A high rate of hepatic, pancreatic and cardiac impairment by iron overload was demonstrated. Ferritin levels could not predict liver, heart or pancreas iron overload as measured by T2* magnetic resonance imaging. There was no correlation between liver, pancreas, liver and myocardial iron overload, neither between ferritin and fraction of labile plasma iron with liver, heart and pancreas T2* values.

To evaluate the role of losartan on left ventricular (LV) function of hypertensive patients. Hypertensive patients (n =19) underwent evaluation of systolic and diastolic LV function, using radionuclide ventriculography (RVG), before and at 3 mo into the treatment with the angiotensin II antagonist losartan. All patients underwent a baseline 12 lead ECG and an echocardiogram (ECHO), which was also repeated at 3 mo into treatment. Results are expressed as mean ± SEM and statistics were performed using paired t-test. A p value <_ 0.05 was considered significant. Treatment with losartan for 3 mo had no effect on LV mass measured by echo (141 ± 5 vs. 139 ± 6 g/m2). The LV ejection fraction, measured by RVG, was unchanged by treatment when compared to the baseline study (58 ± 2 % vs. 57 ± 2% , respectivelly, p = 0.49). Considering all patients involved in the study (n =19), the LV "Peak Filling Rate" (PFR), a parameter of diastolic function measured by RVG, was also unchanged by treatment when compared to baseline (2.5 ± 0.2 EDV/s vs. 2.5 ± 0.3 EDV/s, respectively, p = 0.9). However the analysis of those patients with evidence of diastolic dysfunction (n =12) on the baseline RVG (PFR < 2.5 EVD/s), demonstrated significant improvement of LV filling after therapy with losartan (PFR =1.8 ± 0.1 EDV/s vs. 2.3 ± 0.2 EDV/s, respectively, p = 0.05). This change was associated with improvement of symptoms. Our results demonstrated that hypertensive patients with diastolic dysfunction on radionuclide ventriculography have significant improvement of ventricular filling at 3 mo into treatment with losartan. (Hypertens Res 1999; 22: 155-159)

Magnetic Ressonance Imaging (MRI) using T2 star (T2*) tecnique appears to be a very useful method for monitoring iron overload and iron chelation therapy in thalassaemia. In Brazil, we have around 400 thalassaemic major patients all over the country. They were treated with hipertransfusion protocols and desferroxamine and/or deferiprone chelation. We developed a cooperative program with the Brazilian Thalassaemic Patients Association (ABRASTA) in order to developT2* tecnique in Brazil to submit brazilian patients to an annual iron overload monitoring process with MRI.. We performed the magnetic ressonance T2* using GE equipment (GE, Milwaukee USA), with validation to chemical estimation of iron in patients undergoing liver biopsy. Until now, 60 patients were scanned, median age=23,2 (12–54); gender: 18 male (30%) and 42 female (70%). The median ferritin levels were 2030 ng/ml (Q1=1466; Q3=3296). As other authors described before, there was a curvilinear inverse correlation between iron concentration by biopsy, liver T2*(r=0,92) and also there were a correlation with ferritin levels. We also correlated myocardial iron measured by T2* with ventricular function.. As miocardial iron increased, there was a progressive decline in ejection fraction and no significant correlation was found between miocardial T2* and the ferritin levels. Liver iron content can be predicted by ferritin levels. On the other hand, cardiac disfunction is the most important cause of mortality among thalassaemic patients. Since Miocardio iron content cannot be predicted from serum ferritin or liver iron, and ventricular function can only detect those with advance disease, intensification and combination of chelation therapy, guided by T2* MRI tecnique should reduce mortality from the reversible cardiomyopathy among thalassaemic patients.

Hereditary hemochromatosis is highly prevalent in those with northern European ancestry (1 in 8 individuals are heterozygous and 1 in 100 – 200 are homozygous). It is characterized by laboratory tests as ferritin &gt; 150 ng/mL, transferrine saturation &gt; 40% and HFE mutations (C282Y and H63D). Presently the indications for treatment (therapeutic phlebotomies, TP) are based solely on the ferritin levels. It is possible that patients with moderate or even high levels of ferritin do not have iron overload. Performing liver biopsies would be an option for the actual evaluation, though invasive and risky. A non-invasive method to evaluate this deposition would be helpful in order to determine which patients actually demand TP. To evaluate if the use of Magnetic Ressonance Image (MRI) is a method for measuring tissue iron and could be a new guide for the indication of therapeutic phlebotomies, nineteen patients (mean age 43,47 y.o, +/− 9,85, gender = 16 male, 3 female) with hereditary hemochromatosis were scanned with T2- star (T2*) (GE equipment, Milwaukee, USA). The median of ferritin level was 594 (21–9300) The MRI method was previously validated to chemical estimation of iron in thalassemic major patients undergoing liver biopsies. The evaluated organs were liver and heart. All patients were in normal range of myocardial T2*. The images of four patients (25%), showed liver iron deposition. Eleven patients who presented serum ferritin levels below 600 ng/ml showed no liver iron deposition. Just one among five patients (20%), who presented ferritin levels between 601 and 1000 ng/ml showed hepatic iron overload. The three patients with ferritin levels higher than 1000 ng/ml had liver iron deposition quantified using liver T2* MRI techique. MRI T2* showed that some patients who would have an indication for TP based on laboratory tests, might avoid these procedures based on image results of internal organs. These patients can have an image follow up in order to decide when would be the appropriate time to start TP. This method can also be used to evaluate the efficacy of TP in patients who have already received this treatment. A larger group of patients would have to be evaluated in order to validate these results.

4052 Poster Board III-987 Background Frequent transfusions of red blood cells are considered standard therapy for patients with β-thalassemia. However, this can lead to transfusional iron overload and subsequent end-organ damage with decrease in life-expectancy. Ferritin is the most widely available non-invasive method for assessing iron stores and iron overload in chronically transfused patients. However, it can also be elevated in inflammatory conditions. MRI has been proposed as a non-invasive method for detection and quantification of iron stores in specific organs. Most studies utilizing MRI for detection of iron overload have focused on the heart and liver, and it is unknown if MRI could satisfactory detect iron overload in other potentially involved organs such as pancreas. Aims To evaluate and correlate the level of iron accumulation in different organs and serum ferritin concentrations for 6 months before imaging studies in patients with β-thalassemia receiving chronic transfusion therapy. Methods MRI was used to asses iron content in three different organs (heart, liver, and pancreas) in patients with a diagnosis of β-thalassemia. Validation of the MRI technique was done by determining liver iron concentration (LIC) from 11 liver biopsies. LIC was determined by atomic absorption spectrometry and was correlated with liver T2* measurement obtained with MRI. There was a significant, curvilinear, inverse correlation between liver T2* MRI measurements and the LIC by Pearson′s method (r =-0.878, p=0.001). We used Pearson′s coefficient of correlation to assess association between T2* measurements among different organs (heart, liver and pancreas) and between organs and serum ferritin levels. Results We evaluated 115 patients with a diagnosis of β-thalassemia that were receiving chronic transfusion therapy. Mean age was 21,25 years (range 7-54 years) and 43% were male. Mean T2* value in the liver was 3.91 ± 3.95 ms, indicating significant liver siderosis (T2*<6.3ms) in most patients (92.1%). Mean value of myocardial T2* was 24.96 ± 14.17 ms and the incidence of cardiac siderosis (T2*<20ms) was 36%. Additionaly, 19% of the patients (22/115) had severe cardiac siderosis (T2* <10ms). Mean T2* value in pancreas was 11.12 ± 11.20 ms, and pancreatic iron deposition (T2* < 21ms) was found in 83.5% of patients. There was no significant correlation between liver and pancreas iron overload (r =0.249), and liver and myocardial iron overload (r =0.149). There was a moderate correlation among pancreas and myocardial iron overload (r =0.546; p=0.001). Mean serum ferritin level was 2,676.5 +/- 2,051.7 ng/mL (range 59-12,362 ng/mL). There was no significant correlation among ferritin serum level and liver, heart and pancreas T2* values (r =-0.397; r =-0.220; r =-0.295). Conclusion Iron overload of liver, heart and pancreas, measured by MRI T2*, could not be predicted by ferritin levels in patients with β-thalassemia. Pancreatic iron overload can be measured by MRI, but we could not predict pancreatic hemosiderosis by detection of iron overload in others organs (except for a moderate correlation among pancreas and heart iron overload). Given that direct calibration of MRI with pancreas biopsies is not possible, further studies are necessary to validate this technique. Disclosures: No relevant conflicts of interest to declare.