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Osteoprotegerin, Thiazolidinediones Treatment, and Silent Myocardial Ischemia in Type 2 Diabetic Patients

¹ Service des Maladies Métaboliques, CHU Montpellier, Hôpital Lapeyronie, Montpellier, France
² UFR de Médecine, Université Montpellier 1, Montpellier, France
³ CHU Montpellier & INSERM CIC 0001, Montpellier, France
⁴ Service des Maladies Endocriniennes, CHU Montpellier, Hôpital Lapeyronie, Montpellier, France
⁵ Service de Cardiologie B, CHU Montpellier, Hôpital Arnaud de Villeneuve, Montpellier, France
⁶ Service de Médecine Nucléaire, CHU Montpellier, Hôpital Lapeyronie, Montpellier, France
⁷ Service de Biochimie, CHU Montpellier, Hôpital Lapeyronie, Montpellier, France
⁸ UFR de Médecine, Université Montpellier, Montpellier, France

Address correspondence and reprint requests to Antoine Avignon, Metabolic Disease Department, Lapeyronie Hospital, 371, Av Doyen G. Giraud, 34295, Montpellier Cedex 5, France. E-mail: a-avignon@chu-montpellier.fr

Abbreviations: ECG, electrocardiogram • MPI, myocardial perfusion imaging • SMI, silent myocardial infarction • TZD, thiazolidinedione

The first 20% of the full text of this article appears below.

	INTRODUCTION

 
Thiazolidinediones (TZDs) are widely prescribed for the treatment of type 2 diabetes. They were reported to have vasculoprotective properties like a reduction in carotid artery intima-media thickness progression (1) but may also reduce bone formation and favor bone loss (2,3). The decoy receptor osteoprotegerin, a member of the receptor activator of nuclear factor-B ligand/osteoprotegerin system, involved in osteoclast development and function (4), might also be a regulator of vascular calcification and an indicator of vascular disease (5). In diabetic patients, this latter point is supported by our previous data showing a positive association between silent myocardial ischemia (SMI) and osteoprotegerin levels (6,7). We tested, in a case-control study, the a priori hypothesis that TZDs might be associated with decreased osteoprotegerin levels and lower prevalence of SMI in patients treated with TZDs.

	RESEARCH DESIGN AND METHODS—

 
A total of 198 consecutive asymptomatic non–insulin-treated type 2 diabetes patients (age 60.1 ± 9.1, 68% male, A1C 8.1 ± 1.7%, BMI 30.7 ± 4.6 kg/m²) with one or more additional risk factor underwent SMI screening, using dipyridamole combined with exercise myocardial perfusion imaging (MPI) as previously described (6,7). SMI was defined as positive MPI (mean activity <70% of the maximal myocardium activity in 3 of 20 segments) and/or positive exercise electrocardiogram (ECG) (horizontal or descending ST segment depression . . . [Full Text of this Article]

	RESULTS—

 

	CONCLUSIONS—

 

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