Neurocritical Care

, Volume 5, Issue 2, pp 102–107

Cardiovascular predictors of in-patient mortality after subarachnoid hemorrhage

  • Sirisha Yarlagadda
  • Pam Rajendran
  • Jacob C. Miss
  • Nader M. Banki
  • Alexander Kopelnik
  • Alan H. B. Wu
  • Nerissa Ko
  • Adrian W. Gelb
  • Michael T. Lawton
  • Wade S. Smith
  • William L. Young
  • Jonathan G. Zaroff
Original Article

DOI: 10.1385/NCC:5:2:102

Cite this article as:
Yarlagadda, S., Rajendran, P., Miss, J.C. et al. Neurocrit Care (2006) 5: 102. doi:10.1385/NCC:5:2:102

Abstract

Background and Purpose

Whether cardiac dysfunction contributes to morbidity and mortality after subarachnoid hemorrhage (SAH) remains controversial. The objective of this study was to test the hypothesis that cardiovascular abnormalities are independently related to in-patient mortality after SAH.

Methods

This was a prospective cohort study of patients with aneurysmal SAH. Heart rate and blood pressure were measured, a blood sample was obtained, and echocardiography was performed on three study days, starting as soon after admission as possible. The cardiovascular predictor variables were heart rate, systolic blood pressure (SBP), cardiac troponin I (cTi) level, B-type natriuretic peptide (BNP) level, and left ventricular ejection fraction. The primary outcome measure was in-patient mortality. The association between each predictor variable and mortality was quantified by multivariate logistic regression, including relevant covariates and reporting odds ratios (OR) and 95% confidence intervals (CI).

Results

The study included 300 patients. An initial BNP level greater than 600 pg/mL was markedly associated with death (OR 37.7, p<0.001). On the third study day (9.1±4.1 days after SAH symptom onset), a cTi level greater than 0.3 mg/L (OR 7.6, p=0.002), a heart rate of 100 bpm or greater (OR 4.9, p=0.009), and a SBP less than 130 mmHg (OR 6.7, p=0.007) were significantly associated with death.

Conclusions

Cardiovascular abnormalities are independent predictors of in-patient mortality after SAH. Though these effects may be explained by a reduction in cerebral perfusion pressure or other mechanisms, further research is required to determine whether or not they are causal in nature.

Key Words

Subarachnoid hemorrhage natriuretic peptides troponin echocardiography 

Copyright information

© Humana Press Inc 2006

Authors and Affiliations

  • Sirisha Yarlagadda
    • 1
  • Pam Rajendran
    • 2
  • Jacob C. Miss
    • 1
  • Nader M. Banki
    • 1
  • Alexander Kopelnik
    • 1
  • Alan H. B. Wu
    • 3
  • Nerissa Ko
    • 2
  • Adrian W. Gelb
    • 4
  • Michael T. Lawton
    • 5
  • Wade S. Smith
    • 2
  • William L. Young
    • 4
  • Jonathan G. Zaroff
    • 1
  1. 1.Department of MedicineUniversity of California San FranciscoSan Francisco
  2. 2.Department of NeurologyUniversity of California San FranciscoSan Francisco
  3. 3.Department of Laboratory MedicineUniversity of California San FranciscoSan Francisco
  4. 4.Department of Anesthesia and Perioperative CareUniversity of California San FranciscoSan Francisco
  5. 5.Department of NeurosurgeryUniversity of California San FranciscoSan Francisco

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