Cerebral embolism and atrial septal aneurysm

Cerebral embolism and atrial septal aneurysm

325 Cerebral G.Ruotolo, embolism and atrial septal anewysm P.Gamti, G. Muccati, N.Greco, SMauuca Zm Genaml Medidne Unit, Regionsl Hc+lal ‘A.Pugliese”...

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325 Cerebral G.Ruotolo,

embolism and atrial septal anewysm P.Gamti, G. Muccati, N.Greco, SMauuca Zm Genaml Medidne Unit, Regionsl Hc+lal ‘A.Pugliese” C&warn, Recent studies report atrial septal aneurysm,

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disease are absent. I.B., a 37 years old woman, was hospitalized into our unit for relapsing syncopal event. She reported non-treated borderline hypertension. During the hospital stay she underwent a left facial-brachiocrural hemiparesis. Clinical examination showed a mild overweight. jugular pulse was normal, carotid auscultation did not point out any murmur, pulse was rhythmic with a 72 beatslmin frequency, blood pressure was 150/85 mmHg. Heart sounds were effective and no murmurs or clicks could be appreciated. Laboratory tests, enclosed hemocoagulative tests, C and S proteins were normal Supraortic trunks doppler ultrasonography, standard electrocardiogram and chest radiograph were normal. Brain CT pointed out a big hypodensity area in the right hippocampal region and other little lesions in both hemispheres, in particular to white matter, (0 be referred to multiple ischemic events. The patient was dischargerd with a diagnosis of brain vascular disease with left hemiparesis outcome and an antiplatelet treatment by acetylsalicylic acid. After nine months she was again hospitalized for persisting syncopal events. During the hospital stay electrocardiogram showed an anterolateral myocardial infarction. Transthoracic and later on transesophageal echocardiograms (TTE TEE) showed an atrial septal aneurysm, whilst color doppler ultrasound showed a mild leftto-right shunt. Anticoagulants (acenocoumarol) were added to treatment. After two years follow-up, the patient IS asymptomatic and without syncopal events. Finally, we may suppose that cerebral embolism and probably myocardial infarction are to be awarded to atrial septal aneurysm. Therefore, all the patients with a brain ischemia of unknown etiology should submit to TTE and if necessary TEE, in order to diagnose unknown heart anomalies.

Age related macular degeneratlcn is a leadlng carse of adult blindness in indusrrzalized r.atlxs. It occurs ln two defined forms--an atrophic or dry form that atrects approximately 35% of patients. and a wet form. The wet type macular degeneration occurs 1n 15% of these patients and is caused by s~Jbfove.31 necvascularlzatlon in the choroidal membrsne. Leakage and bleeding 15 common from vessels vhlch leads to blindness which causes a buldup of tension at the lnawlar region with visual acuity compromised. This drsease process affects 11% of the populstlon between the ages of 65 and 74, and 27.9% or‘ those zlder than 74 years. Various treatment regimens have progress of age reiated macular very limlted success. These have steroids.

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Thrombosis and vasculltis associated with CBREW.New insight to rm old ch~llmge. J.E. Naschi~ and D. Yesburun, Haif% Israel. Cancer-associated vascuIopathies are rtiewed, iocluding rare and insticientt); variants, with emphasis on aspects that may suggest the presence of a hidden cancer. Deep venous thrombosis was associated with a sign&&y higher fkequency of malignancy during the ti 6 months after diagnosis. Malignancies were found using simple clinical and diagnostic methods, additional screening was not cost-&cient. Other sigrw associated with deep venous thrombosis that increased the probability of an occult cancer were age older than 50 years, multiple sites of venous thrombosis, associated venous and arterial thromboembolism, tlmmboembolism resistant to watfatin therapy, and pamneoplashc sylldrome. Among VasCUlitiEqndrotnes, only cutaneous leukocytocIae.tic VasCUIitiB prapettting aikr the age of 50 years was consktentIy associated with cancer. J3e role of coaguL%tion studies a8 SigtlaISof the neoplastic etiology of vascUIopathies is comidered, as is the promisii cancer procoagulant assay and the modified whole blood recalcifxation time. These tests could serve as global cancer screening tests that are not specilic for any specific type of cancer. Both tests are most sensitive to detect stage I and II cancer and may not be positive in advanced cancer. The patiophysiologic mechanisms iowhzd in the cancer-associated vascuIopatbies are discussed with emphasis on tumor interaction with the end&e&I Iining, adherence of tumor cells to endoth&i cells, and injury of endothelium by tumor cells. The dysfunction of endotheIi.4 celh at a distance fram the tumor and met&ass is attributed to effects of humoral mediatom and peptides such as tumor necrosis factor, hyperhomocysteinenua, antiphospholipid antibodies, acute phase reactants, and certain poorly characterized factors, and may be regarded a paraneoplastic phenomenon. This paraneoplastic endothelial dysfunction may prevent the in situ release of vasodilator substances, platelet aotiaggregants and anticoagulants, and is a likely mechanism of vasospasm and thrombosis. The recently recognized role of intlammation and hyperhmnocysteinemia in the pathogenesii of cancer-associated tbromboembolism may be the basis for prophylactic intervention.

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