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Letters to the Editor / Clinical Neurology and Neurosurgery 116 (2014) 104–108 ∗ Correspondence
to: Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo 113-8602, Japan. Tel.: +81 3 3822 2131; fax: +81 3 5685 3065. E-mail address: [email protected] 5 August 2013 Available online 15 November 2013
http://dx.doi.org/10.1016/j.clineuro.2013.08.033
Effect of antithrombotic state on clinical outcomes following angiography negative subarachnoid hemorrhage Keywords: Subarachnoid hemorrhage Intracranial hemorrhage Stroke Anticoagulants
Dear Sir, I have read, with great interest, a recently published article in Clinical Neurology and Neurosurgery by Dalbjerg et al. titled ‘Risk factors and short-term outcome in patients with angiographically negative subarachnoid hemorrhage’ [1]. The authors retrospectively analyzed 95 patients who presented with spontaneous, angiographically negative subarachnoid hemorrhage (nSAH) and identified anticoagulant therapy (p = 0.02) as a significant predictor of unfavorable outcome. The authors thoughtfully acknowledge the limited nature of the study based on the relatively few number of patients who were receiving antithrombotic therapy. However, there remain a number of other limitations which may potentially decrease the clinical relevance of the results. First, the authors did not distinguish between perimesencephalic and non-perimesencephalic nSAH. Not only does non-perimesencephalic nSAH comprise one-third of nSAH cases, a recent study by Dalyai et al. reported significant differences between the two groups with regard to both yield of repeat angiography (higher in the non-perimesencephalic cohort) and clinical outcome (worse in non-perimesencephalic cohort) [2]. Perhaps of even greater concern is that 78% of patients in this study did not receive catheter angiography. Modern computed tomography angiography (CTA) detects even small aneurysms with very high sensitivity and specificity, 97% and 95%, respectively, based on a recent study [3]. Nevertheless, CTA remains inferior to catheter angiography for the detection of vascular lesions, especially ones which are inherently difficult to detect such as perforator artery aneurysms [4].
Second, there is no distinction among the different forms of antithrombotic medication in the outcomes analysis. The hematologic effect of a non-steroidal anti-inflammatory drug, such as ibuprofen, may be profoundly different than that of an antiplatelet medication such as clopidogrel. These differences may be quantified with platelet function assays since reduced platelet activity has been linked to increased SAH volume and hydrocephalus in a similar patient cohort [5]. It would be interesting to study, in a larger patient population, the comparison between outcomes in nSAH patients on medications affecting clotting factors (i.e. warfarin) versus those affecting platelet function (i.e. aspirin). Lastly, the medical reason for antithrombotic therapy was not delineated. In the study by Hui et al., the patients on antithrombotic medications had relatively higher hemorrhage volumes [6]. However, since the current study has a similar distribution of Fisher grade in patients with and without antithrombotic state, a potential explanation for the worse outcomes in patients on antithrombotic therapy is poorer underlying medical condition. References [1] Dalbjerg SM, Larsen CC, Romner B. Risk factors and short-term outcome in patients with angiographically negative subarachnoid hemorrhage. Clin Neurol Neurosurg 2013;115(8):1304–7. [2] Dalyai R, Chalouhi N, Theofanis T, Jabbour PM, Dumont AS, Gonzalez LF, et al. Subarachnoid hemorrhage with negative initial catheter angiography: a review of 254 cases evaluating patient clinical outcome and efficacy of short- and longterm repeat angiography. Neurosurgery 2013;72(4):646–52. [3] Zhang H, Hou C, Zhou Z, Zhou G, Zhang G. Evaluating of small intracranial aneurysms by 64-detector CT angiography: a comparison with 3-dimensional rotation DSA or surgical findings. J Neuroimaging 2012 [Epub ahead of print]. [4] Ding D, Starke RM, Jensen ME, Evans AJ, Kassell NF, Liu KC. Perforator aneurysms of the posterior circulation: case series and review of the literature. J Neurointerv Surg 2012;5:546–51. [5] Naidech AM, Rosenberg NF, Maas MB, Bendok BR, Batjer HH, Nemeth AJ. Predictors of hemorrhage volume and disability after perimesencephalic subarachnoid hemorrhage. Neurology 2012;78(11):811–5. [6] Hui FK, Schuette AJ, Moskowitz SI, Gupta R, Spiotta AM, Obuchowski NA, et al. Antithrombotic states and outcomes in patients with angiographically negative subarachnoid hemorrhage. Neurosurgery 2011;68(1):125–30 [discussion 130–1].
Dale Ding ∗ University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, 22908, USA ∗ Correspondence
to: University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, VA 22908, USA. Tel.: +1 434 924 2203; fax: +1 434 982 5753. E-mail address: [email protected] 30 July 2013 Available online 14 November 2013 http://dx.doi.org/10.1016/j.clineuro.2013.10.026
Letters to the Editor / Clinical Neurology and Neurosurgery 116 (2014) 104–108 ∗ Correspondence
to: Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo 113-8602, Japan. Tel.: +81 3 3822 2131; fax: +81 3 5685 3065. E-mail address: [email protected] 5 August 2013 Available online 15 November 2013
http://dx.doi.org/10.1016/j.clineuro.2013.08.033
Effect of antithrombotic state on clinical outcomes following angiography negative subarachnoid hemorrhage Keywords: Subarachnoid hemorrhage Intracranial hemorrhage Stroke Anticoagulants
Dear Sir, I have read, with great interest, a recently published article in Clinical Neurology and Neurosurgery by Dalbjerg et al. titled ‘Risk factors and short-term outcome in patients with angiographically negative subarachnoid hemorrhage’ [1]. The authors retrospectively analyzed 95 patients who presented with spontaneous, angiographically negative subarachnoid hemorrhage (nSAH) and identified anticoagulant therapy (p = 0.02) as a significant predictor of unfavorable outcome. The authors thoughtfully acknowledge the limited nature of the study based on the relatively few number of patients who were receiving antithrombotic therapy. However, there remain a number of other limitations which may potentially decrease the clinical relevance of the results. First, the authors did not distinguish between perimesencephalic and non-perimesencephalic nSAH. Not only does non-perimesencephalic nSAH comprise one-third of nSAH cases, a recent study by Dalyai et al. reported significant differences between the two groups with regard to both yield of repeat angiography (higher in the non-perimesencephalic cohort) and clinical outcome (worse in non-perimesencephalic cohort) [2]. Perhaps of even greater concern is that 78% of patients in this study did not receive catheter angiography. Modern computed tomography angiography (CTA) detects even small aneurysms with very high sensitivity and specificity, 97% and 95%, respectively, based on a recent study [3]. Nevertheless, CTA remains inferior to catheter angiography for the detection of vascular lesions, especially ones which are inherently difficult to detect such as perforator artery aneurysms [4].
Second, there is no distinction among the different forms of antithrombotic medication in the outcomes analysis. The hematologic effect of a non-steroidal anti-inflammatory drug, such as ibuprofen, may be profoundly different than that of an antiplatelet medication such as clopidogrel. These differences may be quantified with platelet function assays since reduced platelet activity has been linked to increased SAH volume and hydrocephalus in a similar patient cohort [5]. It would be interesting to study, in a larger patient population, the comparison between outcomes in nSAH patients on medications affecting clotting factors (i.e. warfarin) versus those affecting platelet function (i.e. aspirin). Lastly, the medical reason for antithrombotic therapy was not delineated. In the study by Hui et al., the patients on antithrombotic medications had relatively higher hemorrhage volumes [6]. However, since the current study has a similar distribution of Fisher grade in patients with and without antithrombotic state, a potential explanation for the worse outcomes in patients on antithrombotic therapy is poorer underlying medical condition. References [1] Dalbjerg SM, Larsen CC, Romner B. Risk factors and short-term outcome in patients with angiographically negative subarachnoid hemorrhage. Clin Neurol Neurosurg 2013;115(8):1304–7. [2] Dalyai R, Chalouhi N, Theofanis T, Jabbour PM, Dumont AS, Gonzalez LF, et al. Subarachnoid hemorrhage with negative initial catheter angiography: a review of 254 cases evaluating patient clinical outcome and efficacy of short- and longterm repeat angiography. Neurosurgery 2013;72(4):646–52. [3] Zhang H, Hou C, Zhou Z, Zhou G, Zhang G. Evaluating of small intracranial aneurysms by 64-detector CT angiography: a comparison with 3-dimensional rotation DSA or surgical findings. J Neuroimaging 2012 [Epub ahead of print]. [4] Ding D, Starke RM, Jensen ME, Evans AJ, Kassell NF, Liu KC. Perforator aneurysms of the posterior circulation: case series and review of the literature. J Neurointerv Surg 2012;5:546–51. [5] Naidech AM, Rosenberg NF, Maas MB, Bendok BR, Batjer HH, Nemeth AJ. Predictors of hemorrhage volume and disability after perimesencephalic subarachnoid hemorrhage. Neurology 2012;78(11):811–5. [6] Hui FK, Schuette AJ, Moskowitz SI, Gupta R, Spiotta AM, Obuchowski NA, et al. Antithrombotic states and outcomes in patients with angiographically negative subarachnoid hemorrhage. Neurosurgery 2011;68(1):125–30 [discussion 130–1].
Dale Ding ∗ University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, 22908, USA ∗ Correspondence
to: University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, VA 22908, USA. Tel.: +1 434 924 2203; fax: +1 434 982 5753. E-mail address: [email protected] 30 July 2013 Available online 14 November 2013 http://dx.doi.org/10.1016/j.clineuro.2013.10.026
