Key result
Oral high-dose atorvastatin loading did not significantly reduce levels of NT-proBNP (P=0.845), hsCRP (P=0.105), or other biomarkers of inflammation and renal injury compared to no statin in patients with acute heart failure.
Why the study?
Does high-dose atorvastatin loading improve biomarkers related to inflammation and renal injury in patients hospitalized with acute heart failure?
RCT (n=49)
Open-label
Randomly assigned
No
Does high-dose atorvastatin loading improve biomarkers related to inflammation and renal injury in patients hospitalized with acute heart failure?
High-dose atorvastatin loading is safe but does not significantly reduce biomarkers of inflammation or renal injury during hospitalization in patients with acute heart failure.
Answers are grounded in this paper and cite their sources.
High-dose atorvastatin loading confers no biomarker benefit in acute HF; challenges expectations of rapid anti-inflammatory effects from statin initiation.
BACKGROUND: High-dose statin loading is known to reduce periprocedural myocardial infarction and contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention. However, the clinical role of high-dose statin loading in patients with acute heart failure (AHF) remains unknown. METHODS AND RESULTS: In a prospective, single-center, randomized, controlled, open-label pilot study, patients hospitalized with AHF were randomly assigned to receive oral high-dose atorvastatin loading (80 mg for 3 days, followed by 10 mg/day until discharge) or no statin therapy, on top of optimal HF treatment. The primary outcome measures were changes to the level of biomarkers related to inflammation and renal injury from admission to hospital day 4. No significant changes in the levels of NT-proBNP (-2,627±4,956 vs. -2,981±6,951 pg/ml, P=0.845), hsCRP (-6.1±16.4 vs. -2.1±16.2 mg/L, P=0.105), cystatin C (0.002±0.185 vs. 0.009±0.216 mg/L, P=0.904), ACR (-886.3±1,984.9 vs. -165.6±825.2 mg/day, P=0.124) were observed in either group. In-hospital mortality (4.3% vs. 3.8%, P>0.999) and all-cause mortality at 90 days (4.3% vs. 3.8%, P>0.999) were not significantly different between groups. CONCLUSIONS: This pilot study showed that oral high-dose atorvastatin loading may be used safely in patients with AHF, but is not effective in reducing the levels of circulating biomarkers related to inflammation and renal injury during hospitalization.
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Oh et al. (2014) conducted an RCT in Acute Heart Failure (n=49). Atorvastatin vs. No statin therapy was evaluated on Change in NT-proBNP from admission to hospital day 4 (pg/ml) (p=0.845). Oral high-dose atorvastatin loading did not significantly reduce levels of NT-proBNP (P=0.845), hsCRP (P=0.105), or other biomarkers of inflammation and renal injury compared to no statin in patients with acute heart failure.
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