Heparin-associated Antiplatelet Antibodies Research Articles

Heparin-Induced Thrombocytopenia Following Cardiac Surgery is Associated With Poor Outcome

The outcome of cardiac surgical patients with clinically diagnosed heparin-induced thrombocytopenia (HIT) was studied. Retrospective, observational study. University hospital. All cardiac surgical patients with diagnosed HIT after cardiac surgery between January 2002 and December 2004, and concurrently, consecutive patients without HIT. None Measurements and Main Results: 3465 patients were treated postoperatively in the cardiac surgical intensive care unit during the study period. Clinical suspicion of HIT arose when platelet count markedly fell several days after surgery and HIT was proven by a positive enzyme immunoassay in 20 patients. Thrombocytopenia (35.5 [22] x 10(9)/L, median [interquartile range]) developed within 7 (6) days. HIT patients received significantly more platelet transfusions perioperatively than controls (p < 0.001). Thromboembolic complications occurred in 70% of HIT patients, but in none of non-HIT patients (14/20 v 0/20, p = 0.001). Intensive care unit stay was longer in HIT patients than in controls (16.5 [11.0] v 1.0 [3.0] days, p < 0.001). Nine HIT patients died (45%), while all control patients survived. Mortality was related to thrombotic complications in seven HIT patients (35%). The incidence of HIT in association with low-molecular-weight heparin use after cardiac surgery was low. HIT was associated with perioperative platelet transfusions and carried a remarkably high risk of thromboembolic complications and death. In order to reduce morbidity and mortality, early recognition of heparin-associated antiplatelet antibodies and alternative anticoagulation strategies need to be implemented.

Heparin-Associated Antiplatelet Antibodies Increase Morbidity and Mortality in Hemodialysis Patients

Heparin-Associated Antiplatelet Antibodies Increase Morbidity and Mortality in Hemodialysis Patients

Heparin-associated antiplatelet antibodies increase morbidity and mortality in hemodialysis patients

Patients are frequently exposed to heparin during hemodialysis (HD) to prevent thrombosis of the extracorporeal circuit. Other groups with frequent heparin exposures have a high rate of development of heparin-associated antiplatelet antibodies (HAAb). We sought to define the prevalence of HAAb in HD patients and evaluate their effects. A chart listing of all patients undergoing HD at our tertiary care institution during a six-year period was obtained. Charts of patients who tested positive for HAAb were reviewed. A cohort of randomly selected HD patients who tested negative for HAAb was analyzed as a control group. In our sample, 3.7% of HD patients were positive for HAAb. Morbidity, as defined by thromboembolic (TEC) or hemorrhagic complications, was higher in the HAAb-positive group compared with the control patients (60% vs 8.7%, P < .05), and the mortality rate (mortality directly related to TECs) was also higher in the HAAb-positive patients (28.6% vs 4.35%, P < .05). Contrary to reports of HAAb in patients undergoing HD without increased morbidity and mortality, we found significant increases in both morbidity and mortality. The elevated morbidity and mortality may represent ongoing endothelial and platelet activation from repeated heparin exposures. Reduced morbidity and mortality will likely require early recognition of HAAb and alteration of anticoagulation in HD patients.

Heparin-induced thrombocytopenia: twenty-nine years later.

To determine the current frequency, types of patients, indications for testing, morbidity and mortality, and management of heparin-induced thrombocytopenia (HIT). Between December 1998 and July 2001, the charts of 102 inpatients that tested positive for heparin-associated antiplatelet antibodies (HAAb) were reviewed. There were 33,941 inpatients, 10,348 of them having received unfractionated or low molecular weight heparins. HAAb were determined by platelet aggregometry. There were 58 males and 44 females with a mean age of 56 years. The majority (72%) of patients were admitted to a surgical service (23% were admitted to medicine, and 5% were admitted to obstetrics/pediatrics). Indications for testing included one or more low platelet counts (n = 51), unexplained arterial (n = 33) or venous (n = 6) thromboses, resistance to anticoagulation (n = 1), prior history of HAAb (n = 3), organ transplant (n = 17), or other indication (n = 4). The HAAb "patterns" were variable, with patients having antibodies only to bovine (n = 7) or porcine heparin (n = 5), bovine and porcine heparins (n = 17), enoxaparin (n = 3), fragmin (n = 7), or all 4 heparins (n = 43). The HIT-related mortality was 6.9%, and the morbidity was 30% with 19 arterial and 7 venous thromboses and 5 bleeding events. Management consisted of discontinuation of heparin in 95 patients. Twenty-five patients did not require continued anticoagulation. When needed, anticoagulation was continued with a direct thrombin inhibitor (n = 32), enoxaparin (n = 16), warfarin (n = 15), or aspirin (n = 7). Seven patients continued to receive unfractionated heparin (n = 4) or low molecular weight heparin (n = 3). HIT occurs in 0.99% of inpatients receiving heparin and remains an important nondiscriminatory contributor to their morbidity and mortality. Patients receiving any form of heparin who develop a decreasing platelet count, unexplained thrombosis, or resistance to heparin anticoagulation should be tested for HAAb. If HAAb are detected, patients must not receive the sensitizing heparin(s).

Lepirudin is a safe and effective anticoagulant for patients with heparin-associated antiplatelet antibodies

Objective: The purpose of this study was to determine whether lepirudin, a direct thrombin inhibitor, is a safe and effective anticoagulant for patients with heparin-associated antiplatelet antibodies (HAAbs). Methods: The charts of HAAb-positive patients who received lepirudin were reviewed. Lepirudin use was analyzed for indication, duration, and effectiveness of anticoagulation, and for adverse events. HAAb presence was determined by platelet aggregation. Results: Eighteen HAAb-positive patients received lepirudin: 9 had previous documentation of HAAb, 6 had thrombocytopenia while receiving heparin; and 3 had HAAb after a thrombotic event. The indications for lepirudin anticoagulation included thromboembolism prophylaxis (5), arterial thromboses (5), pulmonary embolus (3) or deep venous thrombosis (1), and one each for atrial fibrillation, myocardial infarction, artificial heart valves, and hemodialysis access. The average duration of therapy was 4.04 days. Fifteen patients achieved adequate anticoagulation (activated partial thromboplastin time [aPTT] ratio > 2.0) with lepirudin. Seven patients had aPTTs that were sometimes supratherapeutic (aPTT > 100 seconds) but did not bleed. In all patients who had heparin-induced thrombocytopenia, platelet counts were normalized while they received lepirudin. There were two complications: one patient fell and had a calf hematoma (aPTT ratio 3.24), and one patient who received lepirudin during nine separate hospitalizations had epistaxis (aPTT ratio 2.86) during her ninth hospitalization. Another patient received lepirudin during two hospitalizations without an adverse event. Conclusion: Lepirudin is a safe and effective anticoagulant for patients with HAAbs. The platelet counts of all patients with heparin-induced thrombocytopenia were normalized while they received lepirudin. Careful monitoring of the aPTT and avoidance of trauma while patients are receiving lepirudin are recommended. (J Vasc Surg 2001;34:17-20.)

The role of heparin-associated antiplatelet antibodies in the outcome of arterial reconstruction

Purpose: This study was designed to determine the incidence rate of heparin-associated antiplatelet antibodies (HAAb) in patients who require major vascular reconstruction and to determine whether the HAAb were associated with perioperative thrombotic events. Methods: One hundred six patients who underwent elective arterial reconstruction for cerebrovascular occlusive disease (n = 48), aortoiliac occlusive disease (n = 13), aortoiliac aneurysm (n = 17), mesenteric arterial occlusive disease (n = 1), or infrainguinal arterial occlusive disease (n = 28) prospectively underwent evaluation from July 1, 1996, to June 30, 1997. Heparin-associated antibody tests (with a two-point platelet aggregation assay) and platelet counts (via Coulter counter) were performed before surgery and on or after the 4th day after vascular reconstruction. Arterial reconstruction thromboses were established by means of duplex ultrasound scanning or angiography. Acute myocardial infarction (AMI) and venous thromboses were diagnosed with clinical criteria and duplex ultrasound scanning, respectively. A significant decrease in platelet count was defined as a platelet count of less than 100,000/mm 3 or as a more than 30% drop in the platelet count. Results: Twenty-two patients (21%) had at least one positive HAAb assay: one assay was positive before surgery only (after angiography), six were positive both before and after surgery, and 15 were positive after surgery only. There were three perioperative deaths—one in the HAAb-positive group and two in the HAAb-negative group. Ten thrombotic events occurred in the perioperative period. Four thrombotic events (three operative site thromboses and one AMI) occurred in the HAAb-positive group (18.2%). All of these patients were undergoing heparin therapy. Of the six patients (with three operative site thromboses, two deep venous thromboses, and one AMI) in the HAAb-negative group (7%; P = .21), three were undergoing heparin therapy. No patient who was HAAb positive with a thrombotic event had thrombocytopenia or a significant decrease in platelet count. Conclusion: The frequent exposure to heparin by patients with peripheral vascular disease is associated with a high incidence rate (21%) of HAAb formation, which makes it one of the more common hypercoagulable conditions in these patients. The patients who were HAAb positive had a 2.6-fold increase in perioperative thrombotic events. Thrombocytopenia or decreasing platelet counts were not reliable clinical markers for identifying patients who were HAAb positive. It is suggested that all patients who have undergone heparin therapy and who have an unexplained perioperative thrombotic event develop should undergo testing for HAAb. (J Vasc Surg 1999;29:779-86.)

Heparin-bonded grafts induce platelet aggregation in the presence of heparin-associated antiplatelet antibodies

Purpose: Thromboresistant synthetic grafts should decrease the frequency of graft thromboses and could be useful in bypasses to small arteries and to arteries with compromised flow. Heparin-bonded grafts (HBG) have been developed. Studies were done to determine whether the heparin bond is permanent and whether the HBG would aggregate platelets in the presence of heparin-associated antiplatelet antibodies (HAAbs). Methods: We studied an 8 mm HBG from company A (HBGA) and 8 mm and 6 mm HBGs from company B (HBGB-8 and HBGB-6), none of which is available for clinical use in the United States. Five 1 cm long segments of HBGA, HBGB-8, and HBGB-6 were incubated for 24 hours in 5 ml of plasma, 10 ml of saline, or 10 ml of Ringer's lactate. After incubation, 1 ml was obtained from each solution and assayed for heparin. Segments of each graft that leached off an equivalent of 1 U of heparin/ml (i.e., 1 mm 2 of HBGA, 5 mm 2 of HBGB-8, and 20 mm 2 of HBGB-6) were incubated with 0.15 ml of plasma with HAAbs (six samples per graft) for 30 minutes at 25° C. The grafts were removed, and 0.1 ml of normal-donor, platelet-rich plasma was added. The samples were placed in an aggregometer and allowed to react until positive aggregation occurred or 27 minutes had elapsed. Segments of non–heparin-bonded polyester grafts served as controls. Results: Heparin leached off all grafts in plasma (mean values: HBGA, 83.4 U of heparin/ml; HBGB-8, 4 U of heparin/ml; HBGB-6, 6.2 U of heparin/ml). In normal saline, the mean heparin concentrations were lower (HBGA, 10.8 U of heparin/ml; HBGB-8, 0 U of heparin/ml; HBGB-6, 0.01 U of heparin/ml. The mean heparin concentration after incubation in Ringer's lactate were 10 U of heparin/ml for HBGA, 0 U of heparin/ml HBGB-8, and 0.22 U of heparin/ml HBGB-6. All of the HBGs induced platelet aggregation inHAAb-positive plasma. None of the control grafts induced platelet aggregation in HAAb-positive plasma. Conclusions: All HBGs leeched heparin into plasma, and all induced platelet aggregation in the presence of HAAbs. The possibility of sensitizing patients to heparin leeching from a HBG with the activation of platelets and secondary thrombosis strongly suggests that HBG be used with great caution. Other methods for inducing graft thromboresistance should be developed.(J Vasc Surg 1998;27:896-901.)

Reduced morbidity and mortality rates of the heparin-induced thrombocytopenia syndrome

Purpose: We reported a 61% morbidity rate and a 23% mortality rate for the heparin-induced thrombocytopenia (HIT) syndrome in 1983. We subsequently reported in 1987 that with early recognition, immediate cessation of the administration of heparin, and platelet function inhibition, the morbidity rate could be reduced to 23% and the mortality rate to 12%. One hundred recent cases of patients with heparin-associated antiplatelet antibodies (HAAb) have been reviewed to determine whether aggressive screening, early diagnosis, and alternate management could further reduce morbidity and mortality rates. Methods: The consecutive records of 100 patients with positive platelet aggregation tests were reviewed. Sixty-six patients were male. The patients' ages ranged from 23 days to 92 years. The patients were from vascular (28), cardiothoracic (42), and other (30) services. HIT was suspected in patients who received heparin and had falling platelet counts, platelet counts less than 100,000/mm 3, or new thromboembolic or hemorrhagic events. Results: Heparin was not offered to six patients with known HAAb. Twelve patients were successfully treated with antiplatelet therapy and limited reexposure to heparin, and 75 patients were successfully treated with early diagnosis and prompt cessation of heparin. Alternate forms of anticoagulation therapy were used selectively. Seven patients had 11 complications. Three of the seven patients were treated successfully with warfarin anticoagulation and aspirin (2) or with aspirin alone (1). A fourth patient was treated with thrombectomy, hematoma evacuation, and aspirin. A fifth patient underwent thrombolysis and coronary angioplasty in addition to receiving warfarin and aspirin. The sixth patient required two thrombectomies and warfarin. A seventh patient required two thrombectomies and aspirin. HIT was responsible for one of 17 deaths. Conclusions: A 7.4% morbidity rate and a 1.1% mortality rate have been achieved in patients with HAAb by aggressive screening, early recognition of HIT, and prompt cessation of the administration of heparin. Platelet function inhibitors and other anticoagulants, including nonreacting low molecular weight heparin, are important adjuncts in the management of the thromboembolic disorders associated with HIT. (J Vasc Surg 1998;27:309-16.)

Danaparoid. A review of its pharmacology and clinical use in the management of heparin-induced thrombocytopenia.

Danaparoid, a low molecular weight heparinoid consisting of a mixture of heparan, dermatan and chondroitin sulfates, has well established antithrombotic activity. The drug has a high antifactor Xa to antifactor IIa (thrombin) activity ratio, a low tendency to cause bleeding and minimal effects on the fibrinolytic system. Danaparoid has a low cross-reactivity rate with heparin-associated antiplatelet antibodies (0 to 20%; mean approximately 10%). This represents a significant advantage over low molecular weight heparins (LMWHs) as a potential replacement agent for unfractionated heparin (UFH) in patients with immune-mediated (type II) heparin-induced thrombocytopenia (HIT). In a worldwide compassionate-use programme involving a total of 667 patients with HIT to date, 93% of danaparoid treatment courses were considered to be successful. Thrombocytopenia resolved in 91% of episodes. In a multicentre randomised comparative trial of danaparoid and dextran in patients with HIT plus thrombosis (HITT), significantly more danaparoid than dextran recipients had resolution of thromboses, and an effective clinical response was achieved in significantly more danaparoid recipients. Results of a retrospective case-controlled study of danaparoid and ancrod in patients with HITT showed significantly fewer new or progressive thromboses with danaparoid. In the compassionate-use programme, danaparoid was associated with a mortality rate of 10.4% during treatment (up to 3.5 years) and 7.8% during the follow-up period (3 months). 14 of 114 deaths during the follow-up period were considered to be related to danaparoid therapy. A mortality rate of 23.5% was reported in patients accepted for but not treated with, danaparoid. Mortality rates with danaparoid, ancrod and dextran in the comparative studies were similar (7, 11 and 12%, respectively). Severe bleeding was reported in 3.1% of patients in the compassionate-use programme, persistent or recurrent thrombocytopenia in 2.6% and new thromboembolic events/extension of existing thrombosis in 1.7%. The incidence of bleeding was similar with danaparoid and dextran in a comparative trial. Although in vitro cross-reactivity does not always translate into clinical cross-reactivity, testing is currently recommended, when possible, before initiation of danaparoid therapy. Thus, danaparoid appears to be an effective and well tolerated replacement agent for UFH in many patients with HIT who require further anticoagulation. The drug has low cross-reactivity with HIT-associated antibodies. Further comparative trials are needed to confirm these promising findings.

Heparin-induced thrombocytopenia in the newborn

This pilot study was initiated to determine whether heparin-induced thrombocytopenia occurs in the newborn and whether thromboembolic complications in the newborn could be related to heparin-induced thrombocytopenia. Thirty-four infants in whom thrombocytopenia (< 70,000/mm3) (n = 23), precipitous (30% to 50%) fall in platelet count (n = 5), or thromboses (n = 6) developed while they were receiving heparin were studied. Heparin-associated antiplatelet antibodies were demonstrated in 14 infants by platelet aggregation testing. The average gestational age (29 ± 6 weeks); birth weight (1300 ± 945 gm); and platelet count at birth (234,000/mm3 ± 111,000/mm3) of these 14 infants did not differ statistically from the 20 infants without heparin-associated antiplatelet antibodies. An umbilical artery catheter was inserted in all infants except a single patient from each group. Aortic thrombosis was documented by abdominal ultrasonography in 11 of 13 (85%) infants with heparin-associated antiplatelet antibodies. One patient died with a midgut volvulus before the aorta could be examined. Five aortic thromboses were detected in the 20 infants without heparin-associated antiplatelet antibodies. Bleeding was not associated with the heparin-induced thrombocytopenia. One patient with previously demonstrated thrombocytopenia and heparin-associated antiplatelet antibodies had recurrent thrombocytopenia when reexposed to heparin; her platelet count recovered after heparin withdrawal. Thus heparin-induced thrombocytopenia does occur in preterm and term infants receiving heparin and is associated with arterial thromboses. Therefore infants receiving any form or amount of heparin must be carefully monitored for heparin-induced thrombocytopenia. In the absence of new or continued thrombohemorrhagic events, an infant receiving heparin should have platelet count determinations at a minimum of 2- to 3-day intervals. New or continued thromboembolism or a falling platelet count suggest the presence of heparin-induced thrombocytopenia, which should be confirmed by aggregation testing.

Heparin-induced thrombocytopenia in the newborn

This pilot study was initiated to determine whether heparin-induced thrombocytopenia occurs in the newborn and whether thromboembolic complications in the newborn could be related to heparin-induced thrombocytopenia. Thirty-four infants in whom thrombocytopenia (less than 70,000/mm3) (n = 23), precipitous (30% to 50%) fall in platelet count (n = 5), or thromboses (n = 6) developed while they were receiving heparin were studied. Heparin-associated antiplatelet antibodies were demonstrated in 14 infants by platelet aggregation testing. The average gestational age (29 +/- 6 weeks); birth weight (1300 +/- 945 gm); and platelet count at birth (234,000/mm3 +/- 111,000/mm3) of these 14 infants did not differ statistically from the 20 infants without heparin-associated antiplatelet antibodies. An umbilical artery catheter was inserted in all infants except a single patient from each group. Aortic thrombosis was documented by abdominal ultrasonography in 11 of 13 (85%) infants with heparin-associated antiplatelet antibodies. One patient died with a midgut volvulus before the aorta could be examined. Five aortic thromboses were detected in the 20 infants without heparin-associated antiplatelet antibodies. Bleeding was not associated with the heparin-induced thrombocytopenia. One patient with previously demonstrated thrombocytopenia and heparin-associated antiplatelet antibodies had recurrent thrombocytopenia when reexposed to heparin; her platelet count recovered after heparin withdrawal. Thus heparin-induced thrombocytopenia does occur in preterm and term infants receiving heparin and is associated with arterial thromboses. Therefore infants receiving any form or amount of heparin must be carefully monitored for heparin-induced thrombocytopenia.1+

Thrombocytopenia Associated With Heparin-Coated Catheters in Patients With Heparin-Associated Antiplatelet Antibodies

Thrombocytopenia was associated with the presence of heparin-coated pulmonary artery catheters in 12 patients with heparin-associated antiplatelet antibodies. The thrombocytopenia persisted so long as the heparin-coated catheters were in place, even when all other sources of heparin were discontinued. The high morbidity and mortality associated with heparin-induced thrombocytopenia mandates that heparin administration cease and that all heparin-coated catheters be removed from patients with heparin-associated antiplatelet antibodies.

Thrombocytopenia associated with heparin-coated catheters in patients with heparin-associated antiplatelet antibodies

Thrombocytopenia associated with heparin-coated catheters in patients with heparin-associated antiplatelet antibodies

Reexposure to heparin of patients with heparin-associated antibodies

Four patients with heparin-associated antiplatelet antibodies who were not receiving platelet function-inhibiting agents received heparin during surgery, angiography, or hemodialysis. Three of the four patients had complications that were attributed to heparin-induced platelet aggregation. The complications included a superficial femoral artery thrombosis, a thrombotic stroke after a carotid endarterectomy, and recurring thrombosis of a graft inserted for dialysis. Nine patients received aspirin (325 mg b.i.d.) or dipyridamole (Persantine) (200 to 300 mg daily) before reexposure to 5000 to 12,000 units of heparin during 11 vascular procedures. The procedures included two carotid endarterectomies, three aortofemoral bypasses, one femoropopliteal bypass, two femorotibial in situ saphenous vein bypasses, one iliofemoral thrombectomy, one bilateral iliac artery angioplasty, and one axillobifemoral bypass. Platelet counts averaged 173,000/mm3 before heparin reexposure, fell to an average of 86,000/mm3 within 24 hours of heparin reexposure, and returned to normal within 48 hours after the reexposure. None of these patients had a thromboembolic or hemorrhagic complication. Patients with heparin-associated antiplatelet antibodies are at risk for developing thrombocytopenia and thromboembolic complications on reexposure to heparin. The platelet function-inhibiting agents, aspirin and Persantine, protect the patients from the thromboembolic complications but not the thrombocytopenia associated with limited heparin reexposure.

Hidden 19S IgM rheumatoid factors

Purpose: This study was designed to determine the incidence rate of heparin-associated antiplatelet antibodies (HAAb) in patients who require major vascular reconstruction and to determine whether the HAAb were associated with perioperative thrombotic events. Methods: One hundred six patients who underwent elective arterial reconstruction for cerebrovascular occlusive disease (n = 48), aortoiliac occlusive disease (n = 13), aortoiliac aneurysm (n = 17), mesenteric arterial occlusive disease (n = 1), or infrainguinal arterial occlusive disease (n = 28) prospectively underwent evaluation from July 1, 1996, to June 30, 1997. Heparin-associated antibody tests (with a two-point platelet aggregation assay) and platelet counts (via Coulter counter) were performed before surgery and on or after the 4th day after vascular reconstruction. Arterial reconstruction thromboses were established by means of duplex ultrasound scanning or angiography. Acute myocardial infarction (AMI) and venous thromboses were diagnosed with clinical criteria and duplex ultrasound scanning, respectively. A significant decrease in platelet count was defined as a platelet count of less than 100,000/mm3 or as a more than 30% drop in the platelet count. Results: Twenty-two patients (21%) had at least one positive HAAb assay: one assay was positive before surgery only (after angiography), six were positive both before and after surgery, and 15 were positive after surgery only. There were three perioperative deaths—one in the HAAb-positive group and two in the HAAb-negative group. Ten thrombotic events occurred in the perioperative period. Four thrombotic events (three operative site thromboses and one AMI) occurred in the HAAb-positive group (18.2%). All of these patients were undergoing heparin therapy. Of the six patients (with three operative site thromboses, two deep venous thromboses, and one AMI) in the HAAb-negative group (7%; P = .21), three were undergoing heparin therapy. No patient who was HAAb positive with a thrombotic event had thrombocytopenia or a significant decrease in platelet count. Conclusion: The frequent exposure to heparin by patients with peripheral vascular disease is associated with a high incidence rate (21%) of HAAb formation, which makes it one of the more common hypercoagulable conditions in these patients. The patients who were HAAb positive had a 2.6-fold increase in perioperative thrombotic events. Thrombocytopenia or decreasing platelet counts were not reliable clinical markers for identifying patients who were HAAb positive. It is suggested that all patients who have undergone heparin therapy and who have an unexplained perioperative thrombotic event develop should undergo testing for HAAb. (J Vasc Surg 1999;29:779-86.)

Heparin-coated catheters and heparin-induced thrombocytopenia

Ten patients with heparin-coated pulmonary artery catheters had heparin-induced thrombocytopenia, which persisted after all other sources of heparin were discontinued. The thrombocytopenia occurred in approximately 0.4% of the patients receiving heparin-coated catheters and remitted when the catheters were removed. The platelet counts averaged 59,000/mm3 at the time of the diagnosis and recovered to an average of 143,000/mm3 by 3 days (range 2 to 4 days) after removal of the heparin-coated catheters. One patient required a second catheter 31 days after the first catheter had been removed. When the second heparin-coated catheter was inserted, the platelet count decreased from 307,000/mm3 to 102,000/mm3 in 4 days. Segments of heparin-coated pulmonary artery catheters were placed in platelet-rich plasma and incubated with serum from patients with known heparin-associated antiplatelet antibodies or with serum from volunteers with no exposure to heparin. The heparin-coated catheters induced platelet aggregation in all samples containing serum from patients with heparin-induced thrombocytopenia. However, platelet aggregation did not occur when the catheters were incubated with the serum of the volunteers. Non-heparin-coated catheters failed to produce platelet aggregation when incubated with either sera. The high mortality and morbidity rates associated with heparin-induced thrombocytopenia mandate that afflicted patients receive no more heparin, at least until the heparin-associated antiplatelet antibodies are no longer detectable. Patients with heparin-coated catheters who have thrombocytopenia should be tested for the presence of heparin-associated antiplatelet antibodies. If heparin-induced thrombocytopenia is confirmed, the catheters must be removed if the thrombocytopenia is to be reversed and complications avoided.