Back to 85th Annual Meeting
Back to Program Outline

11. Heparin-induced Thrombocytopenia Type II is Frequent and Leads to Serious Complications in Patients on Mechanical Circulatory Support
Soren Schenk, Latif Arusoglu, Kazutomo Minami, Michiel Morshuis, Peter Sarnowsksi, Reiner Koerfer, Aly El- Banayosy; Bad Oeynhausen, Germany

Objective: Heparin-induced thrombocytopenia type II (HIT II), an antibody-mediated platelet activation, can have disastrous consequences for patients on mechanical circulatory support (MCS), but reports on this therapeutic challenge are limited. We analyzed coagulation systems and outcome.
Methods: Between January and August 2004, 40 patients were placed on MCS using various devices and heparin post-implant. Platelet count [ptl; 100,000/ml], partial thromboplastin time [PTT; sec], international normalized ratio [INR], and thromboelastography (TEG) were monitored. HIT II+ was defined by the presence of PF4 antibodies and a drop of ptl below 100.
Results: HIT II was confirmed in 8 (20%) patients after a mean of 7.5 days post-implant. There was an early drop in platelet counts that did not differ between HIT II- and HIT II+ patients [from ptl of 154 ± 67 pre-implant to 95 ± 54 on day 3 post-implant (HIT II-) vs 133 ± 59 to 76 ± 75 (HIT II+); P NS]. Similarly, no differences were observed until day 6 post-implant for PTT [PTT of 46 ± 8 (HIT II-) vs 43 ± 9 (HIT II+); P NS] and INR (INR of 1.4 ± 0.6 vs 1.6 ± 0.7; P NS). TEG thrombus formation time [K; min] and thrombus maximal elastance [ME] also did not differ on day 3 post-implant. However, patients diagnosed as HIT II+ were in a much more procoagulant state by day 6, showing more rapid thrombus formation [K of 6.7 ± 10.4 (HIT II-) vs 3.6 ± 2.6 (HIT II+); P = .06] and more solid blood clots, resistant to thrombolysis [ME of 105 ± 109 (HIT II-) vs 239 ± 192 (HIT II+); P < .05]. Once diagnosed as HIT II+, patients were treated with r-hirudin, alprostadil, or dextran, yet these agents did not allow for safe, effective anticoagulation in most cases. There were 5 major thromboembolic events in HIT II+ patients, directly causing the death of 3 patients, and seriously complicating the hospital course in 2 patients. Only 3 (38%) patients had no thromboembolic events; they are alive on MCS awaiting transplant.
Conclusions: This is the largest series on HIT II in patients on MCS, and it is the first to document their high prevalence and inferior outcome. The data additionally suggest that sophisticated coagulation analyses, such as TEG, should complement standard monitoring to reveal the procoagulant state during the development of HIT II. Because one out of five patients was affected, and a positive diagnosis was associated with serious complications, we recommend testing for HIT II systematically in patients on MCS.

Back to 85th Annual Meeting
Back to Program Outline