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European Heart Journal 2008 29(1):12-20; doi:10.1093/eurheartj/ehm529
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.

Weighing up the cardiovascular benefits of thiazolidinedione therapy: the impact of increased risk of heart failure

Erland Erdmann1,* and Robert G. Wilcox2

1 Department of Cardiology, University of Cologne, Kerpener Street 62, Cologne 50937, Germany
2 University Hospital Nottingham, Nottingham, UK

Received 14 August 2007; revised 16 October 2007; accepted 29 October 2007.

* Corresponding author. Tel: +49 221 478 4503, Fax: +49 221 478 6275. Email: erland.erdmann{at}uni-koeln.de

Type 2 diabetes and heart failure commonly occur together and this combination is associated with poor outcomes. The relationship is likely to be multifactorial and also may involve a specific, though ill-defined, diabetic cardiomyopathy. Glucose-lowering therapies may also be associated with an increased risk of heart failure. Data from recent large-scale clinical trials have drawn particular attention to the thiazolidinediones that appear to increase the risk of heart failure in patients with type 2 diabetes. Although pioglitazone therapy has been shown to decrease the risk of macrovascular events, the overall cardiovascular benefit needs to be addressed together with the apparent increase in heart failure risk. In this review, we provide appropriate context for assessing this balance from several perspectives. First, we consider the high underlying risk of heart failure already present in type 2 diabetes. Secondly, we highlight a potential distinction between genuine heart failure due to cardiac dysfunction and thiazolidinedione-associated oedema that may simply unmask previously undiagnosed cardiac dysfunction without itself having any direct impact on heart muscle. Most importantly, we emphasize the apparent lack of any long-term mortality consequences and a relative improvement in outcomes associated with thiazolidinedione-induced ‘heart failure’ and discuss the potential mechanisms underlying this apparent paradox. Finally, we review the current guidelines for thiazolidinedione use and heart failure and suggest potential future strategies for avoiding and/or minimizing this association.

Key Words: Heart failure • Oedema • Pioglitazone • Rosiglitazone • Thiazolidinediones • Type 2 diabetes


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