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Fluvastatin reduces soluble P-selectin and ICAM-1 levels in hypercholesterolemic patients: role of nitric oxide

M Romano1, A Mezzetti, C Marulli

  • 1Institute of Medical Pathology and Mediterranean Medicine, University of Messina, Italy.

Journal of Investigative Medicine : the Official Publication of the American Federation for Clinical Research
|May 24, 2000
PubMed

Insights

Fluvastatin, a statin, significantly reduced adhesion molecules P-selectin and ICAM-1 in hypercholesterolemia patients. This lipid-lowering therapy also improved nitric oxide generation, suggesting a biochemical basis for its cardiovascular benefits.

Area of Science:

  • Biochemistry
  • Cardiovascular Medicine
  • Pharmacology

Background:

  • 3-hydroxy-3-methylglutaryl-coenzymeA (HMG-CoA) reductase inhibitors (statins) are crucial for reducing atherosclerosis-related cardiovascular events.
  • Adhesion molecules like P-selectin and ICAM-1 are implicated in atherosclerosis pathogenesis.
  • The impact of fluvastatin on these adhesion molecules was investigated.

Purpose of the Study:

  • To evaluate the effect of fluvastatin on plasma levels of P-selectin and ICAM-1 in patients with type IIa hypercholesterolemia.
  • To explore the relationship between fluvastatin treatment, adhesion molecules, and markers of endothelial function.

Main Methods:

  • A double-blind, randomized study involving 26 patients with type IIa hypercholesterolemia.
  • Patients received either fluvastatin (80 mg/d) or a placebo for 12 weeks.
  • Plasma levels of P-selectin and ICAM-1 were measured using enzyme immunoassay.

Main Results:

  • Fluvastatin significantly reduced P-selectin levels by 31% (P=0.0015) and ICAM-1 levels by 13.7% (P=0.0033).
  • Fluvastatin also decreased urinary 11-dehydro-TXB2 and von Willebrand Factor levels.
  • Increased nitric oxide (NO) generation was observed, with an inverse correlation between NO levels and P-selectin, 11-dehydro-TXB2, and LDL.

Conclusions:

  • Fluvastatin effectively lowers key adhesion molecules involved in atherosclerosis.
  • The observed increase in nitric oxide generation may contribute to the beneficial effects of statins.
  • These findings provide a biochemical rationale for the clinical efficacy of HMG-CoA reductase inhibitors in managing hypercholesterolemia.
Abstract

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