Changes in platelet count as a marker of myocardial iron uptake after administration of ferric carboxymaltose in patients with heart failure.
Mollar A., García-Conejo C., Revuelta-López E., Cardells I., López R., Del Canto I., de la Espriella R., Lopez-Lereu MP., Monmeneu JV., Maceira A., Lakhal-Littleton S., Almenar L., Cases A., Peiró M., Bayés-Genís A., Núñez J.
Iron deficiency (ID) treated with ferric carboxymaltose (FCM) previously showed reduced platelet count; however, no studies have evaluated its biological significance in heart failure. In the current study, we aimed to: (a) assess the changes in platelet count at 7 and 30 days post-FCM, and (b) explore its association with non-invasive surrogates of myocardial iron uptake and left systolic function in patients with ID and heart failure with left ventricular ejection fraction < 50% (HFrEF and HFmrEF). This post-hoc analysis of a randomized, double-blind, FCM vs. placebo clinical trial (Myocardial-IRON Trail) involved 45 outpatients with HFrEF and HFmrEF and ID in which the platelet count value was available. Platelet count, cardiac magnetic resonance T1-mapping and 3D-global longitudinal strain (CMR-GLS) were assessed at baseline, 7, and 30 days. Linear regression models were used to evaluate the between-treatment differences and endpoints. The mean (SD) age was 71 ± 8 years, and 32 (71%) were men. At 30 days, we found a significant reduction in platelet count in those treated with FCM (p-value = 0.027). In those treated with FCM, the greater 30-day decrease in platelets showed lower 30-day changes in T1-mapping (p = 0.024) and CMR-GLS (p = 0.028). After administration of FCM, we found a significant 30-day reduction in platelet count. The greater platelet count reduction was related to lower myocardial iron repletion and a smaller improvement in left ventricular systolic function.