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Post-hoc analysis of a randomized trial shows reduced platelet count with ferric carboxymaltose in heart failure, indicating impacts on systolic function.
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.
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Mollar et al. (2026) studied this question.
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