TY - JOUR
T1 - Left ventricular dysfunction and cerebral infarction from vasospasm after subarachnoid hemorrhage
AU - Temes, Richard E.
AU - Tessitore, Elena
AU - Schmidt, J. Michael
AU - Naidech, Andrew M.
AU - Fernandez, Andres
AU - Ostapkovich, Noeleen D.
AU - Frontera, Jennifer A.
AU - Wartenberg, Katja E.
AU - Di Tullio, Marco R.
AU - Badjatia, Neeraj
AU - Connolly, E. Sander
AU - Mayer, Stephan A.
AU - Parra, Augusto
N1 - Funding Information:
Acknowledgment This research was supported in part by a Grant-in-Aid (No. 9750432N) from the American Heart Association to Dr Mayer.
Copyright:
Copyright 2011 Elsevier B.V., All rights reserved.
PY - 2010/12
Y1 - 2010/12
N2 - Background: Although neurogenic stunned myocardium (NSM) after aneurysmal subarachnoid hemorrhage (SAH) is well described, its clinical significance remains poorly defined. We investigated the influence of left ventricular (LV) dysfunction and cerebral vasospasm on cerebral infarction, serious cardiovascular events, and functional outcome after SAH. Methods: Of the 481 patients enrolled in the University Columbia SAH Outcomes Project between 10/96 and 05/02, we analyzed a subset of 119 patients with at least one echocardiogram, serial transcranial Doppler (TCD) data, and with no prior history of cardiac disease. LV dysfunction was defined as an ejection fraction <40% on echocardiography. Infarction from vasospasm was adjudicated by the study team after comprehensive review of all clinical and imaging data. Functional outcome was assessed at 15 and 90 days with the modified Rankin Scale (mRS). Results: Eleven percent of patients had LV dysfunction (N = 13). Younger age, hydrocephalus, and complete filling of the quadrigeminal and fourth ventricles were associated with LV dysfunction (all P < 0.05). Despite a similar frequency of pre-existing hypertension, 0% of patients with LV dysfunction reported taking antihypertensive medication, compared to 35% of those without (P = 0.009). There was a significant association between LV dysfunction and infarction from vasospasm after adjusting for clinical grade, age, and peak TCD flow velocity (P = 0.03). Patients with LV dysfunction also had higher rates of hypotension requiring vasopressors (P = 0.001) and pulmonary edema (P = 0.002). However, there was no association between LV dysfunction and outcome at 14 days after adjustment for established prognostic variables. Conclusions: LV dysfunction after SAH increases the risk of cerebral infarction from vasospasm, hypotension, and pulmonary edema, but with aggressive ICU support does not affect short-term survival or functional outcome. Antihypertensive medication may confer cardioprotection and reduce the risk of catecholamine-mediated injury after SAH.
AB - Background: Although neurogenic stunned myocardium (NSM) after aneurysmal subarachnoid hemorrhage (SAH) is well described, its clinical significance remains poorly defined. We investigated the influence of left ventricular (LV) dysfunction and cerebral vasospasm on cerebral infarction, serious cardiovascular events, and functional outcome after SAH. Methods: Of the 481 patients enrolled in the University Columbia SAH Outcomes Project between 10/96 and 05/02, we analyzed a subset of 119 patients with at least one echocardiogram, serial transcranial Doppler (TCD) data, and with no prior history of cardiac disease. LV dysfunction was defined as an ejection fraction <40% on echocardiography. Infarction from vasospasm was adjudicated by the study team after comprehensive review of all clinical and imaging data. Functional outcome was assessed at 15 and 90 days with the modified Rankin Scale (mRS). Results: Eleven percent of patients had LV dysfunction (N = 13). Younger age, hydrocephalus, and complete filling of the quadrigeminal and fourth ventricles were associated with LV dysfunction (all P < 0.05). Despite a similar frequency of pre-existing hypertension, 0% of patients with LV dysfunction reported taking antihypertensive medication, compared to 35% of those without (P = 0.009). There was a significant association between LV dysfunction and infarction from vasospasm after adjusting for clinical grade, age, and peak TCD flow velocity (P = 0.03). Patients with LV dysfunction also had higher rates of hypotension requiring vasopressors (P = 0.001) and pulmonary edema (P = 0.002). However, there was no association between LV dysfunction and outcome at 14 days after adjustment for established prognostic variables. Conclusions: LV dysfunction after SAH increases the risk of cerebral infarction from vasospasm, hypotension, and pulmonary edema, but with aggressive ICU support does not affect short-term survival or functional outcome. Antihypertensive medication may confer cardioprotection and reduce the risk of catecholamine-mediated injury after SAH.
KW - Cerebral infarction
KW - Echocardiography
KW - Left ventricular dysfunction
KW - Neurogenic stunned myocardioum
KW - Subarachnoid hemorrhage
KW - Vasospasm
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U2 - 10.1007/s12028-010-9447-x
DO - 10.1007/s12028-010-9447-x
M3 - Article
C2 - 20945116
AN - SCOPUS:78649707632
SN - 1541-6933
VL - 13
SP - 359
EP - 365
JO - Neurocritical Care
JF - Neurocritical Care
IS - 3
ER -
