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Myocardial T2* is not affected by ageing, myocardial fibrosis, or impaired left ventricular function
Paul Kirk1, Gillian C Smith, Michael Roughton
1Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital and Imperial College, London, United Kingdom.
Insights
Myocardial T2* measurements are not significantly affected by age, impaired left ventricular function, or myocardial fibrosis from infarction. This indicates T2* is a robust biomarker for cardiac conditions.
Area of Science:
- Cardiology
- Biomedical Imaging
- Magnetic Resonance Imaging
Background:
- Myocardial T2* is a magnetic resonance imaging (MRI) technique sensitive to iron concentration.
- Age, left ventricular dysfunction, and myocardial fibrosis can alter cardiac structure and function.
- Understanding potential confounding factors for T2* is crucial for accurate cardiac assessment.
Purpose of the Study:
- To investigate the impact of aging, impaired left ventricular function, and myocardial fibrosis on myocardial T2* values.
- To determine if these factors confound T2* measurements in cardiac MRI.
Main Methods:
- Myocardial T2* was measured in 126 subjects.
- Subjects included healthy individuals across a range of ages, patients with impaired left ventricular function, and patients with chronic myocardial infarction affecting the septum.
- Exclusion criteria included cardiac iron loading.
Main Results:
- No significant correlation was found between myocardial T2* and age in healthy subjects.
- Myocardial T2* values were not significantly different in patients with impaired left ventricular function compared to normals.
- Ejection fraction did not correlate with T2* in patients with left ventricular impairment.
- Septal myocardial T2* in patients with infarction was not significantly different from normals.
Conclusions:
- Myocardial T2* measurements remain stable despite increasing age, impaired left ventricular function, or myocardial fibrosis due to infarction.
- These findings suggest that myocardial T2* is a robust imaging biomarker, unaffected by common cardiac structural and functional alterations.
Purpose:
To evaluate the influence of alterations in myocardial structure and function from increasing age, myocardial fibrosis, or impaired left ventricular function on myocardial T2*.
Materials And Methods:
Myocardial T2* was measured in 126 subjects without cardiac iron loading, of whom 63 were normals of varying ages, 39 were patients with impaired left ventricular function from various nonsiderotic cardiac causes, and 24 were patients with chronic myocardial infarction affecting the interventricular septum (where myocardial T2* measurements are normally made).
Results:
The median (Q1, Q3) of myocardial T2* in the normals was 36.3 ms (31.6, 45.4). There was no significant correlation between myocardial T2* and age (R(2) = 0.04; P = 0.11). In the patients with impaired left ventricular function, the median myocardial T2* was 35.5 ms (31, 42.2) (P = 0.34 versus normals). There was no significant correlation between ejection fraction and T2* in patients with left ventricular impairment (R(2) = 0.03; P = 0.33). In the patients with septal infarction, the median septal myocardial T2* was 35.4 ms (32.7, 43) (P = 0.81 vs normals).
Conclusion:
There was no significant change in myocardial T2* associated with any alterations of myocardial structure and function occurring with increasing age, impairment of left ventricular function or septal fibrosis from chronic myocardial infarction. These results indicate that myocardial T2* measurements are robust to these potential confounding parameters.
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