Asymptomatic carotid bruit and stenosis: a reappraisal.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F M Yatsu.
Explore the source record for details and available documents.
Hemodynamic data were obtained in 9 patients (mean age 65 yrs) with carotid territory cerebral infarct within the preceding 24 hours (mean 14 +/- 8) as part of a pilot study testing the feasibility and safety of hypervolemic hemodilution. Pulmonary arterial catheters (PACs) were placed without complication in all patients, and after baseline measurements were obtained, up to 1500 cc of 6% hetastarch in 0.9% sodium chloride was administered the first day and up to 1000 cc per day the second and third days. Pulmonary wedge pressure (PWP) rose from 6.3 +/- 3.5 to 14.4 +/- 3.4 mm Hg (p less than 0.001) without development of congestive heart failure in any patient. This was accompanied by a drop in hematocrit (Hct) from 40.3 +/- 3.4 to 32.9 +/- 2.0 (p less than 0.001) and rise in cardiac output (CO) from 4.3 +/- 1.0 to 5.3 +/- 0.6 (p less than 0.05). Phlebotomy of 250 cc was performed in 2 patients and 500 cc in one in order to reduce Hct to desired levels. The volume of fluid needed to raise PWP to 15 was unpredictable (2361 +/- 1106 cc) and therefore PACs were necessary to monitor the rate and volume of fluid administration. The data show that PWP is sufficiently low and Hct sufficiently high following stroke in most patients that hemodilution by volume expansion with phlebotomy added if necessary can be undertaken safely with appropriate monitoring of hemodynamic function, and that this therapy results in optimal reduction of Hct and increased CO without risk of hypotension.
In order to assess the impact of variations in stroke care on outcomes, and to make geographic comparisons, the three Community Hospital-Based Stroke Programs in North Carolina, Oregon, and New York, aggregated their data on 4,132 hospitalized stroke patients. Complete demographic data or "Major Profile" were obtained on 2,390 (57.8%) of the 4,132 stroke patients. This includes those patients on whom informed patient and physician consents were obtained during the hospitalization. Of the major profile patients, 1,490 (62.3%) were followed for periods up to one year, 502 (21.0%) were lost to followup and 398 (16.6%) died within the one year followup period. Incomplete demographic data or "Minor Profile" were observed on 1,742 (42.1%) of the 4,132 patients. Minor profile includes those who died before comprehensive interviews were completed or those for whom informed consent for an interview could not be obtained. Of the minor profile group, 813 (46.7%) died in hospital, and 929 (53.3%) were alive when discharged from the hospital. This paper, which describes the programs, data collection procedures, and study cases, also highlights specific issues on stroke diagnosis, risk factors associated with stroke, and the influence of interventions on stroke outcomes. We conclude that: 1) the merging of data on hospitalized stroke cases from rural and urban hospitals in geographically distinct regions can be used in the study of stroke diagnosis, the use of diagnostic tests, and the effect of interventions on stroke outcomes; and 2) these data are consistent with the hypothesis that part of the national decline in mortality from stroke is due to a decline in stroke severity.
The three Community Hospital-based Stroke Programs collected data on 4132 stroke patients admitted to acute care hospitals during 1979 and 1980. White female stroke patients were older than the white male, nonwhite female and nonwhite male stroke patients. Nearly one-fourth (23%) of stroke patients were employed at the time of the event. Most (77%) of the patients were hospitalized for first stroke episodes. Eighty-three percent of the patients had at least one of the four major risk factors for stroke, namely, hypertension, diabetes, transient ischemic attacks and cardiac disease. Half (49%) of the patients were alert at the time of admission. The three diagnostic categories included infarction (60%), stroke not otherwise specified (30%) and hemorrhage (10%). Fourteen days was the median length of hospitalization; 50% of the stroke patients were discharged to a home setting, 31% were institutionalized and 19% died while in the hospital. The mean Barthel Index score for 2400 patients at the time of discharge was 61.8 (normal is 100). Of those patients who were working at the time of the stroke, 22% returned to work. In comparison to the patients in the National Survey of Stroke, patients in this Study were less severe at the time of admission (49% of patients in the National Survey of Stroke were stuporous or comatose compared to 21% of the patients in the current Study). The inhospital fatality was 30.7% in the National Survey of Stroke, and 19.7% in the current Study.
Foam cells are lipid-laden macrophages derived primarily from circulating mononuclear cells and are a characteristic feature of atheromatous lesions. The exact role of these foam cells in the pathogenesis of atherosclerotic lesions remains uncertain, but one potential function is to take-up and process excess interstitial arterial lipoproteins, suggested by their extraordinary ability to engulf enormous quantities of modified low density lipoproteins by the so-called "scavenging pathway." To test this possibility, monocytes from 15 atherothrombotic brain infarct patients and age and sex matched controls were isolated and cultured for 7-8 days in 20% normal serum. The monocyte-derived macrophages were investigated for their ability to bind, internalize and degrade both native and modified (acetylated) LDL labelled with 125Iodine. While native LDL was metabolized similarly, stroke macrophages displayed significantly reduced ability to scavenge modified LDL. These findings suggest that insufficient processing of interstitial arterial cholesterol by monocyte-derived macrophages may contribute to the aggravation of atheroma formation. This inadequacy is likely further compromised by reduced levels of serum high density lipoprotein since the absence of a cholesterol-acceptor will promote the slow but continued accumulation of lipids and the formation of foam cells.
Explore the source record for details and available documents.
The therapeutic efficacy of prostacyclin in nonhemorrhagic cerebral infarction was assessed in a placebo-controlled double-blind trial. A total of 80 patients with stroke onset within 24 hours were randomized into placebo (37 patients) and prostacyclin (43 patients) groups. Demographic data and risk factors were comparable. Patients in the prostacyclin group received a continuous i.v. infusion of prostacyclin at an average rate of 8.5 ng/kg/min for an average of 64 hours. The placebo group received vehicle only in a similar fashion. During treatment hemodynamic changes were more prominent in the patients receiving prostacyclin and included reduction of systolic and diastolic blood pressure and increase in pulse rate. In contrast there was only a slight (but significant) reduction of diastolic blood pressure in the placebo group. Neurologic deficit scores were determined on admission, at Day 3, and at Weeks 1, 2, and 4. Mean neurologic deficit scores upon entry were comparable in the placebo and prostacyclin groups, and a significant improvement in the score for neurologic deficit was noted in both. The placebo group tended to fare better throughout the study, with a significant difference in neurologic deficit score favoring the placebo group at Week 2 (p = 0.0048). Two patients in the placebo and one in the prostacyclin group died. The only difference in adverse reactions was flushing (6 patients in prostacyclin vs. 0 in placebo group, p less than 0.05). The results of this study suggest a lack of therapeutic efficacy of prostacyclin in a defined population of patients with nonhemorrhagic cerebral infarction.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The permissible duration of brain ischemia without sustaining damage is short. Less clear are the mechanisms accounting for the vulnerability of brain to ischemic insults. Neurochemical factors implicated include impairment of energy synthesis by mitochondria and of energy-dependent processes such as synaptic transmission, ATPase activity, membrane conductance and altered protein and lipid synthesis. To clarify the vulnerability of energy metabolism, we investigated energy availability and synthesis in our model of global cerebral ischemia. Our studies evaluated in vitro mitochondrial ATP synthesis and the in vivo quantitation of the cortical adenylate pool. Results of our investigations support a growing body of evidence showing the energy state to be relatively stable to ischemia. We conclude that an energy-dependent process of brain is primarily vulnerable to ischemia.