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Plaque Rupture After Short Periods Of Fat Feeding In The Apolipoprotein E-knockout Mouse: Model Characterization And Effects Of Pravastatin Treatment.

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Plaque rupture after short periods of fat feeding in the apolipoprotein E-knockout mouse: model characterization and

Jason Johnson1, Kevin Carson, Helen Williams

  • 1Bristol Heart Institute, University of Bristol, Bristol, United Kingdom.

Circulation
|March 23, 2005

View abstract on PubMed

Summary
This summary is machine-generated.

Plaque rupture sharply increases in mice after 8 weeks of a high-fat diet. Pravastatin treatment effectively reduces plaque rupture, even when initiated after plaques have formed.

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Area of Science:

  • Cardiovascular Research
  • Atherosclerosis Studies
  • Pharmacological Interventions

Background:

  • Investigating the timeline of plaque development and rupture in apolipoprotein E-knockout mice.
  • Examining the impact of pravastatin on early and established atherosclerotic plaques.

Purpose of the Study:

  • To determine the critical time point for plaque rupture in a mouse model.
  • To evaluate the efficacy of pravastatin in preventing and treating plaque rupture.

Main Methods:

  • Apolipoprotein E-knockout mice fed a high-fat diet, with analysis at weekly intervals.
  • Assessment of plaque rupture incidence and buried fibrous caps.
  • Administration of pravastatin at different stages of plaque development.

Main Results:

  • A significant increase in plaque rupture observed after 8 weeks of high-fat diet (62% vs 3%).
  • Pravastatin reduced buried fibrous caps by 43% (P<0.0001) without affecting cholesterol levels.
  • Delayed pravastatin treatment reduced plaque rupture incidence by 36% (P<0.0001).

Conclusions:

  • High-frequency plaque rupture occurs in brachiocephalic arteries after 8 weeks of high-fat feeding in this mouse model.
  • Pravastatin effectively inhibits early plaque rupture and is beneficial for established unstable plaques.