Activation of coagulation and fibrinolytic pathways in patients with left ventricular assist devices Talia Spanier, MDa, Mehmet Oz, MDa, Howard Levin,

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Activation of coagulation and fibrinolytic pathways in patients with left ventricular assist devices Talia Spanier, MDa, Mehmet Oz, MDa, Howard Levin, MDb, Alan Weinberg, MSc, Kathy Stamatis, MSc, David Stern, MDa,d, Eric Rose, MDa, Ann Marie Schmidt, MDa,b The Journal of Thoracic and Cardiovascular Surgery Volume 112, Issue 4, Pages 1090-1097 (October 1996) DOI: 10.1016/S0022-5223(96)70111-3 Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 1 Assessment of routine coagulation parameters in patients with LVADs and patients with end-stage heart failure (ESHF). Plasma was obtained by peripheral venipuncture from the patients with LVADs or end-stage heart failure as described in the text. Parameter (normal control) values were obtained from the clinical coagulation laboratory of Columbia Presbyterian Medical Center. Mean values ± standard deviation for prothrombin time, activated partial thromboplastin time, and levels of platelets and fibrinogen are depicted within the bar graphs. No significant differences were noted except that patients with end-stage heart failure had higher levels of fibrinogen than patients with LVADs and normal control subjects (p < 0.02). The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1090-1097DOI: (10.1016/S0022-5223(96)70111-3) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 1 Assessment of routine coagulation parameters in patients with LVADs and patients with end-stage heart failure (ESHF). Plasma was obtained by peripheral venipuncture from the patients with LVADs or end-stage heart failure as described in the text. Parameter (normal control) values were obtained from the clinical coagulation laboratory of Columbia Presbyterian Medical Center. Mean values ± standard deviation for prothrombin time, activated partial thromboplastin time, and levels of platelets and fibrinogen are depicted within the bar graphs. No significant differences were noted except that patients with end-stage heart failure had higher levels of fibrinogen than patients with LVADs and normal control subjects (p < 0.02). The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1090-1097DOI: (10.1016/S0022-5223(96)70111-3) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 1 Assessment of routine coagulation parameters in patients with LVADs and patients with end-stage heart failure (ESHF). Plasma was obtained by peripheral venipuncture from the patients with LVADs or end-stage heart failure as described in the text. Parameter (normal control) values were obtained from the clinical coagulation laboratory of Columbia Presbyterian Medical Center. Mean values ± standard deviation for prothrombin time, activated partial thromboplastin time, and levels of platelets and fibrinogen are depicted within the bar graphs. No significant differences were noted except that patients with end-stage heart failure had higher levels of fibrinogen than patients with LVADs and normal control subjects (p < 0.02). The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1090-1097DOI: (10.1016/S0022-5223(96)70111-3) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 1 Assessment of routine coagulation parameters in patients with LVADs and patients with end-stage heart failure (ESHF). Plasma was obtained by peripheral venipuncture from the patients with LVADs or end-stage heart failure as described in the text. Parameter (normal control) values were obtained from the clinical coagulation laboratory of Columbia Presbyterian Medical Center. Mean values ± standard deviation for prothrombin time, activated partial thromboplastin time, and levels of platelets and fibrinogen are depicted within the bar graphs. No significant differences were noted except that patients with end-stage heart failure had higher levels of fibrinogen than patients with LVADs and normal control subjects (p < 0.02). The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1090-1097DOI: (10.1016/S0022-5223(96)70111-3) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 2 Assessment of thrombin generation in patients with LVADs and in patients with end-stage heart failure (ESHF). Peripheral blood was obtained as described in the text and plasma was assayed as described for F1+2 and TAT. Mean values ± standard deviation are shown within the bar graphs. Levels of F1+2 and TAT were significantly higher in patients with LVADs than in patients with end-stage heart failure and than the normal control values (p < 0.002 and p < 0.0001, respectively). The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1090-1097DOI: (10.1016/S0022-5223(96)70111-3) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 3 Assessment of activation of fibrinolysis in patients with LVADs and patients with end-stage heart failure (ESHF). Peripheral blood was obtained as described in the text and plasma was assayed as described for levels of D-dimers and FDPs. Mean values ± standard deviation are shown within the bar graphs. Levels of D-dimers were significantly higher in patients with LVADs than in patients with end-stage heart failure and than the normal control values (p < 0.002 and p < 0.002, respectively). Levels of FDPs were significantly higher in patients with LVADs than in patients with end-stage heart failure and than the normal control values (p < 0.0001 and p < 0.0001, respectively). The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1090-1097DOI: (10.1016/S0022-5223(96)70111-3) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 4 Elevation of soluble thrombomodulin in patients with LVADs: a possible marker of endothelial perturbation. Peripheral blood was obtained as described in the text and plasma was assayed as described for levels of soluble thrombomodulin. Mean values of soluble thrombomodulin ± standard deviation are shown within the bar graphs. Levels of soluble thrombomodulin were significantly higher in patients with LVADs than the normal control values (p < 0.002). There was no significant difference in levels of soluble thrombomodulin in patients with LVADs and patients with end-stage heart failure sustained without anticoagulation. The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1090-1097DOI: (10.1016/S0022-5223(96)70111-3) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 5 Soluble thrombomodulin. We postulate that soluble thrombomodulin, likely derived from the integral membrane protein constitutively expressed by the endothelium, is shed and/or proteolyzed as a result of endothelial perturbation caused by the presence of the LVAD. Such inciting causes as the presence of microemboli in a procoagulant milieu, altered flow characteristics with cellular activation, and/or other vascular factors associated with the LVAD itself are likely contributory factors. The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1090-1097DOI: (10.1016/S0022-5223(96)70111-3) Copyright © 1996 Mosby, Inc. Terms and Conditions

Fig. 6 Coagulation cascade/fibrinolysis. As demonstrated by our studies, evidence exists for significant thrombin generation (as reflected by increased levels of TAT and F1+2) and fibrinolysis (increased levels of D-dimers and FDPs) in patients with LVADs compared with values for the normal control population and values for patients with end-stage heart failure not supported by LVAD or anticoagulant therapy. The mechanism(s) underlying the generation of a procoagulant state are not yet clear. For example, it is not known whether activation of the intrinsic and/or extrinsic pathways of coagulation underlie these findings. Closed arrows are indicative of the procoagulant pathway resulting in the formation of a fibrin clot. Open arrows follow the fibrinolytic pathway. Dotted arrows and open font signify the markers of these pathways reported in this study. The Journal of Thoracic and Cardiovascular Surgery 1996 112, 1090-1097DOI: (10.1016/S0022-5223(96)70111-3) Copyright © 1996 Mosby, Inc. Terms and Conditions