1/4. Acute myocardial infarction as the presenting symptom of acute myeloblastic leukemia with extreme hyperleukocytosis.This case report deals with an unusual leukostatic complication in a 56-year-old woman with acute myeloblastic leukemia (AML) and extreme hyperleukocytosis (316 x 10(9)/L) who presented with acute myocardial infarction (MI). After leukopheresis the patient achieved hemodynamic stabilization and rapid neurologic recovery of encephalopathy that had also developed after the infarction. Considering the central role of WBC in the remodeling of post MI myocardial tissue, it was obvious that administration of chemotherapy with its subsequent inevitable pancytopenia could impose an increased risk for further cardiac complications including myocardial rupture. Nevertheless, cytarabine-based induction chemotherapy was initiated 3 days after admission, and she achieved prolonged complete remission. coronary angiography disclosed segmental atherosclerosis, but the only significant obstruction was in the right coronary artery. The patient died with relapsed leukemia 7 years later without recurrence of any cardiac symptoms or signs. autopsy disclosed segmental coronary atherosclerosis involving the LAD (60% obstruction), suggesting that atherosclerosis was a predisposing risk factor. Additional compromise to blood perfusion due to leukostasis had led to this unusual complication of AML involving a major vessel. This is the first documented case of leukostasis causing coronary artery occlusion as well as the first report of successful induction chemotherapy for AML during a myocardial infarction.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/4. plasma concentrations of complement-activation complexes correlate with disease activity in patients diagnosed with isolated central nervous system vasculitis.Isolated central nervous system (CNS) vasculitis is rare medium- sized vessel disease limited to intracerebral vessels. The two most common symptoms of this inflammatory disorder observed at entry to a hospital are headaches and mild memory deficits. Further progression of this disease may result in focal neurologic alterations and seizures. Currently, the most common laboratory abnormality noted is an elevated erythrocyte sedimentation rate. The complement (C) system is known to play a role in many inflammatory processes; it may also be involved in CNS vasculitis. In this longitudinal study of patients with CNS vasculitis, we detected C activation by highly sensitive and specific assays that are capable of identifying breakdown products formed after C activation: C3a des arg, C4a des arg, C5a des arg, C1rC1s-C1-inhibitor complex, and terminal C complex (C5b-9). We present two cases of documented CNS vasculitis in which serial measurements of these C-activation products correlate with disease activity. Our results indicate that a temporal association exists between C activation and the clinical presentation of CNS vasculitis. We conclude that physicians should monitor C-activation by-products in plasma when they attempt to follow the clinical course of CNS vasculitis.- - - - - - - - - - ranking = 2keywords = vessel (Clic here for more details about this article) |
3/4. Altered sensorium, confusion, and vertical gaze paresis: the top of the basilar syndrome.The term "top of the basilar" has been used in reference to a group of signs and symptoms of midbrain, diencephalic, and posteroinferior hemispheric dysfunction. It has been attributed to ischemia in the territory of second- and third-order vessels that arise from the uppermost portion of the basilar artery. We report our experience with four patients who had alteration of consciousness, confusion, and vertical gaze paresis accompanied by other physical abnormalities. Extensive evaluation did not help in documenting the lesions or in understanding their pathogenesis. The top of the basilar syndrome is a not uncommon form of stroke and carries a variable prognosis. Treatment by anticoagulation may prevent further infarction in selected patients who are seen early.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
4/4. Temporary neurological deterioration after extracranial-intracranial bypass.Five patients who experienced temporary neurological deterioration after extracranial to intracranial bypass procedures are reported in detail. These patients suffered transient ischemic attacks or more prolonged deficits usually of a different nature than the preoperative symptoms. All patients had a good outcome and the spells ceased; the neurological deficits improved within a maximum of 2 weeks. Obvious causes of deterioration such as intra- or extracerebral hematomas, occlusion of a previously stenotic vessel, or graft occlusion were ruled out by computed tomography and angiography in each case. Intraoperative causes of neurological deterioration such as anesthetic effect, hypotension, and temporary occlusion of the cortical vessel or sacrifice of its small branches were not likely to be the cause of the deficits because in each case, the patient awoke satisfactorily and deterioration occurred hours to days later. In each case, postoperative angiography showed good perfusion of at least one major division of the middle cerebral territory. Anticoagulation with heparin in three patients did not change the clinical course. In one patient who was not anticoagulated, embolism could have been responsible for a single prolonged ischemic event, but in the other patients thromboembolism does not seem likely to have been responsible for the deficits. The cause of the deterioration in these patients remains unexplained. We speculate that hyperperfusion of chronically ischemic brain tissue and shifts in the watershed region resulting from the new flow pattern after bypass grafting are two mechanisms that may have been of importance in the etiology of these deficits.- - - - - - - - - - ranking = 2keywords = vessel (Clic here for more details about this article) |