Maximum Arterial Contrast Concentrations With Computed Tomography and Left Ventriculography: Implications for Contrast Nephrotoxicity Risk

Abstract

Contrast nephropathy occurs more frequently after cardiac angiography, which usually includes left ventriculography via direct left ventricular injection, than after contrast-enhanced computed tomography (CT), despite the usually higher intravenous contrast dose used for CT. To determine whether maximum renal arterial contrast concentration is higher after left ventriculography, we assessed this parameter for both procedures. Contrast concentration in abdominal aortic blood during contrast-enhanced CT was measured by performing CT densitometry of aortic blood before contrast, and in the arterial phase, in 100 adults undergoing abdominal CT. Densities were converted to contrast concentrations by scanning water phantoms containing 20 graded concentrations of contrast and comparing their densities to patient data. Because it was impossible to perform CT densitometry during cardiac angiography, aortic contrast concentrations were calculated from standard contrast doses and injection rates with the range of clinically encountered cardiac output rates, assuming ultimate steady state for blood/contrast mixing and normal data distribution. Maximum aortic (and hence renal arterial) concentrations were significantly higher (range, 6.68%-15.90%) after ventriculography than after CT (1.22%-5.80%). Because ventricular injection times are much shorter than published initial-appearance-to-maximum-concentration times after intravenous administration, the rate of change of contrast concentration is also higher after ventriculography than after CT. Higher maximum renal arterial contrast concentration may be responsible for the greater risk of nephropathy after cardiac angiography than after doses for CT. The faster rate of change of renal arterial contrast concentration after ventriculography may also increase the likelihood of renal toxicity. Maximum renal arterial contrast concentration, and/or the rapidity of change of this parameter, may be partly responsible for the risk of nephropathy. Controlling these factors might permit reduction of nephropathy risk; they also suggest avenues of research into the pathophysiology of contrast nephropathy.