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Biomedical subjects

G J Hankey

Publications and source records attributed to G J Hankey.

At least 73 records · Page 4Linked to original sources
PubMed1996

Streptokinase for acute ischemic stroke with relationship to time of administration: Australian Streptokinase (ASK) Trial Study Group.

OBJECTIVES: To determine whether the administration of 1.5 million units of streptokinase intravenously within 4 hours of the onset of acute ischemic stroke would reduce morbidity and mortality at 3 months and whether outcomes may be better for those receiving therapy within 3 hours of stroke onset compared with those receiving it after 3 hours. DESIGN: Randomized, double-blind, placebo-controlled trial with 3-month follow-up. PARTICIPANTS: A total of 340 patients, aged 18 to 85 years, with moderate to severe strokes were randomized from 40 centers throughout Australia from June 1992 to November 1994. INTERVENTION: Administration of 1.5 million units of streptokinase or placebo intravenously in 100 mL of normal saline over 1 hour. MAIN OUTCOME MEASURE: Combined death and disability score (Barthel index <60) 3 months after the stroke. RESULTS: Using an intention-to-treat analysis with a combined death and disability score at 3 months after stroke as the primary end point, we found a nonsignificant overall trend toward unfavorable outcomes for streptokinase vs placebo (relative risk [RR] of unfavorable outcome, 1.08; 95% confidence interval [CI], 0.74-1.58) and an excess of hematomas (13.2%[12.6% symptomatic] in the treated group, 3% [2.4% symptomatic] for placebo [P<.01]). However, poor outcomes were confined to patients receiving therapy more than 3 hours after stroke onset (RR of unfavorable outcome, 1.22; 95% CI, 0.80-1.86). In contrast, among the 70 patients who were entered into the trial within 3 hours of stroke onset, there was a trend toward improved outcomes for those who received streptokinase (RR of unfavorable outcome, 0.66; 95% CI, 0.28-1.58), and this outcome pattern was significantly better than for those receiving therapy after 3 hours (P=.04). Streptokinase administration resulted in excess deaths in the group treated after 3 hours (RR, 1.98; 95% CI, 1.18-3.35), but not among those treated within 3 hours (RR, 1.11; 95% CI, 0.38-3.21). CONCLUSION: The administration of streptokinase within 4 hours of acute ischemic stroke increased morbidity and mortality at 3 months. While treatment within 3 hours of stroke was safer and associated with significantly better outcomes than later treatment, it showed no significant benefit over placebo. The timing of thrombolytic therapy for acute stroke is critical.

Acute Disease↗
PubMed1996

The risks and benefits of antithrombotic therapy in chronic atrial fibrillation.

As the risks of adverse effects of warfarin and aspirin in certain patients with chronic atrial fibrillation are high, intervention with these agents should be targeted towards those who will derive most benefit. Clearer guidelines are emerging to identify those patients and to standardise current prescribing practices.

Anticoagulants↗
PubMed1995

Asymptomatic carotid stenosis: how should it be managed?

OBJECTIVE: To discuss the implications of recent studies on carotid endarterectomy for asymptomatic carotid stenosis. DATA SOURCES: Trials of the effectiveness of carotid endarterectomy in asymptomatic carotid stenosis, including the Asymptomatic Carotid Atherosclerosis Study (ACAS). RESULTS: In the ACAS study, carotid endarterectomy for asymptomatic moderate to severe carotid stenosis (60%-99% luminal obstruction) reduced the absolute risk of ipsilateral stroke or death at five years by 5.9%. This means that about 17 patients need to be operated on to prevent one stroke or death over five years. To operate on all Australians with asymptomatic 60%-99% carotid stenosis would cost an estimated $A1.24 billion and prevent 800 strokes per year, or only 3% of all first strokes in Australia. RECOMMENDATIONS: In order to identify who will benefit from carotid endarterectomy and who will remain symptom-free without it, patients should continue to be allocated to the ongoing Asymptomatic Carotid Surgery Trail. Otherwise, carotid endarterectomy should be reserved for patients at high risk of stroke (i.e., with 95%-99% carotid stenosis) who are medically fit for surgery and willing to take the small short term risk of surgery for a possible greater long term benefit.

Adult↗
PubMed1995

Transient ischaemic attacks.

Each day, about 25 Australians experience a transient ischaemic attack of the brain or eye. These people need to be distinguished from those who suffer "funny turns" due to other causes because, as a group, they have a significant risk of stroke and other vascular events. This risk can be substantially reduced through control of vascular risk factors, use of long term antithrombotic medication and, in some cases, carotid endarterectomy. Strategies for stroke prevention need to involve both the "high risk" and population "mass" approach, which are complementary.

Anticoagulants↗
PubMed1994

Mechanism of stroke complicating cardiopulmonary bypass surgery.

BACKGROUND: Stroke is a devastating complication of cardiopulmonary bypass (CPB) surgery which occurs in 1 to 5% of cases. Strategies to reduce its incidence require a knowledge of the underlying pathology and aetiology. AIMS: To determine the incidence, pathology and aetiology of stroke complicating CPB. METHODS: Prospective review of clinical, operative and cranial CT scan findings in all cases of stroke complicating CPB procedures in our institution over an 18 month period. RESULTS: Twenty-one (1.6%, 95% CI 0.9-2.3%) cases of stroke were identified from 1336 CPB procedures. Cranial CT scan, performed in all but one patient, was normal in three patients or consistent with ischaemic stroke in 17 patients. There were no cases of haemorrhagic infarction or intracerebral haemorrhage. It was difficult to differentiate embolic and borderzone infarcts in two cases. After considering the clinical, operative and CT scan features together, 12 (57%, 95% CI 36-78%) of the cases were felt to be embolic in origin and nine (43%, 95% CI 22-64%) due to hypoperfusion in a borderzone. CONCLUSIONS: This study demonstrates that stroke remains an important complication of CPB procedures with an incidence in our series of 1.6%. The pathologic type of stroke is predominantly ischaemic in nature due to either cerebral embolism or borderzone infarction. Strategies for stroke prevention in patients undergoing CPB should be targeted primarily at these two mechanisms.

Adult↗
PubMed1994

Validation of a clinical classification for subtypes of acute cerebral infarction.

The validity of a clinical classification system was assessed for subtypes of cerebral infarction for use in clinical trials of putative stroke therapies and clinical decision making in a population based stroke register (n = 536) compiled in Perth, Western Australia in 1989-90. The Perth Community Stroke Project (PCSS) used definitions and methodology similar to the Oxfordshire Community Stroke Project (OCSP) where the classification system was developed. In the PCSS, 421 cases of cerebral infarction and primary intracerebral haemorrhage (PICH), confirmed by brain imaging or necropsy, were classified into the subtypes total anterior circulation syndrome (TACS), partial anterior circulation syndrome (PACS), lacunar syndrome (LACS), and posterior circulation syndrome (POCS). In this relatively unselected population, relying exclusively on LACS for a diagnosis of PICH had a very low sensitivity (6%) and positive predictive value (3%). Comparison of the frequencies and outcomes (at one year after the onset of symptoms) for each subgroup of first ever cerebral infarction in the PCSS (n = 248) with the OCSP (n = 543) registers showed uniformity only for LACI. For example, there were 27% of cases of TACI in the PCSS compared with 17% in the OCSP (difference = 10%; 95% confidence interval (95% CI) 4% to 16%) and 15% of cases in the PCSS compared with 24% in the OCSP were POCI (difference = 9%; 95% CI 3% to 15%). Case fatalities and long-term handicap across the subgroups were not significantly different between studies, but the frequencies of recurrent stroke were significantly greater for POCI in the OCSP compared with the PCSS. Although this classification system defines subtypes of stroke with different outcomes, simple clinical measures-level of consciousness, paresis, disability, and incontinence at onset-are more powerful predictors of death or dependency at one year. It is concluded that simple clinical measures that reflect the severity of the neurological deficit should complement this classification system in clinical trials and practice.

Acute Disease↗
PubMed1993

Why is the outcome of transient ischaemic attacks different in different groups of patients?

The outcomes of each of three large cohorts of patients with transient ischaemic attacks, which were studied in the same country at much the same time with the same methods, were compared and found to be quite different from each other. The differences in outcome were related not only to different strategies of treatment but also to differences in the prevalence and level of important prognostic factors (for example, case mix) and other factors such a the time delay from transient ischaemic attack to entry into the study and the play of chance. The implications for purchasers of health care are that they cannot rely solely on non-randomised comparisons of outcome of patients treated in competing units as a measure of the quality of care (which has only rather modest effects) without accounting for other factors that may influence outcome such as the nature of the illness, the case mix, observer bias, and the play of chance.

Aged↗
PubMed1993

Can the long term outcome of individual patients with transient ischaemic attacks be predicted accurately?

The prognosis of individual patients with transient ischaemic attacks (TIAs) is extremely variable; some patients are at high risk and others at low risk of a serious vascular event. Prediction equations of outcome were developed, based on eight clinical prognostic factors, from a cohort of 469 hospital-referred TIA patients ("training" data set), that enable high (and low) risk patients to be identified and for whom costly and risky treatments may (or may not) be targeted. The study aimed to determine whether these equations are externally valid and can predict outcome, with reliability and discrimination, in two independent cohorts of TIA patients ("test" data sets): 1653 TIA patients in the UK-TIA aspirin trial and 107 TIA patients in the Oxfordshire Community Stroke Project. Predicted outcomes agreed closely with the observed outcomes in the "test" data sets (reliability) for all outcome events at low five year risk (< 30%) but the estimates of risk were less precise in groups predicted to have a high five year risk (> 40%). The prediction equations were fairly accurate in discriminating between patients who subsequently suffered the outcome event of interest and those who survived free of the event at five years after the TIA, particularly at lower cut-off levels distinguishing high and low risk (for example, < 30% vs > 30% at five years). It is very difficult to achieve perfect discrimination because there is no single important prognostic factor for TIA patients that indicates whether a patient is going to suffer an event or not. These equations can be used to provide a reliable estimate of the absolute five year risk of a serious vascular event in hospital-referred TIA patients but they cannot, as yet, be used with confidence to distinguish patients at high risk from patients at low risk.

Aged↗
PubMed1992

Transient ischaemic attacks: which patients are at high (and low) risk of serious vascular events?

The aims of this study were to determine the important prognostic factors at presentation which identify patients with transient ischaemic attacks (TIA) who are at high risk (and low risk) of serious vascular events and to derive a prediction model (equation) for each of the major vascular outcome events. A cohort of 469 TIA patients referred to a University hospital, without prior stroke, were evaluated prospectively and followed up over a mean period of 4.1 years (range 1-10 years). The major outcome events of interest were 1) stroke 2) coronary event and 3) stroke, myocardial infarction or vascular death (whichever occurred first). Prognostic factors and their hazard ratios were identified by means of the Cox proportional hazards multiple regression analysis. The significant adverse prognostic factors (in order of strength of association) for stroke were an increasing number of TIAs in the three months before presentation, increasing age, peripheral vascular disease, left ventricular hypertrophy and TIAs of the brain (compared with the eye); the prognostic factors for coronary event were increasing age, ischaemic heart disease, male sex, and a combination of carotid and vertebrobasilar TIAs at presentation; and for stroke, myocardial infarction or vascular death they were increasing age, peripheral vascular disease, increasing number of TIAs in the three months before presentation, male sex, a combination of carotid and vertebrobasilar TIAs at presentation, TIAs of the brain (compared with the eye), left ventricular hypertrophy and the eye), left ventricular hypertrophy and the eye), left ventricular hypertrophy and the presence of residual neurological signs after the TIA. Prediction models (equations) of both the relative risk and absolute risk of each of the major outcome events were produced, based on the presence or level of the significant prognostic factors and their hazard. Before it can be concluded that our equations accurately predict prognosis and can be generalised to other populations, their predictive power needs to be validated in other, independent samples of TIA patients (which we are currently doing).

Aged↗
PubMed1991

Prognosis and prognostic factors of retinal infarction: a prospective cohort study.

OBJECTIVE: To determine the prognosis and adverse prognostic factors in patients with retinal infarction due to presumed atheromatous thromboembolism or cardiogenic embolism. DESIGN: Prospective cohort study. SETTING: University hospital departments of clinical neurology. PATIENTS: 99 patients with retinal infarction, without prior stroke, referred to a single neurologist between 1976 and 1986 and evaluated and followed up prospectively until death or the end of 1986 (mean follow up 4.2 years). INTERVENTIONS: Cerebral angiography (55 patients), aspirin treatment (37), oral anticoagulant treatment (eight), carotid endarterectomy (13), cardiac surgery (six), and peripheral vascular surgery (two). MAIN OUTCOME MEASURES: Death, stroke, coronary events, contralateral retinal infarction; survival analysis confined to 98 patients with retinal infarction due to presumed artheromatous thromboembolism or cardiogenic embolism (one patient with giant cell arteries excluded), and Cox's proportional hazards regression analysis, including age as a prognostic factor. RESULTS: During follow up 29 patients died (21 of vascular causes and eight of non-vascular or unknown causes), 10 had a first ever stroke, 19 had a coronary event, and only one developed contralateral retinal infarction. A coronary event accounted for more than half (59%) of the deaths whereas stroke was the cause of only one death (3%). Over the first five years after retinal infarction the actuarial average absolute risk of death was 8% per year; of stroke 2.5% per year (7.4% in the first year); of coronary events 5.3% per year, exceeding that of stroke; and of stroke, myocardial infarction, or vascular death 7.4% per year. Prognostic factors associated with an increased risk of death were increasing age, peripheral vascular disease, cardiomegaly, and carotid bruit. Adverse prognostic factors for serious vascular events were increasing age and carotid bruit for stroke, and increasing age, cardiomegaly, and carotid bruit both for coronary events and for stroke, myocardial infarction, or vascular death. CONCLUSIONS: Patients who present with retinal infarction due to presumed atherothromboembolism or cardiogenic embolism are at considerable risk of a coronary event. The risk of stroke, although high, is not so great. Not all strokes occurring after retinal infarction relate directly to disease of the ipsilateral carotid system, although this is probably the most common cause. Few patients experience contralateral retinal infarction. Non-arteritic retinal infarction should be diagnosed or confirmed by an ophthalmologist, and the long term care of patients with the condition should involve a physician who has an active interest in managing vascular disease.

Age Factors↗