Do plasma levels of brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) increase in diastolic dysfunction as well as in systolic dysfunction?

摘要

After the structure of atrial natriuretic peptide was established,1 a Japanese group isolated the brain (also known as B-type) natriuretic peptide (BNP) from porcine brain extracts in 1988 by monitoring the relaxant activity of the chick rectum.2 Subsequent studies demonstrated that BNP is a cardiac hormone that is mainly expressed in the heart, where its concentration is considerably higher than in the human or rodent brain.3 It is well known that mechanical stress, such as pressure and volume overload, neurohumoral factors, and cytokines stimulate the gene expression of BNP and levels of myocardial BNP mRNA and circulating BNP and N-terminal proBNP (NT-proBNP) are remarkably increased in patients with congestive heart failure (HF).4 Clinical studies also showed that BNP levels correlate well with the left ventricular end-diastolic pressure (LVEDP) and ejection fraction (LVEF). Therefore, BNP is considered to function as an emergency defense against ventricular overload in disease states and it has been used as a marker of ventricular function or stress. However, there are few studies that have investigated whether BNP may be used as a marker of LV diastolic function in patients with coronary artery disease (CAD).