Protein C Pathway, Inflammation, and Pump Thrombosis in Patients With Left Ventricular Assist Devices.

Use of left ventricular assist devices (LVADs) for management of advanced heart failure is becoming increasingly common; however, device associated thrombosis remains an important cause of mortality in this patient population. We hypothesize that inflammation in LVAD implanted patients dysregulates the protein C pathway, creating a hypercoagulable state leading to thrombosis. Plasma samples from 22 patients implanted with the Thoratec HeartMate II LVAD were analyzed by commercial ELISAs.

Profiling Heparin-Induced Thrombocytopenia (HIT) Antibodies in Hospitalized Patients With and Without Diabetes.

Heparin (H) anticoagulation in populations characterized by elevated platelet factor 4 (PF4) frequently elicits PF4/H antibodies, presenting a risk of heparin-induced thrombocytopenia. Recent studies have shown that anti-PF4/H enzyme-linked immunosorbent assays (ELISAs) detect antibodies in individuals never exposed to heparin. Platelet factor 4/H cross-reactive antibodies may result from PF4-mediated defense responses to injury or infection.

Identification of Novel Hemostatic Biomarkers of Adverse Clinical Events in Patients Implanted With a Continuous-Flow Left Ventricular Assist Device.

Heart failure affects over 5 million people in the United States. Its rising prevalence and the limited supply of donor hearts is increasing the use of mechanical cardiac support with the implantation of continuous-flow ventricular assist devices (CF-VAD). Patients with CF-VAD implants are at risk of complications, specifically adverse hemostatic events such as nonsurgical bleeding and thrombosis.

Apixaban as an alternate oral anticoagulant for the management of patients with heparin-induced thrombocytopenia.

Due to the pronounced hypercoagulable state in heparin-induced thrombocytopenia (HIT), alternatives to heparin that do not interact with HIT antibodies are needed for anticoagulation management. This study was designed to determine whether the oral factor Xa inhibitor apixaban could be used. Functional platelet activation with apixaban in the presence of HIT antibodies was evaluated by the (14)C-serotonin release assay (SRA; washed platelets) and the heparin-induced platelet aggregation assay (PA-HIT; platelet-rich plasma).

Left ventricular assist device-induced coagulation and platelet activation and effect of the current anticoagulant therapy regimen.

Left ventricular assist devices (LVADs) are mechanical pumps that enhance cardiac function in patients with heart failure. In all, 7 patients with an LVADs (1.8 international normalized ratio warfarin, 81 mg aspirin) were evaluated monthly for 3 months for platelet and coagulation activation (controls: 5 healthy adults and 5 patients having warfarin).

Comparative studies on branded enoxaparin and a US generic version of enoxaparin.

Enoxaparin, a complex, biologically derived low-molecular-weight heparin, is approved for a range of clinical indications. This study was carried out to compare the potency profile and pharmacodynamic responses of branded enoxaparin (Lovenox; Sanofi, US) with a generic enoxaparin (enoxaparin sodium injection, USP). Five batches of each product were tested.

Murine monoclonal antibody to platelet factor 4/heparin complexes as a potential reference standard for platelet activation assays in heparin-induced thrombocytopenia.

Quality control of the platelet activation assays to diagnose heparin-induced thrombocytopenia (HIT), (14)C-serotonin release assay (SRA) and platelet aggregation test (PAT) has yet to be established due to lack of reference standards and the difficulty of obtaining significant amounts of HIT antibodies from patients with HIT. We prepared a murine monoclonal antibody to human platelet factor 4 (hPF4)/heparin complexes (HIT-MoAb) and investigated the platelet activating action of HIT-MoAb by using SRA and PAT. The HIT-MoAb activated human platelets at low heparin concentration and the platelet activations were inhibited at high heparin concentration in both SRA and PAT.

A colorimetric, metabolic dye reduction assay detects highly activated platelets: application in the diagnosis of heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is caused by antibodies, elicited in response to heparin anticoagulant therapy, which can cause extreme platelet activation and result in a highly procoagulant state. Most diagnostic tests for HIT antibodies measure in vitro platelet activation by detecting aggregation or granule release responses. This study demonstrates that the high level of activation by HIT antibodies leads to a rapid breakdown of platelet metabolic activity.