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Biomedical subjects

C Mugnaini

Publications and source records attributed to C Mugnaini.

11 recordsLinked to original sources

[The nimodipine therapy of acute focal cerebral ischemia (minor stroke). A clinical study with an assessment of regional cerebral blood flow by SPECT].

Aim of the study is the evaluation of therapeutic effectiveness of nimodipine in acute focal cerebral ischaemia. Thirty patients affected by minor ischaemic stroke divided in two randomized groups have been studied consecutively: all the patients were treated with standard therapy, nimodipine was delivered in addition only to the patients of the first group. Both clinical evaluation using Mathew scale, modified by Gelmers, and flowmetric evaluation with SPECT were performed at different times. The results haven't shown any significant statistical difference in the effectiveness of the therapy between the two groups even if a positive clinical trend was evidenced in the group treated with nimodipine. The flowmetric study has shown the poor homogeneity of the groups from a physiopathological point of view not-with-standing the two groups were similar for the clinical severity, sex, age and vascular risk factors. We conclude that is advisable to carry out further trials in which the comparison study groups are more numerous and balanced also from a physiopathological point of view.

Acute Disease↗

Increased fibrinopeptide A formation and thromboxane A2 production in patients with ischemic heart disease: relationships to coronary pathoanatomy, risk factors, and clinical manifestations.

In 98 patients with ischemic heart disease (IHD), independent of their clinical status (previous myocardial infarction, spontaneous angina or effort angina), a hypercoagulable state (indicated by significant elevation of fibrinopeptide A plasma level) and an increased platelet biologic activity were observed. Moreover, plasma fibrinopeptide A concentration and platelet aggregation were remarkably higher in patients with frequently occurring spontaneous clinical manifestations (active disease) than in IHD patients with relatively quiescent symptoms. Abnormalities of blood clotting and platelet changes were not significantly altered by the presence of severity of coronary angiographic fixed obstruction in IHD. Multiple regression analysis indicated that hypercoagulability and increased platelet biologic activity were not a consequence of differences in risk factor patterns in IHD patients compared to control subjects.

Blood Coagulation↗

Increased platelet aggregation due to plasma-aggregating activity. Identification of the responsible factors.

Platelet-poor plasmas (PPPs) from 52 out of 71 patients affected by different diseases and selected for increased amounts of circulating platelet aggregates, incubated at 37 degrees C for 30 min with control platelet-rich plasma (PRP; cross-matching test) induced the formation of platelet aggregates, stimulated the production of malondialdehyde and enhanced ADP-induced aggregation. 31 control PPPs were consistently negative at cross-matching test. Gel chromatography of plasmas on agarose 4% allowed the identification of four different fractions (A, B, C, D) provided with aggregating activity. Fraction A eluted at the void volume was to be identified with the von Willebrand factor, whereas B, C and D fractions, eluted at the same elution volumes as activated factor X were mainly composed of factor X (fraction B) and activated factor X (fractions C and D). Thrombin activity was absent in all the fractions provided with aggregating activity. Also, from control PPPs negative at cross-matching tests, the same fractions could be obtained, although of 5--10 times lower aggregating potency, thus explaining the negative cross-matching tests. These findings stress the role of some extraplatelet factors related to hypercoagulability in platelet hyperaggregability.

Adenosine Diphosphate↗

[Clinical diagnosis of pulmonary embolism: validity of a score system and its correlation with therapeutic choices in a case series of 51 patients].

The Authors have used, on a group of 51 patients, a score-system for the clinical diagnosis of pulmonary embolism. This system is based on clinical examination of the patients and utilizes a different value for each sign and symptom: each sign and symptom correspond to a positive number. Every patients was also undergone instrumental tests to confirm the diagnosis (i.e.: perfusion lung scanning and venous doppler) according to previously defined diagnostic program. A good relationship between the instrumental diagnosis and clinical probability was found with above mentioned score-system. The AA believe that this score-system is valid and that it can be used in elaborating diagnostic decision, particularly in those cases in which the diagnosis is not established by the instrumental tests and in which is not possible to perform pulmonary angiography.

Diagnosis, Differential↗

[The patient with carotid reversible cerebral ischemic attack. Clinico-instrumental pathogenetic diagnosis].

Reversible ischemic attacks (RIA) in the carotid territory may be caused by different pathogenetic diseases (atheroembolism, cardioembolism, lacunar infarcts, hemodynamics crisis); peculiar therapeutic treatment has to be related to each pathophysiologic evidence. A pathogenetical and diagnostical approach based on clinical and instrumental data is suggested by the Authors; by this way it was possible to obtain a right pathogenetic diagnosis in 82% of a 144 patients series affected by carotid RIA.

Adult↗