Key result
Iopamidol during catheterization linked to ~17 µmol/L higher creatinine and rare acute cardiovascular complications.
Why the study?
The incidence of cardiovascular and renal toxicity from a nonionic contrast agent during cardiac catheterization, along with the predictive value of electrolytes and urinalysis results for contrast-induced nephropathy, needed to be determined.
What is the incidence and what are the predictors of cardiovascular and renal toxicity when using the nonionic contrast agent iopamidol for diagnostic cardiac catheterization?
Cohort (n=1,144)
Nonrandomized
No
What is the incidence and what are the predictors of cardiovascular and renal toxicity when using the nonionic contrast agent iopamidol for diagnostic cardiac catheterization?
Answers are grounded in this paper and cite their sources.
Diagnostic cardiac catheterization with the nonionic contrast agent iopamidol causes a small but significant rise in serum creatinine, with baseline renal insufficiency (serum creatinine >= 106.1 mumol/L) being the only confirmed predictor of contrast-induced nephrotoxicity.
Study objective To determine the incidence of cardiovascular and renal toxicity of a nonionic contrast agent when used for cardiac catheterization, and to assess the value of electrolytes and urinalysis results as predictors of nephropathy induced by a contrast agent. Study design Nonrandomized trial using a criterion standard and a cohort analytic study with a 48-hour follow-up. Setting Referral-based university hospital. Patients Convenience sample of patients having diagnostic cardiac catheterization. Renal function and clinical status were evaluated at baseline in 1,144 patients; at 24 hours in 1,077 (94%); and at 48 hours in 663 (57%). Interventions After patients received saline for hydration, coronary angiography and left ventriculography were done with iopamidol (average dose, 203 +/- 56 cc). Measurements and main results The definite and possible incidence of major acute cardiovascular complications from nonionic contrast media was 0.2% and 0.7%, respectively. The mean serum creatinine level increased 11.5 mumol/L from baseline at 24 hours (P less than 0.0001) and 16.8 mumol/L from baseline at 48 hours (P less than 0.0001). Results in a randomly selected training sample were studied to determine predictors of a rise in serum creatinine of 44.2 mumol/L or more. The baseline serum creatinine level and age were significant predictors of renal injury, but hypertension, diabetes mellitus, congestive heart failure, vascular disease, the volume of contrast agent injected or baseline values of urinary variables did not predict nephrotoxicity. In an independent validation sample, only the baseline serum creatinine level was confirmed as a predictor of nephrotoxicity, whereas age was not. A model that predicted contrast-induced nephropathy by the serum creatinine level showed an exponential increase in the risk for nephrotoxicity if the baseline level was 106.1 mumol/L or higher. Conclusions Patients have a small but significant rise in serum creatinine after cardiac catheterization with a nonionic contrast agent. Baseline renal insufficiency is the only confirmed predictor of nonionic contrast-induced nephrotoxicity.
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Charles J. Davidson (1989) conducted a cohort in Diagnostic cardiac catheterization (n=1,144). Iopamidol (nonionic contrast agent) with saline hydration was evaluated on Major acute cardiovascular complications and mean change in serum creatinine (MD 16.8 mumol/L, p=<0.0001). Iopamidol contrast during cardiac catheterization caused major acute cardiovascular complications in 0.2% of patients and increased mean serum creatinine by 16.8 mumol/L at 48 hours.
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