The microvascular effects of insulin resistance and diabetes on cardiac structure, function, and perfusion: a
Abdulghani M Larghat1, Peter P Swoboda2, John D Biglands3
1Multidisciplinary Cardiovascular Research Centre & Leeds Institute of Genetics, Health and Therapeutics, University of Leeds, Leeds LS2 9JT, UK Department of Cardiology and Internal Medicine, Tripoli Medical Centre, Faculty of Medicine, University of Tripoli, Tripoli, Libya.
Insights
Type 2 diabetes leads to increased left-ventricular mass and torsion, with reduced myocardial perfusion reserve. This suggests microvascular disease contributes to cardiac dysfunction in diabetic patients.
Area of Science:
- Cardiology
- Diabetology
- Medical Imaging
Background:
- Type 2 diabetes mellitus is a known risk factor for heart failure.
- Understanding the mechanisms linking diabetes and heart failure is crucial for patient outcomes.
Purpose of the Study:
- To investigate cardiac structure, function, and perfusion in patients with and without type 2 diabetes.
- To elucidate the relationship between diabetes, microvascular function, and cardiac remodeling.
Main Methods:
- Comprehensive cardiovascular magnetic resonance (CMR) assessment in 65 patients (19 diabetes, 46 non-diabetes including prediabetes and controls).
- Analysis of left-ventricular (LV) mass, relative wall mass (RWM), Lagrangian circumferential strain, LV torsion, and myocardial perfusion reserve (MPR).
- Invasive coronary angiography performed to exclude significant coronary stenosis (>30%).
Main Results:
- Diabetic patients exhibited significantly higher LV mass (112.8 ± 39.7 g) compared to non-diabetics (91.5 ± 21.3 g, P=0.01) and prediabetics (90.3 ± 18.7 g, P=0.02).
- LV torsion angle was significantly increased in diabetics (9.65 ± 1.90°) versus non-diabetics (8.59 ± 1.91°, P=0.047).
- Myocardial perfusion reserve (MPR) was significantly lower in diabetics (2.10 ± 0.76 mL/g/min) compared to non-diabetics (2.84 ± 1.25 mL/g/min, P=0.01).
- MPR showed significant negative correlations with early diastolic strain rate (r=-0.310, P=0.01) and LV torsion (r=-0.306, P=0.01).
Conclusions:
- Patients with type 2 diabetes demonstrate increased LV mass, LV torsion, and reduced MPR.
- A significant association between decreased MPR and increased LV torsion suggests a mechanistic link between diabetic microvascular disease and cardiac dysfunction.
Aims:
Type 2 diabetes mellitus is an independent risk factor for the development of heart failure. To better understand the mechanism by which this occurs, we investigated cardiac structure, function, and perfusion in patients with and without diabetes.
Methods And Results:
Sixty-five patients with no stenosis >30% on invasive coronary angiography were categorized into diabetes (19) and non-diabetes (46) which was further categorized into prediabetes (30) and controls (16) according to the American Diabetes Association guidelines. Each patient underwent comprehensive cardiovascular magnetic resonance assessment. Left-ventricular (LV) mass, relative wall mass (RWM), Lagrangian circumferential strain, LV torsion, and myocardial perfusion reserve (MPR) were calculated. LV mass was higher in diabetics than non-diabetics (112.8 ± 39.7 vs. 91.5 ± 21.3 g, P = 0.01) and in diabetics than prediabetics (112.8 ± 39.7 vs. 90.3 ± 18.7 g, P = 0.02). LV torsion angle was higher in diabetics than non-diabetics (9.65 ± 1.90 vs. 8.59 ± 1.91°, P = 0.047), and MPR was lower in diabetics than non-diabetics (2.10 ± 0.76 vs. 2.84 ± 1.25 mL/g/min, P = 0.01). There was significant correlation between MPR and early diastolic strain rate (r = -0.310, P = 0.01) and LV torsion (r = -0.306, P = 0.01). In multivariable linear regression analysis, non-diabetics waist-hip ratio, but not body mass index, had a significant association with RWM (Beta = 0.34, P = 0.02).
Conclusion:
Patients with diabetes have increased LV mass, LV torsion, and decreased MPR. There is a significant association between decreased MPR and increased LV torsion suggesting a possible mechanistic link between microvascular disease and cardiac dysfunction in diabetes.
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