Historically, most thalassemia-major patients died from iron-induced cardiomyopathy. Cardiac T2* MRI quantifies myocardial iron non-invasively - enabling early identification and targeted intensive chelation that has substantially changed survival.
Why the Heart is Different #
Iron does not distribute uniformly. Cardiac iron lags hepatic iron in uptake and is slower to mobilise - meaning patients with normal ferritin and acceptable LIC can still have significant cardiac iron. Missing it is dangerous.
Cardiac T2* Interpretation #
| Cardiac T2* | Implication |
|---|---|
| > 20 ms | Normal |
| 10-20 ms | Mild-to-moderate cardiac iron - intensify monitoring |
| < 10 ms | Significant cardiac iron - aggressive chelation and cardiology co-management |
| < 6 ms | Severe cardiac iron - urgent intensive chelation; risk of cardiac decompensation |
Who Should Be Screened? #
- Thalassemia major from age 8-10 annually
- Long-term transfused SCD, MDS patients with high iron burden
- Any patient with persistently elevated ferritin / LIC
Deferasirox and Cardiac Iron #
Studies show sustained deferasirox therapy (24-36 months) is associated with improvement in cardiac T2* from values below 20 ms toward normal. Combination chelation (deferasirox + deferoxamine or deferiprone) is sometimes used under specialist supervision for severe cardiac iron.
Cardiology Integration #
Cardiac T2* should be interpreted alongside LVEF (echocardiography or cardiac MRI), arrhythmia screening (Holter as indicated) and symptomatic assessment. Advanced cardiac iron (T2* < 6 ms with LVEF decline) requires urgent intensive chelation plus standard heart failure management.
See Pharmacodynamics.