title: Elevated cardiac troponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage.
abstract: OBJECTIVE
  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 >or=2 and/or Hunt/Hess grade >or=3. Serum cTnI was collected on Days 1 to 5; cohort dichotomized into peak cTnI >or=0.3 ng/mL (elevated) or cTnI <0.3 ng/mL. Relationships among cTnI and aSAH severity, 12-lead electrocardiography early (<or=4 days) and late (>or=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 >or=0.3 ng/mL. cTnI >or=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 >or=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 >or=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 >or=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.
authors.affiliation: University of Pittsburgh Schools of Nursing, Pittsburgh, PA, USA. mhra@pitt.edu
authors.forename: Marilyn
authors.initials: M
authors.lastname: Hravnak
authors.forename: J Michael
authors.initials: JM
authors.lastname: Frangiskakis
authors.forename: Elizabeth A
authors.initials: EA
authors.lastname: Crago
authors.forename: Yuefang
authors.initials: Y
authors.lastname: Chang
authors.forename: Masaki
authors.initials: M
authors.lastname: Tanabe
authors.forename: John
authors.initials: J
authors.lastname: Gorcsan
authors.forename: Michael B
authors.initials: MB
authors.lastname: Horowitz
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D004452:Echocardiography / Q000379:methods; D004562:Electrocardiography / Q000379:methods; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013345:Subarachnoid Hemorrhage / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D019210:Troponin I / Q000097:blood*; D055815:Young Adult
chemical_list: D015415:Biomarkers; D019210:Troponin I