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J Thorac Cardiovasc Surg 2003;126:1636-1637
© 2003 The American Association for Thoracic Surgery
Brief communications |
a Department of Thoracic and Cardiovascular Surgery, Hôpital Henri Mondor, Créteil, France,
b Department of Hematology, Hôpital Lariboisière, Paris, France
Received for publication February 28, 2003; accepted for publication April 22, 2003. * Address for reprints: Rémi Houël, MD, Department of Thoracic and Cardiovascular Surgery, Hôpital Henri Mondor, 51 Avenue du Maréchal de Lattre de Tassigny, Créteil, France.
Anticoagulation in patients implanted with ventricular assist devices is widely performed with aspirin, heparin, and anti–vitamin K therapy. Nonetheless, a variable antiplatelet effect of aspirin is well-known in healthy subjects. Moreover, the efficacy of aspirin may be reduced in the days after coronary artery bypass grafting surgery.1 Its efficacy has not been reported during the chronic phase of mechanical support with an external ventricular assist device. We report a resistance to aspirin that did respond to an increased daily oral intake and that could be observed as long as 6 weeks after device implantation.
Methods
Patient selection
Fifteen patients were studied prospectively during 6 weeks after implantation of an external ventricular assist device (Thoratec Laboratories Corporation, Pleasanton, Calif). Two patients were female. Median age was 44.3 years, range was 16.6 to 58.6 years. Indications for emergent device implantation were persistent primary cardiogenic shock complicating acute myocardial infarction in 7 patients, acute myocarditis in 2 patients, and end-stage dilated cardiomyopathy in 6 patients. Seven patients were supported by an intra-aortic balloon pump before device implantation. Median duration of support was 72 days (range 28-360 days). Mechanical support was biventricular in 10 patients. Three patients died while on support of sepsis in 1 case, intracranial hemorrhage in 1 case, and device dysfunction in 1 case.
Surgical technique and anticoagulation protocol
Implantation was performed by a standard technique. All patients were implanted under cardiopulmonary bypass and moderate hypothermia. Median cardiopulmonary bypass duration was 162 minutes (range 96-339 minutes). After surgery, anticoagulation was started within 8 to 12 hours with intravenous heparin to achieve an anti-Xa activity between 0.3 and 0.4 IU/L. Aspirin was started after 24 hours with a starting dose of 250 mg daily (except for 1 patient who had a starting dose of 400 mg daily). Aspirin doses were then adjusted according to in vitro platelet function tests and depending on clinical and biologic status. Anti–vitamin K therapy was started after removal of chest drains and extubation to maintain the international normalized ratio between 3 and 4. Fresh blood drawn for platelet function studies was collected once every week after implantation. A resistance to aspirin therapy was considered to have occurred when in vitro testing showed a persistent platelet aggregation in the presence of arachidonic acid despite daily administration of aspirin.
Results
Figure 1 shows the numbers of patients during follow up after device implantation with persistent in vitro platelet aggregation in the presence of arachidonic acid and despite daily aspirin administration. This was observed in 6 of 15 patients.
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Figure 2 shows the mean dose of aspirin administered per day and its temporal trends after device implantation. Two patients had an interruption in treatment because of severe bleeding complications in the third and fourth postoperative weeks (hemothorax and intracranial bleeding).
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Aspirin resistance has been reported in patients after coronary artery bypass grafting and was associated with an increased recruitment of new platelets in the days after surgery.1 After ventricular assist device implantation, we did observe a persistent in vitro platelet aggregation as late as 6 weeks after implantation and despite high doses of aspirin (>150 mg/d). In healthy subjects a dose of 100 mg/d is associated with the absence of in vitro platelet aggregation.2 When flow conditions are changed, however, as in patients with atherosclerosis, a higher dose of aspirin is necessary to preserved the absence of thromboxane A2 production by platelets. This mechanism of resistance to aspirin has been associated with a prothrombotic effect of erythrocytes on platelet reactivity.3 Also, experimentally increased shear stress has been seen to overcome the effect of intravenous aspirin.4 Finally, increased platelet activation is also produced by thrombin generation and cytokine production (interleukin 6 and 8) independently of thromboxane production.5 In patients with external ventricular assist device, all these conditions (increased shear stress, prolonged inflammatory reaction, prolonged cytokine production, thrombin generation) combine to induce a persistent platelet activation and resistance to the antiplatelet effect of aspirin. Although our observation was expected, we observed as many as 30% of patients with a persistent platelet response to arachidonic acid. However, a higher dose of aspirin restored the efficacy of aspirin regarding in vitro platelet aggregation.
Aspirin resistance in the prolonged postoperative course of patients implanted with external ventricular assist device is frequent and necessitates close monitoring. However, it will respond to increased oral intake of aspirin up to 500 mg/d.
References
This article has been cited by other articles:
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  D. Loisance Mechanical circulatory support systems--future opportunities Eur. J. Cardiothorac. Surg., December 1, 2004; 26(Suppl_1): S48 - S53. [Abstract] [Full Text] [PDF]
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