Risk factors

Teasing out the role of myocardial fibrosis in diabetes

Almost a third of patients with type 2 diabetes and without coronary artery disease have diffuse myocardial fibrosis on cardiovascular magnetic resonance imaging, Australian research shows.

A study compared 49 patients with well-controlled type 2 diabetes (duration ~11 years) and no significant coronary artery disease recruited from the Royal Prince Alfred Hospital (RPAH) Diabetes Centre with 18 healthy age and sex-matched controls.

CMR imaging found no difference between patients and controls in absolute or indexed left ventricular mass, global wall thickness, or LV mass/volume ratio.

However patients with diabetes had higher myocardial native T1, T2, and myocardial extracellular volume (ECV) compared to controls.

“Raised T1 and T2 values suggest ongoing myocardial inflammation consistent with a role a chronic inflammatory state in the development of diabetic cardiomyopathy,” the study said.

The study, published in the International Journal of Cardiology, found 22% of patients had focal late gadolinium enhancement (LGE), none of whom had sub-endocardial enhancement.

“Coronary microvascular dysfunction is commonly seen in patients with diabetes and is a likely contributor, though not formally assessed in our study,” the researchers said.

Higher ECV (>30%), found in 27% of patients, was also associated with lower peak VO2 on cardiopulmonary exercise testing.

“Diffuse myocardial fibrosis with reduced systolic and diastolic reserve, altered cardiac function and ultimately reduced O2 delivery may contribute to the lower exercise capacity documented in patients with T2DM,” they said.

No patients had ischaemia diagnosed on stress ECG.

Plasma metabolomics showed increased circulating choline and cysteamine were associated with increased ECV and reduced peak VO2. Isoleucine was associated with the presence of focal LGE (β-coefficient 14.7, p=0.04).

“The association of choline to both peak VO2 max and diffuse cardiac fibrosis measured by ECV is, to our knowledge, novel and requires further research to examine its predictive utility, and whether it has a causal role in fibrosis in diabetic cardiomyopathy or as a therapeutic target.”

The study, led by Dr Mark Dennis from RPAH and the University of Sydney, concluded that the new associations between metabolites and both ECV and peak VO2 warrant future more focused research.

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