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Cardiac function and brain-type natriuretic peptide in first-time flash pulmonary edema
Jacob P Dal-Bianco1, Allan S Jaffe, Malcolm R Bell
1Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Mayo Clinic Proceedings
|March 5, 2008
Summary
First-time flash pulmonary edema (FPE) is often caused by coronary artery disease and hypertension. Diastolic dysfunction is key, with lower brain-type natriuretic peptide (BNP) levels in preserved ejection fraction patients despite similar pressures.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Biomarkers
Background:
- Flash pulmonary edema (FPE) is a critical condition requiring prompt assessment.
- Understanding the role of left ventricular (LV) function and brain-type natriuretic peptide (BNP) in first-time FPE is crucial for diagnosis and management.
Purpose of the Study:
- To evaluate left ventricular (LV) systolic and diastolic function.
- To assess brain-type natriuretic peptide (BNP) levels in patients experiencing their first episode of FPE.
Main Methods:
- Retrospective analysis of patients with first-time FPE from 2000-2004.
- Inclusion criteria: BNP assessment and echocardiography within 24 hours of presentation.
- Patients categorized by reduced (LVEF < 50%) versus preserved (LVEF ≥ 50%) LV ejection fraction.
Main Results:
- Thirty-seven patients met criteria; 73% had reduced LVEF.
- Common causes included coronary artery disease and hypertension.
- Preserved LVEF group had lower BNP levels (535 pg/mL vs 1320 pg/mL, P=.01) despite similar elevated LV filling pressures.
- Reduced early diastolic mitral annulus velocity (myocardial relaxation) observed in nearly all patients.
Conclusions:
- Coronary artery disease and hypertension are primary triggers for first-time FPE.
- Diastolic dysfunction appears to be a prerequisite for FPE.
- BNP levels are elevated in all FPE patients but are significantly lower in those with preserved LVEF, even with similar LV filling pressures.
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