Key result
High-dose atorvastatin fails to reduce contrast-induced nephropathy over regular-dose in primary angioplasty.
Why the study?
The efficacy of high-dose atorvastatin in preventing contrast-induced nephropathy in STEMI patients undergoing primary angioplasty was uncertain.
Does high-dose atorvastatin prevent contrast-induced nephropathy in patients with ST-elevation myocardial infarction undergoing primary angioplasty?
RCT (n=218)
Does high-dose atorvastatin prevent contrast-induced nephropathy in patients with ST-elevation myocardial infarction undergoing primary angioplasty?
Absolute Event Rate: 5.5% vs 10.2%
p-value: p=0.193
High-dose atorvastatin loading does not significantly reduce the overall incidence of contrast-induced nephropathy in STEMI patients undergoing primary PCI, though subgroup analyses suggest potential benefit in elderly patients and those with baseline renal insufficiency.
High-dose atorvastatin may reduce CIN risk in STEMI primary angioplasty; leaves open need for confirmatory randomized trials.
AIMS: To evaluate the efficacy of high-dose atorvastatin on contrast-induced nephropathy (CIN) occurrence in patients with ST-elevation myocardial infarction undergoing primary angioplasty. METHODS: We studied whether 80 mg atorvastatin loading and its subsequent use for 5 days (high-dose group) could prevent CIN as compared to those who received 10 mg atorvastatin (regular-dose group) in patients with ST-elevation myocardial infarction undergoing primary angioplasty. The primary endpoint was incidence of CIN, defined as an at least 25% or at least 0.5 mg/dl increase in baseline serum creatinine within 5 days after contrast administration. The secondary endpoint was an in-hospital 1 and 6-month renal function change, and a composite of all-cause mortality, myocardial infarction, renal failure requiring dialysis, heart failure, and target vessel revascularization. RESULTS: One hundred and ten patients were allocated to high dose and 108 to regular dose from August 2007 to February 2009. CIN incidence was 5.5% (6/110) in the high-dose group and 10.2% (11/108) in the regular-dose group, which is a nonsignificant difference (P = 0.193). CIN occurred significantly less in the high-dose than in the regular-dose group in subgroups of renal insufficiency (creatinine clearance ≤60 ml/min) [0% (0/28) vs. 16.7% (5/30); P = 0.024] and in the elderly patients who were at least 70 years old [4% (1/25) and 23.1% (6/26); P = 0.048]. Serum creatinine level tended to decrease in the high-dose group and increase in the regular-dose group, but the change was not statistically different (P = 0.093). The composite of clinical outcomes at 6 months was comparable in the high-dose and regular-dose groups (7.9 and 13.1%; P = 0.26). CONCLUSION: High-dose atorvastatin pretreatment does not seem to prevent CIN in patients receiving primary angioplasty. However, it has the potential to lower CIN in patients with renal insufficiency and in the elderly.
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Jo et al. (2014) conducted an RCT in ST-elevation myocardial infarction undergoing primary angioplasty (n=218). Atorvastatin vs. 10 mg atorvastatin was evaluated on Incidence of contrast-induced nephropathy (CIN), defined as an at least 25% or at least 0.5 mg/dl increase in baseline serum creatinine within 5 days after contrast administration (p=0.193). High-dose atorvastatin did not significantly reduce contrast-induced nephropathy compared to regular-dose atorvastatin in patients undergoing primary angioplasty (5.5% vs 10.2%; P=0.193).
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