Otic artery and its clinical importance

Three primitive arteries - trigeminal, otic, and hypoglossal - are named according to their close relationship with the 5th, 8th, and 12th cranial nerves. While the incidence of permanent trigeminal artery ranges from 0.06% to 0.6%, the persistent primitive otic artery has been documented on fewer occasions.When the human embryo is 4 mm in length, these arteries serve as transitional anastomoses between the primi­tive internal carotid arteries and the bilateral longitudinal neural arterial plexus.The primitive otic artery originates from the primitive internal carotid artery and joins the basilar artery. It re­gresses at the 30th day of embryogenesis. Persistent primitive otic artery remains in adulthood and it is also called ‘`acoustic artery``. It originates from the petrous part or the C2 part of the internal carotid artery. Sometimes, as a part of another pattern, the persistent primitive otic artery arises from the persistent primitive hypoglossal ar­tery at cervical level.Hypoplasia or aplasia of the vertebral and posterior communicating arteries can be seen with the presence of per­sistent primitive otic artery. Also an angiomatous malformation, the occluded unilateral internal carotid artery and bilateral vertebral arteries are visualized in some cases.Knowledge about persistent carotid-vertebrobasilar anastomoses between the anterior and posterior head circu­lation can be of vital significance during invasive procedures like angiography and surgical operations

Intravenous NPA for the treatment of infarcting myocardium early: InTIME-II, a double-blind comparison on of single-bolus lanoteplase vs accelerated alteplase for the treatment of patients with acute myocardial infarction

Aims to compare the efficacy and safety of lanoteplase, a single-bolus thrombolytic drug derived from alteplase tissue plasminogen activator, with the established accelerated alteplase regimen in patients presenting within 6 h of onset of ST elevation acute myocardial infarction. Methods and Results 15 078 patients were recruited from 855 hospitals worldwide and randomized in a 2:1 ratio to receive either lanoteplase 120 KU. kg-1 as a single intravenous bolus, or up to 100 mg accelerated alteplase given over 90 min. The primary end-point was all-cause mortality at 30 days and the hypothesis was that the two treatments would be equivalent. By 30 days, 6.61% of alteplase-treated patients and 6.75% lanoteplase-treated patients had died (relative risk 1.02). Total stroke occurred in 1.53% alteplase- and 1.87% lanoteplase-treated patients (ns); haemorrhagic stroke rates were 0.64% alteplase and 1.12% lanoteplase (P=0.004). The net clinical deficit of 30-day death or non-fatal disabling stroke was 7.0% and 7.2%, respectively. By 6 months, 8.8% of alteplase-treated patients and 8.7% of lanoteplase-treated patients had died. Conclusion Single-bolus weight-adjusted lanoteplase is an effective thrombolytic agent, equivalent to alteplase in terms of its impact on survival and with a comparable risk-benefit profile. The single-bolus regimen should shorten symptoms to treatment times and be especially convenient for emergency department or out-of-hospital administration. (C) 2000 The European Society of Cardiology