PubMed · 12967358
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Elizabeth Warburton. 2003. Stroke management.. https://pubmed.ncbi.nlm.nih.gov/12967358/
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HISTORY AND CLINICAL FINDINGS: A 61-year-old man was admitted to hospital because of right-sided hypaesthesia. Additionally he reported a brief speech disturbance some weeks before. Neurological examination indicated right-sided sensomotoric hemiparesis and left-sided upper quadrant anopia. 6 years ago recurrent transient ischaemic attacks (TIA) was diagnosed caused by paradoxical embolism through a persistent foramen ovale (PFO). The PFO was closed with a 45 mm Sideris button occluder device. After this, he reported no symptoms of cerebral ischaemia and he did not take any antiplatelet therapy. INVESTIGATIONS: Transesophageal echocardiography (TEE) showed a left atrial thrombus attached to the occluder. Cerebral computed tomography revealed infarction in regions supplied by the right posterior cerebral artery and left media cerebral artery. As additional risk factor for thrombosis a heterozygous factor V Leiden mutation was diagnosed. DIAGNOSIS: Multiple cerebral infarctions caused by a thrombus attached to an occluder system 6 years after interventional closure of persistent foramen ovale in a patient with heterozygous factor V Leiden mutation. TREATMENT AND COURSE: The patient was anticoagulated (phenprocoumon) and the thrombus gradually dissolved. CONCLUSION: A thrombosis on a Sideris occluder device may cause cerebral infarctions even years after transcatheter closure of a PFO.
We compared the efficacy, safety, and impact on postoperative hospital length of stay and inpatient hospital costs of low-molecular-weight heparin with that of unfractionated heparin as a "bridge" to achieving therapeutic levels of anticoagulation with warfarin in patients with newly implanted prosthetic heart valves. The patients who received low-molecular-weight heparin had a shorter length of stay and decreased postoperative costs compared with the control subjects receiving unfractionated heparin.
Sphingolipids contribute to modulation of two opposing cell processes, cell growth and apoptotic cell death; ceramide and sphingosine promote the latter and sphingosine-1-phosphate triggers the former. Thrombin, a pro-inflammatory protease that is regulated by the blood coagulation cascade, exerts similar effects depending on cell type. Here we report a new mechanism for cross-talk between sphingolipid metabolism and thrombin generation. Sphingosine and sphinganine, but not ceramide or sphingosine-1-phosphate, down-regulated thrombin generation on platelet surfaces (IC(50) = 2.4 and 1.4 microm for sphingosine and sphinganine, respectively) as well as in whole plasma clotting assays. Thrombin generation was also inhibited by glucosylsphingosine, lysosphingomyelin, phytosphingosine, and primary alkylamines with >10 carbons. Acylation of the amino group ablated anticoagulant activities. Factor Va was required for the anticoagulant property of sphingosine because prothrombin activation was inhibited by sphingosine, sphinganine, and stearylamine in the presence but not in the absence of factor Va. Sphingosine did not inhibit thrombin generation when Gla-domainless factor Xa was used in prothrombinase assays, whereas sphingosine inhibited activation of Gla-domainless prothrombin by factor Xa/factor Va in the absence of phospholipids (IC(50) = 0.49 microm). Fluorescence spectroscopy studies showed that sphingosine binds to fluorescein-labeled factor Xa and that this interaction required the Gla domain. These results imply that sphingosine disrupts interactions between factor Va and the Gla domain of factor Xa in the prothrombinase complex. Thus, certain sphingolipids may be bioactive lipid mediators of thrombin generation such that certain sphingolipid metabolites may modulate proteases that affect cell growth and death, blood coagulation, and inflammation.