Low-dose aspirin and stroke. "It ain't necessarily so".
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Biomedical subjects
Publications and source records attributed to J W Norris.
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BACKGROUND AND PURPOSE: Silent cerebral infarction is often found on computed tomographic scan in patients with asymptomatic carotid stenosis, but its relation to the arterial stenosis is uncertain. METHODS: We compared computed tomographic scans and carotid Doppler in 115 patients with asymptomatic carotid stenosis, 203 with carotid transient ischemic attacks and carotid stenosis, and 63 with transient ischemic attacks but without carotid stenosis. There was no group with normal carotid arteries for comparison. RESULTS: Lesions seen on CT scan were most common in the transient ischemic attack with carotid stenosis group (47%) compared with the other groups (30%, 19%) (p less than 0.001). Cerebral infarcts ipsilateral to the carotid stenosis were found in 10% of patients with mild (35-50%) stenosis, 17% in moderate (50-75%) stenosis, and 30% with severe (greater than 75%) carotid stenosis (p less than 0.001). In patients with asymptomatic carotid stenosis, 68% of infarcts were ipsilateral to the stenosis; in those with transient ischemic attacks and carotid stenosis, 86% of infarcts were ipsilateral to the stenosis. CONCLUSIONS: The more severe the carotid stenosis, the higher the incidence of cerebral infarction ipsilateral to the stenosis. This finding applied to central infarcts as well as to peripheral infarcts in both symptomatic and asymptomatic patients. Silent cerebral infarction may be an indication for carotid endarterectomy in asymptomatic patients.
We examined the baseline characteristics of patients in the Ticlopidine Aspirin Stroke Study (TASS) to determine if the effects of the two treatments in preventing stroke differed in various subgroups. Patients with the following characteristics did less well on aspirin: elevated creatinine, hypertension or diabetes requiring treatment, or treatment with anticoagulant or antiplatelet drugs prior to their qualifying TIA or stroke. Women and patients with vertebrobasilar symptoms did particularly well on ticlopidine. We performed arteriography in 1,188 patients with carotid qualifying events. The frequency of stroke in patients with abnormal arteriograms ipsilateral to their symptoms was slightly higher than in those with normal carotid arteries. Ticlopidine was more effective in patients without carotid stenosis. Ticlopidine is more effective than aspirin in preventing strokes in patients having warning TIAs. The patients who benefit most from ticlopidine may be women, those who have vertebrobasilar symptoms, those with cerebral ischemic symptoms while on aspirin or anticoagulant therapy, and patients with diffuse atherosclerotic disease rather than high-grade carotid stenosis.
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The role of extracranial occlusive lesions in the pathogenesis of ischemic stroke is well established. The management of asymptomatic carotid bruit or stenosis is still highly controversial, however. This article reviews in detail the currently available data in order to assist clinicians in the management of patients with asymptomatic neck bruits or stenosis.
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Cardiac catheterization in a 55-year-old man, presenting with chronic chest pain and new T wave inversion, showed apical left ventricular (LV) hypertrophy and a large intercoronary connection between the posterior descending artery (PDA) and left anterior descending (LAD). Although the LAD was normal, selective angiography of the right coronary artery (RCA) filled the LAD retrogradely. Possible mechanisms and the literature are reviewed.
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BACKGROUND AND PURPOSE: We sought to determine the risks of stroke, myocardial ischemia, and vascular death in patients with asymptomatic carotid stenosis. METHODS: Six hundred ninety-six patients with asymptomatic carotid stenosis referred to the Doppler laboratory were followed prospectively for a mean time of 41 months. These patients were studied both clinically and by carotid Doppler ultrasound, including evaluation of the effect of stroke risk factors. RESULTS: Transient ischemic attacks occurred in 75 patients and stroke in 29, while 132 had ischemic cardiac events. Five patients died from stroke and 59 from cardiac causes. Annual stroke rate was 1.3% in patients with carotid stenosis less than or equal to 75% and 3.3% in those with stenosis greater than 75%. Ipsilateral stroke rate was 2.5% in patients with greater than 75% carotid stenosis. Annual cardiac event rate was 8.3% and death rate 6.5% in patients with severe carotid stenosis. CONCLUSIONS: With carotid stenosis less than or equal to 75%, the stroke rate is negligible (1.3% annually) whereas the combined risk of cardiac ischemia and vascular death is as high as 9.9%. With stenosis greater than 75%, combined transient ischemic attack and stroke rate is 10.5% per year, with 75% of events ipsilateral to the stenosed artery.
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Much of the published data concerning the outcome in patients with transient ischaemic attacks and stroke was produced before the development of computerised tomography, and when the risk factors for cerebrovascular disease were different in quality and quantity. Outcome data also depend on the definition of the original disorders, which remain controversial and are often poorly described. Recent advances in laboratory diagnosis, such as imaging of the brain and extra- and intra-cranial blood vessels, have also made definition more complex. Strokes due to carotid artery stenosis differ in outcome from those due to cardiac embolism; the most benign group is that of lacunar strokes. Recent trials indicate a more serious prognosis for patients with carotid stenosis than previously believed, although these data are affected by referral bias. Outcome data will need to be updated in the future as more becomes known about the aetiology and pattern of cerebrovascular disease.
The natural history of asymptomatic carotid stenosis was prospectively and systematically studied in 500 patients by clinical observation and carotid Doppler ultrasonography. In the 40% of carotid arteries (398) with an initial stenosis of over 35%, there were apparently two separate populations, with a cutoff point of 85% stenosis. There were 79 ischemic cerebral events (54 transient ischemic attacks and 25 strokes) among the 500 patients during 60 months of follow-up, predominantly in the severe-stenosis (more than 75%) group, with few events occurring in the near-or total-occlusion (95% to 100% stenosis) group; the highest incidence was in patients whose arteries had 75% to 90% stenosis. These observations indicate a critical degree of carotid stenosis at which stroke risk becomes maximal, declining as the artery becomes occluded. These findings suggest that there may be a "window" for carotid endarterectomy in patients with asymptomatic carotid stenosis, when the stroke risk may be high enough (5.5%/year) to warrant surgery.
We correlated the clinical and pathologic findings in 77 consecutive carotid plaques removed at endarterectomy to determine the clinical role of intraplaque hemorrhage. Intraplaque hemorrhages of various severity were seen in 86% of plaques. They were, for the most part, deeply located (63%) and infrequently connected with the lumen. They related closely to the severity of carotid stenosis, but bore no relationship to the timing of symptoms. Luminal thrombus was infrequently seen, and was always microscopic. Hemorrhage into carotid plaque appears to represent an index of the severity of the stenosis and plaque instability rather than to play a direct role in the pathogenesis of transient ischemic attacks or stroke.
Physiological adaptation to weightlessness requires changes in cardiovascular system parameters to maintain homeostasis in the presence of cephalic fluid shifts. The cerebral circulation must respond immediately to these systemic changes or impairment of cerebral function will occur. Blood flow velocities of the middle cerebral artery were measured by transcranial Doppler (TCD) ultrasound in NASA's KC-135 aircraft from four healthy subjects in the supine position. Transcranial Doppler data with accompanying acceleration information were analyzed in three segments in each parabola. Cardiac cycles for each segment of all 20 parabolas were pooled for individual subjects. A Student's t test on the data revealed statistically significant differences in the mean and peak frequencies, systolic/diastolic ratios and Doppler power between positive 2 gz and microgravity (10(-2) gz) as well as between positive 2 gz and negative 2 gz. Velocity waveform profiles differed for the first one third of each segment, with a more resistive waveform developing during the last two thirds. Changes in systemic arterial resistance and/or raised intracranial pressure may contribute to these TCD waveform changes.
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Fibrous membrane formation on the anterior surface of an intraocular lens with occlusion of the pupil was noted in five patients having phacoemulsification and one patient having planned extracapsular cataract extraction. Initial onset of pain and decreased vision ranged from eight to 36 postoperative days. Since these patients did not respond fully to steroid therapy, the neodymium:YAG laser was used to disrupt the fibrinous membrane which occluded the pupil. In all but one case, the fibrinous reaction responded to laser therapy. Generally, less energy was required when laser therapy was initiated early in the treatment plan.
We achieved a unique and timely recording of cerebral activity in a 70 year old woman immediately pre- and post-stroke, while studying the effect of acute cerebral infarction on sleep-electroencephalogram (EEG) patterns. Normal patterns, except for increased wakefulness, were recorded during two pre-infarct polysomnograms. Immediately following cerebral infarction increased delta activity was recorded from the infarcted hemisphere only. Initially, REM sleep could not be recorded from either side; however, on the third post infarct day REM sleep returned. Background EEG levels from both hemispheres became progressively slower, flatter and simpler. In addition, sleep spindles and the distinctive saw-tooth wave forms of sleep almost disappeared. At one year post-stroke sleep-EEG rhythm recordings from both hemispheres became more similar except for persisting delta activity from the left hemisphere. Unexpected deterioration of sleep-EEG pattern recordings from the undamaged hemisphere taken during the patient's clinical recovery remains unexplained. Serial sleep recording may facilitate the study of brain recovery, activity and reorganization following stroke.