Original Paper Received: July 23, 2013 Accepted: September 29, 2013 Published online: January 21, 2014
Eur Neurol 2014;71:203–207 DOI: 10.1159/000356198
Brain Natriuretic Peptide upon Admission as a Biological Marker of Short-Term Mortality after Intracerebral Hemorrhage Yoshino Goya a, b Kensaku Shibazaki a Kenichiro Sakai a Junya Aoki a Jyunichi Uemura a Naoki Saji a Katsunori Isa b Yusuke Ohya b Kazumi Kimura a
a
Department of Stroke Medicine, Kawasaki Medical School, Kurashiki, and b Department of Cardiovascular Medicine, Nephrology and Neurology, University of the Ryukyus Graduate School of Medicine, Nishihara, Japan
Key Words Brain natriuretic peptide · Intracerebral hemorrhage · Mortality
Abstract Background and Purpose: The purpose of the present study was to test the hypothesis that plasma brain natriuretic peptide (BNP) is associated with short-term mortality after intracerebral hemorrhage (ICH). Methods: We prospectively enrolled 271 patients (median age 72 years; 109 females) who were admitted within 24 h of ICH onset between April 2007 and July 2011 and in whom plasma BNP levels were measured upon admission. The patients were assigned to two groups according to survival within 1 month of ICH. Factors associated with mortality were determined by multivariate logistic regression analysis. Results: Within 1 month of ICH, 48 (17.7%) of the 271 enrolled patients died. The median (interquartile range) level of plasma BNP was significantly higher in the group of non-survivors than in the group of survivors [102.5 (48.7–205.0) vs. 32.4 (17.3–85.0) pg/ml; p < 0.001]. A cutoff BNP level of 60.0 pg/ml could predict death within 1 month of ICH. Multivariate logistic regression analysis showed that a plasma BNP of >60.0 pg/ml (OR 4.7; 95% CI
© 2014 S. Karger AG, Basel 0014–3022/14/0714–0203$39.50/0 E-Mail [email protected] www.karger.com/ene
1.43–15.63; p = 0.011) was independently associated with mortality within 1 month after ICH. Conclusions: A high BNP level upon admission is associated with mortality within 1 month after ICH. © 2014 S. Karger AG, Basel
Introduction
Intracerebral hemorrhage (ICH) is a significant cause of adult disability and mortality. Previous studies have identified several clinical [1–6], radiographic [4, 7] and laboratory variables [8–10] that are associated with mortality after ICH. Brain natriuretic peptide (BNP) is a 32-amino acid polypeptide with a 17-amino acid ring structure that has diuretic and vasodilator properties [11]. It is primarily released from the ventricular myocardium and is a biomarker of congestive heart failure. BNP is also a predictive marker of mortality in various disorders [12–16] and in a general community-based population [17]. Plasma BNP levels become elevated for unknown reasons during the acute phase of subarachnoid hemorrhage [18], ischemic stroke [19, 20] and ICH [21]. Plasma BNP Dr. Yoshino Goya Department of Stroke Medicine, Kawasaki Medical School 577 Matsushima Kurashiki City, Okayama 701-0192 (Japan) E-Mail yoozii50 @ gmail.com
is also an independent predictor of neurological function at the time of discharge after ICH [21]. However, the relationship between BNP and mortality after ICH has not been fully examined. The present study tested the hypothesis that admission plasma BNP levels in patients with ICH can serve as a marker of mortality within 1 month after ICH.
Methods We prospectively enrolled consecutive patients who were admitted to our stroke center within 24 h of ICH onset between April 2007 and July 2011. Patients with ICH related to aneurysms, vascular malformation, dissection, tumor, hemorrhagic transformation of ischemic stroke and traumatic ICH were excluded. Plasma BNP was not measured in patients who underwent emergency surgery, and these patients were also excluded. Patients or caregivers were interviewed by telephone or in writing 1–3 months after ICH. Death was defined as all-cause mortality within 1 month after the date of admission. We compared patients who remained alive with those who died. This study complied with the Declaration of Helsinki with regard to human investigations, and the Ethics Committee of Kawasaki Medical School Hospital approved the study protocol. Acute ICH diagnosed by stroke neurologists was confirmed by computed tomography (CT) or magnetic resonance imaging. We assessed age, sex, prior coronary artery disease (CAD), prior ICH, prior ischemic stroke, vascular risk factors, preadmission warfarin therapy, preadmission antiplatelet therapy, systolic and diastolic blood pressure upon admission, National Institutes of Health Stroke Scale (NIHSS) score on admission, location of ICH, hematoma volume, hemoglobin, HbA1c, blood glucose, C-reactive protein (CRP) and plasma BNP. We evaluated vascular risk factors for hypertension (defined as therapy with antihypertensive agents, a systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg before stroke onset), diabetes mellitus (defined as therapy with oral hypoglycemia agents or insulin, or glycosylated hemoglobin ≥6.4%), hyperlipidemia (defined as therapy with antihyperlipidemic agents or serum total cholesterol ≥220 mg/dl) and atrial fibrillation [AF; diagnosed by 12-lead electrocardiography (ECG) and continuous ECG or 24-hour Holter ECG monitoring]. Patients were assessed within 24 h of onset (baseline) using cranial CT according to the protocol of our Radiology Department, with an image matrix of 340 × 340 and a slice width of 8–10 mm. The ICH volume was measured using the A × B × C/2 formula [22]. The location of the ICH was classified according to the location of the largest blood hematoma as the putamen, thalamus, lobe, brainstem or cerebellum. Plasma BNP Measurements Baseline blood samples were collected into tubes containing aprotinin and EDTA from the peripheral veins of all patients upon admission. Plasma was then isolated and stored at –80 ° C. Plasma BNP concentrations were accurately measured within 11 min using a chemiluminescence enzyme immunoassay that sandwiches human BNP between one monoclonal antibody that
204
Eur Neurol 2014;71:203–207 DOI: 10.1159/000356198
recognizes the carboxyl-terminal amino acid sequence, and another that recognizes the ring structure of human BNP (Shionogi and Co. Ltd., Osaka, Japan). Normal values of BNP at our hospital are ≤18.4 pg/ml. The minimal detectable concentration of BNP was 3.9 pg/ml. The investigators were not blinded to the BNP findings. Statistical Analysis We compared the clinical characteristics, including BNP levels, between the two groups using the χ2 and Mann-Whitney U tests. Factors associated with plasma BNP levels were assessed using the Mann-Whitney U test and linear regression analysis. Optimal cutoffs for each continuous variable to discriminate the likelihood of death from survival within 1 month of ICH were determined from receiver operating characteristic (ROC) curves. Factors with a probability of 60.0 and ≤60.0 pg/ml.
Elevated plasma BNP levels upon admission were independently associated with mortality within 1 month after ICH (mortality rates 31.1 and 13.5% for patients with BNP levels >60.0 and ≤60.0 pg/ml, respectively). To the best of our knowledge, a relationship between BNP and mortality after ICH has never been reported. BNP is a valuable predictive marker of mortality in congestive heart failure [12], acute coronary syndrome [13, 14], cardiomyopathy [15], dialysis-dependent chronic renal failure [16] and even in a community-based population [17]. Therefore, admission BNP levels of patients 206
Eur Neurol 2014;71:203–207 DOI: 10.1159/000356198
with ICH would provide prognostic information for clinicians and help guide patient management. One explanation for the increased plasma BNP levels in the group of non-survivors is that ICH causes changes in neuroendocrine factors including catecholamines that affect the cardiac ventricles. Plasma BNP is elevated in takotsubo cardiomyopathy that is occasionally complicated with ICH [23, 24]. Therefore, we suspect that secGoya/Shibazaki/Sakai/Aoki/Uemura/Saji/ Isa/Ohya/Kimura
ondary cardiac disease due to ICH was a frequent complication in the group of non-survivors. We assess and manage cardiac function as soon as possible after admission if patients have BNP >60.0 pg/ml, as this might help to decrease mortality. Further prospective studies involving pathophysiology are required to confirm this notion. This study had several limitations. Firstly, we did not evaluate cardiac function upon admission. This should be investigated in detail in a similar study. Secondly, we did
not investigate neuroendocrine responses to stress, for example vasopressin and catecholamine. We conclude that admission levels of BNP can predict mortality within 1 month after ICH onset.
Disclosure Statement The authors have no conflicts of interest.
References 1 Ruiz-Sandoval JL, Chiquete E, Romero-Vargas S, Padilla-Martínez JJ, González-Cornejo S: Grading scale for prediction of outcome in primary intracerebral hemorrhages. Stroke 2007;38:1641–1644. 2 Cheung RT, Zou LY: Use of the original, modified, or new intracerebral hemorrhage score to predict mortality and morbidity after intracerebral hemorrhage. Stroke 2003; 34: 1717– 1722. 3 Dandapani BK, Suzuki S, Kelley RE, ReyesIglesias Y, Duncan RC: Relation between blood pressure and outcome in intracerebral hemorrhage. Stroke 1995;26:21–24. 4 Flaherty ML, Haverbusch M, Sekar P, Kissela B, Kleindorfer D, Moomaw CJ, Sauerbeck L, et al: Long-term mortality after intracerebral hemorrhage. Neurology 2006;66:1182–1186. 5 Naidech AM, Batjer HH, Bernstein RA: Prior antiplatelet therapy and outcome following intracerebral hemorrhage: a systematic review. Neurology 2011;76:1607. 6 Passero S, Ciacci G, Ulivelli M: The influence of diabetes and hyperglycemia on clinical course after intracerebral hemorrhage. Neurology 2003;61:1351–1356. 7 Hemphill JC, Bonovich DC, Besmertis L, Manley GT, Johnston SC: The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke 2001;32:891–897. 8 Diedler J, Sykora M, Hahn P, Heerlein K, Schölzke MN, Kellert L, et al: Low hemoglobin is associated with poor functional outcome after non-traumatic, supratentorial intracerebral hemorrhage. Crit Care 2010; 14:R63. 9 Kimura K, Iguchi Y, Inoue T, Shibazaki K, Matsumoto N, Kobayashi K, et al: Hyperglycemia independently increases the risk of early death in acute spontaneous intracerebral hemorrhage. J Neurol Sci 2007;255:90–94.
BNP and Mortality in ICH
10 Di Napoli M, Godoy DA, Campi V, del Valle M, Piñero G, Mirofsky M, et al: C-reactive protein level measurement improves mortality prediction when added to the spontaneous intracerebral hemorrhage score. Stroke 2011; 42:1230–1236. 11 Sudoh T, Kangawa K, Minamino N, Matsuo H: A new natriuretic peptide in porcine brain. Nature 1988;332:78–81. 12 Kociol RD, Horton JR, Fonarow GC, Reyes EM, Shaw LK, O’Connor CM, et al: Admission, discharge, or change in B-type natriuretic peptide and long-term outcomes: data from Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) linked to Medicare claims. Circ Heart Fail 2011;4:628– 636. 13 Suzuki S, Yoshimura M, Nakayama M, Mizuno Y, Harada E, Ito T, et al: Plasma level of B-type natriuretic peptide as a prognostic marker after acute myocardial infarction: a long-term follow-up analysis. Circulation 2004;110:1387–1391. 14 Omland T, Persson A, Ng L, O’Brien R, Karlsson T, Herlitz J, et al: N-terminal pro-B-type natriuretic peptide and long-term mortality in acute coronary syndromes. Circulation 2002;106:2913–2918. 15 Ishikawa C, Tsutamoto T, Fujii M, Sakai H, Tanaka T, Horie M: Prediction of mortality by high-sensitivity C-reactive protein and brain natriuretic peptide in patients with dilated cardiomyopathy. Circ J 2006;70:857–863. 16 Westenbrink BD, Hovinga TK, Kloppenburg WD, Veeger NJ, Janssen WM: B-type natriuretic peptide and interdialytic fluid retention are independent and incremental predictors of mortality in hemodialysis patients. Clin Nephrol 2011;76:373–379.
17 Wallén T, Landahl S, Hedner T, Nakao K, Saito Y: Brain natriuretic peptide predicts mortality in the elderly. Heart 1997; 77: 264– 267. 18 Fukui S, Katoh H, Tsuzuki N, Ishihara S, Otani N, Ooigawa H, et al: Focal brain edema and natriuretic peptides in patients with subarachnoid hemorrhage. J Clin Neurosci 2004; 11:507–511. 19 Nakagawa K, Yamaguchi T, Seida M, Yamada S, Imae S, Tanaka Y, et al: Plasma concentrations of brain natriuretic peptide in patients with acute ischemic stroke. Cerebrovasc Dis 2005;19:157–164. 20 Shibazaki K, Kimura K, Iguchi Y, Okada Y, Inoue T: Plasma brain natriuretic peptide can be a biological marker to distinguish cardioembolic stroke from other stroke types in acute ischemic stroke. Intern Med 2009; 48: 259–264. 21 James ML, Blessing R, Phillips-Bute BG, Bennett E, Laskowitz DT: S100b and brain natriuretic peptide predict functional neurological outcome after intracerebral haemorrhage. Biomarkers 2009;14:388–394. 22 Kothari RU, Brott T, Broderick JP, Barsan WG, Sauerbeck LR, Zuccarello M, et al: The ABCs of measuring intracerebral hemorrhage volumes. Stroke 1996;27:1304–1305. 23 Deininger MH, Radicke D, Buttler J, Scheufler KM, Freiman T, Zentner JF: Tako-tsubo cardiomyopathy: reversible heart failure with favorable outcome in patients with intracerebral hemorrhage. Case report. J Neurosurg 2006;105:465–467. 24 Shiromoto T, Shibazaki K, Kimura K, Sakai K: A case of cerebellar hemorrhage complicated with takotsubo cardiomyopathy – usefulness of plasma brain natriuretic peptide measurement. Rinsho Shinkeigaku 2012; 52: 778–781.
Eur Neurol 2014;71:203–207 DOI: 10.1159/000356198
207
Copyright: S. Karger AG, Basel 2014. Reproduced with the permission of S. Karger AG, Basel. Further reproduction or distribution (electronic or otherwise) is prohibited without permission from the copyright holder.
Eur Neurol 2014;71:203–207 DOI: 10.1159/000356198
Brain Natriuretic Peptide upon Admission as a Biological Marker of Short-Term Mortality after Intracerebral Hemorrhage Yoshino Goya a, b Kensaku Shibazaki a Kenichiro Sakai a Junya Aoki a Jyunichi Uemura a Naoki Saji a Katsunori Isa b Yusuke Ohya b Kazumi Kimura a
a
Department of Stroke Medicine, Kawasaki Medical School, Kurashiki, and b Department of Cardiovascular Medicine, Nephrology and Neurology, University of the Ryukyus Graduate School of Medicine, Nishihara, Japan
Key Words Brain natriuretic peptide · Intracerebral hemorrhage · Mortality
Abstract Background and Purpose: The purpose of the present study was to test the hypothesis that plasma brain natriuretic peptide (BNP) is associated with short-term mortality after intracerebral hemorrhage (ICH). Methods: We prospectively enrolled 271 patients (median age 72 years; 109 females) who were admitted within 24 h of ICH onset between April 2007 and July 2011 and in whom plasma BNP levels were measured upon admission. The patients were assigned to two groups according to survival within 1 month of ICH. Factors associated with mortality were determined by multivariate logistic regression analysis. Results: Within 1 month of ICH, 48 (17.7%) of the 271 enrolled patients died. The median (interquartile range) level of plasma BNP was significantly higher in the group of non-survivors than in the group of survivors [102.5 (48.7–205.0) vs. 32.4 (17.3–85.0) pg/ml; p < 0.001]. A cutoff BNP level of 60.0 pg/ml could predict death within 1 month of ICH. Multivariate logistic regression analysis showed that a plasma BNP of >60.0 pg/ml (OR 4.7; 95% CI
© 2014 S. Karger AG, Basel 0014–3022/14/0714–0203$39.50/0 E-Mail [email protected] www.karger.com/ene
1.43–15.63; p = 0.011) was independently associated with mortality within 1 month after ICH. Conclusions: A high BNP level upon admission is associated with mortality within 1 month after ICH. © 2014 S. Karger AG, Basel
Introduction
Intracerebral hemorrhage (ICH) is a significant cause of adult disability and mortality. Previous studies have identified several clinical [1–6], radiographic [4, 7] and laboratory variables [8–10] that are associated with mortality after ICH. Brain natriuretic peptide (BNP) is a 32-amino acid polypeptide with a 17-amino acid ring structure that has diuretic and vasodilator properties [11]. It is primarily released from the ventricular myocardium and is a biomarker of congestive heart failure. BNP is also a predictive marker of mortality in various disorders [12–16] and in a general community-based population [17]. Plasma BNP levels become elevated for unknown reasons during the acute phase of subarachnoid hemorrhage [18], ischemic stroke [19, 20] and ICH [21]. Plasma BNP Dr. Yoshino Goya Department of Stroke Medicine, Kawasaki Medical School 577 Matsushima Kurashiki City, Okayama 701-0192 (Japan) E-Mail yoozii50 @ gmail.com
is also an independent predictor of neurological function at the time of discharge after ICH [21]. However, the relationship between BNP and mortality after ICH has not been fully examined. The present study tested the hypothesis that admission plasma BNP levels in patients with ICH can serve as a marker of mortality within 1 month after ICH.
Methods We prospectively enrolled consecutive patients who were admitted to our stroke center within 24 h of ICH onset between April 2007 and July 2011. Patients with ICH related to aneurysms, vascular malformation, dissection, tumor, hemorrhagic transformation of ischemic stroke and traumatic ICH were excluded. Plasma BNP was not measured in patients who underwent emergency surgery, and these patients were also excluded. Patients or caregivers were interviewed by telephone or in writing 1–3 months after ICH. Death was defined as all-cause mortality within 1 month after the date of admission. We compared patients who remained alive with those who died. This study complied with the Declaration of Helsinki with regard to human investigations, and the Ethics Committee of Kawasaki Medical School Hospital approved the study protocol. Acute ICH diagnosed by stroke neurologists was confirmed by computed tomography (CT) or magnetic resonance imaging. We assessed age, sex, prior coronary artery disease (CAD), prior ICH, prior ischemic stroke, vascular risk factors, preadmission warfarin therapy, preadmission antiplatelet therapy, systolic and diastolic blood pressure upon admission, National Institutes of Health Stroke Scale (NIHSS) score on admission, location of ICH, hematoma volume, hemoglobin, HbA1c, blood glucose, C-reactive protein (CRP) and plasma BNP. We evaluated vascular risk factors for hypertension (defined as therapy with antihypertensive agents, a systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg before stroke onset), diabetes mellitus (defined as therapy with oral hypoglycemia agents or insulin, or glycosylated hemoglobin ≥6.4%), hyperlipidemia (defined as therapy with antihyperlipidemic agents or serum total cholesterol ≥220 mg/dl) and atrial fibrillation [AF; diagnosed by 12-lead electrocardiography (ECG) and continuous ECG or 24-hour Holter ECG monitoring]. Patients were assessed within 24 h of onset (baseline) using cranial CT according to the protocol of our Radiology Department, with an image matrix of 340 × 340 and a slice width of 8–10 mm. The ICH volume was measured using the A × B × C/2 formula [22]. The location of the ICH was classified according to the location of the largest blood hematoma as the putamen, thalamus, lobe, brainstem or cerebellum. Plasma BNP Measurements Baseline blood samples were collected into tubes containing aprotinin and EDTA from the peripheral veins of all patients upon admission. Plasma was then isolated and stored at –80 ° C. Plasma BNP concentrations were accurately measured within 11 min using a chemiluminescence enzyme immunoassay that sandwiches human BNP between one monoclonal antibody that
204
Eur Neurol 2014;71:203–207 DOI: 10.1159/000356198
recognizes the carboxyl-terminal amino acid sequence, and another that recognizes the ring structure of human BNP (Shionogi and Co. Ltd., Osaka, Japan). Normal values of BNP at our hospital are ≤18.4 pg/ml. The minimal detectable concentration of BNP was 3.9 pg/ml. The investigators were not blinded to the BNP findings. Statistical Analysis We compared the clinical characteristics, including BNP levels, between the two groups using the χ2 and Mann-Whitney U tests. Factors associated with plasma BNP levels were assessed using the Mann-Whitney U test and linear regression analysis. Optimal cutoffs for each continuous variable to discriminate the likelihood of death from survival within 1 month of ICH were determined from receiver operating characteristic (ROC) curves. Factors with a probability of 60.0 and ≤60.0 pg/ml.
Elevated plasma BNP levels upon admission were independently associated with mortality within 1 month after ICH (mortality rates 31.1 and 13.5% for patients with BNP levels >60.0 and ≤60.0 pg/ml, respectively). To the best of our knowledge, a relationship between BNP and mortality after ICH has never been reported. BNP is a valuable predictive marker of mortality in congestive heart failure [12], acute coronary syndrome [13, 14], cardiomyopathy [15], dialysis-dependent chronic renal failure [16] and even in a community-based population [17]. Therefore, admission BNP levels of patients 206
Eur Neurol 2014;71:203–207 DOI: 10.1159/000356198
with ICH would provide prognostic information for clinicians and help guide patient management. One explanation for the increased plasma BNP levels in the group of non-survivors is that ICH causes changes in neuroendocrine factors including catecholamines that affect the cardiac ventricles. Plasma BNP is elevated in takotsubo cardiomyopathy that is occasionally complicated with ICH [23, 24]. Therefore, we suspect that secGoya/Shibazaki/Sakai/Aoki/Uemura/Saji/ Isa/Ohya/Kimura
ondary cardiac disease due to ICH was a frequent complication in the group of non-survivors. We assess and manage cardiac function as soon as possible after admission if patients have BNP >60.0 pg/ml, as this might help to decrease mortality. Further prospective studies involving pathophysiology are required to confirm this notion. This study had several limitations. Firstly, we did not evaluate cardiac function upon admission. This should be investigated in detail in a similar study. Secondly, we did
not investigate neuroendocrine responses to stress, for example vasopressin and catecholamine. We conclude that admission levels of BNP can predict mortality within 1 month after ICH onset.
Disclosure Statement The authors have no conflicts of interest.
References 1 Ruiz-Sandoval JL, Chiquete E, Romero-Vargas S, Padilla-Martínez JJ, González-Cornejo S: Grading scale for prediction of outcome in primary intracerebral hemorrhages. Stroke 2007;38:1641–1644. 2 Cheung RT, Zou LY: Use of the original, modified, or new intracerebral hemorrhage score to predict mortality and morbidity after intracerebral hemorrhage. Stroke 2003; 34: 1717– 1722. 3 Dandapani BK, Suzuki S, Kelley RE, ReyesIglesias Y, Duncan RC: Relation between blood pressure and outcome in intracerebral hemorrhage. Stroke 1995;26:21–24. 4 Flaherty ML, Haverbusch M, Sekar P, Kissela B, Kleindorfer D, Moomaw CJ, Sauerbeck L, et al: Long-term mortality after intracerebral hemorrhage. Neurology 2006;66:1182–1186. 5 Naidech AM, Batjer HH, Bernstein RA: Prior antiplatelet therapy and outcome following intracerebral hemorrhage: a systematic review. Neurology 2011;76:1607. 6 Passero S, Ciacci G, Ulivelli M: The influence of diabetes and hyperglycemia on clinical course after intracerebral hemorrhage. Neurology 2003;61:1351–1356. 7 Hemphill JC, Bonovich DC, Besmertis L, Manley GT, Johnston SC: The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke 2001;32:891–897. 8 Diedler J, Sykora M, Hahn P, Heerlein K, Schölzke MN, Kellert L, et al: Low hemoglobin is associated with poor functional outcome after non-traumatic, supratentorial intracerebral hemorrhage. Crit Care 2010; 14:R63. 9 Kimura K, Iguchi Y, Inoue T, Shibazaki K, Matsumoto N, Kobayashi K, et al: Hyperglycemia independently increases the risk of early death in acute spontaneous intracerebral hemorrhage. J Neurol Sci 2007;255:90–94.
BNP and Mortality in ICH
10 Di Napoli M, Godoy DA, Campi V, del Valle M, Piñero G, Mirofsky M, et al: C-reactive protein level measurement improves mortality prediction when added to the spontaneous intracerebral hemorrhage score. Stroke 2011; 42:1230–1236. 11 Sudoh T, Kangawa K, Minamino N, Matsuo H: A new natriuretic peptide in porcine brain. Nature 1988;332:78–81. 12 Kociol RD, Horton JR, Fonarow GC, Reyes EM, Shaw LK, O’Connor CM, et al: Admission, discharge, or change in B-type natriuretic peptide and long-term outcomes: data from Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) linked to Medicare claims. Circ Heart Fail 2011;4:628– 636. 13 Suzuki S, Yoshimura M, Nakayama M, Mizuno Y, Harada E, Ito T, et al: Plasma level of B-type natriuretic peptide as a prognostic marker after acute myocardial infarction: a long-term follow-up analysis. Circulation 2004;110:1387–1391. 14 Omland T, Persson A, Ng L, O’Brien R, Karlsson T, Herlitz J, et al: N-terminal pro-B-type natriuretic peptide and long-term mortality in acute coronary syndromes. Circulation 2002;106:2913–2918. 15 Ishikawa C, Tsutamoto T, Fujii M, Sakai H, Tanaka T, Horie M: Prediction of mortality by high-sensitivity C-reactive protein and brain natriuretic peptide in patients with dilated cardiomyopathy. Circ J 2006;70:857–863. 16 Westenbrink BD, Hovinga TK, Kloppenburg WD, Veeger NJ, Janssen WM: B-type natriuretic peptide and interdialytic fluid retention are independent and incremental predictors of mortality in hemodialysis patients. Clin Nephrol 2011;76:373–379.
17 Wallén T, Landahl S, Hedner T, Nakao K, Saito Y: Brain natriuretic peptide predicts mortality in the elderly. Heart 1997; 77: 264– 267. 18 Fukui S, Katoh H, Tsuzuki N, Ishihara S, Otani N, Ooigawa H, et al: Focal brain edema and natriuretic peptides in patients with subarachnoid hemorrhage. J Clin Neurosci 2004; 11:507–511. 19 Nakagawa K, Yamaguchi T, Seida M, Yamada S, Imae S, Tanaka Y, et al: Plasma concentrations of brain natriuretic peptide in patients with acute ischemic stroke. Cerebrovasc Dis 2005;19:157–164. 20 Shibazaki K, Kimura K, Iguchi Y, Okada Y, Inoue T: Plasma brain natriuretic peptide can be a biological marker to distinguish cardioembolic stroke from other stroke types in acute ischemic stroke. Intern Med 2009; 48: 259–264. 21 James ML, Blessing R, Phillips-Bute BG, Bennett E, Laskowitz DT: S100b and brain natriuretic peptide predict functional neurological outcome after intracerebral haemorrhage. Biomarkers 2009;14:388–394. 22 Kothari RU, Brott T, Broderick JP, Barsan WG, Sauerbeck LR, Zuccarello M, et al: The ABCs of measuring intracerebral hemorrhage volumes. Stroke 1996;27:1304–1305. 23 Deininger MH, Radicke D, Buttler J, Scheufler KM, Freiman T, Zentner JF: Tako-tsubo cardiomyopathy: reversible heart failure with favorable outcome in patients with intracerebral hemorrhage. Case report. J Neurosurg 2006;105:465–467. 24 Shiromoto T, Shibazaki K, Kimura K, Sakai K: A case of cerebellar hemorrhage complicated with takotsubo cardiomyopathy – usefulness of plasma brain natriuretic peptide measurement. Rinsho Shinkeigaku 2012; 52: 778–781.
Eur Neurol 2014;71:203–207 DOI: 10.1159/000356198
207
Copyright: S. Karger AG, Basel 2014. Reproduced with the permission of S. Karger AG, Basel. Further reproduction or distribution (electronic or otherwise) is prohibited without permission from the copyright holder.
