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High-dose atorvastatin improves hypercholesterolemic coronary endothelial dysfunction without improving the

Munir Boodhwani1, Yasunari Nakai, Pierre Voisine

  • 1Division of Cardiothoracic Surgery and Cardiology, Beth Israel Deaconess Medical Center, 110 Francis St, LMOB 2A, Boston, Massachusetts 02215, USA.

Circulation
|July 6, 2006
PubMed

Insights

High-dose atorvastatin improved endothelial function in hypercholesterolemic swine but did not enhance myocardial perfusion. The drug's effects on angiogenesis were linked to molecular changes, including increased endostatin and decreased vascular endothelial growth factor.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Molecular Biology

Background:

  • 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have shown biphasic effects on myocardial angiogenesis.
  • Endothelial function in coronary disease can be restored by statins.
  • Investigating high-dose atorvastatin's impact on angiogenesis in chronic myocardial ischemia is crucial.

Purpose of the Study:

  • To investigate the functional and molecular effects of high-dose atorvastatin on the endogenous angiogenic response.
  • To assess atorvastatin's impact on myocardial angiogenesis in hypercholesterolemic swine with chronic ischemia.

Main Methods:

  • Yucatan pigs were fed normal or high-cholesterol diets, with or without atorvastatin (3 mg/kg/day) for 13 weeks.
  • Chronic ischemia was induced by ameroid constrictor placement.
  • Microvessel relaxation, myocardial perfusion, and protein expression were assessed.

Main Results:

  • High-cholesterol diet impaired microvessel relaxation, which atorvastatin normalized.
  • Collateral-dependent myocardial perfusion was reduced in both cholesterol-fed groups.
  • Atorvastatin increased Akt phosphorylation, decreased vascular endothelial growth factor, and increased endostatin expression.

Conclusions:

  • Atorvastatin improved hypercholesterolemia-induced endothelial dysfunction but did not improve collateral-dependent perfusion.
  • Increased endostatin and decreased vascular endothelial growth factor expression, alongside Akt activation, may explain the diminished angiogenic response.
  • High-dose atorvastatin's effects on angiogenesis are complex and warrant further investigation.
Abstract

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