Europace Advance Access published online on January 18, 2008
Europace, doi:10.1093/europace/eum291
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
CASE REPORT
Coronary sinus atresia and persistent left superior vena cava with the presence of thrombus complicating implantation of a left ventricular pacing lead
Department of Cardiology, Catharina Hospital, Michelangelolaan 2, Eindhoven, 5623 EJ, The Netherlands
Manuscript submitted 1 November 2007. Accepted after revision 11 December 2007.
* Corresponding author. Tel: +31 40 2397765; fax: +31 40 2447885. E-mail address: carlgr{at}cze.nl
 |
Abstract |
|---|
 Top Abstract IntroductionDiscussionConclusionAcknowledgementsReferences |
|---|
A 68-year-old male with heart failure and a suitable candidate for resynchronization therapy was referred to our hospital because of a failed coronary sinus (CS) lead implant. Catheterization of the CS initially also failed in our department but a left coronary angiogram revealed atresia of the CS and drainage of the coronary venous system via a persistent left superior vena cava (PLSVC). Implantation of a CS lead through the PLSVC could be accomplished after a selective angiogram, even in spite of the presence of a large thrombus at the junction of PLSVC and CS.
Key Words: Coronary sinus atresia, Thrombus formation, Cardiac resynchronization therapy, Persistent left superior vena cava
|
Introduction |
|---|
|
TopAbstractIntroductionDiscussionConclusionAcknowledgementsReferences |
|---|
Implantation of a coronary sinus (CS) lead for left ventricular (LV) pacing in cardiac resynchronization therapy (CRT) may be complicated by the inability to catheterize the CS. Failure to enter the CS is mainly related to anatomical barriers like the Thebesius valve at the ostium of the CS, present in 75% of the patients.1
Very rarely, communication between the CS and the right atrium is absent and the CS is draining via a persistent left superior vena cava (PLSVC) into the left innominate vein.2–4 We recently encountered this venous anomaly during implantation of a CS lead complicated by the presence of a large thrombus at the junction of the CS and the PLSVC. Implantation of a CS lead was successful in spite of these abnormalities.
Case report
A 68-year-old male with ischaemic cardiomyopathy was referred to our hospital for CRT because in a previous attempt, the CS could not be catheterized. During this attempt, a bipolar atrial lead and a ventricular lead were implanted. He had a history of a previous CABG for left main coronary artery stenosis. The LV ejection fraction was 20% and the ECG showed a complete left bundle branch block with a QRS complex of 160 ms and a prolonged PR interval of 290 ms. At the time of admission, he was in New York Heart Association Class III despite optimal medical treatment.
At the second attempt, also from the left pectoral area, catheterization of the CS ostium failed again. During this attempt, a left coronary angiogram was performed to visualize the venous phase of the coronary circulation. Although visualization remained suboptimal with all angiograms, it could be deduced that there was an abnormal run off of the coronary circulation towards a PLSVC. Because drainage of this PLSVC into the innominate vein was anticipated, an angiogram was made from the left subclavian vein. This confirmed the presence of a PLSVC connecting with the innominate vein (Figure 1). Subsequently, the PLSVC was selectively catheterized with a right Judkins coronary angiography catheter, and an angiogram performed from this vessel showed a dilated proximal portion of the PLSVC that was connected to the proximal segment of the CS. It also revealed the presence of a large thrombus in the proximal segment of the PLSVC (Figures 2 and 3). In spite of the presence of the thrombus, implantation of a CS lead in a posterior branch was attempted. The CS was cannulated via the PLVCS with a standard 9F Attain 6216A-MB2 guide catheter (Medtronic, Minneapolis, MN, USA), and a 6F Medtronic Attain 6248 DEL inner catheter selectively positioned in the posterior branch. After obtaining a selective angiogram via the inner catheter, a guide wire was advanced distally in the posterior vein. The Attain 6248 was exchanged for a Medtronic 4194 bipolar CS lead, which was advanced distally into the posterior tributary (Figure 4). The stimulation threshold was 1.3 V at 0.5 ms pulse duration with a lead impedance of 968 
. The guide catheter was removed by a standard slitter technique. Although fragmentation of the thrombus was noted after instrumentation of the PLVCS, there were no clinical signs of embolization. Subsequently, a Medtronic 6931-65 Sprint Fidelis shock lead was positioned in the right ventricular septum. All leads were connected to a Medtronic Concerto C174AWK ICD that was implanted subcutaneously in the left pectoral area. The previously implanted bipolar right ventricular lead was capped and abandoned.
|
|
|
|
The system was haemodynamically optimized by invasive measurement of LV dP/dtmax, which increased from 848 to 1006 mmHg/s after optimization of AV and V–V interval. Dalteparin was administered subcutaneously within 2 h after the procedure and continued twice daily in a weight-adjusted dosage until adequate anticoagulation with oral warfarin was obtained. Two months after implantation, the patient was clinically improved without further clinical thrombo-embolic complications.
|
Discussion |
|---|
|
TopAbstractIntroductionDiscussionConclusionAcknowledgementsReferences |
|---|
A persistent left vena cava superior is a well-known anomaly with an incidence between 1.0–2.0% in the general population and up to 10% in patients with associated cardiovascular defects.5
–7 Winter8 reviewed and analysed 174 patients with PLSVC collected from the world literature and his personal experience from the Hahnemann Hospital. In this cohort of 174 patients, he reported 9 patients in whom the usual ostium of the CS into the right atrium was closed. He stated that ‘In each of these cases CS blood takes a circuitous course through the PLSVC and innominate anastomosis to the right superior vena cava and right atrium’. These data indicate that an incidence of the CS atresia is much lower than the incidence of the PLVCS. This is in contrast with the calculated incidence of this anomaly in our experience. Two cases were encountered in a cohort of 558 consecutive patients who had CRT devices implanted between November 1999 and July 2007, which is an incidence of 0.36%. The third patient described in this case report is not included in this calculation because the patient was not part of the cohort of consecutive patients, but a patient selected because of an unsuccessful attempt in a referring hospital.
The discrepancy between the data of Winter and our experience regarding the incidence of CS atresia can be explained by the fact that insertion of diagnostic catheters or pacemaker leads from the left pectoral venous route in the case of CS atresia will easily follow the normal route towards the right atrium without noticing the presence of this venous anomaly. Only when intubation of the CS by a catheter or pacing lead is necessary and it fails, the presence of this venous anomaly may be anticipated. In patients with only a PLSVC, catheters and pacemaker leads inserted from the left upper thoracic site will easily follow the course of the PLSVC and attract the attention of the operator to this variant.
Failed catheterization of the CS in CRT is recently reported by Gras et al.9 in 4.8% of patients in the CARE-HF trial. However, it is not mentioned whether in those cases a coronary arteriogram has been performed to demonstrate or exclude the presence of CS atresia. We previously reported a patient with a similar anatomy in whom intubation of the CS from the right atrium failed and the presence of the PLSVC as drainage of the CS could be demonstrated by a left coronary angiogram.4 Also in this patient, implantation of the CS lead through the PLSVC in the presence of CS atresia was successfully performed. This variant of PLSVC has been described earlier by Peele3 in 1932 and Beyerlein2 already back in 1914.
The presence of a thrombus in the CS is rarely reported, and in the cases without CS, anomaly related to surgical trauma during mitral valve replacement10 and intracardiac repair of tetralogy of Fallot.11 The 14 year interval between bypass surgery (1993) and CRT-D implantation (2007) makes a relationship between surgery and the presence of thrombus in the CS unlikely in our patient. To the best of our knowledge, there is only one report in which the presence of a thrombus in a patient with CS ostial atresia and a PLSVC was accidentally discovered in an 82-year-old patient without previous symptoms.12 In this patient, anticoagulant therapy with warfarin was initiated, and the patient recovered without further clinical complications. In our patient, we decided to accept the potential risk of pulmonary emboli by catheter and lead manipulation during implantation because epicardial lead placement was not an attractive alternative due to his poor physical condition and previous cardiothoracic surgery. Although there were angiographic signs of fragmentation of the thrombus after lead placement, there were no clinical signs of pulmonary emboli in the follow-up after initiation of oral anticoagulant therapy with warfarin. With respect to the risk of thrombo-embolization, abandonment of the procedure followed by institution of anticoagulation therapy for 3 months prior to another attempt for CS lead implantation could have been considered as an alternative. The latter is probably even a safer approach in the prevention of pulmonary embolism and could be regarded as first choice, although a second surgical intervention always carries the risk of procedure complications like pocket infection.
|
Conclusion |
|---|
|
TopAbstractIntroductionDiscussionConclusionAcknowledgementsReferences |
|---|
In case of failure to catheterize the CS, a left coronary artery angiogram should be performed to visualize the coronary venous anatomy. Presence of CS atresia combined with a PLSVC does not hinder a successful implantation of a CS lead. If a thrombus is present in the CS–PLSVC junction, abandonment of the procedure and institution of anticoagulant therapy followed by implantation of the CS lead in a later phase should be considered. This approach prevents the potential risk of pulmonary embolism, but necessitates a second surgical procedure.
|
Acknowledgements |
|---|
|
TopAbstractIntroductionDiscussionConclusionAcknowledgementsReferences |
|---|
We wish to thank Dr Nobuhiro Tanaka for the interpretation of the article in Japanese language mentioned in reference 12.
Conflict of interest: B.M.V.G. is clinical advisor for Medtronic Trading NL BV, Heerlen, the Netherlands.
|
References |
|---|
|
TopAbstractIntroductionDiscussionConclusionAcknowledgementsReferences |
|---|
[1] Wright RR, Anson BJ, Cleveland HC. The vestigial valves and the interatrial foramen of the adult human heart. Anat Rec (1948) 100:331–51.[Medline]
[2] Beyerlein E. Die persistierende Vena cava superior sinistra als Abflussrohr fxr den Coronarvenenblut. Frankfurter Zeitschr für Pathol (1914) 327–332. Bd15.
[3] Peele TL. A case of a closed coronary sinus and left superior vena cava. Anat Rec (1932) 54:83–6.[CrossRef]
[4] Van Gelder BM, Elders J, Bracke FA, Meijer A. Implantation of a biventricular pacing system in a patient with a coronary sinus not communicating with the right atrium. Pacing Clin Electrophysiol (2003) 26:1294–6.[CrossRef][Medline]
[5] Fraser RS, Dvorkin J, Rossall RE, Eidem R. Left superior vena cava. A review of associated heart lesions, catheterization data and roentgenologic findings. Am J Med (1961) 31:711.[CrossRef][Web of Science][Medline]
[6] Cha EM, Khoury GH. Persistent left superior vena cava. Radiology (1972) 103:375–9.[Web of Science][Medline]
[7] Noah EN, Moore GW, Hutchins GM. Pathogenesis of persistent left superior vena cava with a coronary sinus connection. Pediatr Pathol (1991) 11:261–9.[CrossRef][Medline]
[8] Winter FS. Persistent left superior vena cava; survey of world literature and report of thirty additional cases. Angiology (1954) 5:90–134.
[9] Gras D, Böcker D, Lunati M, Wellens HJJ, Calvert M, Freemantle N, et al, on behalf of the CARE-HF Study steering committee Investigators. Implantation of cardiac resynchronization therapy systems in the CARE-HF trial: procedural success rate and safety. Europace (2007) 9:516–22.
[10] Hazan MB, Byrnes DA, Elmquist TH, Mazzara JT. Angiographic demonstration of coronary sinus thrombosis: a potential consequence of trauma to the coronary sinus. Cathet Cardiovasc Diagn (1982) 8:405–8.[CrossRef][Web of Science][Medline]
[11] Bapat VN, Hardikar AA, Porwal MM, Agrawal NB, Tendolkar AG. Coronary sinus thrombosis after cannulation during cardiopulmonary bypass. Ann Thorac Surg (1996) 62:1506–7.
[12] Matsui H, Kobayashi N, Nasu M, Takahashi Y, Ito M, Sate Y, et al. Coronary sinus ostial atresia with thrombus: a case report. J Cardiol (2005) 45:269–75. (Article in Japanese).[CrossRef][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||