The prevalence of type 2 diabetes (T2D) has reached a pandemic scale. Systemic chronic inflammation dominates the diabetes pathophysiology and has been implicated as a causal factor for the development of vascular complications. Heart failure (HF) is regarded as the most common cardiovascular complication of T2D and the diabetic diagnosis is an independent risk factor for HF development. Key molecular mechanisms pivotal to the development of diabetic cardiomyopathy include the NF-κB pathway and renin–angiotensin–aldosterone system, in addition to advanced glycation end product accumulation and inflammatory interleukin overexpression. Chronic myocardial inflammation in T2D mediates structural and metabolic changes, including cardiomyocyte apoptosis, impaired calcium handling, myocardial hypertrophy and fibrosis, all of which contribute to the diabetic HF phenotype. Advanced cardiovascular magnetic resonance imaging (CMR) has emerged as a gold standard non-invasive tool to delineate myocardial structural and functional changes. This review explores the role of chronic inflammation in diabetic cardiomyopathy and the ability of CMR to identify inflammation-mediated myocardial sequelae, such as oedema and diffuse fibrosis.

Aims Recently developed in-line automated cardiovascular magnetic resonance (CMR) myocardial perfusion mapping has been shown to be reproducible and comparable with positron emission tomography (PET), and can be easily integrated into clinical workflows. Bringing quantitative myocardial perfusion CMR into routine clinical care requires knowledge of sex- and age-specific normal values in order to define thresholds for disease detection. This study aimed to establish sex- and age-specific normal values for stress and rest CMR myocardial blood flow (MBF) in healthy volunteers. Methods and results A total of 151 healthy volunteers recruited from two centres underwent adenosine stress and rest myocardial perfusion CMR. In-line automatic reconstruction and post processing of perfusion data were implemented within the Gadgetron software framework, creating pixel-wise perfusion maps. Rest and stress MBF were measured, deriving myocardial perfusion reserve (MPR) and were subdivided by sex and age. Mean MBF in all subjects was 0.62 ± 0.13 mL/g/min at rest and 2.24 ± 0.53 mL/g/min during stress. Mean MPR was 3.74 ± 1.00. Compared with males, females had higher rest (0.69 ± 0.13 vs. 0.58 ± 0.12 mL/g/min, P < 0.01) and stress MBF (2.41 ± 0.47 vs. 2.13 ± 0.54 mL/g/min, P = 0.001). Stress MBF and MPR showed significant negative correlations with increasing age (r = −0.43, P < 0.001 and r = −0.34, P < 0.001, respectively). Conclusion Fully automated in-line CMR myocardial perfusion mapping produces similar normal values to the published CMR and PET literature. There is a significant increase in rest and stress MBF, but not MPR, in females and a reduction of stress MBF and MPR with advancing age, advocating the use of sex- and age-specific reference ranges for diagnostic use.