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Association of imaging markers of myocardial fibrosis with metabolic and functional disturbances in early diabetic cardiomyopathy
Citation
Jellis, C and Wright, J and Kennedy, D and Sacre, J and Jenkins, C and Haluska, B and Martin, J and Fenwick, J and Marwick, TH, Association of imaging markers of myocardial fibrosis with metabolic and functional disturbances in early diabetic cardiomyopathy, Circulation: Cardiovascular Imaging, 4, (6) pp. 693-702. ISSN 1941-9651 (2011) [Refereed Article]
Copyright Statement
Copyright 2011 American Heart Association
DOI: doi:10.1161/circimaging.111.963587
Abstract
Background—Metabolic and vascular disturbances contribute to diabetic cardiomyopathy, but the role of interstitial fibrosis in early disease is unproven. We sought to assess the relationship between imaging markers of diffuse fibrosis and myocardial dysfunction and to link this to possible causes of early diabetic cardiomyopathy.
Methods and Results—Hemodynamic and metabolic data were measured in 67 subjects with type 2 diabetes mellitus (age 60±10 years) with no cardiac symptoms. Myocardial function was evaluated with standard echocardiography and myocardial deformation; ischemia was excluded by exercise echocardiography. Calibrated integrated backscatter was calculated from parasternal long-axis views. T1 mapping was performed after contrast with a modified Look-Locker technique using saturation recovery images. Amino-terminal propeptides of procollagens type I and III, as well as the carboxy-terminal propeptide of procollagen type I, were assayed to determine collagen turnover. Subjects with abnormal early diastolic tissue velocity (Em) had shorter postcontrast T1 values (P=0.042) and higher calibrated integrated backscatter (P=0.007). They were heavier (P=0.003) and had worse exercise capacity (P<0.001), lower insulin sensitivity (P=0.003), and blunted systolic tissue velocity (P=0.05). Postcontrast T1 was associated with diastolic dysfunction (Em r=0.28, P=0.020; E/Em r=−0.24, P=0.049), impaired exercise capacity (r=0.30, P=0.016), central adiposity (r=−0.26, P=0.046), blood pressure (systolic r=−0.30, P=0.012; diastolic r=−0.49, P<0.001), and insulin sensitivity (r=0.30, P=0.037). The association of T1 with E/Em (β=−0.31, P=0.017) was independent of blood pressure and metabolic disturbance. Amino-terminal propeptide of procollagens type III was linked to diastolic dysfunction (Em r=−0.32, P=0.008) and calibrated integrated backscatter (r=0.30, P=0.015) but not T1 values.
Conclusions—The association between myocardial diastolic dysfunction, postcontrast T1 values, and metabolic disturbance supports that diffuse myocardial fibrosis is an underlying contributor to early diabetic cardiomyopathy.
Methods and Results—Hemodynamic and metabolic data were measured in 67 subjects with type 2 diabetes mellitus (age 60±10 years) with no cardiac symptoms. Myocardial function was evaluated with standard echocardiography and myocardial deformation; ischemia was excluded by exercise echocardiography. Calibrated integrated backscatter was calculated from parasternal long-axis views. T1 mapping was performed after contrast with a modified Look-Locker technique using saturation recovery images. Amino-terminal propeptides of procollagens type I and III, as well as the carboxy-terminal propeptide of procollagen type I, were assayed to determine collagen turnover. Subjects with abnormal early diastolic tissue velocity (Em) had shorter postcontrast T1 values (P=0.042) and higher calibrated integrated backscatter (P=0.007). They were heavier (P=0.003) and had worse exercise capacity (P<0.001), lower insulin sensitivity (P=0.003), and blunted systolic tissue velocity (P=0.05). Postcontrast T1 was associated with diastolic dysfunction (Em r=0.28, P=0.020; E/Em r=−0.24, P=0.049), impaired exercise capacity (r=0.30, P=0.016), central adiposity (r=−0.26, P=0.046), blood pressure (systolic r=−0.30, P=0.012; diastolic r=−0.49, P<0.001), and insulin sensitivity (r=0.30, P=0.037). The association of T1 with E/Em (β=−0.31, P=0.017) was independent of blood pressure and metabolic disturbance. Amino-terminal propeptide of procollagens type III was linked to diastolic dysfunction (Em r=−0.32, P=0.008) and calibrated integrated backscatter (r=0.30, P=0.015) but not T1 values.
Conclusions—The association between myocardial diastolic dysfunction, postcontrast T1 values, and metabolic disturbance supports that diffuse myocardial fibrosis is an underlying contributor to early diabetic cardiomyopathy.
Item Details
| Item Type: | Refereed Article |
|---|---|
| Keywords: | diabetic cardiomyopathies, fibrosis, magnetic resonance, diastolic dysfunction |
| Research Division: | Biomedical and Clinical Sciences |
| Research Group: | Cardiovascular medicine and haematology |
| Research Field: | Cardiology (incl. cardiovascular diseases) |
| Objective Division: | Health |
| Objective Group: | Clinical health |
| Objective Field: | Clinical health not elsewhere classified |
| UTAS Author: | Marwick, TH (Professor Tom Marwick) |
| ID Code: | 90907 |
| Year Published: | 2011 |
| Web of Science® Times Cited: | 100 |
| Deposited By: | Menzies Institute for Medical Research |
| Deposited On: | 2014-05-01 |
| Last Modified: | 2014-06-06 |
| Downloads: | 0 |
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