 |
|
Electrocardiographic Findings Predict Short-term Cardiac Morbidity After Transient Ischemic Attack
Jacob S. Elkins, MD;
Stephen Sidney, MD, MPH;
Daryl R. Gress, MD;
Alan S. Go, MD;
Allan L. Bernstein, MD;
S. Claiborne Johnston, MD, PhD
Arch Neurol. 2002;59:1437-1441.
ABSTRACT
| |
Background Current guidelines recommend the use of electrocardiography (ECG) in
the evaluation of transient ischemic attack (TIA), but the data supporting
its value in acute management are sparse.
Objective To determine whether ECG findings are useful as independent predictors
of short-term cardiac or neurologic complications after TIA.
Methods We included patients who presented to 1 of 16 emergency departments
of a health maintenance organization in northern California and received a
diagnosis of TIA from March 1, 1997, through February 28, 1998, for a 90-day
follow-up. A cardiac event was defined as a hospitalization or a death due
to myocardial infarction, ventricular arrhythmia, heart failure, or unstable
angina.
Results Among the 1327 patients with TIA for whom ECG findings were available
for diagnostic coding, cardiac events occurred in 2.9%, strokes in 10.9%,
recurrent TIAs in 13.7%, and deaths in 2.6% during 90-day follow-up. The ECG
findings disclosed a new diagnosis of atrial fibrillation in 28 (2.3%) of
the 1200 patients with no history of this condition. The 90-day risk for a
cardiac event was greater in those who had any abnormal ECG findings (4.2%
vs 0.6%; P<.001). This association remained significant
after adjustment for medical history and examination findings (odds ratio,
6.9; 95% confidence interval, 1.6-29.5; P = .009).
Left ventricular hypertrophy, atrial fibrillation, and atrioventricular conduction
abnormalities were each independently associated with more than doubling of
the risk. The ECG abnormalities were not associated with risk for stroke or
death.
Conclusions Short-term cardiac morbidity is substantial after TIA. Electrocardiographic
findings disclose new atrial fibrillation in a significant portion of patients
with TIA and can identify a group of patients at a substantially higher risk
for short-term cardiac events.
INTRODUCTION
TRANSIENT ISCHEMIC attacks (TIAs) are common and entail a substantial
short-term risk for stroke and other adverse events. Based on estimates of
stroke incidence, approximately 300 000 TIAs occur in the United States
each year.1-2 Within 90 days of
a TIA, approximately 10.5% of patients have a stroke, and 2.5% are hospitalized
for cardiac events.3 During long-term follow-up,
cardiac disease is the most common cause of death in these patients.4-8
Despite the frequency and morbidity of TIA, clinical management varies substantially.9 Consensus guidelines currently recommend the standard
12-lead electrocardiography (ECG) as an initial diagnostic study in the evaluation
of TIA.10-12 Some
benefits of screening ECG in TIA are self-evident; ie, abnormal ECG findings
may indicate a direct cardiac cause of the patient's symptoms or may identify
a condition, such as atrial fibrillation, that would alter treatment in the
secondary prevention of stroke. However, certain ECG findings may also be
relevant to the assessment of short-term cardiac or stroke risk in patients
with TIA. The overall utility of ECG in this context has not been formally
evaluated, and its full implications for clinical management are uncertain.
Previous studies of the relationship between initial ECG findings and
TIA outcome have not focused on short-term risk.4, 13-15
For example, in the largest previous study of the role of ECG in TIA, patients
were enrolled up to 3 months after the index TIA, and more than 50% were enrolled
after 1 month.15-16 Although several
ECG findings have been associated with an increased probability of stroke
and cardiac events in patients with TIA,3, 14-15
it is not known whether their short-term risk is sufficient to prompt urgent
intervention or further testing. To assess the ability of ECG findings to
predict short-term stroke and cardiac events in patients with TIA, we studied
a cohort of patients with a diagnosis of TIA in the emergency departments
of a large health maintenance organization.
SUBJECTS AND METHODS
This study was based on a cohort of patients with a diagnosis of TIA
in the 16 hospitals within Kaiser Permanente of Northern California. Details
of the cohort definition and predictors of stroke risk were described previously3 and are only briefly reviewed herein. Kaiser Permanente
of Northern California is a large health maintenance organization providing
medical care for 2.9 million enrollees with a demographic distribution similar
to that of the regional population. All patients were included in the study
if they received a diagnosis of TIA in the emergency department from March
1, 1997, through February 28, 1998. Patients were excluded if they did not
have emergency department records, were not members of the health care plan,
or had a previous TIA treated in the emergency department during the study
period. Using emergency department records, investigators extracted information
about demographic characteristics, medical history, baseline medications,
TIA symptom details, examination findings attributed to TIA, and treatment
plans according to predefined criteria. A neurologist (S.C.J.) masked to follow-up
events reviewed the medical records of all patients in whom the diagnosis
of TIA was uncertain. Emergency department physicians ordered all cardiac
diagnostic tests at their discretion. The ECG results were abstracted from
the official reports of hospital cardiologists. Abnormal ECG findings included
any of the following diagnoses in the ECG report: acute myocardial infarction,
previous myocardial infarction, ST-T wave changes, left ventricular hypertrophy,
atrial fibrillation, atrioventricular block (first through third degrees),
and bundle branch block.
Patients were followed up for 90 days after presentation with TIA. Incident
stroke, recurrent TIA, death, and hospitalization for cardiac events were
identified from computerized databases and review of medical records. Hospitalizations
outside the Kaiser Permanente system were recorded in a separate database,
which enabled complete follow-up of the cohort. Deaths occurring during the
90-day follow-up were identified from medical records, enrollment files, and
the California Automated Mortality Linkage System.17
Stroke was defined as a rapidly developed clinical sign of focal or global
disturbance of cerebral function lasting more than 24 hours or until death
without an apparent nonvascular cause.18 Strokes
had to be distinguishable from the initial TIA event. Stroke diagnosis required
independent confirmation by 2 neurologists. Diagnosis of recurrent TIA required
confirmation by a reviewing neurologist and a written diagnosis in the medical
record. A cardiac event was defined as a hospitalization or death due to myocardial
infarction, ventricular arrhythmia, heart failure, or unstable angina. To
estimate the cardiac event rate in a geographically similar and age-matched
population, we used codes from the International Classification
of Diseases, Ninth Revision, to identify all cardiac-related hospitalizations
and deaths in patients 30 years and older in Kaiser Permanente of Northern
California for 1997. We then matched the patient population by age using 5-year
increments to calculate an adjusted cardiac event rate for comparison with
our cohort.
The risks for stroke, recurrent TIA, and cardiac events were determined
as the proportion of patients with these events during the 90 days after the
resolution of TIA symptoms. For patients without documentation of symptom
resolution, follow-up began at the time of emergency department discharge.
For univariate analysis of dichotomous outcomes, we used the Fisher exact
test when any cell in a 2 x 2 table was 5 or less; otherwise, we used
the  2 test. We entered all variables that were associated
with the specified outcome (at P<.20) in univariate
analysis into multivariable logistic regression models by removing variables
that were no longer associated with the outcome (at P>.10)
with a backward stepwise elimination approach.19
Continuous variables were dichotomized at prespecified cut points (eg, heart
rate of 80 beats/min; systolic blood pressure of 140 mm Hg) to simplify the
models. Kaplan-Meier life-table analysis was used to illustrate the timing
of follow-up events. All statistical analyses were performed with the Stata
statistical package (Version 6.0; Stata Corp, College Station, Tex).
RESULTS
Among the 1797 patients with a diagnosis of TIA during the study period,
1707 met the inclusion criteria. Electrocardiography was performed in 1365
(80.0%). Those undergoing ECG were more likely to be male and to have a medical
history of hypertension and atrial fibrillation (Table 1). Symptoms of weakness, dizziness, and gait disturbance
were also associated with a greater likelihood of undergoing ECG. The 90-day
risk for cardiac events (2.9% vs 2.9%; P>.99), stroke
(10.8% vs 9.7%; P = .54), and death (2.6% vs 2.9%; P = .71) were not significantly different between the patients
with TIA who underwent ECG and those who did not.
|
|
|
|
Table 1. Demographic Characteristics, Symptoms, and Examination Findings
of the Entire Cohort and the Subgroup Undergoing ECG*
|
|
|
The ECG findings from 1327 patients were available for diagnostic coding.
Of these, findings in 474 (35.7%) were normal. The most common abnormality
was ST-T wave changes (n = 467) (Table 2). A new diagnosis of atrial fibrillation was made in 28 patients
(2.3%) who underwent ECG. An acute myocardial infarction was identified in
3.
|
|
|
|
Table 2. ECG Findings and Their Association With the 90-Day Risk for
Cardiac Events*
|
|
|
During the 90-day follow-up, 145 strokes (10.9%), 182 recurrent TIAs
(13.7%), 39 cardiac events (2.9%), and 34 deaths due to all causes (2.6%)
occurred. By comparison, the 90-day cardiac event rate in age-matched control
subjects was 0.39%. Cardiac events included 11 myocardial infarctions, 21
hospitalizations or deaths due to heart failure, 4 cases of ventricular arrhythmias,
and 3 cases of unstable angina. Nineteen cardiac events (49%) occurred within
the first 30 days of follow-up (Figure 1).
Fifteen cardiac events (38%) occurred in patients without a medical history
of coronary artery disease or heart failure. Three (8%) of the 39 cardiac
events were deaths. Seven patients (18%) with cardiac events died within 90
days.
|
|
|
|
Kaplan-Meier estimates of the cumulative probability of not having
a cardiac event during 90-day follow-up according to electrocardiographic
findings. The y-axis is constricted to illustrate the timing of events.
|
|
|
The prognostic value of ECG findings for adverse events was evaluated
in multivariable models. The ECG findings at the time of TIA were not independent
predictors of stroke, recurrent TIA, or death within 90 days (P>.10). The risk for any adverse cardiac event during the 90-day follow-up
was higher in patients with any abnormal ECG finding (4.2% vs 0.6%; P<.001). This association remained significant after
adjustment for medical history and clinical presentation (odds ratio [OR],
6.9; 95% confidence interval [CI], 1.6-29.5; P =
.009). The ECG findings of left ventricular hypertrophy (OR, 4.4; 95% CI,
2.0-10.1; P<.001), atrial fibrillation (OR, 7.2;
95% CI, 3.0-17.0; P<.001), and atrioventricular
block (OR, 3.3; 95% CI, 1.2-9.3; P = .02) were all
independent risk factors for cardiac events. However, the most common ECG
abnormalities, ST-T wave changes and previous myocardial infarction, were
not independent predictors of cardiac events (P =
.27 and P = .95, respectively). Abnormal ECG findings
had a sensitivity of 92% and a specificity of 36% for predicting short-term
cardiac events. Their positive predictive value for cardiac events was 4%,
whereas their negative predictive value was 99%. Aside from abnormal ECG findings,
other findings from the history or examination that predicted cardiac events
were a history of coronary artery disease or hypertension, a heart rate of
greater than 80 beats/min, or a systolic blood pressure of less than 140 mm
Hg at presentation (Table 3).
|
|
|
|
Table 3. Independent Risk Factors for Cardiac Events Within 90 Days*
|
|
|
At discharge from the emergency department, 898 patients (67.7%) were
treated with aspirin; 192 (14.5%), with heparin sodium or warfarin sodium;
and 157 (11.8%), with ticlopidine hydrochloride. Compared with patients with
normal ECG findings, patients with abnormal ECG findings were more likely
to receive warfarin (14.8% vs 5.7%; P<.001) and
less likely to receive aspirin (64.6% vs 73.2%; P<.001).
No medical treatments, however, were independently associated with cardiac
events (P = .67, P = .13,
and P = .27 for aspirin, ticlopidine, and anticoagulants,
respectively). Abnormal ECG findings predicted hospitalization and death related
to heart failure (P<.001), but their association
with more rare cardiac events (eg, ventricular arrhythmias [P = .17]) was not statistically significant. When heart failure events
were considered exclusively as the outcome of interest, the ECG findings of
atrial fibrillation (OR, 7.3; 95% CI, 2.9-18.3; P<.001)
and left ventricular hypertrophy (OR, 4.7; 95% CI, 1.9-11.3; P<.001) but not atrioventricular block (OR, 3.8; 95% CI, 0.3-50.1; P = .31) remained significantly associated in multivariable
models. A systolic blood pressure of less than 140 mm Hg was also more closely
associated with heart failure events than with cardiac events in general.
COMMENT
Although abnormal resting ECG findings have been associated with an
increased incidence of cardiac morbidity in some studies,20-22
they generally have lacked sufficient sensitivity and specificity to be useful
as prognostic screening tests.23 Although our
cohort consisted of patients with TIA due to all causes, the cardiac event
rate during the 90-day follow-up was high, nearly 7 times the rate of age-matched
controls. Furthermore, abnormal resting ECG findings in our cohort were strong
independent risk factors for short-term cardiac morbidity and had a negative
predictive value of 99% for cardiac events. Our definition of TIA was based
on the clinical impression of emergency department physicians and not on results
of specialized testing or expert review. Although certain subgroups of patients
with TIA may differ with respect to cardiac risk, our findings offer practical
guidance for the management of TIA in the acute care setting, where clinical
findings frequently do not allow for risk stratification based on underlying
pathophysiology. Events diagnosed as TIA likely include some instances of
syncope or presyncope with cardiac causes, but it may not be possible to differentiate
these causes, even with neurologist review.24-25
Electrocardiographic findings do not merely confirm information that
is available from the medical history; 38% of the patients in our cohort who
had cardiac events had no medical history of coronary disease or heart failure.
Furthermore, the pathological changes detected by means of ECG appear to be
better predictors of early cardiac events than medical history alone. For
example, in our cohort and in previous studies, left ventricular hypertrophy
on ECG findings was a significant predictor of cardiac events, whereas a history
of hypertension alone was not.4, 14-15
Previous studies have shown an association of ECG findings with only a long-term
risk for cardiac events after TIA.14-15
In a study with a mean follow-up of 31 months, the ECG findings of old anterior
infarction, T-wave inversion, and left ventricular hypertrophy were each independently
associated with cardiac events in multivariable models.15
Their longer follow-up compared with ours may account for the differences;
some ECG findings may entail a more acute risk, whereas others act as long-term
risk factors or markers for underlying vascular disease.
The results of our study are limited by the nonrandom selection of patients
to undergo ECG. Symptoms and examination findings such as dizziness and gait
abnormality were associated with undergoing ECG. This association may have
selected a group whose TIA symptoms were more likely to be cardiac related.
In most patients, however, ECG was performed, and the cardiac event rates
were nearly identical in patients who underwent ECG and those who did not.
Therefore, the selection of patients for ECG did not appear to be related
to prognosis overall and is unlikely to significantly influence the generalizability
of our findings.
We found a strong association between abnormal ECG findings and cardiac
events in aggregate. However, in the subgroup analysis of specific types of
cardiac events, only heart failure events remained significantly associated
with ECG abnormalities. Cardiac events related to heart failure were the most
common subtype in our cohort and likely account for the association between
cardiac events and low systolic blood pressure.26
Previous investigators have not included hospitalizations related to heart
failure in their assessment of cardiac events after TIA.4, 14-15
Although exacerbations of heart failure may be largely reversible, they can
be triggered by cardiac ischemia and are associated with high rates of mortality.27 Three (14%) of 21 patients who had cardiac events
related to heart failure died within the 90-day follow-up. Furthermore, as
only hospitalizations and death were included, all heart failure events entailed
significant resource consumption and morbidity. The relatively low short-term
rates of myocardial infarction, ventricular arrhythmia, and unstable angina
made it difficult to detect possible associations between these end points
and ECG findings.
CONCLUSIONS
This study confirms the utility of the routine use of ECG in the acute
evaluation of TIA. In addition to the detection of new-onset atrial fibrillation
and myocardial ischemia, the ECG identifies a group of patients with TIA who
are at a substantially higher risk for short-term cardiac morbidity. Given
the high risk for cardiac events after TIA, more extensive medical evaluation
may be indicated in certain subgroups of patients with abnormal ECG findings,
such as those with left ventricular hypertrophy, atrial fibrillation, or atrioventricular
conduction abnormalities. Additional research studies are needed to assess
the incremental effectiveness of timely cardiac diagnostic or therapeutic
interventions in these subgroups.
AUTHOR INFORMATION
Accepted for publication April 9, 2002.
Author contributions: Study
concept and design (Drs Elkins, Gress, and Johnston); acquisition of data (Drs Sidney and Johnston); analysis
and interpretation of data (Drs Elkins, Go, Bernstein, and Johnston); drafting of the manuscript (Drs Elkins and Johnston); critical revision of the manuscript for important intellectual
content (Drs Elkins, Sidney, Gress, Go, Bernstein, and Johnston); statistical expertise (Dr Johnston); obtained funding (Dr Johnston); adminstrative, technical,
and material support (Drs Sidney and Johnston); and study supervision (Dr Gress).
This study was supported by a grant-in-aid from the American Heart Association,
Western States Affiliate, Burlingame, Calif. Dr Johnston is a clinical research
fellow of the National Stroke Association and is supported by grant NS 02042
from the National Institutes of Health, Bethesda, Md.
We thank Carolyn Salazar, Barbara Rowe, RN, and Michael Sorel, MPH,
for their careful analysis.
Corresponding author and reprints: S. Claiborne Johnston, MD, PhD,
Department of Neurology, UCSF Box 0114, University of California, San Francisco,
505 Parnassus Ave, Room M-798, San Francisco, CA 94143-0114 (e-mail: Clay.Johnston{at}ucsfmedctr.org).
From the Department of Neurology, University of California, San Francisco
(Drs Elkins, Gress, and Johnston); the Division of Research, Kaiser Permanente
of Northern California, Oakland (Drs Sidney, Go, and Johnston); and the Department
of Neurology, Kaiser Permanente Medical Center, Santa Rosa, Calif (Dr Bernstein).
REFERENCES
| |
1. Brown RD Jr, Petty GW, O'Fallon WM, Wiebers DO, Whisnant JP. Incidence of transient ischemic attack in Rochester, Minnesota, 1985-1989. Stroke. 1998;29:2109-2113.
FREE FULL TEXT
2. Broderick J, Brott T, Kothari R, et al. The Greater Cincinnati/Northern Kentucky Stroke Study: preliminary
first-ever and total incidence rates of stroke among blacks. Stroke. 1998;29:415-421.
FREE FULL TEXT
3. Johnston SC, Gress D, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000;284:2901-2906.
FREE FULL TEXT
4. Heyman A, Wilkinson WE, Hurwitz BJ, et al. Risk of ischemic heart disease in patients with TIA. Neurology. 1984;34:626-630.
FREE FULL TEXT
5. Wiebers DO, Whisnant JP, O'Fallon M. Reversible ischemic neurologic deficit (RIND) in a community: Rochester,
Minnesota, 1955-1974. Neurology. 1982;32:459-465.
FREE FULL TEXT
6. Whisnant JP. Epidemiology of stroke: emphasis on transient cerebral ischemic attacks
and hypertension. Stroke. 1974;5:68-70.
FREE FULL TEXT
7. Toole JF, Yuson CP, Janeway R, et al. Transient ischemic attacks: a prospective study of 225 patients. Neurology. 1978;28:746-753.
FREE FULL TEXT
8. Muuronen A, Kaste M. Outcome of 314 patients with transient ischemic attacks. Stroke. 1982;13:24-31.
ABSTRACT
9. Johnston SC, Smith WS. Practice variability in management of transient ischemic attacks. Eur Neurol. 1999;42:105-108.
FULL TEXT
|
ISI
| PUBMED
10. Feinberg WM, Albers GW, Barnett HJ, et al. Guidelines for the management of transient ischemic attacks: from the
Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks
of the Stroke Council of the American Heart Association. Circulation. 1994;89:2950-2965.
FREE FULL TEXT
11. Wolf PA, Clagett GP, Easton JD, et al. Preventing ischemic stroke in patients with prior stroke and transient
ischemic attack: a statement for healthcare professionals from the Stroke
Council of the American Heart Association. Stroke. 1999;30:1991-1994.
FREE FULL TEXT
12. Albers GW, Hart RG, Lustep HL, Newell DW, Sacco RL. AHA Scientific Statement: supplement to the guidelines for the management
of transient ischemic attacks: a statement from the Ad Hoc Committee on Guidelines
for the Management of Transient Ischemic Attacks, Stroke Council, American
Heart Association. Stroke. 1999;30:2502-2511.
FREE FULL TEXT
13. Heyden S, Heiss G, Heyman A, et al. Cardiovascular mortality in transient ischemic attacks. Stroke. 1980;11:252-255.
FREE FULL TEXT
14. Hankey GJ, Slattery JM, Warlow CP. Transient ischaemic attacks: which patients are at high (and low) risk
of serious vascular events? J Neurol Neurosurg Psychiatry. 1992;55:640-652.
FREE FULL TEXT
15. Pop GA, Koudstaal PJ, Meeder HJ, Algra A, van Latum JC, van Gijn J for the Dutch TIA Trial Study Group. Predictive value of clinical history and electrocardiogram in patients
with transient ischemic attack or minor ischemic stroke for subsequent cardiac
and cerebral ischemic events. Arch Neurol. 1994;51:333-341.
FREE FULL TEXT
16. Dutch TIA Trial Study Group. A comparison of two doses of aspirin (30 mg vs. 283 mg a day) in patients
after a transient ischemic attack or minor ischemic stroke. N Engl J Med. 1991;325:1261-1266.
ABSTRACT
17. Arellano MG, Petersen GR, Petitti DB, Smith RE. The California Automated Mortality Linkage System (CAMLIS). Am J Public Health. 1984;74:1324-1330.
FREE FULL TEXT
18. WHO MONICA Project Principal Investigators. The World Health Organization MONICA Project (Monitoring Trends and
Determinants in Cardiovascular Disease): a major international collaboration. J Clin Epidemiol. 1988;41:105-114.
FULL TEXT
|
ISI
| PUBMED
19. Kleinbaum DG, Kuppe LL, Morgenstern H. Epidemiologic Research Principles and Quantitative
Methods. New York, NY: Van Nostrand Reinhold Co; 1982.
20. Multiple Risk Factor Intervention Trial Research Group. Baseline rest electrocardiographic abnormalities, antihypertensive
treatment, and mortality in the Multiple Risk Factor Intervention Trial. Am J Cardiol. 1985;55:1-15.
FULL TEXT
| PUBMED
21. Kannel WB, Anderson K, McGee DL, Degatano LS, Stampfer MJ. Nonspecific electrocardiographic abnormality as a predictor of coronary
heart disease: the Framingham Study. Am Heart J. 1987;113:370-376.
FULL TEXT
|
ISI
| PUBMED
22. Knutsen R, Knutsen SF, Curb JD, Reed DM, Kautz JA, Yano K. The predictive value of resting electrocardiograms for 12-year incidence
of coronary heart disease in the Honolulu Heart Program. J Clin Epidemiol. 1988;41:293-302.
FULL TEXT
|
ISI
| PUBMED
23. US Preventive Services Task Force. Guide to Clinical Preventive Services: Report of
the US Preventive Services Task Force. Baltimore, Md: Williams & Wilkins; 1996.
24. Koudstaal PJ, Gerritsma JG, van Gijn J. Clinical disagreement on the diagnosis of transient ischemic attack:
is the patient or the doctor to blame? Stroke. 1989;20:300-301.
FREE FULL TEXT
25. Kraaijeveld CL, van Gijn J, Schouten HJ, Staal A. Interobserver agreement for the diagnosis of transient ischemic attacks. Stroke. 1984;15:723-725.
FREE FULL TEXT
26. Stevenson L, Perloff J. The limited reliability of physical signs for estimating hemodynamics
in chronic heart failure. JAMA. 1989;261:884-888.
FREE FULL TEXT
27. Jaagosild P, Dawson NV, Thomas C, et al for the SUPPORT Investigators. Outcomes of acute exacerbation of severe congestive heart failure:
quality of life, resource use, and survival. Arch Intern Med. 1998;158:1081-1089.
FREE FULL TEXT
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter
What's this?
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
|
Definition and Evaluation of Transient Ischemic Attack: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease: The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists.
Easton et al.
Stroke 2009;40:2276-2293.
ABSTRACT
| FULL TEXT
Noninvasive Cardiac Monitoring for Detecting Paroxysmal Atrial Fibrillation or Flutter After Acute Ischemic Stroke: A Systematic Review
Liao et al.
Stroke 2007;38:2935-2940.
ABSTRACT
| FULL TEXT
Defining Cause of Death in Stroke Patients: The Brain Attack Surveillance in Corpus Christi Project
Brown et al.
Am J Epidemiol 2007;165:591-596.
ABSTRACT
| FULL TEXT
Emergency department evaluation of ischemic stroke and TIA: The BASIC Project
Brown et al.
Neurology 2004;63:2250-2254.
ABSTRACT
| FULL TEXT
A comparison of risk factors for recurrent TIA and stroke in patients diagnosed with TIA
Claiborne Johnston et al.
Neurology 2003;60:280-285.
ABSTRACT
| FULL TEXT
|
