Ann Thorac Surg 2003;76:617-619
© 2003 The Society of Thoracic Surgeons
Case report
Regression of intracardiac heparin-induced thrombosis after aortic root surgery
Frédéric Collart, MDa*,
David Derouck, MDa,
Francois Kerbaul, MDa,
Horea Feier, MDa,
Thierry G. Mesana, PhDa
a Department of Cardiac Surgery, Hôpital de la Timone, University of Marseille, Marseille, France
Accepted for publication January 12, 2003.
* Address reprint requests to Dr Collart, Service de Chirurgie Cardiaque, Hôpital de la Timone, 264 rue St. Pierre, 13385 Marseille Cx 05, France
e-mail: fcollart{at}univ-aix.fr
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Abstract
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Heparin-induced thrombocytopenia and thrombosis syndrome (type II) is associated with thromboembolic complications and a mortality rate up to 30%. We describe a patient who developed intracardiac and aortic Dacron prosthesis heparin-induced thrombosis after aortic root conservative surgery. Successive transoesophageal echocardiographies demonstrated a progressive regression of intracardiac thrombosis with oral anticoagulation by warfarin and antiplatelet therapy combining aspirin and clopidogrel.
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Introduction
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Heparin-induced thrombocytopenia type II (HITT) is an idiosyncratic immune-mediated reaction most commonly caused by an immunoglobulin G antibody that binds to platelets in the presence of heparin and causes platelet activation [1]. Heparin-induced thrombocytopenia type II is defined by a fall of platelet count by more than 50% of the base line value occurring at least 5 days after heparin therapy onset, accompanied by heparin-dependant antiplatelet antibodies detected by the sensitive C-serotonin release assay. The real frequency of HITT is unknown and ranges between 0.2% and 2% [2, 3], although it is more common after full dose intravenous heparin administration. The risk for thromboembolic events in patients with HITT has been reported more than 60% [1]. In contrast, intracardiac thrombosis due to HITT remains exceptional and treatment of this complication is unclear [4, 5]. We describe a patient with multiple intracardiac and aortic prosthesis thrombosis due to HITT after aortic root surgery successfully treated without cardiac reoperation.
A 70-year-old patient underwent elective aortic root remodeling, described by David and Feindel [6], for an ascending aorta aneurysm with a prosthetic Dacron graft. Preoperative platelet count was 213,000 per µL. The immediate postoperative course was uneventful. Anticoagulation therapy with subcutaneous heparin (7500 U three times daily) was necessary because of chronic atrial fibrillation. One week after surgery the patient developed an acute ischemic leg syndrome with a drop of platelet count down to 44,000 per µL. Transthoracic echocardiography was normal. An emergency aortic bifemoral bypass was indicated due to the presence of extensive and disseminated "white clot" in the aortic bifurcation and legs arteries. At the same time heparin-dependent antibodies were detected by the sensitive C-serotonin release assay and treatment with Orgaran (AntiXa levels at 0.5 IU/mL; Orgaran, Roseland, NJ, USA) was started and then switched to oral anticoaglation with warfarin (INR: 3 to 3.5) 5 days after vascular surgery. Platelet count rose back up to 250,000 per µL.
Evolution was satisfactory up to the tenth postoperative day after vascular surgery, when the patient developed a transient ischemic attack. A transoesophageal echocardiographic (TEE) scan demonstrated multiple thrombosis in the right and left atrium, and attached to the proximal and distal suture of the aortic prosthesis (Figs 1 and 2).
An adjunctive therapy with aspirin and clopidogrel was started in
association with warfarin. Eight days later a TEE control illustrated regression of the intracardiac thrombosis. The antiplatelet therapy was continued and a new TEE control 1-month later revealed the total disappearance of intracardiac thrombosis.
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Fig 1. Transesophageal echocardiography images revealed thrombosis (TH) into the left atrium (LA) and in the Dacron aortic graft (AO). (LV = left ventricle.)
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Fig 2. Transesophageal echocardiography images revealed thrombosis (TH) into the right atrium (RA) and near to the proximal suture of the Dacron aortic graft (AO). (LA = left atria; LV = left ventricle.)
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Comment
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This observation demonstrates the urgent need for rapid recognition of HITT because continuing heparin therapy may lead to severe thromboembolic complications. A drop of platelets count below 100,000 per µL with thromboembolic complication suggests the presence of heparin-induced antibodies that need to be confirmed by laboratory tests. This report also demonstrates that, despite rapid diagnosis and treatment of HITT, the risk for severe thrombosis persists for several weeks after exposure to heparin. Warkentin and Kelton [7] indicated in a retrospective study that patients with a diagnosis of isolated HITT without thrombosis have a 30-day risk of thrombosis of more than 50%, despite cessation of heparin administration. This study suggests that alternate anticoagulant or antiplatelet therapy should be necessary when the diagnosis of HITT is done, even without thrombosis complications.
Peripheral vascular thrombosis that occurred in our patient was largely reported previously. But heparin-induced intracardiac and Dacron prosthesis thrombosis remains exceptional. Intracardiac thrombosis may be underestimated in asymptomatic patients and TEE should be systematically performed in all patients with HITT to search for intracardiac thrombosis [5].
The therapeutic strategy in this patient was unclear. Regarding for the risk of a new thromboembolic event in the case of medical treatment, compared with the risk of cardiac reoperation with the difficult management of cardiopulmonary bypass without heparin administration. Thrombolytic agents have been successfully used in life-threatening conditions without bleeding complications [4]. Antiplatelet therapy is a good alternative and, in this patient, association of warfarin, aspirin, and clopidogrel have demonstrated a rapid regression of thrombosis.
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References
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- Brieger D.B., Mak K., Kottke-Marchand K., Topol E.J. Heparin-induced thrombocytopenia. J Am Coll Cardiol 1998;31:1449-1459.[Abstract/Free Full Text]
- Baglin T.P. Heparin induced thrombocytopenia thrombosis (HIT/T) syndrome: diagnosis and treatment. J Clin Pathol 2001;54:272-274.[Abstract/Free Full Text]
- Munver R., Schulman I.C., Wolf D.J., Rosengart T.K. Heparin-induced thrombocytopenia and thrombosis: presentation after cardiopulmonary bypass. Ann Thorac Surg 1994;58:1764-1766.[Abstract]
- Elliott L.D., Lichtenberg R., Johnson S.A., Lewis B.E. Diagnosis and management of right atrial thrombus in heparin-induced thrombocytopenia and thrombosis syndrome with transesophageal echocardiography and thrombolytic therapy. Am Heart J 1996;131:1227-1229.[Medline]
- Movsowitz H.D., Jacobs L.E., Movsowitz C., Kotler M.N., Kajani M. Transesophageal echocardiography in patients with heparin-induced thrombocytopenia and thrombosis. Am Heart J 1993;126:1011-1013.[Medline]
- David T.E., Feindel C.M. An aortic valve sparing operation for patients with aortic incompetence and aneurysm of the ascending aorta. J Thorac Cardiovasc Surg 1992;103:617-622.[Abstract]
- Warkentin T.E., Kelton J.G. A fourteen year study of heparin induced thrombocytopenia. Am J Med 1996;101:502-507.[Medline]
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Abstract
Introduction
