The contribution of an arteriovenous access for hemodialysis to left ventricular hypertrophy

The long-term isolated contribution of hemodialysis arteriovenous access (AVA) to cardiac hemodynamics has not been previously investigated in a prospective manner.

Twelve predialysis patients were studied before and 1 and 3 months after creation of a primary AVA. Evaluation included relevant clinical parameters, echocardiographic studies, and hemodynamic hormones.

After creation of an AVA, there was no change in patient weight, blood pressure or hemoglobin level. Cardiac index increased and systemic vascular resistance decreased. Left ventricular mass (LVM) corrected to height increased from 63.8 +/- 5.5 to 68.9 +/- 4.9 g/m(2.7) at 1 month (P = 0.05) and 72.5 +/- 8.9 g/m(2.7) at 3 months (P < 0.05). This increase in LVM was accounted for mostly by an increase in interventricular septal thickness, whereas left ventricular end-diastolic diameter and posterior wall thickness did not change. The incidence of left ventricular hypertrophy (LVH) increased from 67% at baseline to 83% and 90% at 1 and 3 months, respectively. Left atrial area increased from 17.6 +/- 1.0 cm(2) at baseline to 19.7 +/- 1.3 cm(2) at 1 month (P < 0.01) and 20.2 +/- 1.2 cm(2) at 3 months (P < 0.05). Early diastolic transmitral flow increased from 68.0 +/- 4.2 cm/s at baseline to 85.6 +/- 7.3 and 89.2 +/- 6.5 cm/s at 1 and 3 months, respectively (P < 0.01). Inferior vena cava diameter increased at 1 month and did not change at 3 months. Plasma atrial natriuretic polypeptide levels increased from 268 +/- 35 pg/mL (87 +/- 11 pmol/L) at baseline to 461 +/- 63 pg/mL (150 +/- 20 pmol/L) at 1 month (P < 0.01) and 610 +/- 96 pg/mL (198 +/- 31 pmol/L) at 3 months (P < 0.01). Plasma renin activity and serum aldosterone levels decreased. Plasma angiotensin II, angiotensin-converting enzyme, and endothelin levels did not change.

Creation of a hemodialysis AVA is independently associated with further progression of already existing LVH.