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Intraoperative heparin demonstrated low risk for recurrent HIT
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Patients with previous heparin-induced thrombocytopenia, or HIT, who were re-exposed to heparin demonstrated a low risk for recurrent HIT, yet the development of strong heparin-independent platelet-activating antibodies increased that risk, according to study results.
The analysis included 20 patients who had previous HIT. Of these patients, 17 received intraoperative heparin during cardiac/vascular surgery.
The mean time between heparin re-exposure and initial HIT was 4.4 years (range, 8 weeks to 13.5 years).
Recurrent HIT — demonstrated by seroconversion from a negative baseline to a strong-positive serotonin-release assay and enzyme immunoassay immunoglobulin G — occurred in one patient 7 days after surgery. The patient exhibited newly developed HIT antibodies with strong heparin-independent platelet-activating properties.
None of three patients who received postoperative unfractionated heparin or low–molecular-weight heparin developed seroconversion. However, most of the patients who received intraoperative heparin (n=11; 64%) exhibited an immune response against PF4-dependent antigens (P=.0737).
Nine of the 11 patients who exhibited an immune response demonstrated strong IgG anti-PF4/heparin seroconversions. Eight of these nine also developed positive serotonin-release assay.
The median time to detection of anti-PF4/heparin IgG was 7 days.
“Patients with a history of HIT could have an inherently greater capacity to form platelet-activating HIT antibodies compared with cardiac/vascular surgery patients who do not have a history of previous HIT,” the researchers wrote. “Nevertheless, since it takes at least 5 days post-surgery to form platelet-activating antibodies, and since further heparin use can be avoided during the post-surgical period, it would appear that the frequency of recurrent HIT will likely be low. We believe that our findings therefore support consensus conference recommendations for intraoperative heparin use in patients with a previous history of HIT (provided that platelet-activating antibodies are no longer detectable), and to use an alternative (non-heparin) anticoagulant for postoperative anticoagulation.”
Disclosure: The researchers report lecture honoraria/research funding from and consultant roles with GlaxoSmithKline, Immucor GTI Diagnostics, Instrumentation Laboratories, Paringenix, Pfizer Canada and W.L. Gore.
Perspective
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Harry S. Jacob, MD, FRCPath(Hon)
This is a most welcome confirmation of what many of us have suspected, and it does much to alleviate the fear of reheparinization in patients requiring cardiac-pump surgery. Note that it is the ratio of heparin to PF4, not the level of either alone, that is critical in creating the catastrophic, platelet-activating antigen/antibody complex in HIT. But the circulating level of PF4, usually enormous from platelet damage in the extracorporeal circuit, is unpredictable and uncontrollable. Therefore, the suggestion that heparin can be safely used in cardiac pump patients — those who do not exhibit preoperative elevated ELISA or serotonin-release activities — and that heparin in any form not be used in the postoperative period seems to be a rational guideline. The substitution of prostanoids or bivalirudin for the procedure will probably be rarely necessary in the future.
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