Ivo van der Bilt1, Djo Hasan, Renee van den Brink, Maarten-Jan Cramer, Mathieu van der Jagt, Fop van Kooten, John Meertens, Maarten van den Berg, Rob Groen, Folkert Ten Cate, Otto Kamp, Marco Götte, Janneke Horn, Johan Groeneveld, Peter Vandertop, Ale Algra, Frans Visser, Arthur Wilde, Gabriel Rinkel. 1. From the Departments of Cardiology (I.v.d.B, D.H., R.v.d.B., A.W.) and Intensive Care (J.H.), Academic Medical Center Amsterdam; Department of Cardiology (M.-J.C.), University Medical Center Utrecht; Departments of Intensive Care (M.v.d.J.), Neurology (F.v.K.), and Cardiology (F.t.C.), Erasmus Medical Center Rotterdam; Departments of Intensive Care (J.M.), Cardiology (M.v.d.B.), and Neurosurgery (R.G.), University Medical Center Groningen; Departments of Cardiology (O.K.) and Intensive Care (J.G.), VU University Medical Center; Department of Cardiology (M.G.), Haga Hospital The Hague; Department of Neurosurgical Center Amsterdam (P.V.), Academic Medical Center and VU University Medical Center; Department of Clinical Epidemiology (A.A.), Julius Center for Health Sciences and Primary Care; Departments of Neurology and Neurosurgery (A.A., G.R.), Utrecht Stroke Center, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht; and Stichting CardioZorg (F.V.), Amsterdam, the Netherlands.
Abstract
OBJECTIVE: To assess whether cardiac abnormalities after aneurysmal subarachnoid hemorrhage (aSAH) are associated with delayed cerebral ischemia (DCI) and clinical outcome, independent from known clinical risk factors for these outcomes. METHODS: In a prospective, multicenter cohort study, we performed echocardiography and ECG and measured biochemical markers for myocardial damage in patients with aSAH. Outcomes were DCI, death, and poor clinical outcome (death or dependency for activities of daily living) at 3 months. With multivariable Poisson regression analysis, we calculated risk ratios (RRs) with corresponding 95% confidence intervals. We used survival analysis to assess cumulative percentage of death in patients with and without echocardiographic wall motion abnormalities (WMAs). RESULTS: We included 301 patients with a mean age of 57 years; 70% were women. A wall motion score index ≥1.2 had an adjusted RR of 1.2 (0.9-1.6) for DCI, 1.9 (1.1-3.3) for death, and 1.8 (1.1-3.0) for poor outcome. Midventricular WMAs had adjusted RRs of 1.1 (0.8-1.4) for DCI, 2.3 (1.4-3.8) for death, and 2.2 (1.4-3.5) for poor outcome. For apical WMAs, adjusted RRs were 1.3 (1.1-1.7) for DCI, 1.5 (0.8-2.7) for death, and 1.4 (0.8-2.5) for poor outcome. Elevated troponin T levels, ST-segment changes, and low voltage on the admission ECGs had a univariable association with death but were not independent predictors for outcome. CONCLUSION: WMAs are independent risk factors for clinical outcome after aSAH. This relation is partly explained by a higher risk of DCI. Further study should aim at treatment strategies for these aSAH-related cardiac abnormalities to improve clinical outcome.
OBJECTIVE: To assess whether cardiac abnormalities after aneurysmal subarachnoid hemorrhage (aSAH) are associated with delayed cerebral ischemia (DCI) and clinical outcome, independent from known clinical risk factors for these outcomes. METHODS: In a prospective, multicenter cohort study, we performed echocardiography and ECG and measured biochemical markers for myocardial damage in patients with aSAH. Outcomes were DCI, death, and poor clinical outcome (death or dependency for activities of daily living) at 3 months. With multivariable Poisson regression analysis, we calculated risk ratios (RRs) with corresponding 95% confidence intervals. We used survival analysis to assess cumulative percentage of death in patients with and without echocardiographic wall motion abnormalities (WMAs). RESULTS: We included 301 patients with a mean age of 57 years; 70% were women. A wall motion score index ≥1.2 had an adjusted RR of 1.2 (0.9-1.6) for DCI, 1.9 (1.1-3.3) for death, and 1.8 (1.1-3.0) for poor outcome. Midventricular WMAs had adjusted RRs of 1.1 (0.8-1.4) for DCI, 2.3 (1.4-3.8) for death, and 2.2 (1.4-3.5) for poor outcome. For apical WMAs, adjusted RRs were 1.3 (1.1-1.7) for DCI, 1.5 (0.8-2.7) for death, and 1.4 (0.8-2.5) for poor outcome. Elevated troponin T levels, ST-segment changes, and low voltage on the admission ECGs had a univariable association with death but were not independent predictors for outcome. CONCLUSION: WMAs are independent risk factors for clinical outcome after aSAH. This relation is partly explained by a higher risk of DCI. Further study should aim at treatment strategies for these aSAH-related cardiac abnormalities to improve clinical outcome.
Authors: Benjamin B Kenigsberg; Christopher F Barnett; Jeffrey C Mai; Jason J Chang Journal: Curr Neurol Neurosci Rep Date: 2019-11-13 Impact factor: 5.081
Authors: Charlotte H P Cremers; Ivo A C van der Bilt; Irene C van der Schaaf; Mervyn D I Vergouwen; Jan Willem Dankbaar; Maarten J Cramer; Arthur A M Wilde; Gabriel J E Rinkel; Birgitta K Velthuis Journal: Neurocrit Care Date: 2016-04 Impact factor: 3.210
Authors: Azra Bihorac; Tezcan Ozrazgat-Baslanti; Elizabeth Mahanna; Seemab Malik; Peggy White; Matthew Sorensen; Brenda G Fahy; John W Petersen Journal: Anesth Analg Date: 2016-05 Impact factor: 5.108