Prevention of Contrast-Induced Nephropathy With N-Acetylcysteine or Sodium Bicarbonate in Patients With ST-Segment–Myocardial Infarction

Abstract

Background-Contrast-induced nephropathy (CIN) is a serious condition in patients with ST-segment-elevation myocardial infarction treated with primary percutaneous coronary intervention. We compared the risk of acute CIN and the influence of preventive strategies in patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention. Methods and Results-A total of 720 patients were randomized in the Prevention of Contrast-induced Nephropathy inPatients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention (CINSTEMI) trial. Patients were randomly assigned in a 1:1:1:1 ratio to receive hydration with sodium chloride together with 1 of 4 prophylactic regimes (1) N-acetylcysteine (NAC), (2) sodium bicarbonate (NaHCO 3 ) infusion, (3) NAC in combination with NaHCO 3 , or (4) hydration with sodium chloride infusion alone. Patients in cardiogenic shock were excluded. Acute CIN was defined as an increase in serum creatinine concentration >25% from the baseline value within a 3-day period. Overall, CIN occurred in 141 (21.9%) patients. The prevention treatment with NAC, NaHCO 3 , or the combined NAC and NaHCO 3 did not reduce the rate of CIN significantly compared with hydration with intravenous sodium chloride infusion alone (20.1% versus 20.1% versus 20.8% versus 26.5%; P=NS). However, an increase in serum creatinine >25% from the baseline value to 30 day was significantly lower in patients treated with combined NAC and

Impact of acute kidney injury in elderly (≥80 years) patients undergoing percutaneous coronary intervention

“…Guideline‐recommended strategies for the prevention of AKI include preventive hydration with isotonic saline and the minimization of the amount of contrast media . Efforts to further reduce the incidence of AKI have yielded mixed results and mainly included the use of N‐acetylcysteine and sodium bicarbonate, or the administration of statins or ascorbic acid . Our findings further strengthen the unmet clinical need for novel strategies to reduce the occurrence of AKI in high‐risk patients undergoing PCI.…”

How Strong Is the Evidence for Sodium Bicarbonate to Prevent Contrast-Induced Acute Kidney Injury After Coronary Angiography and Percutaneous Coronary Intervention?

“…Twenty-three were first removed due to duplication. After initial review of the titles and abstracts of the left 33 studies, 3 studies 33–35 comparing N-acetylcysteine (NAC) versus sodium bicarbonate and 1 study regarding hydration with SB pre- and postprocedurally while hydration with SC only postprocedurally were excluded. The remaining 19 studies were further screened into the full texts and 3 studies 36–38 were rejected because of low quality according to the Jadad score.…”

Association Between Acidosis Soon After Reperfusion and Contrast‐Induced Nephropathy in Patients With a First‐Time ST‐Segment Elevation Myocardial Infarction

“…Additionally, some previous reports revealed that hydration with sodium bicarbonate improved acidosis as the rapid increase of intravascular volume was more effective than hydration with sodium chloride for prophylaxis of CIN . In contrast, previous reports have shown that hydration with sodium bicarbonate had no clinical superiority in reducing the risk of CIN than that with sodium chloride . Since there is no evidence that hydration with sodium bicarbonate decreases the risk of hemodialysis or death, the effect of intervention for acidosis prevention may have a limited impact on CIN.…”

“…34,35 In contrast, previous reports have shown that hydration with sodium bicarbonate had no clinical superiority in reducing the risk of CIN than that with sodium chloride. [36][37][38][39] Since there is no evidence that hydration with sodium bicarbonate decreases the risk of hemodialysis or death, the effect of intervention for acidosis prevention may have a limited impact on CIN. Hence, now we conclude that acidosis is useful as a marker of risk stratification for CIN.…”