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SAN DIEGO -- Two prevention strategies again came up short against contrast-induced acute kidney injury (AKI) even in high-risk patients who got percutaneous coronary intervention (PCI) and larger contrast volumes, researchers reported here, leaving operators back to square one with simple saline hydration as the mainstay of renal protection in this setting.

Neither intravenous sodium bicarbonate nor oral N-acetylcysteine was associated with a reduction in serious adverse events (death, dialysis, persistent decline in kidney function), as event rates were between 2.50% and 5.00% across the board at 90 days following PCI.

Specifically, sodium bicarbonate did no better than saline (OR 0.64, 95% CI 0.33-1.24) and acetylcysteine was no better than placebo (OR 1.37, 95% CI 0.71-2.62), according to the study presented here by Santiago Garcia, MD, of the University of Minnesota and the Minneapolis VA Healthcare System, at the annual meeting of the Society for Cardiovascular Angiography and Interventions.

Furthermore, contrast-associated AKI reached 10-13% of patients across treatment groups. Again, sodium bicarbonate performed similarly to saline (OR 0.93, 95% CI 0.65-1.34) and acetylcysteine similarly to placebo (OR 0.98, 95% CI 0.69-1.41).

The type and amount of contrast used were comparable between treatment groups.

"Intravascular volume expansion with isotonic sodium chloride should be considered the standard of care for the prevention of adverse renal outcomes in patients undergoing PCI," Garcia concluded.

He and his collaborators performed a subgroup analysis of the PRESERVE trial, this time with a focus on patients who went on to receive PCI after angiography (n=1,161). Compared with those who did not get stenting (n=3,304), this group had received more contrast (160 ml median versus 75 ml, P<0.01).

PRESERVE had been stopped early after a prespecified interim analysis suggested futility. The doubled-blind trial, featuring a 2 x 2 factorial design, had been conducted in the U.S. (at 53 sites), Australia (13 sites), Malaysia (three sites), and New Zealand (two sites). As reported last year, the findings for the two therapies were negative in the overall study population.

Participants were included in the trial if they were at high risk for renal complications, but were excluded if they had ST-segment elevation myocardial infarction or cardiogenic shock.

The co-moderator of the session at which the study was presented, George Dangas, MD, of Mount Sinai Medical Center in New York City, said that since renal risk can be calculated with relative ease, he hoped more studies on contrast-induced AKI will incorporate risk scores in the future: "I hope study designs from now on take into account previous knowledge in order to make some sense of it all."

Panelist Todd Brinton, MD, of Stanford Health Care in California, wondered if there was really no subgroup that benefited from either intravenous sodium bicarbonate or oral N-acetylcysteine.

Garcia's response: Even PCI recipients who received more than the median contrast volume showed no signal of benefit with either therapy.

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