This Article Full Text Full Text (PDF) All Versions of this Article: 40/11/3478    most recent STROKEAHA.109.556753v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Hravnak, M. Articles by Horowitz, M. B. PubMed PubMed Citation Articles by Hravnak, M. Articles by Horowitz, M. B. Related Collections Electrocardiology Echocardiography Acute Cerebral Hemorrhage Cerebral Aneurysm, AVM, & Subarachnoid hemorrhage

(Stroke. 2009;40:3478.)
© 2009 American Heart Association, Inc.

Original Contributions

Elevated Cardiac Troponin I and Relationship to Persistence of Electrocardiographic and Echocardiographic Abnormalities After Aneurysmal Subarachnoid Hemorrhage

Marilyn Hravnak, RN, PhD; J. Michael Frangiskakis, MD, PhD; Elizabeth A. Crago, RN, MSN; Yuefang Chang, PhD; Masaki Tanabe, MD; John Gorcsan, III, MD Michael B. Horowitz, MD

From the University of Pittsburgh Schools of Nursing (M.H., E.A.C.) and the Medicine Division of Cardiology (J.M.F., J.G.) and Division of Neurosurgery (Y.C., M.B.H.), University of Pittsburgh, Pittsburgh, PA; and Mie University Graduate School of Medicine (M.T.), Tsu City, Mie Prefecture, Japan.

Correspondence to Marilyn Hravnak, RN, PhD, FCCM, 336 Victoria Building, 3500 Victoria Street, Pittsburgh, PA 15261. E-mail mhra{at}pitt.edu

Background and Purpose— Cardiac injury persistence after aneurysmal subarachnoid hemorrhage (aSAH) is not well described. We hypothesized that post-aSAH cardiac injury, detected by elevated cardiac troponin I (cTnI), is related to aSAH severity and associated with electrocardiographic and structural echocardiographic abnormalities that are persistent.

Methods— Prospective longitudinal study was conducted of patients with aSAH with Fisher grade 2 and/or Hunt/Hess grade 3. Serum cTnI was collected on Days 1 to 5; cohort dichotomized into peak cTnI 0.3 ng/mL (elevated) or cTnI <0.3 ng/mL. Relationships among cTnI and aSAH severity, 12-lead electrocardiography early (4 days) and late (7 days), Holter monitoring on Days 1 to 5, and transthoracic echocardiogram (left ventricular ejection fraction and regional wall motion abnormalities) early (Days 0 to 5) and late (Days 5 to 12) were evaluated.

Results— Of 204 subjects, 31% had cTnI 0.3 ng/mL. cTnI 0.3 ng/mL was incrementally related to aSAH severity by admission symptoms (Hunt/Hess P=0.001) and blood load (Fisher P=0.028). More patients with cTnI 0.3 ng/mL had prolonged QTc on early (63% versus 30%, P<0.0001) and late electrocardiography (24% versus 7%, P=0.024). On Holter monitoring, more patients with cTnI 0.3 ng/mL had ventricular tachycardia/fibrillation (22% versus 9%, P=0.018) but not atrial fibrillation/flutter (P=0.241). Cardiac troponin I 0.3 ng/mL was associated with both early ejection fraction <50% (44% versus 5%, P<0.0001) and regional wall motion abnormalities (44% versus 4%, P<0.0001). Regional wall motion abnormalities predominated in basal and midventricular segments and persisted to some degree in 73% of patients affected, whereas ejection fraction <50% persisted in 59% of patients affected.

Conclusions— Cardiac injury is incrementally worse with increasing aSAH severity and associated with persistent QTc prolongation and ventricular arrhythmias. Regional wall motion abnormalities and depressed ejection fraction persist to some degree in the majority of those affected.

Key Words: cardiac arrhythmia • cardiac troponin I • echocardiography • electrocardiography • left ventricular ejection fraction • neurocritical care • SAH • subarachnoid hemorrhage • wall motion abnormality