IMPACT OF IRON DEFICIENCY ON CLINICAL,BIOCHEMICAL AND ECHOCARDIOGRAPHIC PARAMETERS IN HEART FAILURE PATIENTS

Abstract

Objective: Iron deficiency (ID) is prevalent in HF irrespective of the presence of anemia. Objective was to study the impact of iron deficiency on clinico- biochemical and echocardiographic parameters of heart failure patients. Design and method: Sixty adult heart failure patients were included in observational study with consent. Excluded were anemia not attributed to ID,IV iron or blood transfusion administered in last 3 months,Oral iron supplements in previous 4 weeks, dyspnea of non cardiac origin,clinical evidence of ACS, TIA or stroke within the last 30 days,CABG, PTCA, cardiac device implant/resynchronisation therapy or any other cause leading to significant blood loss within the last 30 days. Demographic information and medical history including NYHA grade of Dyspnea at presentation were noted. Iron studies,Nt proBNP levels and echocardiography were performed and appropriate statistical tests were applied. Results: Mean Age of cases was 57 (+/-5) years. Most common presenting symptom was breathlessness in 49(81.7%)patients followed by leg swelling in 46 (76.7%) and chest pain in 34 (56.7%)where as among the signs on examination; raised JVP was recorded in 18 (30%),hepatomegaly in 30(50%), splenomegaly in 17(28.3%),ascites in 19(31.7%),S3 gallop rhythm and basal lung crepitations in 10(16.6%) and 47(78.3%)patients respectively. Majority of patients were in grade2 NYHA. Iron Deficiency as determined by serum ferritin of <100 μg/mL or ferritin 100-300 μg/ml but transferrin saturation less than 20% was present in 43(71.7%)patients whereas in 17 patients(28.3%) it was not observed. Mean serum Iron was 36.417μg/dl,mean serum ferritin was 242.89 μg/ml and mean transferrin saturation was 17.25%. Mean Hb was 10 gm% and mean NTProBNP was 11,324.65 picogm/ml.Mean Ejection fraction was 38%(+/- 12.75%).NtProBNP levels did not show any correlation with iron profile whereas LVEF showed a significant correlation with serum Iron as well as transferrin saturation (p <0.001). Serum iron and Transferrin saturation were significantly reduced with the progression of severity grade (p<0.006&0.001 respectively). Conclusions: Targeting iron deficiency in HF can improve outcomes as it targets mitochondrial dysfunction. This makes ID stand out as a therapeutic target in HF since it is relatively easy to diagnose and treat.