the risk of caval obstruction after atria: repair of transposition of the great arteries even without pacing leads (29-32). Transvenous access to the atrium or ventricle may also be limited by congenital anomalies of the systemic veins or by prior operations such as superior vena cava to pt.u rtoaary artery anastomosis (Glenn shunt), Fontan operation or tricuspid valve replacement (33). fortunately, children with complex anatomy represent a significant proportion of pediatric patients requiring pacing. Epicardial pacing has been used in a large number of children because of small patient size, anatomic consider- ations or the need to perform surgical correction of struc- tural congenital heart disease at the time o implantation. However, epicardial pacing ated with a high incidence of pacing or sensing problems requiring lead repiacement (16,34-40). Pf a reliable epicar- dial pacing lead were available, it might prove to be a good choice as a first pacing system in infants and small children, as well as in older children undergoing concomitant cardiac 07351097/92/$5.00
Transcript
Page 1: STEROID-ELUTING EPiCARDIAi PACING LEADS · The protocol was approved by the Vanderbilt University CommIttee for the Protection of Human Subjects on Febru- ary 7, 1990. This study

Permanent pacing in children presents special problems fat the pediatric cardiologist and the cardiac surgeon (f-17). These include the need to provide pacing for a period that may span many decades, small patient size and the common

presence of structural congenital heart dis patients who require permanent pacing.

infants and children has been performed because of brady- cardia produced by sinus node dysfunction or atrioventric- ular (AV) block. As the role of pacing for treatment (18-20) or prevention (21) of tachycardia expands in this patient

group, the number of pediatric patients undergoing implan- tation of a permanent pacing system will continue to grow.

Over the last decade, transvenous endocardial pacing leads have gained favor for use in smaller and smaller

children including infants and children weighing ~10 kg

From the Division of Pediatric Cardiology and Department of Cardiac and Thoracic Surgery, Vanderbilt University School of Medicine. Nashville. Tennessee. This work was presented in part at the IXth World Symposium on Cardiac Pacing and Electrophysiology, Washington, DC.. May 29, 1991. It was funded in part by agrant from Medtronic, Minneapolis, Minnesota to the Vanderbilt Pediatric Cardiology Development Fund, Vanderbilt University Medical Center.

Manuscript received October 15, 1991; revised manuscript received March 5, 1992. accepted March 25, !992.

Add ess for correspondence: James A. Johns. MD, Division of Pediatric Cardioligy, D-2217 Medical Center North, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2572.

01992 by the American College of Cardiology

(22~27). The pacing and sensing characteristics of thcsc

leads have generally been excellen:. Although t

results are quit2 favorable, there is a poten

obstruction by relatively large transve us leads (281, par- ticularly in children who are likely to r ire multiple pacing ieads over their lifetime. This problem can be of particular

concern because of the risk of caval obstruction after atria:

repair of transposition of the great arteries even without

pacing leads (29-32). Transvenous access to the atrium or

ventricle may also be limited by congenital anomalies of the

systemic veins or by prior operations such as superior vena

cava to pt.u rtoaary artery anastomosis (Glenn shunt),

Fontan operation or tricuspid valve replacement (33).

fortunately, children with complex anatomy represent a

significant proportion of pediatric patients requiring pacing.

Epicardial pacing has been used in a large number of

children because of small patient size, anatomic consider-

ations or the need to perform surgical correction of struc-

tural congenital heart disease at the time o

implantation. However, epicardial pacing

ated with a high incidence of pacing or sensing problems

requiring lead repiacement (16,34-40). Pf a reliable epicar-

dial pacing lead were available, it might prove to be a good

choice as a first pacing system in infants and small children,

as well as in older children undergoing concomitant cardiac

07351097/92/$5.00

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396 JOHNS ET AL. STEROID-ELUTING EPiCARDIAi PACING LEADS

JACC Vol. 20. No. 2 Arlgust 1992:395-b 11

Table 1. Clinical Features of Patients Undergoing Placement of Steroid-Eluting Epicardial Pacing

Pt Age (yr)l Rhythm Concurrent Implantation

No. Gender Cardiac Diagnosis Diagnosis Prior Operahon Operation Technique Chamber F/I_! (wan,! --I__

1 6/M

2 k/F

3 IS/F

4 WM

5 18/M

6 d/F

7 51M

8 ‘IF

9 2/M

IO 3 wk/M

II 13/M

d-TGA

Muscular VSD

Common atrium,

unroofed CS

Mitral atresia

AVSD

AVSD

DILV

d-TGA

DlLV

d-TGA, VSD

DILV. subaorlic

stenosis

12 2/F None

SND

CAVB

SAW

CAVB

SAVB

SAVB

CAVB

SND

CAVB

SAVB

SAW3

CAVB

PA banding

ASD repair. mitral

valve replacement

None

Repair of AVSD

Repair of AVSD

PA banding

Senning

Coorct repair

Arterial switch. VSD

repair

PA bnnding, atria1

septcccomy. BVF

enlargemenl. central shunt,

Glenn shunt

None

None

VSD repair

None

Atrial septectomy.

PA band

Mitral valvuloplasty

None

Glenn shunt

None

None

None

L thoracukomy

Sternoromy

Subxiphoid

R thoracotomy.

subxiphoid

Sternotomy

L thoracotomy

R thoracotomy,

subxiphoid

L thoracotomy

Sternotomy

L thoracotomy

L thoracoromy,

repeat L

thoracotomy

L thoracotomy

LV, RV

RV (2 leads)

RV

RA, RV

RA. RV

LA

RA, LV

LA. LV

WA. LV

LA, LV

LV, replaced with

2 additiomll LV

leeds

LA. LV

3.5

0

84

82

73

77

49

74

38

IO

6

4’

42

ASD = atrial septal defect: AVSD = atrioventricular septal defect; BVF = bulboventriculllr foramen: CAVB = congenital atrioventricuh block; Caarc! =

coarctation of aorta; CS = coronary sinus: DILV = double-inlet left ventricle; d-TGA = dextrolransposition of the great arteries; F = female: F/U = follow-up

interval; L = left: LA = left atrium; LV = left ventricle; M = male: PA = pulmonary artery: Pt = patient: R = right: RA = right atrium: RV = right ventricle:

SAVB = surgical atrioventricular block: SND = sinus node dysfunction; VSD = ventricular septal defect.

surgery or having anatomic abnormalities precluding trans- venous pacing.

The addition of a small amount of steroid to endocardial pacing electrodes has appeared to improve the pacing and sensing characteristics of these electrodes (41-48). Encour- aged by the results obtained with endocardial steroid-eluting pacing electrodes and by animal studies of epicardial pacing electrodes (493). we undertook this study of a new porous- tipped steroid-eluting epicardial pacing electrode in a group of infants and chi!dren requiring epicardial pacing. Our purpose was to evaluate the pacing and sensing characteris- tics of this new lead in infants and children.

Study patients. We studied I2 pediatric patients requiring cardiac pacemaker lead placement over a l-year period from February 1990 to February 1991. Patient characteristics are summarized in Table 1. The patients ranged in age from 3 weeks to 18 years (mean 2 SD 6.4 + 5.9 years) at the time of pacemaker implantation. Eleven patients had underlying structural congenital heart disease (single ventricle in four, d-transposition of the great arteries in three, AV septal defect in two, ventricular septal defect in one and common atrium with unroofed coronary sinus in one). Ten patients had undergone previous cardiac operation, inclading Sen- ning repair in two, AV septal defect repair in two, pulmonary artery banding in two, repair of common atrium with mitral valve replacement in one, repair of coarctation of the aorta in one and arterial switch procedure with ventricular septal

defect repair in one. Two patients bad sinus node dysfunc- tion, five had surgical complete AV block and five had high grade congenital AV block. Four patients had had other pacing leads placed before the study: two of these patients had steroid leads placed because of malfunction of the existing lead and two had placement of additiona! ieads to allow dual-chamber pacing.

Informed written consent was obtained from the parents of all patients and from those patients old enough to consent. The protocol was approved by the Vanderbilt University CommIttee for the Protection of Human Subjects on Febru- ary 7, 1990. This study was part of a multncenter tnal of the lead as an investigational device performed under the control of the Food and Drug Administration.

Characteristics of the lead (Fig. 1). The lead consisted of a porous-tipped electrode platinized with platinum black and coated with dexamethasone sodium phosphate (49,50). The electrode contained app,qximately 1 mg of dexamethasone sodium phosphate in a silicone rubber binder designed to allow elution of the dexamethasone into the area surround- ing the electrode when exposed to body fluids. The electrode was attached to a triangular silicone suture pad with two holes and proximal and distal grooves to allow attachment to the epicardial surface of the heart. The conductor was a 74ilar MP35N nickel alloy conductor with silicone insulation and a standard S-mm unipolar connector. All leads were used in a unipolar configuration.

Surgical technique (Table I). Leads were placed by tho- racotomy (14 leads, eight patients), sternotomy (6 leads, three patients) or the subxiphoid approach (3 leads, three

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JAW Vol. 20. No. 2 August 3992:395-401

pat~e~t§); in two pat~ents~ atriz cotomy and ventricular leads

because of the need fo

cardiac anatomy, previous iac operations at the time of

in one, repair of ventri k-Han1011 atrial septet

banding in one). Eight atria1 leads (4 right and 4 left) and 15 ve~t~c~lar leads (6 right and 9 left)

ln all cases, the lead was he! ventricular epicar ium and pacing a ensirlq characteris- tics of the lead were deiermined. hen a satisfactory position was found (generally the fi r second position tested), the lead was sewn i and the proximal suture groo . After the lead had stabilized for 5 to 10 min, mecsurcmcn:s G% pulse width threshold at 0.8, 1.6, 2.5 and 5 V were obtained, as well as current and voltage thresholds at 0.05, 0.2-, 0.5 and I-ms pulse width. Lead impedance was measured at an amplitude of 2.5 V and a pulse width of 0.5 ms. P or R wave amplitudes and slew rates were also measured. All intraoperative measurements were obtained with a Medtronic model 531 I Pacing System

measurements. Patients underwent follow-up pacemaker lead analysis every week for 6 weeks, at 3 and 6 months, and then every 6 months. At each visit, pulse width threshold was determined at approximately 0.8, 1.6,2,5 and 5 V. (The actual voltages tested varied slightly depending on the pacemaker generator manufacturer, so that for some patients the voltages tested were 1, I.5,2.5 and 5.4 V.) The threshold was determined by decreasing the pulse width until there was failure to capture. The threshold was consid- ered to be the lowest programmable pulse width at which there was consistent capture. Mean pulse width threshold at

rences between atria

ata are expressed as

acement of two ventricular scular ve~trico~ar sepal de flow cardiac output unrel

pacing leads. In two oth patiems, one lead was future use. Follow-up la were obtained on retlraining 13 leads for ean of 53 I 25 weeks (range 6 to

transposition of the great tricular septal defect, who died 14 weeks

after lead placement of graft-versus host disease acquired from traasfusion at the time of arterial switch repair. through the 1st 38 weeks are included for Patient 9, who

congestive heart failure 42 weeks after lead ient 1 I, who had exit block requiring replace- tricular lead 6 weeks after its place

discussed in more detail later. No patient was lost to sed any scheduled lead analysis. calds. Mean pulse width ;hresholds at im-

plantation and throughout the follow-up period are show Table 2 and Figure 2. At imp~a~tatioo, the at a pulse width of 0.5 ms was 0.9 9

rence between the atrial and .O.91 2 0.27 V). The pulse width threshold at

an amplitude of 2.5 V was 0.15 & 0.08 ms and was nearly identical for tbe atrial and ventricular leads. On follow- visits, only pulse width threshold was obtained. Over duration of follow-up, there was no significant change in the

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398 JOHNS ETAL. STEROID-ELUTlNGEPlCARDlAL PACING LEADS

JACC Vol. 20. No. 2 August 1992:395-101

Table 2, Pulse Width Thresholds, Sensing Thresholds and Impedance on All Leads, Atria1 Leads Only and VentriCUiar kads Only 0.8 to 1.0 v 1.5 to I.6 v 2.5 v 5.0 to 5.4 v Sensing impedance

---

Wk n* ms nt 31s rlt ms nt ms nt mV nS R nS

A. All Leads

0 19 0.60 c 0.29 17 0.28 r 0.20 I9 0.15 + 0.08 I9 0.08 + 0.03 19 4.80 + 1.75 17 410~72 19 I 19 0.53 t 0.27 18 0.27 C 0.12 I8 0.15 + 0.08 I9 0.08 i 0.03 I9 4.66 t 1.79 I6 314 rt 55 I9 2 I9 0.46 f 0.22 15 0.27 t 0.16 18 0.16 + 0.07 I9 0.07 r 0.03 I9 4.69 2 1.75 I6 305 + 45 19 3 19 0.45 t 0.26 16 0.27 ? 0.15 I8 0.15 + 0.09 I9 0.07 f 0.03 I9 4.56 ? 1.74 I6 313 243 I9 4 19 0.39 2 0.16 I5 0.31 f 0.29 IS 0.17 It 0.12 I9 0.07 + 0.04 I9 4.63 + 1.68 16 317243 19

5 I9 0.37 r 0.14 I5 0.30 + 0.30 I8 0.15 + 0.11 I8 0.10 f 0.17 I9 4.61 ?r 1.73 16 323 + 36 I9 6 I8 0.38 + 0.18 I4 0.29 e 0.25 I7 0.14 2 0.10 I7 0.07 * 0.04 I7 4.72 2 1.69 I6 319+51 18

I2 I7 0.38 + 0.16 15 0.26 4 0.18 I7 0.14 it 0.08 I7 0.06 + 0.04 I7 4.69 + 1.73 I6 334 r 47 I8 24 I6 0,52 I 0.35 IS 0.24 + 0.13 I5 0.15 c 0.08 I6 0.M + 0.04 I6 4.71 rt 1.70 14 357 2 43 16

52 II OS44 IO.21 II 0.22 + 0.07 II 0.13 + 0.03 II 0.06 + 0.03 II 4.82 ” 1.64 II 368~49 II 78 9 0.45 + 0.22 9 0.21 + 0.07 9 0.13 + 0.03 9 0.07 c 0.03 9 4.89 + 1.66 9 378 + 61 9

B. Atrial Leads Only ~_____l____ “l..--. ,-~ ~~_-._-

0 tl 0.71 + 0.36 7 0.29 + 0.14 8 0.16 ?: 0.08 8 0.08 ” 0.03 8 3.25 k 0.50 8 374 c 44 8

I 8 0.43 * 0.19 8 0.24 C 0.10 8 0.11 to.03 8 0.06 % 0.02 8 3.06 i: 0.63 8 328 ” 65 8 2 8 0.34 9 0.15 8 0.18 ” 0.06 tl 0.12 ?: 0.02 8 0.05 r 0.02 8 3.13 -‘- 0.5s 8 314rt52 8 3 8 0.31 2 0.12 N 0.18 -c 0.07 8 0.11 ” 0.03 8 0.05 ? 0.02 lt 3.00 1 0.56 8 307 c 38 8

4 8 0.32 + 0.16 8 0.18 + 0.07 8 0.11 + 0.02 8 0.05 i: 0.03 8 3.13 c 0.55 8 319244 8 5 8 0.31 t 0.13 8 0.16 + 0.05 8 0.10 + 0.03 8 0.04 + 0.01 8 3.10 + 0.76 8 325 r 33 8

6 7 0.28 + 0.09 7 0.16 + 0.03 7 0.09 * 0.02 7 0.04 2 0.01 7 3.19 c 0.56 8 324 z!z 52 8

12 7 0.25 ” 0.08 7 0.15 + 0.05 7 0.10 lr 0.03 7 0.03 + 0.01 7 3.14 I?: 0.67 8 337 + 50 8 24 7 0.29 T. 0.10 7 0.16 + 0.04 7 0.10 f 0.03 7 0.04 2 0.01 7 3 I4 -c 0.58 7 354 + 45 7 52 5 0.29 2 0.07 5 0.17 f 0.04 5 0.10 + 0.00 5 3.04 t 0.01 5 3.2@ + 0.40 5 356 r 29 5 78 4 0.26 + 0.08 4 0.16 2 0.05 4 0.11 f 0.02 4 0.04 + 0.01 4 3.25 T 0.43 4 362 t 44 4

C. Ventricular Leads Only

0 II 0.52 + 0.20 IO 0.28 ? 0.24 II 0.15 + 0.08 II 0.07 * 0.03 I I 6.17 ” I.25 9 436 + 77 I I I II 0.61 i 0.23 I(! 0.31 r 0.12 IO 0.18 t 0.08 II 0.10 + 0.03 II 6.25 2 0.97 8 304243 II 2 II 0.58 2 0.21 7 0.36 2 0.16 IO 0.19 i 0.08 I I 0.09 + 0.03 II 6.25 + 0.97 a 298 ? 39 I I

3 II 0.58 * 0.29 8 0.35 + 0.15 IO 0.19 + 0.11 II 0.09 + 0.03 I I 6.13 z! 0.93 8 316245 II 4 II 0.4! + 0.11 7 0.42 - 0.34 IO 0.22 2 0.14 II 0.08 -c 0.04 II 6.13 c 0.93 8 316’41 II

s II 0.44 f 0.13 7 0.41 + 0.36 IO 0.19 * 0.14 IO 0.15 ir 0.21 II 6.13 + 0.93 8 322238 II 6 II 0.48 + 0.19 7 0.39 c 0.30 IO 0.18 + 0.11 IO 0.08 + 0.04 IO 6.25 + 0.83 8 315*51 IO

i2 IO 0.50 t 0.12 8 0.35 + 0.19 IO 0.18 ? 0.08 IO 0.08 + 0.03 10 6.25 2 0.83 8 332 2 46 IO 24 9 0.73 f 0.35 8 0.33 t 0.14 a 0.19 + 0.09 9 0.08 + 0.04 9 6.29 k 0.70 7 350 t 42 9

52 6 0.56 t 0.21 6 0.27 t 0.07 6 0.15 2 0.03 6 0.07 f 0.03 6 6.17 k 0.90 6 377 + 42 6

78 5 0.60 I 0.18 5 0.25 * 0.07 5 0.15 + 0.03 5 0.09 ? 0.02 5 6.20 If: 0.98 5 390 t 69 5

*Number of leads for which pulse width threshold was measured. th’umber of leads capturrng nt indicated voltage. $Number of leads for which sensing was measured. DNumber of leads for which impedance was measured.

mean pulse width threshold for all leads, although there were significant d&ereaces in threshold between the atrial and ventricular leads.

For the atrial leads, there was a significant decrease in pulse width threshold with time (Table 28, Fig. iB) (by analysis of variance p < 0.0005 at an amplitude of I V, p < 0.05 at 1.5 V, p = 0.08 at 2.5 V and p < 0.005 at 5.4 V). The decline was most apparent within the 1st week after implan- tation, with little change thereafter. No atrial lead dem- onstrated any significant increase in threshold. and ail follow-up pulse width thresholds were lower than the thresh- olds at implantation.

In contrast to the atrial leads, the ventricular leads showed no significant difference in pulse width threshold

with time. Mean pulse width threshold for the ventricular leads is shown in Table 2C and Figure 2C. Ten of the II ventricular leads showed an increase in pulse width thresh- old to a level greater than that at implantation. The time of the maximal threshold for these ventricular leads ranged from I to 32 weeks (median 3, mean I2 weeks). Despite these increases, the mean pulse width threshold for the ventricular leads at 2.5 V was still only 0.19 + 0.09 ms at 6 months and 0.15 + 0.03 ms at I2 months. By analysis of variance, pulse width threshold for the atrial leads was significantly lower than for the ventricular leads at all amplitudes (p < O.OOOOP at 0.8 to I V, I.5 to 1.6 V and 2.5 V; p < 0.00005 at 5 to 5.4 V).

Patient I I deserves special mention because of a marked

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JACC Vol. 20, No. 2 Au@~st 1992:395-401

0 1 2 3 4 5 6 12245270 Follow-up Duration (weeks)

Atrial Leads

1 .o Volts 6 Volts

Its 12 3 4 5 6 12245278

Follow-up Duration (weak)

Ventricular Leads

1 5 ; 0.9

g. O.&l

; 0.7

f 0.G o! c 0.5

; 0.4

fG z

0.3

% 0.2

z 0.1

0 0 1 2 3 4 5 6 12245276

Follow-up Duratlon (weeks)

Figare 2. Pulse width threshold for all leads (A), atrial leads ( ventricular leads (C), shown as a function of time after implantation. Numbers indicate the number of ltads at each follow-up interval. Strength-duration curves are shown on the Y and Z axes at each follow-up intervai. There was no significant change in threshold over time for all leads (A) or ventricular leads (B), but the threshold for atrial leads (B) decreased significantly.

itxrezse ia threshold Oiier time. This iSyear old boy with a double-inlet left ventricle had developed complete AV block at the time of surgical enlargement of the bulboventricular foramen. He underwent placement of transvenous atrial and ventricular endocardial pacing leads and subsequent anasto- mosis of the right pulmonary artery to the superior vena cava

superior vena cava arose%

tra~svc~o~s access t

6 weeks, there was de at th:: maximal s HI0 possibility of

nd to skew the mean thre

iately at the mini for atrial leads and

illplantation or during follow-up.

s. These data indi- cate that over a period of to h year, pacing and sens characteristics of this new steroid-eluting pacing lead mained excellent. ~~fortu~ate~y, there are few similar pro- spective studies to allow compariso this lead with other epicardial leads. Hengiein et al. (39) pulse width threshold ia several dl t e~doca~dial and epicardial electrodes, and found that there was a substantial increase in pulse width threshold of the epicardial ventricu-

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400 JOHNSETAL. STEROID-ELUTING EPICARDIAL PACING LEADS

JACC Val. 20. No. 2 August 1992:395-401

lar leads, peakilrg at approximately 0.33 ms at 5 V, between 5 weeks and 6 months after pacemaker implantation. The steroid-eluting ventricular leads we tested showed a similar increase, although the peak threshold of our leads Was

considerably lower. Kugler et al. (38), in a retrospective study of two different epicardial leads, reported long-term ventricular pulse width thresholds similar to !hose we ob- served. However, it is difficult to compare our data with theirs because their “chronic” thresholds were obtained at various times at least 6 weeks after pacemaker implantation. At 6 months, our mean atrial lead pulse width threshold at 2.5 V (0.1 + 0.03 ms) was lower than that reported by Ott (50) (0.18 ?Z 0.18 ms), and the difference may be even greater, because some or all of Ott’s thresholds may have

been at a 5-V amplitude. ifferences between atrial and ventricular leads. The dif-

ference in the pulse width threshold between our atrial and ventricular lcads was intcrcsting. Unlike the ventricular leads, virtually all OF which demonstrated an increase in pulse width threshold at least transiently, the atrial leads showed a decrease in pulse width threshold with time. Kugler et al. @I), using a similar epicardial electrode in swine, demonstrated a lower atrial pacing threshold with a steroid-eluting version than with a nonsteroid-eluting ver- sion, but ventricular pacing threshold did not differ between electrodes.

Mechanism of steroid effect. The mechanism by which dexamethasone improves pacing and sensing thresholds is not fully understand: presumably, the drug decreases the fibrous tissue formation or the inflammation around the electrode, allowing more effective stimulation of the myo- cardium (48). Direct electrophysiologic effects of dexam- ethasone may explain some. but not all, of the difference between steroid and nonsteroid-eluting electrodes (52). The platinized porous tip may also play a role in decreasing fibrous tissue formation (53). Karpawich et al, (54) recently compared steroid-eluting and nonsteroid-eluting versions of an epicardial pacing lead and found that initial thresholds were similar, but that the thresholds of the nonsteroid- cluting leads increased with time whereas those of the steroid-eluting leads did not.

Clinical implications. The availability of a reliable atrial epicardial pacing lead will be an important advance for children who are not good candidates for transvenous atriaI leads. In some of these patien!s there is limited or no venous

access to the atrium from the superior vena cava, either because of caval obstruction after atrial repair of transposi- tion of the great arteries or because of a Glenn shunt. In children with AV block who will require pacing for the remainder of their lives, epicardial atrial leads may allow AV

synchrony at an earlier age without the risk of caval obstruc- tion. Karpawich et al. (55) found that fixed rate ventricular

Pacing in puppies predisposes to myoceliular disruption. Some of these changes may be related to the fixed rate pacing rather than to lack of AV synchrony. Rate-responsive (WW pacing may be an alternative with more favorable

hemodynamic effects than those of fixed rate pacing (56-58), but it does not provide AV synchrony. Only with an atri lead that can reliably sense the atrial activity are both A synchrony and rate respcnsiveness possible (2038). In ad- dition, antitachycardia pacing, which is being recognized as an attractive alternative to pharmacologic therapy of su praventricular tachycardias (l8-20), requires reliable atrial sensing and pacing. Finally, lower pacing thresholds with steroid-eluting epicardial pacing leads will allow lower gen- erator outputs with maintenance of an adequate safety margin. Pacing can now be performed in all af our patients using an amplitude of 1.5 to 2.5 V at a 0.5 ms while maintaining a >2:l safety

conclusions. Over a period of up t steroid-eluting epicardial pacing leads have retained excel- lent pacing and sensing characteristics. If these ing early results continue, epicardial steroid-eluting be an attractive option for infants and children requiring pacing. Clearly, transvenous endocardial pacing is tke preferred route for pacing in most older children, but there will continue to be a group of patients who require epicardial pacing because of small patient size, inadequate transvenous access to the atrium or ventricle or the need for concomitant cardiac surgery at the time of pacemaker implantation. The availability of epicarJd leads with reliable pacing and sensing of both the atrium and the ventricle may also allow smaller infants to undergo dual-chamber pacing, giving them the benefits of AV synchrony.

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