B-Type Natriuretic Peptide: Practical Diagnostic use
B-Type Natriuretic Peptide: Practical Diagnostic use
Assessment of brain natriuretic peptide levels may provide important information that can be used in the evaluation of patients with dyspnea and follow-up of heart failure. Brain natriuretic peptide levels have been shown to be useful for evaluating patients in the emergency department and for evaluating patients complaining of dyspnea in the outpatient setting. Brain natriuretic peptide assessment also provides an adjunct to diagnosis of both systolic and diastolic dysfunction, has prognostic value for heart failure and in acute coronary syndromes, and may be a useful measure to guide therapy. Further work needs to be done to establish the best type of assay to use, to determine the optimal cutoff point for what is considered abnormal, and to determine how conditions other than ventricular dysfunction affect brain natriuretic peptide levels.
The approach to diagnosis and evaluation of heart failure is generally based on clinical findings. Echocardiography and functional testing provide important diagnostic and prognostic information, but a reliable objective biochemical marker for diagnosis and monitoring of disease progression in heart failure has been lacking. Recently, investigators have focused on cardiac natriuretic peptides as a potential reliable objective marker for diagnosis and monitoring of heart failure.
Brain natriuretic peptide (BNP), also known as B-type natriuretic peptide, a hormone first isolated in 1988, has been the primary focus of investigation. Two other structurally related peptide hormones are known at this time: atrial natriuretic peptide (ANP) and C-type natriuretic peptide. All of these peptides share a similar structure but have somewhat different physiologic properties. ANP is produced mainly in the cardiac atria, BNP is secreted by the ventricular myocardium, and C-type natriuretic peptide is produced by endothelial cells. The natriuretic peptide system counteracts the renin-angiotensin-aldosterone system in intravascular volume control. BNP and ANP share common physiological secretory triggers and end organ functions. The main stimuli for secretion are thought to be an increase in myocardial stretch and the rise in intraventricular pressure. These hormones potentiate compensatory natriuresis, peripheral vasodilation, and inhibition of the renin-angiotensin-aldosterone system through a cyclic guanosine mono-phosphate-dependent signaling cascade. Furthermore, they have been shown to have an antimitogenic effect on cardiac fibroblasts (Figure). Plasma BNP levels, however, may possess more significant clinical implications because they correlate more closely with ventricular overload than ANP levels. We review the current practical and potential use of BNP levels in diagnosis and follow-up of patients with heart failure.
(Enlarge Image)
Diagram of simplified neuroendocrine cascade in congestive heart failure.
Assessment of brain natriuretic peptide levels may provide important information that can be used in the evaluation of patients with dyspnea and follow-up of heart failure. Brain natriuretic peptide levels have been shown to be useful for evaluating patients in the emergency department and for evaluating patients complaining of dyspnea in the outpatient setting. Brain natriuretic peptide assessment also provides an adjunct to diagnosis of both systolic and diastolic dysfunction, has prognostic value for heart failure and in acute coronary syndromes, and may be a useful measure to guide therapy. Further work needs to be done to establish the best type of assay to use, to determine the optimal cutoff point for what is considered abnormal, and to determine how conditions other than ventricular dysfunction affect brain natriuretic peptide levels.
The approach to diagnosis and evaluation of heart failure is generally based on clinical findings. Echocardiography and functional testing provide important diagnostic and prognostic information, but a reliable objective biochemical marker for diagnosis and monitoring of disease progression in heart failure has been lacking. Recently, investigators have focused on cardiac natriuretic peptides as a potential reliable objective marker for diagnosis and monitoring of heart failure.
Brain natriuretic peptide (BNP), also known as B-type natriuretic peptide, a hormone first isolated in 1988, has been the primary focus of investigation. Two other structurally related peptide hormones are known at this time: atrial natriuretic peptide (ANP) and C-type natriuretic peptide. All of these peptides share a similar structure but have somewhat different physiologic properties. ANP is produced mainly in the cardiac atria, BNP is secreted by the ventricular myocardium, and C-type natriuretic peptide is produced by endothelial cells. The natriuretic peptide system counteracts the renin-angiotensin-aldosterone system in intravascular volume control. BNP and ANP share common physiological secretory triggers and end organ functions. The main stimuli for secretion are thought to be an increase in myocardial stretch and the rise in intraventricular pressure. These hormones potentiate compensatory natriuresis, peripheral vasodilation, and inhibition of the renin-angiotensin-aldosterone system through a cyclic guanosine mono-phosphate-dependent signaling cascade. Furthermore, they have been shown to have an antimitogenic effect on cardiac fibroblasts (Figure). Plasma BNP levels, however, may possess more significant clinical implications because they correlate more closely with ventricular overload than ANP levels. We review the current practical and potential use of BNP levels in diagnosis and follow-up of patients with heart failure.
(Enlarge Image)
Diagram of simplified neuroendocrine cascade in congestive heart failure.
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