OBJECTIVE: The association between smoking and intracranial aneurysms is now well recognized. However, the relationship between tobacco use and outcome after aneurysmal subarachnoid hemorrhage (SAH) is not as well understood and published results are contradictory. The purpose of this study is to examine the degree to which the amount of tobacco exposure/dose impacts delayed neurological deterioration and overall clinical outcome after aneurysmal SAH. METHODS: We reviewed our retrospective database of patients with aneurysmal SAH. We assessed the impact of four independent tobacco variables: smoker (ever smoked), current smoker (actively smoking within the past yr and with at least a 10 pack per yr history of smoking), long-term smoker (at least a 20 pack per yr history), and salient (combination of current and long-term) smoker as well as tobacco dose (categorized according to number of packs per yr) on two outcome variables, delayed neurological deterioration and dichotomized Glasgow Outcome Scale score. Covariates included in the analysis were age, sex, Hunt and Hess grade, Fisher grade, and medical comorbidities. Stepwise elimination with logistic regression was used to arrive at a final multivariate model for each outcome and independent tobacco variable in the presence of covariates. RESULTS: A total of 320 patients were analyzed. As expected, Hunt and Hess grade was a significant predictor of both delayed neurological deterioration and clinical outcome. Tobacco use (smoker variable) showed an independent association with the development of delayed neurological deterioration (P = 0.0409; odds ratio, 1.78; 95% confidence interval, 1.02-3.08). In addition, patients who were long-term or current smokers (salient smoker variable) showed a trend toward a slightly stronger association with the occurrence of delayed neurological deterioration (P = 0.0229; odds ratio, 1.85; 95% confidence interval, 1.09-3.14). No tobacco use variable was associated with clinical outcome (Glasgow Outcome Scale) in the multivariate analysis. CONCLUSION: The duration and timing of tobacco use, rather than the dose of tobacco per se, seem to be risk factors for delayed neurological deterioration after aneurysmal SAH. Although we did not find an association between tobacco use and overall clinical outcome after aneurysmal SAH, these results suggest that the distribution of various patterns of tobacco use within a given data set may influence the overall results.
OBJECTIVE: The association between smoking and intracranial aneurysms is now well recognized. However, the relationship between tobacco use and outcome after aneurysmal subarachnoid hemorrhage (SAH) is not as well understood and published results are contradictory. The purpose of this study is to examine the degree to which the amount of tobacco exposure/dose impacts delayed neurological deterioration and overall clinical outcome after aneurysmalSAH. METHODS: We reviewed our retrospective database of patients with aneurysmalSAH. We assessed the impact of four independent tobacco variables: smoker (ever smoked), current smoker (actively smoking within the past yr and with at least a 10 pack per yr history of smoking), long-term smoker (at least a 20 pack per yr history), and salient (combination of current and long-term) smoker as well as tobacco dose (categorized according to number of packs per yr) on two outcome variables, delayed neurological deterioration and dichotomized Glasgow Outcome Scale score. Covariates included in the analysis were age, sex, Hunt and Hess grade, Fisher grade, and medical comorbidities. Stepwise elimination with logistic regression was used to arrive at a final multivariate model for each outcome and independent tobacco variable in the presence of covariates. RESULTS: A total of 320 patients were analyzed. As expected, Hunt and Hess grade was a significant predictor of both delayed neurological deterioration and clinical outcome. Tobacco use (smoker variable) showed an independent association with the development of delayed neurological deterioration (P = 0.0409; odds ratio, 1.78; 95% confidence interval, 1.02-3.08). In addition, patients who were long-term or current smokers (salient smoker variable) showed a trend toward a slightly stronger association with the occurrence of delayed neurological deterioration (P = 0.0229; odds ratio, 1.85; 95% confidence interval, 1.09-3.14). No tobacco use variable was associated with clinical outcome (Glasgow Outcome Scale) in the multivariate analysis. CONCLUSION: The duration and timing of tobacco use, rather than the dose of tobacco per se, seem to be risk factors for delayed neurological deterioration after aneurysmalSAH. Although we did not find an association between tobacco use and overall clinical outcome after aneurysmalSAH, these results suggest that the distribution of various patterns of tobacco use within a given data set may influence the overall results.
Authors: Wessel E van der Steen; Eva L Leemans; René van den Berg; Yvo B W E M Roos; Henk A Marquering; Dagmar Verbaan; Charles B L M Majoie Journal: Neuroradiology Date: 2019-01-28 Impact factor: 2.804
Authors: David B Seder; J Michael Schmidt; Neeraj Badjatia; Luis Fernandez; Fred Rincon; Jan Claassen; Errol Gordon; Emmanuel Carrera; Pedro Kurtz; Kiwon Lee; E Sander Connolly; Stephan A Mayer Journal: Neurocrit Care Date: 2011-02 Impact factor: 3.210
Authors: Alexander Hammer; Anahi Steiner; Gholamreza Ranaie; Eduard Yakubov; Frank Erbguth; Christian M Hammer; Monika Killer-Oberpfalzer; Hans Steiner; Hendrik Janssen Journal: Sci Rep Date: 2018-08-17 Impact factor: 4.379
Authors: Alexander Hammer; Frank Erbguth; Matthias Hohenhaus; Christian M Hammer; Hannes Lücking; Markus Gesslein; Monika Killer-Oberpfalzer; Hans-Herbert Steiner; Hendrik Janssen Journal: BMC Neurol Date: 2021-01-19 Impact factor: 2.474
Authors: Benjamin W Y Lo; Hitoshi Fukuda; Yusuke Nishimura; Forough Farrokhyar; Lehana Thabane; Mitchell A H Levine Journal: Surg Neurol Int Date: 2015-08-11