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To the editor: Treatment with thiazolidinedione (TZD), an agonist of peroxisome proliferator-activated receptor-γ (PPARγ), has been associated with a significant increase in heart failure in type 2 diabetic patients.1 These ligand-activated nuclear transcription factors (rosiglitazone and pioglitazone) are implicated in adipogenesis and tissue lipid accumulation.2 Indeed, myocyte overexpression of PPARγ, leads to lipotoxic cardiomyopathy in both transgenic mice overexpressing PPARγ and TZD-treated diabetic mice.3 Thus, while PPARγ agonists appear to have beneficial effects on metabolic control,4 their direct actions on myocardium may impair heart function, inducing lipid accumulation. To examine these concerns, we analysed lipid accumulation and PPARγ expression in myocardial biopsy specimens obtained from type 2 diabetic patients with and without TZD treatment who underwent surgical valve replacement for mitral stenosis (MS), and related them to the heart function.
Nineteen non-TZD-treated and 13 TZD-treated (⩾24 weeks of monotherapy in the previous year) type 2 diabetic patients who underwent mitral valve replacement (area⩽1.2 cm2) participated in the study. Patients …