Acipimox does not augment thallium-201 redistribution in the fasting state

Abstract

Background. Recently oral glucose loading and a thallium-glucose insulin infusion have been used to augment myocardial uptake of thallium-201 (Tl-201). Acipimox is a nicotinic-acid derivative that reduces serum free fatty acid (FFA) levels and enhances myocardial glucose uptake. This study was performed to assess the effects of acipimox on Tl-201 redistribution. Methods. Fourteen patients with coronary artery disease underwent 2 successive Tl-201 perfusion studies. Stress was performed by adenosine coupled with ergometer exercise. Patients received either 500 mg of acipimox or placebo immediately after stress, and images were acquired. Redistribution imaging was carried out after 4 hours. Patients returned after 7 to 14 days for a repeat stress protocol, receiving the alternate test article. Both studies were carried out under identical conditions with identical medication with the patient in the fasting state. Image analysis was conducted quantitatively with polar plots and by using segmental uptake as a percentage of maximal counts with a 9-segment model. Results. There were no significant differences between the acipimox and placebo arms of the study of hemodynamic parameters. On polar plot analysis, there were no differences between acipimox and placebo for mean values of stress defect extent (97 ± 16.1 vs 96.5 ± 18.8 pixels), defect severity (532.2 ± 120 vs 537 ± 133.9 standard deviations [SDs]), for defect reversibility (61.7 ± 18 vs 55.4 ± 15.3 SDs), and percentage reversibility (21.2% ± 5.5% vs 19.2% ± 5.8%), respectively. Similarly, on segmental uptake analysis there was no significant difference between the acipimox and placebo arms with regard to the proportion of segments classified as normal, fixed defect, reversible defect, or reverse redistribution. Conclusion. Although acipimox has been shown to augment myocardial glucose uptake and myocardial glucose uptake has been shown to improve cellular uptake of Tl-201, in the fasting state acipimox does not enhance the redistribution after stress. This may be because serum insulin levels are not increased by acipimox, and insulin is instrumental in enhancing the joint transport of glucose and Tl-201 into myocytes.