Volume 13 Supplement 1
Subclinical perfusion deficits in patients with Type 2 diabetes detectable with Cardiovascular Magnetic Resonance Imaging
© Schmidt et al; licensee BioMed Central Ltd. 2011
Published: 2 February 2011
An estimated 200 million people worldwide have type 2 diabetes. Type 2 diabetes is recognized as an independent risk factor for adverse cardiac events, such as myocardial infarction. Cardiovascular disease is the leading cause of death amongst diabetic patients. The subclinical pathophysiology of diabetic heart disease predicts global microvascular disease, prior to the onset of overt ischemic heart disease. Non-invasive screening methods are therefore important for risk stratification of asymptomatic patients. Cardiovascular Magnetic Resonance Imaging (CMR) is a valuable tool for the assessment of subclinical microvascular function in this high-risk population.
To assess the degree of cardiac microvascular dysfunction in individuals type 2 diabetes (T2D) without coronary disease or hypertension, compared to healthy, non-diabetic controls.
This cross sectional pilot data included 2 groups of subjects: Patients diagnosed with type 2 diabetes (HbA1c 7.5-9.9%; mean age 59.3±7.17; n=6), and healthy, non-diabetic age-matched controls (mean age 51.9±10.3; n=10). Medical history and ECG were reviewed to rule out ischemic heart disease. Qualified patients underwent a CMR-Adenosine stress perfusion,
The observed perfusion abnormality supports previous nuclear imaging findings and pathophysiological research of diabetic heart disease and may indicate more diffuse patterns of microvascular disease. Further studies are required to assess the pathophysiologic context and prognostic impact of these findings.
This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.