Erythrocytapheresis is an established therapy for the prevention of stroke in sickle cell disease [1]. We report its use in the prevention of recurrent acute coronary syndromes.A 50-year-old woman, with homozygous sickle cell disease presented in December 2005 with central chest pain, T wave inversion in V1-V3 and biphasic T waves in V4-V6. She was treated with aspirin, clopidogrel, and enoxaparin. Her troponin I peaked at 8.23 lg/L 12 hr later. Cardiac magnetic resonance imaging (MRI) showed subendocardial hyperenhancement in the lateral wall of the left ventricle consistent with an infarct. Coronary angiography showed no obstruction [2]. A long-term red cell exchange program was considered but deferred in the absence of evidence of recurrent myocardial infarction in sickle cell disease.Nine months later the patient presented with central chest pain of sudden onset. Electrocardiography showed new onset atrial fibrillation with T wave inversion across V1-V4. Serum troponin I was elevated at 0Á19 lg/ L and rose to 4Á61 lg/L 12 hr later. Cardiac MRI was unchanged compared with the previous study. Treatment with enoxaparin was commenced and electrocardioversion undertaken, successful only with amiodarone preloading.In light of the recurrence of myocardial infarction, a red cell exchange program to achieve a target hemoglobin S level of <30% was implemented. Thirty-four months after this second event, the patient is maintained on a regular red cell exchange program and remains well in sinus rhythm. We have recommended erythrocytapheresis is continued on an indefinite basis.Although regular red cell transfusions to suppress the level of hemoglobin S are well established in the primary and secondary prevention of stroke in sickle cell disease [1], they have not previously been shown to reduce the risk of recurrent myocardial infarction. We believe hematologists should be aware of the potential benefit of such an approach.
The aims of this study were to determine the outcome and the natural history of GBV-C/hepatitis G virus (HGV) infection and to establish the frequency of acute or persistent infections in multiply-transfused individuals and blood donors. We used a GBV-C/HGV RNA polymerase chain reaction (PCR) and an assay evidencing antibodies to the envelop protein E2, which is considered a marker for virus clearance. Among 16 PCR-positive recipients, 11 were still positive for GBV-C/HGV RNA at the end of the study period; six of the 16 recipients were GBV-C/HGV infected during the study period and thus had a well-defined date of infection. The 16 patients were shown to carry GBV-C/HGV RNA over a mean period of 4.4 years, for a mean observational period (defined as the follow-up period since the first sample positive for GBV-C/HGV RNA) of 5.3 years. Within the limits of the study period, the patients with a well-defined date of infection were positive for GBV-C/HGV RNA during a mean period of 4.7 years. If defined by the presence of GBV-C/HGV RNA for at least 6 months, the persistent infection rate was 100% in this recipient cohort. Serum anti-E2 antibody was evidenced at least once in five (31.2%) recipients and, except in one case, became detectable after the loss of GBV-C/HGV RNA. Among the 11 blood donors, all were still positive for GBV-C/HGV RNA after a mean follow-up period of 7.7 months. The persistent infection rate was 100% in this donor cohort. Once acquired, the infection to GBV-C/HGV generally tends to persist in immunocompetent patients.
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