RESUMO
BACKGROUND: An aneurysm is an abnormal focal dilatation of an artery. Most of the unruptured aneurysms are asymptomatic and discovered incidentally or some of them symptomatic with mass effect or nerve palsy, but rupture of aneurysm results in a potentially life-threatening subarachnoid haemorrhage. Aneurysms with wide necks are defined by neck diameters greater than 4 mm or dome-to-neck ratios less than 2 and are the most difficult to treat with the endovascular method. AIM: This study aimed to analyse the endovascular treatment of intracranial aneurysms with a wide neck. METHODS: The study population included 37 patients with 46 aneurysms referred to the University Clinic of Radiology in Skopje, the Republic of Macedonia for endovascular treatment during the period January 2013 to May 2018. This study included 24 females and 13 males, ranging in age from 25 to 74 years. RESULTS: From total 46 treated aneurysms 13 were ruptured and 33 unruptured. Six patients were with multiple aneurysms. In these study complex aneurysms were treated with combined technique, 5 with balloon-assisted coiling, 25 with stent-assisted coiling, 6 stents, 2 with flow diverter assisted coiling, 6 FD and 2 with partial coil filling without assistance device. CONCLUSION: Aneurysms with wide neck remain a challenge for endovascular treatment. But the development of new techniques and materials in the treatment of aneurysms makes endovascular treatment of intracranial aneurysms safe and feasible.
RESUMO
Prostaglandin F(2alpha) (PGF(2alpha)) is produced during myocardial inflammation and many of the insults that trigger contractile dysfunction also activate prostaglandin synthesis and production. However, although PGF(2alpha) plays a significant role in the cardiac response to inflammation, the effect of this particular compound on the heart was largely studied at the cellular level and probably no due attention was paid to the effect of PGF(2alpha) on the whole heart contractility. Therefore, in the present study we have investigated the effect of PGF(2alpha) on isolated right ventricle of the rat heart. PGF(2alpha) (1nM-1microM) induced concentration-dependent decrease of the amplitude of contractions of the ventricular muscle. Real time RT-PCR has revealed that prostaglandin FP receptors are expressed in the rat myocardium and the level of expression was similar to those of creatine kinase and adenylate kinase, which are proteins abundantly present in the heart. An antagonist of FP receptors, PGF(2alpha) dimetilamide (10nM), abolished negative inotropic effect induced by PGF(2alpha). To examine the possibility that PGF(2alpha) could activate non-FP prostaglandin receptor, we have measured the level of expression of all known prostaglandin receptors in the rat heart. These experiments have shown that the order of expression of prostaglandin receptors in the rat heart is FP>>EP1=TP>EP4>EP3>DP=IP. Based on the obtained results we conclude that PGF(2alpha) induces negative inotropic effect on rat heart by activating FP prostaglandin receptors. This effect of PGF(2alpha) could contribute to cardiac dysfunction in conditions of systemic and myocardial inflammation.
