The effect of rosuvastatin on inflammation, matrix turnover and left ventricular remodeling in dilated

Kaspar Broch1, Erik T Askevold2, Erik Gjertsen3

  • 1Department of Cardiology, Oslo University Hospital Rikshospitalet, Oslo, Norway ; Faculty of Medicine, University of Oslo, Oslo, Norway.

Plos One
|March 4, 2014
PubMed

Insights

Rosuvastatin did not improve left ventricular ejection fraction in patients with dilated cardiomyopathy. While it lowered cholesterol, it did not significantly impact inflammation or extracellular matrix remodeling markers.

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Dilated cardiomyopathy involves left ventricular enlargement and impaired function.
  • Inflammation and extracellular matrix remodeling are implicated in its pathogenesis.
  • Statins, like rosuvastatin, may possess anti-inflammatory and matrix-modulating properties.

Purpose of the Study:

  • To investigate the effect of rosuvastatin on left ventricular remodeling in dilated cardiomyopathy.
  • To determine if rosuvastatin can improve left ventricular ejection fraction.

Main Methods:

  • A multicenter, randomized, double-blind, placebo-controlled trial involving 71 patients.
  • Patients received either 10 mg rosuvastatin or placebo for six months.
  • Left ventricular ejection fraction was assessed via echocardiography and cardiac MRI at baseline and follow-up.

Main Results:

  • Left ventricular ejection fraction improved by 5 percentage points overall, with no significant difference between rosuvastatin and placebo groups.
  • Rosuvastatin significantly reduced low-density lipoprotein cholesterol but did not affect inflammatory markers or extracellular matrix remodeling.
  • No significant difference in left ventricular ejection fraction change was observed between treatment arms.

Conclusions:

  • Rosuvastatin treatment does not improve left ventricular ejection fraction in patients with dilated cardiomyopathy.
  • The drug's effects on inflammation and matrix remodeling were not substantial enough to alter cardiac function in this cohort.
Abstract

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