Prospective, observational study of antiplatelet and coagulation biomarkers as predictors of thromboembolic events after implantation of ventricular assist devices.
BACKGROUND
Long-term success in ventricular assist device (VAD) recipients is limited by thromboembolic events, the prediction of which remains elusive. We evaluated the predictive value of aspirin hyporesponsiveness and markers of coagulation and fibrinolysis.


METHODS
We prospectively enrolled patients scheduled to undergo VAD implantation between June 2004 and March 2006. Once before surgery, daily during hospitalization, and weekly after discharge we assessed platelet function, measured prothrombin activation fragment 1.2 (F1.2) and plasminogen activator inhibitor-1 (PAI-1) concentrations, and evaluated aspirin hyporesponsiveness by whole-blood aggregometry and thromboelastography. All patients received 325 mg oral aspirin daily from at least 7 days before VAD implantation. Follow-up continued until heart transplantation, death or closure of the database.


RESULTS
We included 26 patients (median follow-up 315 days, range 9-833 days). In eight (31%) patients, 14 thromboembolic events occurred at a median of 42 (interquartile range 26-131) days. Only six (43%) events based on whole-blood aggregometry and one (7%) based on thromboelastography coincided with aspirin hyporesponsiveness. Within-patient variability was high for both tests (59% and 567%, respectively). Compared with levels before surgery, PAI-1 concentrations were raised for up to 45 days (P <0.0001) and those of F1.2 for up to 3 days (P = 0.0001) after VAD implantation. PAI-1 and F1.2 levels did not rise significantly further before thromboembolic events.


CONCLUSIONS
Aspirin hyporesponsiveness was not associated with raised risk of future clinical thromboembolic events after VAD implantation. Impaired fibrinolysis, demonstrated by raised PAI-1 concentrations, might, however, indicate a predisposition to such events early after surgery.
Majeed
Farhan
F
Division of Cardiology, University of Maryland School of Medicine, Baltimore, MD, USA.
Kop
Willem J
WJ
Poston
Robert S
RS
Kallam
Seeta
S
Mehra
Mandeep R
MR
D000328:Adult; D000368:Aged; D001241:Aspirin / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000187:drug effects*; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D004351:Drug Resistance; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects; D006333:Heart Failure / Q000628:therapy*; D006353:Heart-Assist Devices / Q000009:adverse effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D010979:Platelet Function Tests; D011237:Predictive Value of Tests; D011446:Prospective Studies; D011516:Prothrombin / Q000378:metabolism; D018570:Risk Assessment; D013916:Thrombelastography; D013923:Thromboembolism / Q000097:blood / Q000209:etiology* / Q000517:prevention & control; D013997:Time Factors
D015415:Biomarkers; D010446:Peptide Fragments; D017395:Plasminogen Activator Inhibitor 1; D010975:Platelet Aggregation Inhibitors; C051321:SERPINE1 protein, human; C045879:prothrombin fragment 1.2; D011516:Prothrombin; D001241:Aspirin