Absence of Relationship of Myocardial T2* to Right Ventricular Function In Thalassaemia Major
Authors: Perifanis Vassilios , Kondou Antonia , Teli Aikaterini , Vlachaki Efthimia , Economou Marina , Tsatra Giannoula , Spanos George P , Athanassiou-Metaxa Miranda 
Published: October 2019

Abstract 5160

Iron-induced cardiac dysfunction is a leading cause of death in transfusion-dependent anemia. Myocardial T2* magnetic resonance imaging (MRI) provides a rapid and reproducible measure of cardiac iron loading and is being increasingly used worldwide for monitoring of transfusion-dependent thalassaemia patients. Recent reports associate myocardial siderosis (T2* <20 ms) with impaired left ventricular (LV) function, as well as with right ventricular (RV) function. As RV dysfunction may play a significant role in heart failure associated with myocardial siderosis the aim of this study was to investigate the relationship between cardiac T2* and RV function in patients treated in a single institution. Methods: A retrospective analysis of 190 well chelated patients with beta-thalassaemia major presenting for their first T2*. MRI scan (examination year 2005) was performed (53.7% male, mean age 26,2±8,3 years). The majority of patients were on Desferrioxamine and 30% were on Deferiprone. Patient's mean ferritin, mean T2* and mean RVEF was 1467±1087 ng/ml, 32,5±15,8ms and 67,9±5,25% respectively. Magnetic resonance images were acquired using a single imager (Philips®, Philips Medical Systems Ltd, Eindhoven, The Netherlands) equipped with a 1.5 Tesla magnet. Each scan included the measurement of heart T2* (mid-septum) together with LV and RV volumes, EF, and mass using previously published techniques. Pearson correlation was used to assess the statistical significance between myocardial T2*, ferritin, RV volumes (End Systolic and End Diastolic), and EF. Results: In 156 patients (Group A) with normal myocardial T2* (>20 ms), the RV ejection fraction (EF) was within the normal range (>55%) in all of them. Mean ferritin, mean T2* and mean RVEF for Group A was 1397±1007ng/ml, 39±11ms and 68,6 ±4,8% respectively. No correlation with feritin was found. In the remaining 34 patients (Group B) with myocardial T2* <20ms, mean ferritin, mean T2* and mean RVEF was 1664±1341ng/ml, 10,8±4,2ms and 64,8±7,35% respectively. Although there was a good correlation between T2* and RVEF for the entire group (A+B) (r=0,312, p=0,001) we did not find a correlation between T2* and RVEF for Group B (r=0,074, p=ns). In the contrary there was a strong correlation between T2* and ferritin for Group B (r=0,382, p=0,0034). There was no other significant correlation between T2* and RESV, REDV for both groups. There was a linear relationship between RV and LVEF for the whole group (r=0,454, p=0,001), for Group A (r=0,269, p=0,015) and more significant for Group B (r=0,720, p=0,001). Conclusions: Myocardial iron deposition by MRI seems not to be associated with RV dysfunction, although it is related to ferritin. The decrease in LV function seen with worsening cardiac iron loading does not necessarily predicts right ventricular dysfunction. The only limitation of our study is that in contrast with other reports the percentage of patients with abnormal T2* was smaller (18%). Larger studies are required to determine the relation of right ventricular function and cardiac iron overload.

Disclosures:

No relevant conflicts of interest to declare.