Aspirin resistance in patients with ventricular assist devices: A follow‐up study

Author:

Flieder Tobias1,Blaesen Sonja1,Schulte Katrin1,Blasberg Jost2,Lauenroth Volker3,Knabbe Cornelius1,Schramm René3,Morshuis Michiel3,Gummert Jan3,Birschmann Ingvild1ORCID

Affiliation:

1. Herz‐ und Diabeteszentrum Nordrhein‐Westfalen Universitätsklinik der Ruhr‐Universität Bochum, Institut für Laboratoriums‐ und Transfusionsmedizin Bad Oeynhausen Germany

2. Institut für Psychosoziale Medizin, Psychotherapie und Psychoonkologie Universitätsklinikum Jena, Friedrich‐Schiller‐Universität Jena Germany

3. Herz‐ und Diabeteszentrum Nordrhein‐Westfalen Universitätsklinik der Ruhr‐Universität Bochum, Klinik für Thorax‐ und Kardiovaskularchirurgie Bad Oeynhausen Germany

Abstract

AbstractBackgroundDespite combined anticoagulation therapy consisting of a vitamin K antagonist and an antiplatelet agent, thromboembolic complications often occur in patients with a left ventricular assist device (LVAD). In addition, bleeding events are also common. Resistance to antiplatelet drugs is a well‐known phenomenon; however, the utilization of laboratory chemistry testing for the presence of such resistance, and then switching therapy, is controversial.MethodsWe tested 132 patients with LVAD (HeartWare n = 57, HeartMate II n = 22, HeartMate 3 n = 53) on acetylsalicylic acid (ASA) therapy for resistance and followed them for a maximum of 7 years regarding pump thrombosis. Light transmission aggregometry (LTA) and impedance aggregometry (IPA) were performed for testing platelet function.ResultsWe could show that patients with ASA resistance displayed an increased risk of pump thrombosis, regardless of the test used (LTA: OR = 6.20, CI [1.86–20.64], p = 0.003; IPA: OR = 12.14, CI [3.00–49.07], p < 0.001). In patients with a HeartMate 3, we could not detect any pump thrombosis associated with aspirin resistance. Furthermore, there was no significant difference in bleeding events between patients with ASA resistance and ASA responders.ConclusionLaboratory testing of ASA resistance seems to be a good tool to detect an increased risk of pump thrombosis, at least for patients with a HeartWare or HeartMate II. The extent to which these thromboses can be prevented with a change of medication has to be investigated in further studies. No pump thrombosis was detected in patients with a HeartMate 3, and the question should be asked as to what constellation of underlying and concomitant diseases must be present to justify ASA therapy for these patients.

Publisher

Wiley

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