Ventricular Dysfunction as a Stimulus for BNP Release

Increased BNP synthesis and secretion may be owing to increased wall stress from ischemia-induced ventricular dysfunction. BNP levels positively correlate with hemodynamic parameters that reflect ventricular dysfunction, including LVEDP, and negatively correlate with left ventricular ejection fraction (LVEF) (31).

A retrospective study reported that 30% of patients who develop heart failure after MI have preserved LVSF and are thought to have "diastolic dysfunction" (32). Since neurohormonal activation occurs in this group of patients, it has also been proposed that a minor degree of left ventricular systolic dysfunction may be present but may not be detectable because BNP decreases afterload and maintains ejection fraction (33). Compared with patients without significant CAD, patients with coronary artery stenoses have elevated BNP levels and LVEDP independent of LVSF (34).

LAD vs. non-LAD culprit lesion Prox/Mid vs Distal LAD lesion Fig. 3. Median concentration of BNP in patients with lesions in LAD artery (black bars) vs lesions in other vessels (white bars) and in patients with lesions in proximal/mid-LAD (black bars) vs distal LAD artery (white bars). (Adapted from ref. 30.)

LAD vs. non-LAD culprit lesion Prox/Mid vs Distal LAD lesion Fig. 3. Median concentration of BNP in patients with lesions in LAD artery (black bars) vs lesions in other vessels (white bars) and in patients with lesions in proximal/mid-LAD (black bars) vs distal LAD artery (white bars). (Adapted from ref. 30.)

Table 3

Potential Beneficial Actions of BNP in CAD

Vascular

Renal

Cardiac

Vasodilaton

Decreased sympathetic tone Natriuresis/diuresis Decreased smooth muscle Increased glomeruler filtration proliferation rate

Increased vascular permeability Increased arterial distensibility

Improved diastolic function Improved hemodynamics Decreased infarct size Preconditioning Decreased cardiac fibrosis

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