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Updated: Apr 17, 2026

Peptide-based Identification of Functional Motifs and their Binding Partners
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Statin therapy decreases N-terminal pro-B-type natriuretic peptide in HIV: randomized placebo-controlled trial

Sahera Dirajlal-Fargo1, Bruce Kinley, Ying Jiang

  • 1aCase Western Reserve University bRainbow Babies and Children's Hospital cCase Medical Center, University Hospitals dMetroHealth Medical Center, Cleveland, Ohio, USA.

AIDS (London, England)
|February 18, 2015
PubMed

Insights

Rosuvastatin significantly reduced N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels in HIV patients, a marker associated with cardiovascular disease risk. This study highlights NT-proBNP

Area of Science:

  • Cardiology
  • Infectious Diseases
  • Pharmacology

Background:

  • HIV-infected individuals face elevated risks for cardiovascular disease (CVD).
  • N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a key CVD predictor in the general population and linked to mortality in HIV patients.

Purpose of the Study:

  • To evaluate the effect of rosuvastatin on NT-proBNP levels in HIV-infected participants.
  • To explore the association of NT-proBNP with CVD risk markers and inflammation in this population.

Main Methods:

  • The SATURN-HIV trial randomized 147 HIV patients to rosuvastatin or placebo for 96 weeks.
  • NT-proBNP levels were measured using ELISA; baseline and changes were compared between groups.
  • Correlations between NT-proBNP, inflammation, and CVD risk markers were analyzed.

Main Results:

  • Baseline NT-proBNP was higher in the rosuvastatin group compared to placebo.
  • Rosuvastatin treatment led to a significant decrease in NT-proBNP levels over 96 weeks versus placebo.
  • Baseline NT-proBNP correlated with measures of atherosclerosis and inflammatory markers; changes correlated with insulin resistance and fat distribution.

Conclusions:

  • Rosuvastatin effectively reduces plasma NT-proBNP in HIV-infected individuals on antiretroviral therapy.
  • NT-proBNP is a valuable biomarker for CVD risk in this population, independent of inflammation.
Abstract

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