ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Ann Thorac Surg 2008;86:639-640. doi:10.1016/j.athoracsur.2008.01.080
© 2008 The Society of Thoracic Surgeons
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Anna Lassia Meyer
Stefan Fischer
Axel Haverich
Martin Strüber
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Meyer, A. L.
Right arrow Articles by Strüber, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meyer, A. L.
Right arrow Articles by Strüber, M.
Related Collections
Right arrow Mechanical Circulatory Assistance

Case Reports

Implantation of a Left Ventricular Assist Device in a Patient With Primary Antiphospholipid Syndrome

Anna Lassia Meyer, MDa, Christian Kuehn, MDa, Clemens Gras, MDb, Doris Malehsa, MDa, Christoph Bara, MDa, Stefan Fischer, MD, MSa, Axel Haverich, MDa, Martin Strüber, MDa,*

a Department of Cardiothoracic, Transplant, and Vascular Surgery, Hannover Medical School, Hannover, Germany
b Department of Anesthesia, Hannover Medical School, Hannover, Germany

Accepted for publication January 28, 2008.

* Address correspondence to Dr Strüber, Department of Cardiothoracic, Transplantation, and Vascular Surgery, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover, 30625, Germany (Email: strueber.martin{at}mh-hannover.de).


   Abstract
Top
 Abstract
Introduction
 Comment
 References
 
The antiphospholipid syndrome is characterized by arterial and venous thrombosis and is associated with the presence of circulating antiphospholipid antibodies. Arterial thrombosis can result in myocardial infarction, which may potentially lead to end-stage heart failure. Here we report our anticoagulation protocol for patients with antiphospholipid syndrome that undergo axial-flow left ventricle assist devices (HeartMate II; Thoratec, Pleasanton, CA) implantation.


   Introduction
Top
 Abstract
 Introduction
Comment
 References
 
The first clinical description of the antiphospholipid syndrome (APS) goes back to Hughes [1] in 1983. Initially, APS was named anticardiolipin syndrome, which was subsequently re-defined to antiphospholipid syndrome [1]. This autoimmune disorder is characterized by recurrent thrombotic events in medium to large vessels in the presence of antiphospholipid antibodies (lupus anticoagulant or anticardiolipin antibodies, or both) [2]. The antiphospholipid syndrome occurs in 2% of the overall population [3].

Thus far, warfarin (Coumadin; Bristol-Myers Squibb, Princeton, NJ) remains the drug of choice in the treatment of patients diagnosed with thrombosis [4]. Previously reported experience suggests that surgery in patients with antiphospholipid syndrome is complicated by the presence of hypercoagulability and thrombosis formation, and is otherwise associated with thrombocytopenia and life-threatening hemorrhage.

Thrombotic events in coronary arteries lead to myocardial infarction and may induce end-stage heart failure. Treatment by implantation of a left ventricular assist device (LVAD) in patients with antiphospholipid syndrome remains a challenge. In addition, anticoagulation in such patients is complex. Currently, no anticoagulation protocol for patients with LVAD has been reported.

We report a 36-year-old man with severe cardiac insufficiency who was evaluated for cardiac transplantation at our institution. The patient's history went back to an extensive myocardial infarction of the anterior wall in 1999 with consequent formation of a giant aneurysm of the anterior wall. At this time, coronary artery disease was excluded by coronary angiography in this patient. At the same time, cerebral insult with aphasia and right-sided hemiparesis occurred. Extensive diagnostic workup revealed antiphospholipid syndrome with a positive anticardiolipin serology and a positive lupus anticoagulant, and the patient was treated with warfarin. Later on, thromboembolic occlusion of the left leg developed in the patient, which was treated with embolectomy and repair of the left femoral artery. In September 2004, a biventricular pacemaker with an implantable cardioverter defibrillator was implanted due to decline of global cardiac function.

In December 2006, the patient was transferred to our hospital due to a decrease in cardiac function with a subsequent "high urgency" listing for heart transplantation. The hemiparesis and aphasia was completely reversible. Echocardiography showed a dilated left ventricle with an end-diastolic dimension of 8.8 cm, an ejection fraction of 10%, and dyskinesia of the apex and the anterior wall. In comparison, the right ventricle seemed to be less dilated and showed only a mild functional decrease. Moderate mitral regurgitation and mild tricuspid regurgitation were observed. An intraventricular thrombus could not be detected at this time.

After progress in heart failure with frustrating stabilization, a high dose of catecholamines (dobutamine 6 µg/kg/min, noradrenaline 0.3 µg/kg/min, and levosimendan 0.19 µg/kg/min), and onset of end-organ failure, the decision for LVAD implantation was made. Serologic testing had demonstrated the presence of immunoglobulin G anticardiolipin antibodies.

As part of the preoperative management, plasmapheresis was performed to eliminate circulating antiphospholipid antibodies the day before LVAD implantation. In addition, transfusion of fresh frozen plasma was applied followed by the instillation of 1,000 mg of the B cell-depleting monoclonal antibody rituximab (MabThera; Roche Pharma AG, Grenzach-Wyhlen, Germany). A second measurement of antiphospholipid antibodies was not done.

The axial flow left ventricular assist device (HeartMate II; Thoratec, Pleasanton, CA) was implanted. Preoperatively, the activated clotting time was 160 seconds. Initiation of cardiopulmonary bypass was preceded by the administration of 600 U/kg of unfractionated heparin. The initial activated clotting time was 762 seconds. After systemic heparinization one million KIU of aprotinin (Trasylol; Bayer Vital GmbH, Leverkusen, Germany) were administered. After termination of the extracorporeal circulation, heparin was antagonized with 350 U/kg of protamin (Protamin Valeant; Valeant Pharmaceuticals Germany GmbH, Eschborn, Germany), and the initial activated clotting time was 141 seconds.

Postoperatively, the patient was transferred to the intensive care unit. During the first 36 hours after implantation blood loss was high at 4,900 mL, which was substituted by fresh frozen plasma, erythrocyte concentrate, and platelets. No anticoagulation therapy was given until the postoperative day 2 when the bleeding had deceased to 50 mL/hour. Consequently, intravenous heparin was applied with a target activated clotting time level between 160 and 180 seconds. After hemodynamic and respiratory stabilization, the patient was extubated on the postoperative day 6.

In the intermediate care unit on postoperative day 17, acetylsalicylic acid (100 mg/day, orally) was added to the medication. After further stabilization, the heparin was switched to warfarin (international normalized ratio, between 2.5 and 3.0).

After 34 days, the patient was discharged in very good condition under anticoagulation therapy with warfarin (international normalized ratio, between 2.5 and 3.0) and acetylsalicylic acid (100 mg/d). Six months later the patient is doing well and he is able to perform his routine daily activities with no need for assistance.


   Comment
Top
 Abstract
 Introduction
 Comment
References
 
Antiphospholipid antibodies belong to a heterogeneous group of auto-antibodies as part of the antiphospholipid syndrome. When the diagnosis of APS is not known before surgery and a catastrophic perioperative event occurs, the chance for a patient to survive seems to be very low [5]. We believe that only one case report of a patient with antiphospholipid syndrome after LVAD implantation was reported. In this case the syndrome was diagnosed based on frozen serum specimen analysis, which had been obtained before LVAD implantation [6]. Management strategies for patients with antiphospholipid syndrome during surgery were described by Agaba and colleagues [7] in 2006. In cardiac surgery, a restrictive strategy of protamin application seems to be advisable in cases of known APS [5].

This is the first report on the successful implantation of an axial flow LVAD in a patient with an antiphospholipid syndrome. The plasma exchange with fresh frozen plasma as the exchange plasma was preoperatively started so as to decrease the antibody load. This procedure is described in patients with catastrophic events associated with APS.

In conclusion, the anticoagulation management is similar in patients with and without APS [8], except for the use of preoperative plasmapheresis and the application of the B cell-depleting anti-CD 20 monoclonal antibody rituximab. This novel strategy allowed for an uneventful LVAD implantation in our patient with APS, and it is the future procedure in the case of an LVAD explantation in this patient.


   References
Top
 Abstract
 Introduction
 Comment
 References
 

  1. Hughes G. Hughes syndrome: the antiphospholipid syndrome-a clinical overview Clin Rev Allergy Immunol 2007;32:3-12.[Medline]
  2. Roubey RA. Antigenic specificities of antiphospholipid autoantibodies implications for clinical laboratory testing and diagnosis of the antiphospholipid syndrome Lupus 1996;5:425-430.[Medline]
  3. Shapiro SS, Thiagarajan P. Lupus anticoagulants Prog Hemost Thromb 1982;6:263-285.[Medline]
  4. Lockshin MD. Update on antiphospholipid syndrome Bull NYU Hosp Jt Dis 2006;64:57-59.[Medline]
  5. Massoudy P, Certin SM, Thielmann M, et al. Aniphospholipid syndrome in cardiac surgery an underestimated coagulation disorder? Eur J Cardiothorac Sur 2005;28:133-137.[Abstract/Free Full Text]
  6. Wadia Y, Thiagarajan P, Delgado R, Allison P, Robertson K, Frazier OH. Antiphospholipid syndrome with anti-prothrombin autoantibodies in a patient with an axial flow left ventricular assist device J Heart Lung Transplant 2005;24:1133-1136.[Medline]
  7. Agaba AE, Charaklias N, Babu-Victor A, et al. Aniphospholipid syndrome: a series of surgical emergencies and the current evidence for its management Ann R Coll Surg Engl 2006;88:370-374.[Medline]
  8. Miller LW, Pagani FD, Russell SD, et al. Use of a continuous-flow device in patients awaiting heart transplantation New Engl J Med 2007;357:885-896.[Abstract/Free Full Text]




This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Anna Lassia Meyer
Stefan Fischer
Axel Haverich
Martin Strüber
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Meyer, A. L.
Right arrow Articles by Strüber, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meyer, A. L.
Right arrow Articles by Strüber, M.
Related Collections
Right arrow Mechanical Circulatory Assistance

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS