HISTORY AND ADMISSION FINDINGS: At the age of 55 years a now 70-year-old man had his aortic valve replaced by a prosthetic (Björk-Shiley) valve, and 11 years later a VDD pacemaker had been implanted. 18 months before the latest admission he had been hospitalized for treatment of staphylococcal endocarditis involving the aortic prothesis. At that time thrombocytopenia developed during heparin administration, diagnosed clinically and with the heparin-induced platelet activity (HIPA) test as type II heparin induced thrombocytopenia. His latest admission was for the diagnosis and treatment of peripheral arterial disease of the right leg (Fontaine stage IIb). INVESTIGATIONS: Right popliteal and pedal pulses were not palpable. He was able to walk pain-free for only 70 m. Doppler sonography demonstrated an arm-leg index on the right of 0.7. Angiography revealed marked stenosis in the right superficial femoral artery and a filiform stenosis in the right popliteal artery. TREATMENT AND COURSE: Both stenoses were relieved by percutaneous transluminal balloon angioplasty, in the course of which 5000 IU heparin were administered as a bolus intraarterially. Postoperative anticoagulation was maintained for 2 days with recombinant hirudin. There was no evidence of platelet reduction or heparin-induced antibodies despite the renewed infusion of heparin. CONCLUSION: Single re-administration of heparin in a patient who had developed a type II heparin-induced thrombocytopenia several years before does not necessarily lead to a booster of antibodies and thus to a reduction of platelets in the peripheral blood. It is a moot point whether the course in this case was an exception or the rule.
HISTORY AND ADMISSION FINDINGS: At the age of 55 years a now 70-year-old man had his aortic valve replaced by a prosthetic (Björk-Shiley) valve, and 11 years later a VDD pacemaker had been implanted. 18 months before the latest admission he had been hospitalized for treatment of staphylococcal endocarditis involving the aortic prothesis. At that time thrombocytopenia developed during heparin administration, diagnosed clinically and with the heparin-induced platelet activity (HIPA) test as type II heparin induced thrombocytopenia. His latest admission was for the diagnosis and treatment of peripheral arterial disease of the right leg (Fontaine stage IIb). INVESTIGATIONS: Right popliteal and pedal pulses were not palpable. He was able to walk pain-free for only 70 m. Doppler sonography demonstrated an arm-leg index on the right of 0.7. Angiography revealed marked stenosis in the right superficial femoral artery and a filiform stenosis in the right popliteal artery. TREATMENT AND COURSE: Both stenoses were relieved by percutaneous transluminal balloon angioplasty, in the course of which 5000 IU heparin were administered as a bolus intraarterially. Postoperative anticoagulation was maintained for 2 days with recombinant hirudin. There was no evidence of platelet reduction or heparin-induced antibodies despite the renewed infusion of heparin. CONCLUSION: Single re-administration of heparin in a patient who had developed a type II heparin-induced thrombocytopenia several years before does not necessarily lead to a booster of antibodies and thus to a reduction of platelets in the peripheral blood. It is a moot point whether the course in this case was an exception or the rule.