Heparin-induced thrombocytopenia from venous thromboembolism treatment.

OBJECTIVES: We aimed to characterize the clinical experiences of patients in whom heparin-induced thrombocytopenia (HIT) complicated heparin therapy for venous thromboembolism (VTE) and who switched to argatroban. DESIGN: A retrospective analysis of previously reported prospective, multicentre, historical-controlled Argatroban-911 and Argatroban-915 studies of argatroban therapy in HIT. SETTING: Inpatient. SUBJECTS: Patients (n = 145) administered heparin for VTE and who developed HIT were identified. INTERVENTIONS: Patients were treated with argatroban 2 mcg kg(-1) min(-1) for up to 14 days, adjusted to maintain activated partial thromboplastin times 1.5 to three times baseline. Patient characteristics, anticoagulation and outcomes were summarized. The primary end-point was a composite of death, amputation, or new thrombosis within 37 days of argatroban initiation. RESULTS: During heparin therapy, platelet counts decreased (mean +/- SD nadir: 78 +/- 67 x 10(9) L(-1)), and 75 (52%) patients developed thrombosis. After heparin was discontinued, patients received argatroban (mean dose 2.1 +/- 1.2 mcg kg(-1) min(-1)) for 6.8 +/- 4.3 days. By day 6 of argatroban therapy, the mean platelet count rose to >150 x 10(9) L(-1). The primary end-point occurred in 41 (28.3%) patients (values of 26-44% are reported for argatroban therapy of HIT from any heparin indication). Seventeen (11.7%) patients, including 12 who had also experienced thrombosis whilst on heparin, developed new thrombosis after argatroban initiation, typically on the day argatroban was discontinued or later (n = 10). Seven (4.8%) patients experienced major bleeding. CONCLUSIONS: For VTE patients with HIT, argatroban provides effective anticoagulation, with outcomes comparable with those reported for other argatroban-treated HIT patients. New thrombosis in this setting occurred most often in patients with existing HIT-associated thrombosis, before HIT recognition or either at/after argatroban discontinuation.

Nonatherosclerotic arterial disease of the extracranial cerebrovasculature.

Extracranial carotid and vertebral arterial disease is most often attributable to underlying atherosclerosis. However, several other diseases may mimic atherosclerosis clinically. These include Takayasu's arteritis, giant cell arteritis, fibromuscular dysplasia, dissections, and aneurysms. It is important to recognize distinguishing characteristics of each condition to determine the appropriate course of treatment and long-term prognosis.

Fibromuscular dysplasia.

Fibromuscular dysplasia is an uncommon angiopathy that occurs in young to middle-aged, predominately female individuals. The disease consists of a heterogeneous group of histologic changes, which ultimately lead to arterial narrowing. Clinical manifestations reflect the arterial bed involved, most commonly hypertension (renal) and stroke (carotid). Fibromuscular dysplasia is a pathologic diagnosis, but the characteristic changes seen on an angiogram can be used to make the diagnosis in the appropriate clinical setting. This noninflammatory disease is a common mimic of vasculitis. A very limited amount of new literature has been published in the past year about this relatively uncommon condition.