Ann Thorac Surg 1999;67:1775-1776
© 1999 The Society of Thoracic Surgeons
Case Reports
Immediate vein graft thrombectomy for acute occlusion after coronary artery bypass grafting
Adam E. Saltman, MD, PhDa,
Walter H. Dzik, MDb,
Sidney Levitsky, MDa
a Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
b Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
Accepted for publication November 2, 1998.
Address reprint requests to Dr Levitsky, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, 110 Francis St, Suite 2C, Boston, MA 02215
e-mail: slevitsk{at}bidmc.harvard.edu
 |
Abstract
|
|---|
A 76-year-old man underwent coronary bypass grafting 3 days after exposure to heparin. Immediately after chest closure, he developed acute graft thrombosis and cardiac arrest in the setting of thrombocytopenia. Immediate graft thrombectomies were performed. Postoperative tests for heparin-induced thrombocytopenia and thrombosis (HITT) were positive. This case represents a dramatic example of HITT after coronary revascularization.
|
Introduction
|
|---|
With the increasing use of Heparin in the treatment of unstable angina and in patients following invasive cardiology procedures, the incidence of Heparin-induced thrombocytopenia and thrombosis (HITT) will increase and present untoward problems following surgical coronary revascularization. Intraoperative strategies to treat acute graft thrombosis in the operating room related to HITT requires further developments, in addition, to mechanical removal of the thrombus as described in this case report.
A 76-year-old man with a subendocardial myocardial infarction was transferred to the our hospital, where cardiac catheterization demonstrated triple vessel disease with a well-preserved left ventricle. The patient had received no heparin exposure before admission, although at cardiac catheterization he received 5,000 units of intravenous heparin. An elective sextuple coronary artery bypass was performed 3 days later utilizing the internal mammary artery and reversed greater saphenous vein. No sequential anastomoses were performed. The target coronary arteries all measured 1.5 mm in diameter or greater. The patient had received no prior heparin exposure. Ten minutes after chest closure, the patient suffered electromechanical dissociation. Open cardiac massage was begun and he was placed immediately on cardiopulmonary bypass. A large amount of fresh red clot was removed from each bypass graft. Patency was confirmed by direct probing of the distal anastomoses. The grafts were closed and the patient was successfully weaned from cardiopulmonary bypass with pharmacologic support. Half of the usual protamine dose was given. The patient received no antifibrinolytic drugs.
The platelet count immediately after surgery was 41,000/mm3; a test for heparin-dependent antiplatelet antibodies was negative at that time. During his postoperative course the patient received no heparin and his thrombocytopenia resolved (Table 1); additional hematologic studies confirmed the diagnosis of heparin-induced thrombocytopenia and thrombosis (Table 2). Pathologic examination of the removed clots showed simple tan, dark-brown clots. No further evidence of thrombotic complication was noted. An echocardiogram performed before discharge showed that his ejection fraction was reduced to 15% with global dysfunction. An ultrafast electron beam computed tomographic scan demonstrated patent grafts to the right posterior descending artery and left anterior descending artery only (Fig 1). The patient was discharged on the 15th postoperative day.
View larger version (141K):
[in this window]
[in a new window]
|
Fig 1. Contrast-enhanced ultrafast electron beam computed tomogram of the heart, obtained on postoperative day 11. The large white arrows indicate the patent right posterior descending artery and left anterior descending artery bypass grafts on the patient’s right (R) and left (L), respectively. The other four bypass grafts are occluded, and therefore are not seen.
|
|
|
Comment
|
|---|
Heparin-induced thrombocytopenia and thrombosis (HITT) is an uncommon but serious complication of heparin therapy. Occurring in only about 2% of patients receiving standard bovine heparin, HITT is associated with an absolute thrombocytopenia and enhanced platelet aggregation. In the absence of prior exposure, HITT typically does not occur for at least 1 week after starting heparin therapy. Patients with a history of heparin exposure, however, may develop HITT within hours of restarting therapy. They develop an antibody directed against the complex of heparin with platelet factor 4 [1].
Platelet thrombi infarct multiple end organs such as the brain, heart, kidney, liver, and bowel. Pulmonary embolism, saphenous vein graft occlusion, [2] and prosthetic valve thrombosis have also been reported. The typical 20%–30% mortality rate appears to be decreasing, probably as a result of earlier diagnosis.
The diagnosis of HITT is largely clinical. Platelet aggregometry, heparin-induced platelet aggregation, and C14 serotonin release are commonly used to detect antiplatelet antibodies. Lumographic detection of platelet-dense granule ATP release [3] and enzyme-linked immunosorbant heparin-PF4 antibody assay [4, 5] are considered to be very sensitive and specific for HITT. In this patient, the original antibody assay was likely negative because he had received over 88,000 units of heparin within a few hours, neutralizing the in vitro test. Repeat testing after several days without heparin administration was positive.
Treatment of HITT is controversial. If possible, all heparin should be stopped preoperatively. Heparin-bonded pump circuits (Carmeda BioActive Surface; Carmeda AB, Stockholm, Sweden), low molecular weight heparins such as enoxaparin and tedelparin, heparinoids such as dermatan and orgaran, and ancrod have been successfully used for cardiopulmonary bypass. For acute treatment of HITT intra- and postoperatively, iloprost (a prostacyclin analog) [6] or abciximab (a monoclonal antiplatelet GPIIb-IIIa receptor antibody) may prove beneficial but are unproved. By only half-reversing anticoagulation with protamine, we allowed an excess of circulating heparin to sequester the antiplatelet antibody, permitting time to institute other anticoagulant regimens. Most importantly, platelet transfusions should be avoided as they will most likely promote further plug formation.
Sometimes, streptokinase, urokinase, and/or tissue plasminogen activator [7] may prove successful at lysing platelet plugs. If these measures fail, however, operation may be necessary to remove larger clots from accessible vessels. This is the first case of which we are aware, however, in which coronary bypass graft thrombectomy was performed with restoration of flow and survival.
|
References
|
|---|
-
Greinacher A., Liebenhoff U., Kiefel V., et al. Heparin-associated thrombocytopenia: the effects of various intravenous IgG preparations on antibody mediated platelet activation: a possible new indication for high dose i.v. IgG. Thromb Haemost 1994;71:641-645.[Medline]
-
Singer R.L., Mannion J.D., Bauer T.L., et al. Complications from heparin-induced thrombocytopenia in patients undergoing cardiopulmonary bypass. Chest 1993;104:1436-1440.[Abstract/Free Full Text]
-
Stewart M.W., Etches W.S., Boshkov L.K., Gordon P.A. Heparin-induced thrombocytopenia: an improved method of detection based on lumi-aggregometry. Br J Haematol 1995;91:173-177.[Medline]
-
Gruel Y., Rupin A., Darnige L., et al. Specific quantification of heparin-dependent antibodies for the diagnosis of heparin-associated thrombocytopenia using an enzyme-linked immunosorbent assay. Thromb Res 1991;62:377-387.[Medline]
-
Greinacher A., Amiral J., Dummel V., et al. Laboratory diagnosis of heparin-associated thrombocytopenia and comparison of platelet aggregation test, heparin-induced platelet activation test, and platelet factor 4/heparin enzyme-linked immunosorbent assay. Transfusion 1994;34:381-385.[Medline]
-
Feng W.C., Singh A.K., Bert A.A., et al. Perioperative paraplegia and multiorgan failure from heparin-induced thrombocytopenia. Ann Thorac Surg 1993;55:1555-1557.[Abstract]
-
Dauerman H.L., Cutlip D.E., Sellke F.W. Intracoronary thrombolysis in the treatment of graft closure immediately after CABG. Ann Thorac Surg 1996;62:280-283.[Abstract/Free Full Text]
Top
Abstract
Introduction
