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Thiazolidinediones may contribute to the intramyocardial lipid accumulation in diabetic myocardium: effects on cardiac function
1 Department of Geriatrics and Metabolic Diseases Second University of Naples, Naples, Italy
2 Cardiovascular Surgery Unit, Sassari Hospital, Sassari, Italy
3 Department of Clinical, Public and Preventive Medicine Second University of Naples, Naples, Italy
4 Department of Cardiovascular Diseases, Agropoli Hospital, Agropoli, Italy
5 Department of Experimental Medicine Second University of Naples, Naples, Italy
Correspondence to:
Professor R Marfella, Second University of Naples, Piazza Miraglia, 1 Naples, 80138 Italy; raffaele.marfella@unina2.it
| The first 150 words of the full text of this article appear below. |
To the editor: Treatment with thiazolidinedione (TZD), an agonist of peroxisome proliferator-activated receptor-
(PPAR), 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 PPAR, leads to lipotoxic cardiomyopathy in both transgenic mice overexpressing PPAR and TZD-treated diabetic mice.3 Thus, while PPAR 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 PPAR 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
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Drugs: cardiovascular system
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Clinical diagnostic tests
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Acute coronary syndromes
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Hypertension
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Mitral valve disease
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