The detection of myocardial fibrosis: an opportunity to reduce cardiovascular risk in patients with diabetes mellitus?

Both type 1 and type 2 diabetes mellitus (DM) are associated with a significant increase in cardiovascular risk. Glycemic control has, unfortunately, not been convincingly shown to reduce cardiovascular risk.1–3 The level at which blood pressure should be controlled also is controversial.4 Thus, there may be a need to focus on new therapeutic targets if we are to reduce cardiovascular risk in patients with either type 1 or type 2 DM. Cardiac and large arteries fibrosis is a frequent occurrence in patients with DM and one of the major factors predisposing to the development of heart failure (HF). Cardiac fibrosis is the consequence of extracellular cardiac matrix remodeling resulting from pathological processes, including ischemia; stretch; inflammation; and specifically in DM, oxidative stress, advanced glycation end products, and several neurohormonal mediators. Cardiac fibrosis may cause myocyte slippage, tissue heterogeneity and dyssynchrony, ventricular dilatation, and contractile dysfunction. Myocardial fibrosis alters myocardial compliance, and associated fibrosis-related large artery stiffness may predispose to diastolic dysfunction and HF with a preserved left ventricular ejection fraction. Cardiac fibrosis also may result in alteration of gap junctions and predispose to arrhythmias and sudden cardiac death.5 Bioimaging and biomarkers of cardiac fibrosis, therefore, may become clinically useful tools, particularly given the potential for cardioprotective and cardioreparative pharmacological strategies.6,7