Resolution of Sickle Cell Crisis Following Administration of Amiodarone.

Sickle cell disease is a prevalent hematologic condition, but some of the factors that lead to erythrocyte sickling are not fully known. A 58-year-old male patient with a history of sickle cell disease (SCD) and paroxysmal atrial fibrillation was transferred from an outside hospital for further management of refractory sickle cell crisis with acute chest syndrome. Before transfer, the patient received antibiotics and multiple packed red blood cell (pRBC) transfusions, with minimal effect on symptoms or anemia. After transfer, the patient developed rapid supraventricular tachycardia and atrial fibrillation (rates >160) with a drop in blood pressure. He was started on IV amiodarone. His heart rate was subsequently better controlled and converted to sinus rhythm the following day. Three days following initiation of amiodarone, the patient, with a hemoglobin count of 6.4 g/dl, required one additional unit of pRBC. On the fourth day, the patient's hemoglobin count rose to 9.4 g/dl, and he reported a marked improvement in symptoms. The improvements in symptoms and hemoglobin count were sustained, and the patient was discharged two days later. This remarkable improvement in anemia and symptoms triggered a search for potential causes. Amiodarone is a complex drug shown to have effects on multiple cell types, including erythrocytes. A recent preclinical study demonstrated reduced sickling and improved anemia in a murine model of SCD. This case report raises the possibility that amiodarone may have contributed to the rapid improvement in anemia and should be further explored in clinical trials. LEARNING POINTS: Prior studies support a link between erythrocyte sickling and membrane lipid composition.Amiodarone may impact erythrocyte pathophysiology by increasing cellular lipids including bis(mono)acylglycerol phosphate (BMP).Drugs with effects on erythrocyte lipid fractions may be beneficial during sickle cell crises.

Beta1-receptor blockade attenuates atherosclerosis progression following traumatic brain injury in apolipoprotein E deficient mice.

Traumatic brain injury (TBI) is associated with cardiovascular mortality in humans. Enhanced sympathetic activity following TBI may contribute to accelerated atherosclerosis. The effect of beta1-adrenergic receptor blockade on atherosclerosis progression induced by TBI was studied in apolipoprotein E deficient mice. Mice were treated with metoprolol or vehicle following TBI or sham operation. Mice treated with metoprolol experienced a reduced heart rate with no difference in blood pressure. Six weeks following TBI, mice were sacrificed for analysis of atherosclerosis. Total surface area and lesion thickness, analyzed at the level of the aortic valve, was found to be increased in mice receiving TBI with vehicle treatment but this effect was ameliorated in TBI mice receiving metoprolol. No effect of metoprolol on atherosclerosis was observed in mice receiving only sham operation. In conclusion, accelerated atherosclerosis following TBI is reduced with beta-adrenergic receptor antagonism. Beta blockers may be useful to reduce vascular risk associated with TBI.