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M Antar

Publications and source records attributed to M Antar.

6 recordsLinked to original sources
PubMed1993

Comparison and spacial correlation of interictal HMPAO-SPECT and FDG-PET in intractable temporal lobe epilepsy.

The respective contribution of interictal HMPAO-SPECT and FDG-PET to the imaging of the epileptogenic zone in intractable temporal lobe epilepsy is not known. Ten consecutive patients with drug resistant focal epilepsy of temporal lobe origin were studied with prolonged noninvasive video-EEG monitoring, magnetic resonance imaging, interictal FDG-PET and HMPAO-SPECT. Five patients demonstrated unitemporal and 5 patients bitemporal interictal and/or ictal EEG epileptiform abnormalities. We developed a 3-dimensional semiquantitative method for interpretation and comparison of FDG-PET and HMPAO-SPECT using a 15-compartment model of the temporal lobe. In all 5 patients with unilateral epileptogenicity, interictal hypometabolism and hypoperfusion were recorded on the side of the EEG abnormalities without discrepancy between PET and SPECT. The severity and the extent of focal abnormalities were consistently greater on PET than on SPECT, in agreement with previously well documented better 'sensitivity' of PET. Among the 5 patients with bitemporal epileptogenicity, results of SPECT and PET were convergent in only 2 cases. In this group, SPECT abnormalities appeared more profound but either SPECT or PET were not constantly correlated with the side of predominant EEG epileptogenicity. Abnormalities on PET and SPECT were more frequently limited to mesiobasal structures among cases with unilateral epileptogenicity and tended to involve neocortical structures in bitemporal cases. We conclude that interictal FDG-PET and HMPAO-SPECT provide the same type of information on the side of the epileptogenic zone in cases with clearly unilateral epileptogenicity, with abnormalities more intense and more extensive on PET.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Detection by echocardiography of a thrombus of the right cavities in acute pulmonary embolism].

Echocardiography evaluates the severity of acute pulmonary embolism from its repercussions on haemodynamics. However, many authors have reported the discovery of thrombosis in the right heart cavities of patients with acute pulmonary embolism. In order to assess the frequency of intracavitary thrombosis and to evaluate the practical problems it raises, we have systematically examined by echocardiography 84 patients hospitalized for severe, acute pulmonary embolism (mean Miller's score: 21). In this series of 39 men and 45 women (mean age 62 years), 9 thrombi were detected, i.e. an incidence of 11%. Depending on the ultrasonographic images they presented, these patients were divided into two groups: 1. Six patients with low mobility thrombi attached to the cardiac wall. All benefited from a medical treatment consisting of heparin in 4 cases and a thrombolytic drug in 2 cases. There was no clinical evidence of recurrent embolism. Echocardiography showed complete disappearance of the thrombi in 5 of these 6 patients and partial regression under heparin therapy in one. 2. Three patients with a large and mobile thrombus threatening to prolapse through the tricuspid valve during atrial systole. It seemed rational to regard such thrombi as carrying a high risk of embolism with recurrences, especially since they had formed in patients already with severe pulmonary embolism. This view was confirmed by a search in the literature which yielded a 40% death rate figure when these thrombi were associated with pulmonary embolism. This high mortality, however, can be reduced by diagnostic and therapeutic measures.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMedDate not supplied

Role of a nonsteroidal anti-inflammatory agent, ibuprofen, in coronary revascularization after acute myocardial infarction.

The efficacy of using a nonsteroidal anti-inflammatory agent such as ibuprofen for the salvage of ischemic and reperfused myocardium was investigated by examining its ability to improve global and regional functions as well as to preserve high-energy phosphate compounds and inhibit creatine kinase release from an isolated in-situ pig heart subjected to 1 h of normothermic regional ischemia followed by 1 h of global hypothermic arrest and 1 h of normothermic reperfusion. Preperfusion of the heart for 15 min prior to ischemic insult with 50 microM ibuprofen failed to mitigate the myocardial reperfusion injury. Ibuprofen, however, functioned as an anti-inflammatory agent, as judged by its ability to inhibit the influx of indium-111-labeled polymorphonuclear leukocytes and chromium-51 (51Cr)-labeled platelets into the ischemic and reperfused heart. It also blocked the cyclooxygenase pathway, as evidenced by the significant reduction of 6-keto-prostaglandin F1 alpha and thromboxane B2 concentrations in the perfusate. Inhibition of cyclooxygenase resulted in increased accumulation of nonesterified fatty acids, particularly arachidonic acid, in the heart. These results suggest that although ibuprofen can inhibit polymorphonuclear leukocyte and platelet influx into the ischemic and reperfused heart, it causes further damage to the already ischemic heart by reducing prostacyclin concentration and increasing free fatty acids in the heart.

6-Ketoprostaglandin F1 alpha↗