Identifying patients at high risk of heparin-induced thrombocytopenia-associated thrombosis with a platelet activation assay using flow cytometry.

To diagnose heparin-induced thrombocytopenia (HIT), detection of platelet-activating antibodies (HIT antibodies) is crucial. However, serum platelet activation profiles vary across patients and depend on test conditions. We evaluated the association between clinical outcomes and platelet-activating profiles assessed by a platelet microparticle assay (PMA), which detects activation of washed platelets induced by HIT antibodies, in 401 consecutive patients clinically suspected of having HIT. We made modifications to the assay, such as donor selection for washed platelets that increased sensitivity. Serum that activated platelets at a therapeutic (but not high) heparin concentration was defined as positive. Of these, serum that activated platelets within 30 minutes or in the absence of heparin was defined as strongly positive. The remaining samples were considered weakly positive. As a result, 97 % and 93 % of patients who tested strongly and weakly positive had clinical profiles consistent with HIT, respectively. The incidence of thromboembolic events (TEEs) after heparin exposure in patients who tested strongly positive, weakly positive, and negative was 61 %, 40 %, and 29 %, respectively. Among patients who did not experience a TEE on the day HIT was suspected, there was no significant difference in the cumulative incidence of subsequent TEEs between patients who tested strongly and weakly positive when argatroban was initiated on the same day (19.0 % vs 7.1 %, p=0.313), but there was a significant difference when argatroban therapy was delayed by one or more days (61.1 % vs 17.6 %, p=0.007). The modified PMA is effective in diagnosing HIT and identifying patients at high risk for HIT-associated TEEs.

Cardiac Resynchronization Therapy-Induced Cardiac Index Increase Measured by Three-Dimensional Echocardiography Can Predict Decreases in Brain Natriuretic Peptide.

OBJECTIVES: First, to examine the perioperative association between increased cardiac index (CI) measured using three-dimensional echocardiography (CI3D), two-dimensional echocardiography (CI2D), and FloTrac/Vigileo (CIFT) (Edwards Lifesciences, Irvine, CA) after cardiac resynchronization therapy (CRT) and decreased brain natriuretic peptide (BNP) 6 months after CRT. Second, to evaluate the accuracy and tracking ability of CI2D and CIFT. DESIGN: A prospective clinical study. SETTING: A cardiac surgery operating room in a single cardiovascular center. PARTICIPANTS: Forty-five patients undergoing elective CRT lead implantation. INTERVENTIONS: CIFT and CI2D were determined simultaneously before and after CRT using CI3D as the reference method. MEASUREMENTS AND MAIN RESULTS: BNP was measured before CRT and 6 months after CRT. Areas under the receiver operator characteristic curves (AUCs) were calculated for each method of measurement to predict BNP decrease. AUC was largest for CI3D (AUC = 0.735, p = 0.017). Bland-Altman analysis revealed that the percentage error was 58% for CIFT and 28% for CI2D. A polar plot analysis showed that the mean angular bias was -7.26° and 0.64°, the radial limits of agreement were 70° and 29.4°, and the concordance rate was 67.7% and 93.8% for CIFT and CI2D, respectively. CONCLUSIONS: CI significantly increased after CRT in patients whose BNP level decreased 6 months after CRT. However, only CI3D could predict decreases in BNP 6 months after CRT. Although CI2D was acceptable compared with CI3D, the tracking ability of CI changes was just below acceptable. CIFT has a wide limit of agreement with CI3D, with a poor tracking ability.

[A case of Rh incompatible transfusion after use of anti-D immunoglobulin for unexpected intraoperative massive hemorrhage].

A 69-year-old woman with Rh-negative blood type was scheduled for total pelvic exenteration. Despite having prepared suspected amount of blood, we were forced to transfuse Rh-positive blood after use of anti-D immunoglobulin (0.25 mg) for unexpected massive hemorrhage. Although some strategies (blood-withdrawal system, vascular embolization, discontinuation of operation, et al.) for reduction of incompatible transfusion were considered, we fortunately could acquire additional matched blood after transfusion of Rh-positive blood (4 units), and the operation was completed. On postoperative days 1-2, we administered anti-D immunoglobulin (each 0.25 mg) prophylactically. It is reported that 0.02 mg immunoglobulin prevents sensitization against 1 ml transfused red cells. In this case, total dose of immunoglobulin was not enough, but antiD antibody was not detected over 6 months nonetheless. Two reasons were speculated for lack of anti-D anti body; this patient was immune-suppressed for chemoradiation against rectal cancer, and remaining Rh-positive red cells in her body were of small amount because of massive hemorrhage. Anyway, anti-D globulin administration with the aim of complete neutralization against incompatible transfusion is considered impossible, as there are few Rh-negative people in Japan. It is necessary to prepare sufficient matched blood for major surgery of Rh-negative patients, and to consider above-described strategies. Unavoidable Rh incompatible transfusion needs long-term (about 6 months) follow-up based on erythrocyte life-span and time of antibody production.