In a recent letter in this journal, Dr. Zingarelli suggests the potential role of bivalirudin in reducing the risk of acute kidney disease (AKI), on top of other not bleeding-related complications, after primary percutaneous coronary intervention. His intuition derives by the observation that in our PRIPITENA study, patients with a transradial approach were more frequently treated with bivalirudin compared with the transfemoral group, and by the fact that by reducing bleedings bivalirudin may reduce the hypovolemia-related cortical glomerular hypoperfusion.

This hypothesis is intriguing and deserves a comment by our group. In the PRIPITENA study, 18.4% of transradial and 3% of transfemoral patients were treated with bivalirudin; of the transradial patients, 64% had a 4-hour postprocedural infusion and 36% did not. Those that received a postprocedural infusion had a lower risk for the occurrence of the primary end point of AKI: 6.4% versus 9.9% (unpublished data). The small population treated with bivalirudin does not allow drawing a definite conclusion but may reinforce the hypothesis of Dr Zingarelli. Furthermore, our cumulative data from the PROBI VIRI and PROBI VIRI 2 studies show a significantly greater risk for the occurrence of AKI with the normal bivalirudin infusion, compared with the 4-hour prolonged one (6.3% vs 4.6%, p = 0.04; unpublished data).

With these data, we want to emphasize that this novel and intriguing finding, however, deserves further ad hoc investigations. The ongoing MATRIX trial, whose results will be published soon, will definitely clarify if a prolonged infusion of bivalirudin is able to further reduce the occurrence of AKI after percutaneous coronary intervention, both with the transradial or the transfemoral approach.