The role of copeptin for diagnose cardiac deterioration in thalassemia major patients

Thalassemia disease is one of the most common hematologic genetic disorders in our country that it can only be cured by stem cell transplantation. If stem cell transplantation is impossible, lifelong regularly blood transfusion is needed. Iron overload, which is caused by regular blood transfusions, damages heart like all other tissues. Cardiac events related with iron overload are still the primary reason for mortality of these patients. Therefore, the clinicians have to realize cardiac complications early and treat them at the right time while they are still reversible. While information about this chronic disease has been increased in the last years, methods of new diagnose, follow-up and treatment have been evaluated. The tests (ferritin, MRI, cardiac markers) used for determining the iron overload and transfusion-related cardiac complications currently are limited capacity and can be insufficient to identify cardiac complications early. The copeptin molecule, which is released by pituiary gland together with arginine vasopressin molecule (AVP) - responsible for fluid and electrolyte balance in human body-and which can be measured easier than AVP in vitro, has been studied in recent years. There have been publications showing relation of copeptin with myocardial infarction and heart failure. It could not be encountered any studies in literature studying copeptin in thalassemia major patients. In this study, methods for early diagnose of cardiac injury in the thalassemia major patients were examined and compared. The patients were divided into groups according to MRI (MRI T2*<20 and T2*≥20), copeptin levels of the patient and control groups were compared. The copeptin levels and PW doppler/PWDD echocardiographies of the patient (n=59) and control groups (n=24) were compared. Some cardiac markers (nt-proANP, nt-proBNP, CK-MB 76 and ultrasensitive troponin I) were also measured besides copeptin and comparison of these markers between the MRI groups was made. As a result, similar to the results in the literature, no significant differences in markers among the groups were determined, except nt-proBNP which was measured at high level in the patients. The reason for no significant difference in copeptin levels is associated that mostly our patients were asymptomatic. Tissue doppler imaging is a well enough method to provide especially determining diastolic dysfunctions, evaluating global functions of heart to measure different areas of heart and evaluate cardiac dynamics. Because of the significant results of myocardial performance index especially measured at PWDD segmentally in our study, it makes us consider that this technique should be used in routine. We suggest that segmental MPI values of patients have to be calculated and evaluated at least once in a year. Finally we want to point that our patient groups were divided into two groups according to their T2* MRI results based on literature. Also PWDD evaluation was made segmentally. Although it is well known that iron overload on septum shows total cardiac iron overload, we suggest that measuring of segmental iron overload by MRI and comparing it with tissue doppler would give us more valuable information and we recommend to care attention about this issue while planning further researches.