Effects of the creation of arteriovenous fistula for hemodialysis on cardiac function and natriuretic peptide levels in CRF.

BACKGROUND Cardiac failure occasionally is caused by the creation of vascular access for hemodialysis. However, the influence of an arteriovenous (AV) fistula on cardiac function has not been fully elucidated. The present study investigated serial changes in cardiac function and hormonal levels after the AV fistula operation. METHODS Sixteen patients with chronic renal failure underwent echocardiographic studies before and 3, 7, and 14 days after the AV fistula operation. Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations were measured before and 1, 3, 6, 10, and 14 days after the operation. RESULTS Creation of an AV fistula produced significant elevations in left ventricular (LV) end-diastolic diameter (+4%), fractional shortening (+8%), and cardiac output (CO; +15%). In LV inflow velocities measured by Doppler echocardiography, deceleration time of the early diastolic filling wave shortened (-12%) and the ratio of the peak velocity of early diastolic to atrial filling (E-A ratio) increased (+18%). The difference in duration of LV inflow and pulmonary venous flow at atrial contraction, a marker of LV end-diastolic pressure, significantly shortened day 14 after the operation (-37%). That is, creation of an AV fistula induced LV diastolic dysfunction toward a restrictive filling pattern. Both ANP and BNP levels increased after the operation, and maximal percentages of increase were observed after 10 days (ANP, +48%; BNP, +68%). In the relationship between cardiac function and hormonal response, the increase in CO was associated with elevation of ANP levels (r = 0.61; P = 0.01), but not BNP levels. Conversely, the increase in E-A ratio correlated only with BNP level elevation (r = 0.60; P = 0.01). CONCLUSION Our observations indicate that creation of an AV fistula has significant effects on cardiac systolic and diastolic performance, and ANP release is induced by volume loading, but BNP release is stimulated by LV diastolic dysfunction.