Evidence Of Acute Infarction Research Articles

Transient Ischemic Attacks: A Modern Approach

Event Abstract Back to Event Transient Ischemic Attacks: A Modern Approach José Biller1* 1 Loyola University Health System, Department of Neurology, United States Learning Objectives: Understand modern definition of TIAs Describe manifestations of carotid and vertebrobasilar TIAs Identify criteria for the administration and quantification of the ABCD2 score Explain recommended evaluation of patients with recent TIAs Identify rationale for medical, surgical, and endovascular management strategies for patients with TIAs Transient ischemic attacks (TIAs) are brief episodes of neurological dysfunction caused by a focal brain or retinal ischemia with clinical symptoms typically lasting less than an hour and without evidence of acute infarction. Following a TIA, the risk of cerebral infarction is increased up to 10 times within 5 years. The risk is highest during the first weeks after the index event, and approximately half of the strokes occur in the first few days. Treatment of acute cerebral ischemia is a very time sensitive medical situation. A recent TIA is an urgent situation necessitating rapid assessment designed to identify and correct underlying stroke risk factors as well as to initial appropriate therapy. Each patient with recurrent neurologic deficit must be individualized. The key to therapy is, whenever possible, the removal or treatment of any triggering mechanisms and modification of risk factors. Antiplatelet therapy is highly effective in reducing the risk of recurrent vascular events and is recommended over warfarin for non-cardioembolic TIAs. Data from large randomized clinical trials have established carotid endarterectomy (CEA) as the standard treatment for severe symptomatic carotid artery stenosis. In centers with a low surgical risk, CEA also provides modest benefit in symptomatic patients with carotid artery stenosis of 50% to 69%. The indications for urgent or emergent CEA remain controversial. The results of the Carotid Revascularization Endarterectomy vs. Stent Trial (CREST) will be briefly discussed. Conference: Paroxysmal Neurology Symposium, Chicago, United States, 7 Apr - 7 Apr, 2010. Presentation Type: Oral Presentation Topic: Abstracts Citation: Biller J (2010). Transient Ischemic Attacks: A Modern Approach. Front. Neurol. Conference Abstract: Paroxysmal Neurology Symposium. doi: 10.3389/conf.fneur.2010.07.00001 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 06 Apr 2010; Published Online: 06 Apr 2010. * Correspondence: José Biller, Loyola University Health System, Department of Neurology, Illinois, United States, jbiller@lumc.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers José Biller Google José Biller Google Scholar José Biller PubMed José Biller Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Characteristics of TIA and its management in a tertiary care hospital in Pakistan

BackgroundTransient ischemic attack (TIA) is described as a brief episode of neurological dysfunction caused by focal brain ischemia, with clinical symptoms typically lasting less than an hour, and without evidence of acute infarction. Recent studies depict TIA as a particularly unstable condition. Risk of stroke is greater than 10% in the first 90 days after an index TIA. The presentation, prognosis and intervention for TIA have not been reported in South-Asians in a developing country.MethodA retrospective chart review was done for 158 patients who were admitted with the diagnosis of TIA, as defined by ICD 9 code 435, from January 2003 to December 2005 at the Aga Khan University Hospital, Karachi, Pakistan. The data was entered and analyzed in SPSS version 14.0.FindingsAmong 158 patients, 57.6% were male and 41.1% were female. The common presenting symptoms were motor symptoms (51.3%), speech impairment (43%), sensory impairment (34.8%) and loss of balance/vertigo (29.1%). The median delay in presenting to the hospital was 4 hours. Those with motor symptoms were found to present earlier. The study showed that only 60.8% of all the patients presenting with TIA received any immediate treatment out of which 44.7% received aspirin. Neuroimaging was used in 91.1% of the patients. Of all the TIA patients 9.1% converted to stroke with 50% doing so within the first 24 hours.ConclusionThe natural history of TIA from this developing nation is comparable to international descriptions. A large percentage of patients are still not receiving any immediate treatment as recommended in available guidelines, even in a tertiary care hospital.

Transient ischemic attack: Definition and natural history

The standard definition of a transient ischemic attack--"a cerebral dysfunction of an ischemic nature lasting no longer than 24 hours with a tendency to recur"--was arrived at arbitrarily and is no longer tenable. Experience shows that attacks are much briefer, usually less than an hour, and many are associated with brain infarction. A newer definition, more consonant with the data, is preferred--"transient ischemic attack is a brief episode of neurological dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than an hour, and without evidence of acute infarction." Patients with transient ischemic attacks require urgent evaluation that includes brain and vascular imaging, blood tests, and often cardiac investigations. Treatment will depend on the nature of the causative cervico-cranial vascular, cardiac, and hematologic abnormalities found on investigation.

Technetium-99m stannous pyrophosphate myocardial scintigraphy. Reliability and limitations in assessment of acute myocardial infarction.

Two hundred-three patients had -echnetium 99m (stannous) pyrophosphate myocardial scintigrams for the evaluation of chest pain and suspected acute myocardial infarction. In addition to routine imaging at 60--90 minutes after injection of the radio-pharmaceutical, the blood pool was imaged immediately in each patient for comparison with routine anterior, left anterior oblique, and left lateral views. Further delayed studies were obtained when residual blood pool activity was identified. Seventy patients had acute myocardial infarction by clinical, electrocardiographic, and enzymatic (CK-MB) criteria. Sixty-five of these 70 patients with acute infarction had positive myocardial scintigrams, with one technically unsatisfactory study. Only four of the 70 patients had negative scintigrams when imaged 18--72 hours after infarction in this study. Technically satisfactory scintigrams were recorded in 125 patients without evidence of infarction. Ninety-six had negative scintigrams at 60--90 minutes, while 19 patients (15%) had precordial activity at 60--90 minutes which was identical in distribution to early blood pool images and cleared with further delay. With these included, the true negative incidence was 92%. Ten of 125 patients had false positive scintigrams; two had recent cardioversion with resultant chest wall damage. The other eight patients had previous infarction 1 1/2 to 72 months earlier and had akinetic segments shown angiographically in the areas of the persistently positive scintigrams. Myocardial scintigraphy correlates well with the presence of other evidence of acute infarction, as well as with the absence of acute infarction when residual blood pool activity is identified. False positive scintigrams can occur following cardioversion and in patients with previous myocardial infarction and resultant ventricular wall motion abnormalities.

Heparin neutralizing activity test in the diagnosis of acute myocardial infarction.

We have previously shown in patients after recovery from a myocardial infarct (post-MI) that the heparin neutralizing activity (HNA) in the plasma is raised and that this activity may come from platelet factor 4 derived from activated platelets. This report concerns 89 patients admitted with acute chest pain; in 54, with evidence of acute infarction, the level of HNA is much higher than in a post-MI group or controls. Over the ensuing weeks the HNA decreases to the post-MI level. In 34 patients the evidence subsequently collected excluded a diagnosis of infarction; in these there were almost always normal amounts of HNA and little overlap with the results from the patients with infarcts. This easy test is therefore likely to prove clinically useful. Its significance is discussed. The platelet count and platelet volume are both abnormal in patients with acute infarction and also in the chest pain group so these tests do not help to discriminate.

Earliest symptoms of coronary heart disease and their recognition.

We have reviewed the histories of 320 patients in whom a diagnosis of coronary heart disease was ultimately established and traced the symptoms back to their first appearance. In 51% the first symptom was effort angina. Difficulties in recognition arose when the symptom was localized to an unusual site, when its occurrence was dependent on a combination of exercise with cold or a recent meal, or when it was induced by excitement rather than by effort. In a quarter of the cases the onset of angina was abrupt, and in these there was usually evidence of acute infarction.In 43% of cases the first symptom was an attack of pain or discomfort in the torso occurring without any discernable precipitating factor. Again, diagnosis was difficult when the pain was in an atypical site and also when it was of brief duration associated with skeletal or abdominal disease which could cause pain at the same site, or if the patient was able to undertake strenuous exertion. In four patients cardiac pain was first experienced during a paroxysm of tachycardia. In 6% of cases the onset was marked by a symptom other than pain-most frequently dyspnoea, tiredness, faintness, or syncope.Clinical examination was of no direct value in diagnosis. Its importance lay in disclosing factors which had to be taken into account in interpreting the electrocardiogram. The electrocardiogram was invaluable, though by no means infallible. In over half of the patients the first tracing showed major abnormalities of coronary type, and nearly a quarter more showed minor S-T/T depression consistent with coronary disease. Ten per cent. showed miscellaneous abnormalities, such as left ventricular hypertrophy or bundle-branch block, and 15% no definite abnormality.There is as yet no completely reliable objective method of diagnosing early coronary heart disease, so that the recognition of symptoms remains of paramount importance.