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  • Poster presentation
  • Open Access

Significance of B-type natriuretic peptide in acute cerebrovascular disease

  • 1,
  • 1 and
  • 1
Critical Care200610 (Suppl 1) :P191

https://doi.org/10.1186/cc4538

  • Published:

Keywords

  • Congestive Heart Failure
  • Ischemic Stroke
  • Pulmonary Embolism
  • Acute Coronary Syndrome
  • Natriuretic Peptide

Introduction

Increased serum N-terminal pro-B-type natriuretic peptide (N-BNP) has been observed in congestive heart failure (CHF), acute coronary syndromes, pulmonary embolism and septic shock. N-BNP elevation has also been linked with ischemic stroke (IS) and aneurysmal subarachnoid hemorrhage (SAH); however, the significance of N-BNP in this setting is unknown. We hypothesized that elevated serum N-BNP may occur independently of CHF in patients with acute cerebrovascular disease.

Design

A case–control study.

Methods

Patients hospitalized with acute IS, SAH, or spontaneous intracerebral hemorrhage (ICH) were evaluated with serum N-BNP testing and transthoracic echocardiography. Patients were classified into two groups (presence or absence of CHF) using modified Framingham criteria.

Results

Sixty-seven patients were evaluated, 37 with IS, 20 with SAH, and 10 with ICH. CHF was present in 36 patients (53%), while elevated N-BNP (>500 pg/ml) was detected in 57 (85%). Patients with and without CHF were not significantly different with regard to demographics, cardiovascular risk factors, stroke subtype, fluid balance, and administration of diuretic, antihypertensive, or vasoactive medications. Systolic and diastolic dysfunction and increased serum troponin I were more common in the CHF group, but these differences were not significant. N-BNP was markedly elevated in both groups, and significantly higher in patients with CHF. At a 500 pg/ml cutoff, the sensitivity, specificity, positive predictive value, and negative predictive value of N-BNP for CHF were respectively 94%, 25%, 58%, and 80%.

Conclusion

Serum N-BNP has limited value for diagnosing CHF in patients with acute cerebrovascular disease. Elevated levels in patients without CHF point to alternative mechanisms of N-BNP production. More work is needed to explore the pathophysiology, diagnostic role, and prognostic significance of N-BNP in this patient group.
Table 1

(abstract P191)

 

CHF (n = 36)

No CHF (n = 31)

P value

Age (years)

65

62

0.8

Males (number of patients)

18

11

0.05

SAH (number of patients)

9

11

0.7

ICH (number of patients)

6

4

0.7

IS (number of patients)

21

16

0.6

N-BNP (pg/ml)

8032 ± 10,110

3014 ± 3823

0.007

Systolic dysfunction (number of patients)

14

6

0.08

Diastolic dysfunction (number of patients)

14

7

0.1

Tropinin I (number of patients)

15

9

0.2

Hospital LOS (days)

17

17

0.8

Death (number of patients)

12

4

0.04

Authors’ Affiliations

(1)
Johns Hopkins University, Baltimore, MD, USA

Copyright

© BioMed Central Ltd 2006

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