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Cardioprotection and myocardial salvage by a disodium disuccinate astaxanthin derivative (Cardax)

Garrett J Gross1, Samuel F Lockwood

  • 1Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.

Life Sciences
|May 4, 2004
PubMed

Insights

This study shows that a novel carotenoid derivative, Cardax, given intravenously, significantly reduced heart muscle damage in a rat model of heart attack. This suggests Cardax could be a potential treatment for myocardial infarction.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Oxidative Stress Biology

Background:

  • Human cardioprotection by carotenoids is suggested by observational studies, but direct evidence for myocardial salvage is limited.
  • Astaxanthin, a carotenoid, has antioxidant properties, but its direct impact on infarct size and myocardial salvage requires investigation.
  • Novel carotenoid derivatives may offer improved therapeutic potential for cardiovascular conditions.

Purpose of the Study:

  • To evaluate the efficacy of a novel carotenoid derivative, disodium disuccinate astaxanthin (Cardax), as a myocardial salvage agent.
  • To determine the dose-dependent effects of Cardax on infarct size in a rat model of myocardial infarction.
  • To investigate the correlation between plasma astaxanthin levels and cardioprotective effects.

Main Methods:

  • A rat model of myocardial infarction was induced by ligating the left anterior descending (LAD) coronary artery for 30 minutes, followed by 2 hours of reperfusion.
  • Animals received daily intravenous (I.V.) pre-treatment with Cardax (25, 50, or 75 mg/kg) or saline vehicle for 4 days prior to the infarct induction.
  • Area at risk (AAR) was quantified using Patent blue dye, and infarct size (IS) was determined by triphenyltetrazolium chloride (TTC) staining.

Main Results:

  • Cardax administration at 50 and 75 mg/kg significantly reduced infarct size (IS) as a percentage of the area at risk (AAR).
  • Mean IS/AAR was reduced to 35% (41% salvage) and 26% (56% salvage) at the higher Cardax doses, respectively, compared to 59% in controls.
  • A significant, linear correlation was observed between infarct size reduction, myocardial salvage, and plasma levels of free astaxanthin.

Conclusions:

  • Intravenous pre-treatment with Cardax demonstrates significant cardioprotective effects and myocardial salvage in a rat infarct model.
  • The cardioprotective efficacy of Cardax is dose-dependent and correlates with plasma astaxanthin levels.
  • Parenteral Cardax shows potential utility in clinical settings for pre-treatment of patients at risk for myocardial infarction.

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