(Circulation. 2007;116:e311.)
© 2007 American Heart Association, Inc.
Correspondence |
Laboratory of Interventional Cardiology and Department of Cardiology, Clinica Mediterranea, Naples, Italy
Laboratory of Interventional Cardiology, "Vita e Salute", University School of Medicine, San Raffaele Hospital, Milan, Italy
Institute of Medical Statistics and Biometry, University of Milan, Milan, Italy
We thank Dr Wetzels for his interest and comments on our Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL).1 We will try to clarify the questions raised.
1. The study was double blinded. Neither the patient nor the interventional cardiologist performing the procedure was aware of the type of treatment. Patients enrolled were randomized the day before contrast exposure. The randomization list was handled by a dedicated nurse. The protocol of infusion (according to the group of treatment) was managed by a nurse and physician not involved in the study.
2. The infusion rate of the sodium bicarbonate solution was in accordance with the protocol reported by Merten et al.2 The initial intravenous bolus was 3 mL · kg–1 · h–1 for 1 hour immediately before contrast injection. After this, patients received the same fluid at a rate of 1 mL · kg–1 · h–1 during contrast exposure and for 6 hours after the procedure. However, in many cases, the contrast exposure started >1 hour after the initial intravenous bolus. This was due to the unpredictable course of the catheterization laboratory schedule in everyday practice. Furthermore, the infusion sometimes lasted >6 hours after the procedure. This may explain why the "theoretical" volume is actually smaller than the "actual" volume infused in the bicarbonate plus N-acetylcysteine (NAC) group.
3. Volume output, although not statistically different, was actually lower in the bicarbonate group compared with the other groups. The total volume of intravenous hydration was lower in the bicarbonate plus NAC group compared with both the saline plus NAC group and the saline plus ascorbic acid plus NAC group. This supports the concept that the mechanism of the effectiveness of sodium bicarbonate in preventing contrast-induced nephropathy is not likely to be a result of larger volume expansion than isotonic saline. We may hypothesize that the higher amount of HCO3– in the proximal convoluted tubule may buffer the higher amount of H+ resulting from cellular hypoxia and facilitate Na+ reabsorption through the electrogenic Na+/HCO3– cotransporter.3
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