Influence of Chronic Ethanol Consumption on the Neurological Severity in Patients With Acute Cerebral Ischemia
Background and Purpose—We tested the hypothesis that excessive chronic ethanol consumption is associated with more severe ischemic strokes.
Methods—We recruited patients with supratentorial cerebral ischemia within 48 hours of symptom onset. We defined heavy drinkers by a weekly consumption of ethanol of ≥300 g and severe strokes by a National Institutes of Health Stroke Scale score≥6.
Results—Of 436 patients, 60 were heavy drinkers. Being a heavy drinker was independently associated with baseline National Institutes of Health Stroke Scale scores ≥6 (odds ratio, 2.35; 95% confidence interval, 1.12–5.26; P=0.023) at the logistic regression analysis. This result was not modified with the propensity analysis.
Conclusion—An excessive chronic ethanol consumption is associated with higher baseline stroke severity.
A chronic and excessive consumption of ethanol is associated with larger infarcts in animals.1 To our knowledge, this effect has not been evaluated in humans. We tested the hypothesis that a chronic excessive consumption of ethanol is associated with a higher severity of the neurological deficit in acute ischemic stroke.
Inclusion and Noninclusion Criteria
We recruited patients with supratentorial ischemic stroke or transient ischemic attack, within 48 hours of symptom onset. Patients were not consecutive, because of the need to obtain consents.
Stroke severity was assessed by the National Institutes of Health Stroke Scale (NIHSS).2 The cause was classified according to the Trial of Org 10172 in Acute Stroke Treatment criteria.3 Definitions used for variables included in the analysis have been previously defined.4,5
At admission, all patients underwent either a noncontrast computed tomographic (CT) scan or an MRI scan.
Assessment of Ethanol Consumption
The assessment of ethanol consumption was declarative. We considered heavy drinkers as patients with a weekly consumption of ethanol of ≥300 g4,5 (ie, 4 standard alcoholic drinks per day). When there was a discrepancy between the declaration and the biological results, we interviewed close relatives or general practitioners. We performed a measurement of carbohydrate-deficient transferrin (CDT) serum level. These results were not available at inclusion, and therefore, they were not used for diagnostic purposes. They were used months later to evaluate patients’ declaration but did not change the classification. A value between 2.1% and 2.5% was considered an area of uncertainty.6 CDT has a better sensitivity and specificity than corpuscular volume and γ-glutamyl transferase for the diagnosis of excessive chronic ethanol consumption.6
We performed statistics with the SPSS 15.0 package for windows. We compared patients with minor strokes (NIHSS scores 0–5) versus severe strokes (NIHSS scores ≥6), for baseline characteristics including ethanol consumption, with the χ2 and Mann–Whitney U tests. Independent variables were selected from the univariable analysis, with a 0.25 level as a screening criterion, the variable heavy drinker being forced into the model. We calculated adjusted odds ratios (adjusted odds ratio) and 95% confidence interval by logistic regression analyses, with NIHSS ≥6 as dependent variable, as in a previous study.4 Correlations between variables were checked for collinearity, which was defined as r>0.6. The last step of analysis consisted of a propensity analysis. Propensity scores have been generated by a logistic regression model. Variables for the propensity score (sex, tobacco consumption, body mass index, aspartate amino transferase, mean corpuscular volume, and unknown cause of stroke) were included step-by-step using an α value of 0.15.
The study was approved by the ethical committee, and patients or a close relative gave a signed informed consent.
The study population consisted of 436 patients with a median age of 70 years (interquartile range, 58–79), 205 women (47.0%), and median NIHSS scores 6 (interquartile range, 1–14), 105 (24.1%) treated with thrombolytic therapy, and 60 (13.8%) classified as heavy drinkers.
The comparison of heavy drinkers and nonheavy drinkers is detailed in Table 1. The dosage of CDT could be performed in 409 patients (93.8%): 51 (13.5%) were misclassified, 34 were self-reported as heavy drinkers with CDT <2.1%, and 17 were self-reported as nonheavy drinkers with CDT>2.5%.
Being classified as a heavy drinker was independently associated with more severe strokes (adjusted odds ratio 2.26; 95% confidence interval 1.06–4.82; P=0.034; Table 2). A supplementary adjustment for propensity score was found and adjusted odds ratio was 2.30 (P=0.051).
We have shown that being a heavy drinker was independently associated with more severe ischemic strokes. Factors associated with the initial severity other than ethanol consumption were those found in other studies. The limitations are the monocenter design, the lack of evaluation of arterial occlusion and dosage of ethanolemine at baseline, and the selection of patients on the possibility to consent.
The classification between heavy and nonheavy drinkers was based on declaration, but agreement between clinical and CDT-based classification was close to 87%. As the specificity of a CDT>2.5% for excessive chronic ethanol consumption is high,7 there were probably <5% of heavy drinker misclassified. Many heavy drinkers had a level of CDT<2.1%, but this is not necessarily a misclassification because this is usually found in 1 of 6 patients with excessive chronic ethanol consumption.7
We found that a chronic ethanol consumption of ≥300 g per week is independently associated with a higher severity of the neurological deficit. There is not necessarily a causal relationship between ethanol consumption and stroke severity, but just a statistical association, that could be related to confounders that were not included in the analysis. Our findings generate a hypothesis that needs confirmation. As an interventional study would not be feasible, this question can be answered only through experimental approaches in animals.
We are grateful to Anne-Marie Bordet who contributed to the data collection.
Sources of Funding
This study was funded by the Programme Hospitalier de Recherche Clinique (Biostroke, Direction Générale de la Santé 2006/0153).
- Received March 4, 2013.
- Accepted April 4, 2013.
- © 2013 American Heart Association, Inc.
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