on August 27, 2009
Published online before print August 27, 2009, doi: 10.1161/STROKEAHA.109.556753
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on April 30, 2009
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. * To whom correspondence should be addressed. 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 Results—Of 204 subjects, 31% had cTnI 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.
Revised on June 5, 2009
Accepted on June 17, 2009
Elevated Cardiac Troponin I and Relationship to Persistence of Electrocardiographic and Echocardiographic Abnormalities After Aneurysmal Subarachnoid Hemorrhage
Marilyn Hravnak RN, PhD*;
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.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.
Key words: cardiac arrhythmia • cardiac troponin I • echocardiography • electrocardiography • left ventricular ejection fraction • neurocritical care • SAH • subarachnoid hemorrhage • wall motion abnormality