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. 2015 Feb 13:14:23.
doi: 10.1186/s12933-015-0187-2.

Cardiac structure and function are altered in type 2 diabetes and non-alcoholic fatty liver disease and associate with glycemic control

Cardiac structure and function are altered in type 2 diabetes and non-alcoholic fatty liver disease and associate with glycemic control

Sophie Cassidy et al. Cardiovasc Diabetol. .

Abstract

Background: Both non-alcoholic fatty liver disease (NAFLD) and Type 2 diabetes increase the risk of developing cardiovascular disease. The metabolic processes underlying NAFLD and Type 2 diabetes are part of an integrated mechanism but little is known about how these conditions may differentially affect the heart. We compared the impact of NAFLD and Type 2 diabetes on cardiac structure, function and metabolism.

Methods: 19 adults with Type 2 diabetes (62 ± 8 years), 19 adults with NAFLD (54 ± 15 years) and 19 healthy controls (56 ± 14 years) underwent assessment of cardiac structure, function and metabolism using high resolution magnetic resonance imaging, tagging and spectroscopy at 3.0 T.

Results: Adults with NAFLD and Type 2 diabetes demonstrate concentric remodelling with an elevated eccentricity ratio compared to controls (1.05 ± 0.3 vs. 1.12 ± 0.2 vs. 0.89 ± 0.2 g/ml; p < 0.05). Despite this, only the Type 2 diabetes group demonstrate significant systolic and diastolic dysfunction evidenced by a reduced stroke index (31 ± 7vs. controls, 38 ± 10, p < 0.05 ml/m2) and reduced E/A (0.9 ± 0.4 vs. controls, 1.9 ± 1.4, p < 0.05) respectively. The torsion to shortening ratio was higher in Type 2 diabetes compared to NAFLD (0.58 ± 0.16 vs. 0.44 ± 0.13; p < 0.05). Significant associations were observed between fasting blood glucose/HbA1c and diastolic parameters as well as the torsion to shortening ratio (all p < 0.05). Phosphocreatine/adenosine triphosphate ratio was not altered in NAFLD or Type 2 diabetes compared to controls.

Conclusions: Changes in cardiac structure are evident in adults with Type 2 diabetes and NAFLD without overt cardiac disease and without changes in cardiac energy metabolism. Only the Type 2 diabetes group display diastolic and subendocardial dysfunction and glycemic control may be a key mediator of these cardiac changes. Therapies should be explored to target these preclinical cardiac changes to modify cardiovascular risk associated with Type 2 diabetes and NAFLD.

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Figures

Figure 1
Figure 1
Cardiac MRI techniques. These include (a) Cardiac cine imaging (top) and cardiac tagging (bottom) at diastole (left) and systole (right), showing how a rectangular grid of nulled signal applied at diastole remains with the tissue through the cardiac cycle, allowing calculation of strain and torsion. (b) Tagging in two parallel sections allows the calculation of the torsion (the longitudinal-circumferential shear angle ϒ) between two short-axis planes a distance d apart with radius r where one short-axis plane rotates through ΔΦ relative to the other. ϒ = tan−1[(2r sin(ΔΦ/2))/d]. (c) Phosphorus spectroscopy from a control subject (PCr/ATP = 1.95). Spectrum presented before correction for saturation due to blood content, flip angle at the cardiac tissue and heart rate.
Figure 2
Figure 2
Measures of cardiac structure and function. (a) eccentricity ratio, (b) longitudinal shortening (c) E/A and (d) torsion to shortening ratio, in control, NAFLD and Type 2 diabetes adults. Data are means ± SE.*Significant difference disease vs. control (p < 0.05). †Significant difference Type 2 diabetes vs. NAFLD (p < 0.05).
Figure 3
Figure 3
Associations between glycemic control and measures of cardiac function. Triangle = Control, Square = NAFLD, Circle = Type 2 diabetes. Relationships between (a) fasting glucose and early filling percentage, (b) fasting glucose and torsion to shortening ratio, (c) HbA1c and E/A and (d) HbA1c and early filling rate, are presented in the figure. HbA1c, haemoglobin A1c.
Figure 4
Figure 4
Postulated interactions between cardiac parameters across controls, NAFLD and Type 2 diabetes.

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