CASE REPORT
Possible compications
Su sub avian
crush
syndrome
S.A.M. Said, C.H.J.M. Ticheler, C.M. Stassen, A. Derks, H.T. Droste
A 70-year-old woman with symptomatic Mobitz type II atrioventricular block underwent implantation of a dual-chamber pacemaker 11 years ago. The leads were inserted through a percutaneous puncture of the right subdavian vein, using standard techniques. Both leads were passive fixation leads. Due to battery failure and end of life criteria, the pulse generator (PG) had been routinely replaced six years previously. Predischarge pacemaker control revealed norm pacing, sensing thresholds and impedance for both leads. Because of a syncopal attack subsequent to lead fractures, most likely secondary to right subdavian cuh syndrome (SCS) of both leads, she underwent a double lead re-implantation one year after PG replacement by access via left subclavian vein puncture. After a symptom-free period of few years she was re-analysed because of palpitations, dizziness, angina pectoris and tiredness. Pulmonary embolisation and myocardial perfusion defects were detected udlising scintigraphic techniques. Chest X-ray revealed the crushed atrial lead dislocated from the right subclavian region and lodged into the right ventricle towards the inferior septum. Because she was symptomatic, a retrieval tednique was applied and the crushed atrial lead was pulled back from the right ventricle and securely fixed to its former position. On maintnce medical treatment, she remains well. (Neth Heartj 2005;13: 92-7.) SA.M. Said A. Deut H.T. Droste
Department of Cardiology, Twente Hospital Group, Hengelo C.HJ.M. Ticheler C.M. Stasen Departments of Nuclear Medicine and Radiology, Twente Hospital Group, Hengelo Correspondence to: S.A.M. Said Department of Cardiology, Hospital ZGT, location Hengelo, Geerdinksweg 141, 7555 DL Hengelo E-mail address: [email protected]
92
Key words: subclavian crush syndrome, pulmonary embolisation, lead migration, myocardial perfusion defect, retraction technique
facemaker lead insulation defects and conductor r fracture are not rare. Venous complications and pulmonary embolisation may occur. Pacemaker electrode failure due to the subclavian crush syndrome (SCS) often appears in the first three months postimplant and usually occurs within five years after implantation.1l2 The current case is unique because the SCS occurred seven years post-implant giving rise to atrial and ventricular lead fractures and insulation breaks producing pacing failure and causing recurrence of symptoms. Jacobs et al. studied 49 explanted fractured leads and found that all leads were inserted by conventional percutaneous subclavian venous puncture.3 After dissecting cadavers with percutaneous subclavian puncture of pacemakers, central venous catheters and defibrillators, Magney and colleagues reported that almost all leads or catheters passed through the medial subclavicular musculotendinous complex (MSMC) before entering the vein. Furthermore, they demonstrated that leads trapped in the MSMC are exposed to unnecessary compression as they move with the clavicle.4 It has been suggested that the use of cephalic vein cut-down or a more lateral percutaneous puncture of the subdavian vein would eliminate lead compression or crush syndrome.5 In our case, new pacing leads were implanted using a more lateral percutaneous venipuncture access ofthe left subclavian vein. The crushed atrial lead, which was found to have migrated and lodged into the right ventricle, could possibly be incriminated for irritative dysrhythmias and myocardial and pulmonary defects. The migrated atrial lead was retracted and firmly fixed to the right subclavian region. Cao report A 70-year-old woman, a nonsmoker, was referred for analysis of palpitations of recent onset and complaints of being easily fatigued. She had undergone a DDDNctherlands Heart Journal, Volume 13, Number 3, March 2005
Possible complications of subclavian crush syndrome
.0 10 7
M. W MW. vwllll stAwm NAE Mg W T&I 3 M " 99 14!12
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........ *
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;
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ff;
i
j:
-......
Eli
illI l......... 11 l
......
...... i:2,
.........
Figure 1M Tekmetric rythm sip dpcingpacingfailure withut ventricular escape
rhythm.
pacemaker implantation because of symptomatic atnoventricular (Mobitz II) heart block 11 years ago. A 294-03 Relay DDD pacemaker, Biopore 432-02 atrial lead and Biopore 430-02 ventricular lead were implanted. Acute atrial and ventricular impedance were 512 Ohm, and 500 Ohm, respectively. Follow-up took place every four months. Due to battery failure, the PG
was
replaced (17 February 1998) by
a
Vitatron
Diamond DDD pacemaker. In July 1998, the impedance ofthe atrial and ventricular leads unexpectedly decreased hold and
to
400 and 437 Ohm,
sensing
levels
were at
respectively. implantation
Thresvalues.
On 24 June 1999, the patient presented with a subcapital fracture of the left foot due to a syncopal attack. The ECG depicted periods with pacing failure without ventricular escape rhythm (figure IA). A detailed chest X-ray of the right infraclavicular region revealed two fractured leads at the level of the first rib and the clavicle. The insulation defect of both leads was well appreciated (figure iB). The site of fracture could not be reached for repair of the leads, therefore she underwent re-implantation of two new
Figure lB. Detailed chest X-ray ofte right infraclavicular area demonstratingdoubk kadfracture (arrows) at thekvel of thefirst rib and th clavick.
Ndherlanbd Heart Journal, Vohlmc 13, Number 3, March 2005
93
Possible complications of subclavian crush syndrome
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05-08-33
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32
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r Apex
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38
it
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Figure 2A. Dipypidamok MIBI stress test illustrating an irreversibk inftrior wall myocardial defect.
leads from the left side. During this procedure, both atrial and ventricular electrodes were inserted from a more lateral approach through percutaneous puncture of the left subclavian vein. The case was presented at the heart team meeting, and it was decided not to retrieve the seven-year-old crushed leads because of increased risk of cardiac damage. The fractured 'crushed' electrodes were retained and fixed to the right subdavian region and remained distally connected to the myocardium. Then they were capped and subcutaneously sutured with Vicryl in the right infra-
94
clavicular region. Routine chest radiograph demonstrated a proper position ofthe new electrodes and a good fixation of the old fractured 'crushed' leads. During the whole follow-up period (1992-1999) there were no significant alterations in body weight or length. The current symptoms, besides palpitation and tiredness, were dizziness, shortness of breath on exertion and angina pectoris NYHA functional dass II. The 48hour ambulatory ECG monitoring revealed normal DDD pacing alternating with sinus rhythm, premature ventricular contractions and periods of paroxysmal
Netherlands Heart Journal, Volume 13, Number 3, March 2005
Possible complications of subclavian crush syndrome
Figure 2B. Coronary angiogramsshowing normal left (leftpanel) and right (rightpanel) coronary arteries. The migrated crushed atrial lead (CAL) is well appreciated.
atrial fibrillation and flutter. Repeated transthoracic echocardiographic studies demonstrated a normokinetic normal-sized left ventricle with mild mitral and tricuspid regurgitation. Maximal exercise tolerance testing revealed normal physical capacity. The test was terminated due to angina pectoris and fatigue. Pharmacological MIBI stress test depicted a small irreversible myocardial defect in the inferior wall (figure 2A).
Figure 2C Plain X-ray in left lateralposition revealing the crushed atrial lead (CAL) migrated and dislodged into the right ventricle. Netherlands Heart Journal, Volume 13, Number 3, March 2005
Coronary arteriography and contrast ventriculography studies illustrated normal coronary arterial anatomy and distribution with normokinetic left ventricle (figure 2B left and right panels). The fractured fragment ofthe atrial lead was detected whirling in the right ventricle. It migrated from the right infraclavicular region and lodged into the right ventricle (figure 2C). Its proximal tip remained connected to the right atrial appendage. This fragment of the atrial lead may have wandered around causing, by traction forces and mechanical irritation, atrial and ventricular arrhythmias. Pulmonary perfusion-ventilation scintigraphy showed a solitary perfusion defect in the left upper lobe with ventilation mismatch as usually seen by foreign body embolisation (probably insulation material). On 8 April 2004, the old atrial lead was pulled back to the site of the right subclavian vein using percutaneous right subclavian venous access. In this setting an angled wire loop retriever was successfully utilised. The right subclavian venous puncture was performed by Doppler-guided needle because ofthe presence of crushed atrial and ventricular leads in the vein. The crushed atrial lead was again, after light traction, securely sutured to the subcutaneous tissue in the subclavian area (figure 3). After this uncomplicated procedure, she remained well. She was treated with oral anticoagulation at INRlevel between 1.8 and 4.1, digoxin 0.25 mg and 200 mg flecainide/day. Discussion Pacing lead fracture occurs infrequently (1 to 4%) but causes potentially catastrophic complications of permanent pacing systems. Because of statistical 95
Possible complications of subclavian crush syndrome
Figure 3. Plain X-ray in antero-posteriorposition: Before (kftpanel) and after (riqhtpanel) retraction of the crushed atrial lead (CAL).
difference (p=0.08) in lead fracture between subclavian and cephalic vein access, it has been suggested that cephalic vein approach may be preferable.6 Lead fracture occurred in 3.4% of cases reported by Kazama et al. within five years post-implant. They identified two particular sites of lead fracture: one within the pacemaker pocket due to fixation ligature and the other at the subclavian venipuncture point between the clavicle and the first rib.2 Seven years post-implant, our patient had developed a fracture in both the atrial and ventricular leads due to the subclavian crush syndrome (SCS). Because there is no direct cause of the lead fractures such as loss of body weight and/or length, clavicle or rib fractures, it could be concluded that the fractures were most likely caused by lead compression between clavicle and first rib, as illustrated in (figure 4). Measurement of lead impedance can provide important information about the integrity ofthe pacing electrodes and this information can be used in an early stadium to detect isolation defects in vulnerable pacing leads. It has been reported that SCS occurred in both conventional and thin leads implanted in the same patient.7 Furthermore, when subclavian venipuncture is used, SCS may even develop in patients with transvenous defibrillator systems.8 In the current case, after implantation of dual pacing leads using the left subclavian vein, the symptoms recurred. Ambulatory ECG recording showed atrial and ventricular dysrrhythmias. This may be due to traction of the atrial tissue and mechanical irritation of the right ventricle. Scintigraphic pulmonary and myocardial and angiographic coronary analysis demonstrated pulmonary and cardiac defects with normal coronary anatomy and left ventricular function. 96
Because of the recurrence of symptoms and the pulmonary and cardiac damage it was decided to retrieve the crushed atrial lead back to its former site in the right subclavian region. This was successfully performed by using an angled wire loop retriever. Pulmonary embolism (PE) has been reported in association with permanent transvenous pacing
leads.9"10
Figure 4. Anatomical landmarks for subclavian crush syndrome illustrated by the yellow shaded area. I=Sternocleidomastoid muscle, 2=Internaljugular vein, 3=Subclavian vein, 4=Clavicle, 5=First rib.
Netherlands Heart Journal, Volume 13, Number 3, March 2005
Possible complications of subclavian crush syndrome
Reversible inferolateral myocardial perfusion defect with normal coronary arteries has been described by Erdogan and colleagues in a patient with a permanent dual chamber pacemaker implantation and an activefixation ventricular lead insertion in the right ventricular outflow tract.1' In contrast to their case, the present patient was paced in the right ventricle apical region and showed irreversible inferior myocardial perfusion defect. Possible mechanisms responsible for these defects may be factors related to technical processing, myocardial bridging and anomalous coronary anatomy, attenuation artifacts (because of low energy emission of thallium-201 which results in important tissue attenuation and scatter giving rise to degrading the scintigraphic images), or ischaemia in the presence of small vessel disease, coronary vasospasm, hypertension with or without hypertrophy, left bundle branch block, paced rhythm and valvular heart disease.'2-'6 It has been suggested that the use ofcephalic vein cut-down or a more lateral percutaneous puncture of the subclavian vein would eliminate lead compression or crush syndrome.5'6 Also the internal jugular vein has been used as a venous access for permanent pacing leads implantation.6"7 After re-implantation of dual leads from a more lateral venous access of the left subclavian vein and retraction of the migrated atrial lead from the right ventricle she remained well. c
4 5
6
7
8
9 10
11 12
13
14
Acknowledgement The authors would like to thank Mr. A. Onrust, Mr. M. Mintjens, H. Schutte and G. Horstink for their technical assistance during the preparation of this manuscript.
15 16 17
References 1
2
3
Gupta K, Villareal RP, Rasekh A, Massumi A. Pacemaker lead entrapment syndrome. Tex HeartJ2003;30:84-5. Kazama S, Nishiyama K, Machii M, Tanaka K, Amano T, Nomoura K, et al. Long-term follow up of ventricular endocardial pacing leads: Complications, electrical performance, and longevity of 561 ventricular leads. Jpn HeartJ 1993;34:193-200. Jacobs DM, Fink AS, Miller RP, Anderson WR, McVenes RD, Lessar JF, et al. Anatomical and morphological evaluation of pace-maker lead compression. Pacing Clin Ekctrophysiol 1993;16: 434-44.
Netheriands Heart Journal, Volume 13, Number 3, March 2005
18
Magney JE, Parsons JA, Flynn DM, Hunter DW. Pacemaker and defibrillator lead entrapment: case studies. Pacing Clin Electrophysiol 1995;18:1509-17. Magney JE, Staplin DH, Flynn DM, Hunter DW. A new approach to percutaneous subclavian venipuncture to avoid lead fracture or central venous catheter occlusion. Pacing Clin Ekctrophysiol 1993; 16:2133-42. Gallik DM, Ben-Zur UM, Gross JN, Furman S. Lead fracture in cephalic versus subclavian approach with transvenous implantable cardioverter defibrillator systems. Pacing Clin Electrophysiol 1996; 19:1089-94. Weiner S, Patel J, Jadonath RL, Goldner BG, Gross JN. Lead failure due to the subclavian crush syndrome in a patient implanted with both standard and thin bipolar spiral wound leads. Pacing Clin Ekctrophysiol 1999;22:975-6. Roelke M, O'Nunain SS, Osswald S, Garan H, Harthorne JW, Rusl JN. Subclavian crush syndrome complicating transvenous cardioverter defibrillator systems. Pacing Clin Electrophysiol 1995;18: 973-9. Theiss W, WirtzfeldA. Pulmonary embolization of retained transvenous pacemaker electrode. Br HeartJ 1976;38:326-30. Said SAM, Ticheler CHJM. Early pulmonary embolism following transvenous permanent dual chamber pacemaker implantation. Electrocardiographic and scintigraphic evaluation. Cardiologie 2000;7:21-4. Erdogan 0, Altun A, Durmus-Altun G, Ozbay G. Inferolateral myocardial perfusion defect caused by right ventricular outflow tract pacing. PACE 2004;27:808-11. Fuller CM, Raizner AE, Chahine RA, et al. Exercise induced coronary artery spasm: Angiographic demonstration, documentation of ischemia by myocardial scintigraphy and results of pharmacological intervention. AmJ Cardiol 1980;46:500-6. Pichard AD, Gorlin R, Smith H, et al. Coronary flow studies in patients with left ventricular hypertrophy ofthe hypertensive type. Evidence for impaired coronary vascular reserve. Am J Cardiol 1981;47:547-53. Cannon RO III, Watson RM, Douglas RR, et al. Angina caused by reduced vasodilator reserve of small coronary arteries. JAm Coil Cardiol 1983;1:1359-73. Hirzel HO, Markus S, Nuesch K, et al. Thallium-201 scintigraphy in complete LBBB. Amj Cardiol 1984;53:764-9. Bailey IK, Come PC, Kelly DT, et al. Thallium-201 myocardial perfusion imaging in aortic valve stenosis. Am JCardiol 1977;40: 889-99. Said SAM, Bucx JJJ, Stassen CM. Failure of subclavian venipuncture: the internal jugular vein as a useful alternative. IntJ Cardiol 1992;35:275-8. Moses HW, Taylor GJ, Schneider JA, Dove JT, eds. A practical guide of cardiac pacing. Boston/Toronto: Little, Brown and Company, 1983.
97
Possible compications
Su sub avian
crush
syndrome
S.A.M. Said, C.H.J.M. Ticheler, C.M. Stassen, A. Derks, H.T. Droste
A 70-year-old woman with symptomatic Mobitz type II atrioventricular block underwent implantation of a dual-chamber pacemaker 11 years ago. The leads were inserted through a percutaneous puncture of the right subdavian vein, using standard techniques. Both leads were passive fixation leads. Due to battery failure and end of life criteria, the pulse generator (PG) had been routinely replaced six years previously. Predischarge pacemaker control revealed norm pacing, sensing thresholds and impedance for both leads. Because of a syncopal attack subsequent to lead fractures, most likely secondary to right subdavian cuh syndrome (SCS) of both leads, she underwent a double lead re-implantation one year after PG replacement by access via left subclavian vein puncture. After a symptom-free period of few years she was re-analysed because of palpitations, dizziness, angina pectoris and tiredness. Pulmonary embolisation and myocardial perfusion defects were detected udlising scintigraphic techniques. Chest X-ray revealed the crushed atrial lead dislocated from the right subclavian region and lodged into the right ventricle towards the inferior septum. Because she was symptomatic, a retrieval tednique was applied and the crushed atrial lead was pulled back from the right ventricle and securely fixed to its former position. On maintnce medical treatment, she remains well. (Neth Heartj 2005;13: 92-7.) SA.M. Said A. Deut H.T. Droste
Department of Cardiology, Twente Hospital Group, Hengelo C.HJ.M. Ticheler C.M. Stasen Departments of Nuclear Medicine and Radiology, Twente Hospital Group, Hengelo Correspondence to: S.A.M. Said Department of Cardiology, Hospital ZGT, location Hengelo, Geerdinksweg 141, 7555 DL Hengelo E-mail address: [email protected]
92
Key words: subclavian crush syndrome, pulmonary embolisation, lead migration, myocardial perfusion defect, retraction technique
facemaker lead insulation defects and conductor r fracture are not rare. Venous complications and pulmonary embolisation may occur. Pacemaker electrode failure due to the subclavian crush syndrome (SCS) often appears in the first three months postimplant and usually occurs within five years after implantation.1l2 The current case is unique because the SCS occurred seven years post-implant giving rise to atrial and ventricular lead fractures and insulation breaks producing pacing failure and causing recurrence of symptoms. Jacobs et al. studied 49 explanted fractured leads and found that all leads were inserted by conventional percutaneous subclavian venous puncture.3 After dissecting cadavers with percutaneous subclavian puncture of pacemakers, central venous catheters and defibrillators, Magney and colleagues reported that almost all leads or catheters passed through the medial subclavicular musculotendinous complex (MSMC) before entering the vein. Furthermore, they demonstrated that leads trapped in the MSMC are exposed to unnecessary compression as they move with the clavicle.4 It has been suggested that the use of cephalic vein cut-down or a more lateral percutaneous puncture of the subdavian vein would eliminate lead compression or crush syndrome.5 In our case, new pacing leads were implanted using a more lateral percutaneous venipuncture access ofthe left subclavian vein. The crushed atrial lead, which was found to have migrated and lodged into the right ventricle, could possibly be incriminated for irritative dysrhythmias and myocardial and pulmonary defects. The migrated atrial lead was retracted and firmly fixed to the right subclavian region. Cao report A 70-year-old woman, a nonsmoker, was referred for analysis of palpitations of recent onset and complaints of being easily fatigued. She had undergone a DDDNctherlands Heart Journal, Volume 13, Number 3, March 2005
Possible complications of subclavian crush syndrome
.0 10 7
M. W MW. vwllll stAwm NAE Mg W T&I 3 M " 99 14!12
*
.1=~~~~~~~~~~....
l, lil ., j l t ! jl l S
....
......
S 1
A
5V nkITM *IIf-?- 2 'w EE e miaiwt~Ii ow DIT. OT4 -ft- .sm
........ *
.....
i--6. ..6 .h * ---t ,-
**
.
s ,1 1
I
..
.
I knsi. X X 1 -i1 1 1 1r !_E ! --
I:E
*
7 INK 155
7A
......... |
'-jr-I
11! !:; lj
i | I d ffi L s !1B;||f^|;
;
iZ1 |
ff;
i
j:
-......
Eli
illI l......... 11 l
......
...... i:2,
.........
Figure 1M Tekmetric rythm sip dpcingpacingfailure withut ventricular escape
rhythm.
pacemaker implantation because of symptomatic atnoventricular (Mobitz II) heart block 11 years ago. A 294-03 Relay DDD pacemaker, Biopore 432-02 atrial lead and Biopore 430-02 ventricular lead were implanted. Acute atrial and ventricular impedance were 512 Ohm, and 500 Ohm, respectively. Follow-up took place every four months. Due to battery failure, the PG
was
replaced (17 February 1998) by
a
Vitatron
Diamond DDD pacemaker. In July 1998, the impedance ofthe atrial and ventricular leads unexpectedly decreased hold and
to
400 and 437 Ohm,
sensing
levels
were at
respectively. implantation
Thresvalues.
On 24 June 1999, the patient presented with a subcapital fracture of the left foot due to a syncopal attack. The ECG depicted periods with pacing failure without ventricular escape rhythm (figure IA). A detailed chest X-ray of the right infraclavicular region revealed two fractured leads at the level of the first rib and the clavicle. The insulation defect of both leads was well appreciated (figure iB). The site of fracture could not be reached for repair of the leads, therefore she underwent re-implantation of two new
Figure lB. Detailed chest X-ray ofte right infraclavicular area demonstratingdoubk kadfracture (arrows) at thekvel of thefirst rib and th clavick.
Ndherlanbd Heart Journal, Vohlmc 13, Number 3, March 2005
93
Possible complications of subclavian crush syndrome
Lw
w%.o
05-08-33
j%
,F
l iiL
s %. r,%L-%
3004
%.O
Ant a
x
S 0
X Inf
i ~ ~ ~r MnIl%I-xL
Ir%n
0
t
A
p
VL-
24
26
26
28
28 ato
30~~~ s 30
32
34
36
30
32
t
34
36
38
Vert i ca 1 LA
Septa 1
5 t
r Apex
e
L a
Infer 101
Horizontal LA
Anter i or
5
Latera 1
s
26
O28
30
26
28
30
SI.O
S
34
36
t
34
36
36
t
p
base 32
Short Axis
Apex Ant L a t
p I
I n f er 10o
Horizontal LA
Rnter i or
S
I .
Se So
Base
S t r
e
S
30
32
S
34
36
38
it
nf
0. Sp Pk
1
t
-*
A
Figure 2A. Dipypidamok MIBI stress test illustrating an irreversibk inftrior wall myocardial defect.
leads from the left side. During this procedure, both atrial and ventricular electrodes were inserted from a more lateral approach through percutaneous puncture of the left subclavian vein. The case was presented at the heart team meeting, and it was decided not to retrieve the seven-year-old crushed leads because of increased risk of cardiac damage. The fractured 'crushed' electrodes were retained and fixed to the right subdavian region and remained distally connected to the myocardium. Then they were capped and subcutaneously sutured with Vicryl in the right infra-
94
clavicular region. Routine chest radiograph demonstrated a proper position ofthe new electrodes and a good fixation of the old fractured 'crushed' leads. During the whole follow-up period (1992-1999) there were no significant alterations in body weight or length. The current symptoms, besides palpitation and tiredness, were dizziness, shortness of breath on exertion and angina pectoris NYHA functional dass II. The 48hour ambulatory ECG monitoring revealed normal DDD pacing alternating with sinus rhythm, premature ventricular contractions and periods of paroxysmal
Netherlands Heart Journal, Volume 13, Number 3, March 2005
Possible complications of subclavian crush syndrome
Figure 2B. Coronary angiogramsshowing normal left (leftpanel) and right (rightpanel) coronary arteries. The migrated crushed atrial lead (CAL) is well appreciated.
atrial fibrillation and flutter. Repeated transthoracic echocardiographic studies demonstrated a normokinetic normal-sized left ventricle with mild mitral and tricuspid regurgitation. Maximal exercise tolerance testing revealed normal physical capacity. The test was terminated due to angina pectoris and fatigue. Pharmacological MIBI stress test depicted a small irreversible myocardial defect in the inferior wall (figure 2A).
Figure 2C Plain X-ray in left lateralposition revealing the crushed atrial lead (CAL) migrated and dislodged into the right ventricle. Netherlands Heart Journal, Volume 13, Number 3, March 2005
Coronary arteriography and contrast ventriculography studies illustrated normal coronary arterial anatomy and distribution with normokinetic left ventricle (figure 2B left and right panels). The fractured fragment ofthe atrial lead was detected whirling in the right ventricle. It migrated from the right infraclavicular region and lodged into the right ventricle (figure 2C). Its proximal tip remained connected to the right atrial appendage. This fragment of the atrial lead may have wandered around causing, by traction forces and mechanical irritation, atrial and ventricular arrhythmias. Pulmonary perfusion-ventilation scintigraphy showed a solitary perfusion defect in the left upper lobe with ventilation mismatch as usually seen by foreign body embolisation (probably insulation material). On 8 April 2004, the old atrial lead was pulled back to the site of the right subclavian vein using percutaneous right subclavian venous access. In this setting an angled wire loop retriever was successfully utilised. The right subclavian venous puncture was performed by Doppler-guided needle because ofthe presence of crushed atrial and ventricular leads in the vein. The crushed atrial lead was again, after light traction, securely sutured to the subcutaneous tissue in the subclavian area (figure 3). After this uncomplicated procedure, she remained well. She was treated with oral anticoagulation at INRlevel between 1.8 and 4.1, digoxin 0.25 mg and 200 mg flecainide/day. Discussion Pacing lead fracture occurs infrequently (1 to 4%) but causes potentially catastrophic complications of permanent pacing systems. Because of statistical 95
Possible complications of subclavian crush syndrome
Figure 3. Plain X-ray in antero-posteriorposition: Before (kftpanel) and after (riqhtpanel) retraction of the crushed atrial lead (CAL).
difference (p=0.08) in lead fracture between subclavian and cephalic vein access, it has been suggested that cephalic vein approach may be preferable.6 Lead fracture occurred in 3.4% of cases reported by Kazama et al. within five years post-implant. They identified two particular sites of lead fracture: one within the pacemaker pocket due to fixation ligature and the other at the subclavian venipuncture point between the clavicle and the first rib.2 Seven years post-implant, our patient had developed a fracture in both the atrial and ventricular leads due to the subclavian crush syndrome (SCS). Because there is no direct cause of the lead fractures such as loss of body weight and/or length, clavicle or rib fractures, it could be concluded that the fractures were most likely caused by lead compression between clavicle and first rib, as illustrated in (figure 4). Measurement of lead impedance can provide important information about the integrity ofthe pacing electrodes and this information can be used in an early stadium to detect isolation defects in vulnerable pacing leads. It has been reported that SCS occurred in both conventional and thin leads implanted in the same patient.7 Furthermore, when subclavian venipuncture is used, SCS may even develop in patients with transvenous defibrillator systems.8 In the current case, after implantation of dual pacing leads using the left subclavian vein, the symptoms recurred. Ambulatory ECG recording showed atrial and ventricular dysrrhythmias. This may be due to traction of the atrial tissue and mechanical irritation of the right ventricle. Scintigraphic pulmonary and myocardial and angiographic coronary analysis demonstrated pulmonary and cardiac defects with normal coronary anatomy and left ventricular function. 96
Because of the recurrence of symptoms and the pulmonary and cardiac damage it was decided to retrieve the crushed atrial lead back to its former site in the right subclavian region. This was successfully performed by using an angled wire loop retriever. Pulmonary embolism (PE) has been reported in association with permanent transvenous pacing
leads.9"10
Figure 4. Anatomical landmarks for subclavian crush syndrome illustrated by the yellow shaded area. I=Sternocleidomastoid muscle, 2=Internaljugular vein, 3=Subclavian vein, 4=Clavicle, 5=First rib.
Netherlands Heart Journal, Volume 13, Number 3, March 2005
Possible complications of subclavian crush syndrome
Reversible inferolateral myocardial perfusion defect with normal coronary arteries has been described by Erdogan and colleagues in a patient with a permanent dual chamber pacemaker implantation and an activefixation ventricular lead insertion in the right ventricular outflow tract.1' In contrast to their case, the present patient was paced in the right ventricle apical region and showed irreversible inferior myocardial perfusion defect. Possible mechanisms responsible for these defects may be factors related to technical processing, myocardial bridging and anomalous coronary anatomy, attenuation artifacts (because of low energy emission of thallium-201 which results in important tissue attenuation and scatter giving rise to degrading the scintigraphic images), or ischaemia in the presence of small vessel disease, coronary vasospasm, hypertension with or without hypertrophy, left bundle branch block, paced rhythm and valvular heart disease.'2-'6 It has been suggested that the use ofcephalic vein cut-down or a more lateral percutaneous puncture of the subclavian vein would eliminate lead compression or crush syndrome.5'6 Also the internal jugular vein has been used as a venous access for permanent pacing leads implantation.6"7 After re-implantation of dual leads from a more lateral venous access of the left subclavian vein and retraction of the migrated atrial lead from the right ventricle she remained well. c
4 5
6
7
8
9 10
11 12
13
14
Acknowledgement The authors would like to thank Mr. A. Onrust, Mr. M. Mintjens, H. Schutte and G. Horstink for their technical assistance during the preparation of this manuscript.
15 16 17
References 1
2
3
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