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Etiology, Duration, and Prognosis of Transient Ischemic Attacks
An Analysis From the German Stroke Data Bank
Christian Weimar, MD;
Klaus Kraywinkel, MD;
Joachim Rödl, MD;
André Hippe, MD;
Lutz Harms, MD;
Antje Kloth, MD;
Hans-Christoph Diener, MD;
for the German Stroke Data Bank Collaborators
Arch Neurol. 2002;59:1584-1588.
ABSTRACT
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Context A transient ischemic attack (TIA) has been arbitrarily defined as a
focal cerebral ischemic deficit lasting less than 24 hours.
Objective To determine if TIAs of short duration (<1 hour) and long duration
(1 hour to <24 hours) differ from each other and from ischemic stroke (IS).
Design, Setting, and Patients Inception cohorts of 1429 patients with acute TIAs and 5206 patients
with IS were prospectively documented in 15 German medical centers with neurology
departments and acute stroke units. Outcome after 3 months was assessed in
72.8% of the patients with TIAs.
Main Outcome Measures Risk factor distribution, etiology, and prognosis of TIAs and IS.
Results Patients with TIAs, especially those with symptoms lasting less than
1 hour, were significantly more likely to have a history of TIAs and less
likely to have diabetes mellitus, arterial hypertension, or atrial fibrillation
at admission compared with those with IS. Cardioembolic etiologies were less
frequent and unknown etiologies more frequent among patients with TIAs than
those with IS. Functional outcome and mortality did not differ significantly
in patients with TIAs of different durations.
Conclusion This study demonstrates differences in comorbidity and etiology among
patients with TIAs of different durations and IS.
INTRODUCTION
THE NATIONAL Institute of Neurological Disorders and Stroke's "Classification
of Cerebrovascular Diseases III"1 defines transient
ischemic attacks (TIAs) as brief episodes of focal loss of brain function
lasting less than 24 hours that are thought to be due to ischemia, that can
usually be localized to a portion of the brain supplied by 1 vascular system
(left or right carotid or vertebrobasilar system), and for which no other
cause can be found. The incidence of first-time TIAs constitutes roughly one
quarter of the incidence of initial cerebrovascular events.2-8
Although TIAs are generally regarded as significant risk factors for subsequent
stroke, the criterion of symptoms lasting less than 24 hours has been criticized
as having little relevance for diagnosis and secondary prevention.9 To date, only 1 study with small patient numbers has
investigated the clinical characteristics of patients with different durations
of neurological deficits following cerebral ischemia. It found a higher frequency
of cardiac and large-vessel disease among patients with long-duration TIAs.10
To fulfill one of the predefined aims of the German Stroke Data Bank,
we investigated the hypothesis that short- (<1 hour) and long-duration
TIAs (1 hour to <24 hours) differ in terms of risk factor distribution,
etiology, and prognosis compared with ischemic stroke (IS).
PATIENTS AND METHODS
Data were prospectively collected between 1998 and 1999 within the German
Stroke Data Bank of the German Stroke Foundation (Stiftung Deutsche Schlaganfall-Hilfe,
Gütersloh) in 23 hospitals with neurology departments and acute stroke
units. Each one serves a catchment area of more than 100 000 inhabitants
and is the main source of care for patients with stroke in its region. Prospectively
collected data included age, sex, times of the event and admission, risk factors,
vascular comorbidity, prior medication use, National Institutes of Health
Stroke Scale (NIHSS) score at admission, functional independence on the Barthel
Index and modified Rankin scale before the event and after admission, results
of additional clinical investigations such as cerebral imaging, extracranial
ultrasonography, and transesophageal echocardiography, Trial of Org 10172
in Acute Stroke Treatment (TOAST) classification,11
complications, length of stay in the documenting hospital, and medications
for secondary prevention at discharge. Follow-up interviews after 3 and 12
months assessed functional independence on the Barthel Index and modified
Rankin scale or cause of death in patients with TIAs and IS. Data were collected
using a standardized questionnaire based on an extensive manual, as well as
video training for the assessment of the NIHSS score.
The NIHSS assesses deficits in 15 neurological functions on a scale
of 0 (no deficit) to 42. The modified Rankin scale quantifies overall functional
status on a score of 0 (no handicap) to 5 (bedridden, incontinent, and requiring
constant nursing care and attention).12 Risk
factors were defined as follows: arterial hypertension as a history of elevated
blood pressure (>160/90 mm Hg) on 2 independent readings before stroke or
the use of antihypertensive medication; diabetes mellitus as a history of
elevated blood glucose levels on 2 independent readings before stroke, elevated
glycosylated hemoglobin level (>7.5%) at admission, or the use of antidiabetic
medication; hypercholesterolemia as a history of elevated total cholesterol
levels (>220 mg/dL [>5.69 mmol/L]) on 2 independent readings before stroke
or the use of lipid-lowering medication; and smoking currently or during the
last 5 years. Information on risk factors and other comorbidity was obtained
primarily from the patient; additional information was collected from relatives
and primary care physicians.
A diagnosis of TIA was made in cases of clinical deficits lasting less
than 24 hours regardless of an infarction seen on cerebral imaging scans.1 The duration of TIAs was stratified into intervals
of less than 1 hour, 1 to less than 12 hours, and 12 to less than 24 hours.
For the purpose of this analysis, the latter 2 categories respresent long-duration
TIAs (1 to <24 hours). The etiological classification was based on the
TOAST criteria and was scored according to a standardized protocol by the
investigators at each site.11, 13
After a final consistency check with the source data at each site, questionnaires
were sent to the data management centers at the University of Essen (Essen,
Germany) and the German Stroke Foundation. They were rechecked by 2 physicians
for completeness and consistency of the classification with additional diagnostic
results. Questions regarding missing or implausible data were directed to
the treating neurologist. Data were entered into the database in duplicate
by trained personnel. Data quality was further ensured with monthly reports
and clinical site visits. All patients gave informed consent if their personal
data were to be transferred to the data management center for central follow-up.
Otherwise the follow-up was performed in the documenting center, and the results
were forwarded to the data management center. To assess outcome after both
recurrent TIAs and IS, we considered all information obtained from the patient,
relatives, and treating physicians.
A total of 9296 patients with TIAs or IS were recruited for this study.
Of these, all 2661 patients from 8 of the participating centers were excluded
because we could not rule out a selection bias in these hospitals. Thus, our
analyses include 6635 patients from 15 centers. Follow-up after 3 months (median,
102 days; range, 70-150 days) was obtained in 1040 (72.8%) of the patients
with TIAs, and the results were considered to indicate the respective patients'
status after 3 months. Of the patients with TIAs, 1.4% refused to participate
in the follow-up, 7% could not be contacted during the follow-up window, and
18.8% were not contacted at all, partly because of limited funding for central
follow-up or lack of staff to ensure local inquiries by the participating
centers (Figure 1). Comparison of
the patients included in the follow-up and those lost to follow-up showed
no significant differences in age, sex, duration of symptoms, prior stroke,
prior TIAs, ischemic heart disease, arterial hypertension, or diabetes mellitus.
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Figure 1. Flowchart of patient inclusion.
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Statistical analysis was performed using SPSS version 9.0 statistical
software (SPSS Inc, Chicago, Ill). Continuous variables are presented as mean
and median. Categorical variables are presented as percentages. For statistical
comparisons between patients with TIAs of different durations and patients
with IS, as well as the comparison of short- and long-duration TIAs, we used
the Fisher exact test for categorical variables and the 2-tailed t test for continuous variables. To account for multiple testing, P<.01 was considered significant.
RESULTS
Of the 6635 patients with cerebral ischemia included in this analysis,
1429 patients (21.5%) had a final diagnosis of TIA, and 5206 (78.5%) had a
final diagnosis of IS. Among those with TIAs, neurological symptoms were completely
resolved in less than 1 hour in 423 patients (29.7%), in 1 to less than 12
hours in 429 patients (30.1%), and in 12 to less than 24 hours in 577 patients
(40.5%).
The frequencies of comorbidity and risk factors are listed in Table 1. There were only minor differences
in age, sex, and prior functional independence between patients with different
durations of TIAs and those with IS. The rates of prior TIAs and hypercholesterolemia
were significantly higher in patients with TIAs than in those with IS, whereas
the rates of smoking, arterial hypertension, diabetes mellitus, and atrial
fibrillation at admission were significantly lower in patients with TIAs.
Patients with symptoms lasting less than 1 hour reported the highest rates
of prior TIAs and hypercholesterolemia but had the lowest rates of prior stroke
and atrial fibrillation at admission.
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Table 1. Demographic Characteristics, Comorbidity, and Risk Factors
of All Patients With TIAs and IS*
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The median delay between the event and admission was 135 minutes in
patients with TIAs compared with 111 minutes in patients with IS. At admission,
57% of patients with TIAs had some neurological deficits according to the
NIHSS: usually limb weakness (25%), facial weakness (22%), sensory deficits
(21%), or aphasia (11%). The mean NIHSS score at admission was 1.8 (median,
1).
Additional examinations were performed in similar percentages of patients
with TIAs and IS. These included cerebral imaging (TIAs and IS: 99.9%), extracranial
ultrasonography (TIAs: 97.7%; IS: 95.9%), and transesophageal echocardiography
(TIAs: 32.6%; IS: 35.9%). Table 2
indicates the frequency of pathologic findings on these examinations. Patients
with TIAs had significantly fewer ipsilateral stenoses with more than a 50%
reduction in diameter on extracranial ultrasonography and fewer cardiac sources
of embolism on transesophageal echocardiography than patients with IS. In
addition, prior infarctions detected using cerebral imaging were significantly
less frequent in patients with short-duration compared with long-duration
TIAs.
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Table 2. Frequency of Clinically Relevant Pathologic Findings in Additional
Investigations in Patients With TIAs and IS*
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The frequencies of TOAST classification etiologies are presented in Table 3. The use of this classification
system resulted in a high percentage of unknown etiologies. Among patients
with TIAs, small vessel disease was significantly more common and cardioembolic
causes were significantly less common compared with patients with IS. Compared
with long-duration TIAs, short-duration TIAs were classified significantly
more often as large artery atherosclerosis and less often as small vessel
disease.
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Table 3. TOAST Classification in Patients With TIAs and IS*
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The mean length of stay in the documenting hospital was 7.7 days (median,
7 days) for patients with TIAs and 11.9 days (median, 10 days) for patients
with IS. At the time of discharge from the hospital, 82% of patients with
TIAs were prescribed platelet inhibitors (49% receiving aspirin), 12% were
prescribed oral anticoagulants, 4.5% were given intravenous heparin (most
of these patients were transferred to another hospital), and 1.5% were discharged
without any preventive medication. Of the patients with IS, 69.4% were given
platelet inhibitors (43.7% receiving aspirin), 18.4% were prescribed oral
anticoagulants, 6.2% received intravenous heparin, and 6.0% were given no
preventive medication.
By the 3-month follow-up visit, 18 patients (1.7%) with TIAs had died
(Figure 2) compared with 551 patients
(14.0%) with IS. Only 3 patients with TIAs had died due to a new stroke. Although
more patients with short-duration TIAs experienced a recurrent cerebrovascular
event during their hospital stay than those with long-duration TIAs (data
not shown), there was no significant difference in functional outcome after
3 months (Table 4).
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Figure 2. Mortality rates up to 3 months
after a transient ischemic attack (TIA) or ischemic stroke (IS) in patients
available for follow-up. Asterisk indicates significance (P<.01) vs IS.
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Table 4. Mortality and Global Outcome After 3 Months in Patients With
TIAs Who Were Reached for Follow-up*
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COMMENT
In this large, hospital-based cohort study, we investigated the hypothesis
that TIAs of varying duration differ from each other and from IS in terms
of etiology, risk factor distribution, and prognosis. Because this was not
an epidemiological study, the population can be considered representative
only for specialized stroke care facilities. However, the prevalence of TIAs
in all patients with cerebral ischemia (21.5%) was similar to that observed
in epidemiological studies.3-4,8
In contrast, the prevalence of long-duration TIAs (70%) was unexpectedly high.
This might be explained by the fact that patients with singular symptoms of
shorter duration are less likely to see a physician or be admitted to the
hospital. Whereas epidemiological studies to date have not investigated the
duration of symptoms in TIAs, other hospital-based studies have reported a
mean duration of 207 minutes and symptoms lasting more than 30 minutes in
50% of all patients with TIAs.14-15
Risk factors such as atrial fibrillation, arterial hypertension, diabetes
mellitus, and smoking were significantly less frequent in patients who had
TIAs compared with those with IS. An inverse relationship was seen for hypercholesterolemia
and prior TIAs. Several population-based studies have shown no significant
differences in risk factor distribution between TIAs and IS, which could be
because of the exclusion of more severe strokes as well as smaller patient
numbers.16-18
Among patients with short-duration TIAs, the frequency of prior TIAs
was significantly elevated, whereas that of prior stroke was significantly
reduced. Apart from small vessel disease, which was diagnosed more often in
patients with TIAs, known etiologies such as cardioembolic events were reduced;
a high percentage of etiologies remained unknown in these patients. However,
the classification of large artery atherosclerosis was more frequent among
patients who had TIAs with symptoms lasting less than 1 hour and patients
with IS than among those who had TIAs with symptoms lasting 1 hour or more.
This contrasts with the results of a small study by Kimura et al,10 which found an increase in pathologic vascular findings
with increasing duration of symptoms. Because the diagnostic workup after
a TIA was very similar to that after IS, the high percentage of unknown etiologies
according to the TOAST criteria might be indicative both of transient pathologic
findings and diagnostic uncertainty regarding TIAs.
The mortality rate of patients with TIAs was slightly lower in our study
than in a large hospital-based study in San Francisco, Calif, that reported
a mortality rate of 2.6% within the first 90 days, of which 44% of deaths
were due to a new stroke.14 The overall 90-day
stroke recurrence rate in that study was 10.5%, more than half of which occurred
within the first 2 days after the initial TIA. This suggests that TIAs must
be considered serious events requiring immediate action. Similarly, a smaller
population-based study in Rochester, Minn, reported a 3-month stroke recurrence
rate of 10% following TIAs.7 A study from Oxford,
England, reported stroke in 8.8% of patients with TIAs during the first 6
months after the event and 11.6% during the first year, but it excluded all
patients who experienced a stroke prior to inclusion in the study.19 In our study, recurrent TIAs and stroke could not
be reliably differentiated and are therefore the subject of an ongoing study.
Although several studies have proposed possible predictors for stroke
recurrence after TIAs,14, 20-24
only 1 has attempted an external validation.24
Because the prognostic models identified in these studies had low predictive
accuracy, we did not analyze possible predictors for recurrent cerebral ischemia.
Some investigators have suggested that the differences between cerebral
ischemias of different duration are quantitative rather than qualitative.25 However, the arbitrary definition of TIA as an episode
lasting less than 24 hours has little relevance for clinical decision making,
nor is it supported by modern imaging techniques.26
Our results support the concept of short-duration TIA as an additional entity,
as do those of an earlier study.10
Our study has several limitations. In most of the participating hospitals,
patients were included consecutively and without the application of selection
criteria. We cannot exclude the possibility that some patients with short-duration
TIAs may have been systematically missed, which could have influenced our
results. We were also unable to ensure complete follow-up of all patients.
Nevertheless, a comparison between the patients included in the study and
those lost to follow-up showed no significant differences in baseline characteristics.
In conclusion, we found differing etiologies and risk factors for short-
and long-duration TIAs and IS. Whereas patients with short-duration TIAs showed
the highest prevalence of prior TIAs and hypercholesterolemia as strong risk
factors for cerebrovascular disease, they had a low prevalence of prior stroke
and visible prior infarction. Whether this corresponds to a predominant risk
of recurrent TIAs rather than stroke is the subject of an ongoing study. Meanwhile,
any TIA should be regarded as a serious event requiring a complete etiologic
workup and appropriate medical prevention strategies to prevent recurrent
cerebral ischemia with potentially more disastrous consequences.
AUTHOR INFORMATION
Accepted for publication April 24, 2002.
Author contributions: Study concept and design (Drs Weimar, Rödl, and Diener); acquisition of data (Drs Weimar, Rödl, Hippe, Harms, and Kloth); analysis
and interpretation of data (Drs Weimar, Kraywinkel, and
Harms); drafting of the manuscript (Drs Weimar and
Kraywinkel); critical revision of the manuscript for important intellectual
content (Drs Rödl, Hippe, Harms, Kloth, and Diener); statistical expertise (Drs Diener and Kraywinkel); obtained funding (Drs Weimar and Diener);
administrative, technical, and material support (Dr Weimar); study supervision (Drs Weimar and Diener).
This study was supported by the Stiftung Deutsche Schlaganfall-Hilfe,
Gütersloh, Germany; Heinz-Nixdorf-Foundation, Essen, Germany; Bayer,
Leverkusen, Germany; Bristol-Myers-Squibb, Munich, Germany; Boehringer Ingelheim,
Ingelheim, Germany; Glaxo-Wellcome (now GlaxoSmithKline), Munich; Janssen-Cilag,
Neuss, Germany; Knoll, Ludwigshafen, Germany; Sanofi-Synthelabo, Berlin, Germany;
and Schering, Berlin.
We thank the Stiftung Deutsche Schlaganfall-Hilfe for help with data
collection.
German Stroke Data Bank Collaborators
Departments of Neurology and Principal Investigators
in Germany
Klinikum Minden, Minden: Joerg Glahn, MD. Krankenhaus München-Harlaching, Munich: Martin L.
J. Wimmer, MD. University of Essen, Essen: Christian
Weimar, MD. University of Homburg, Homburg: Michael
P. Roth. University of Leipzig, Leipzig: Dietmar
S. Schneider, MD. Benjamin Franklin University, Berlin: Christian Koennecke, MD. Asklepiosklinik Salzhausen,
Nidda–Bad Salzhausen: Gerhard-Michael v. Reutern, MD. University of Greifswald, Greifswald: Jochen Machetanz, MD. University of Rostock, Rostock: Antje Kloth, MD. St Katharinen Hospital, Frechen: Rolf Adams, MD. University of Magdeburg, Magdeburg: Michael Goertler, MD. University of Jena, Jena: Joachim Roether, MD. University
of Ulm, Ulm: Matthias Riepe, MD. Bürgerhospital
Stuttgart, Stuttgart: Elisabeth Schmid, MD. Krankenanstalten
Gilead, Bielefeld: Angela Schacker, MD.
Corresponding author and reprints: Christian Weimar, MD, Neurologische
Klinik der Universität-GHS Essen, Hufelandstr 55, 45122 Essen, Germany
(e-mail: stroke.med{at}uni-essen.de).
From the Departments of Neurology, University of Essen, Essen (Drs
Weimar, Kraywinkel, and Diener), Klinikum Nürnberg Süd, Nuremberg
(Dr Rödl), University of Greifswald, Greifswald (Dr Hippe); University
Charité Berlin, Berlin (Dr Harms), and University of Rostock, Rostock
(Dr Kloth), Germany.
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