Lactate dehydrogenase (LDH) as a predictor of left atrial remodeling in patients with sickle cell anemia.

Authors

Fábio Galvão, Felipe Soares Maia, Mabel Rodrigues Rios, Jersey Heitor da Silva Maues, Bruno Deltreggia Benites, Samuel de Souza Medina, Paula de Melo Campos, José Roberto Matos-Souza, Fernando Ferreira Costa, Wilson Nadruz, Sara Teresinha Olalla Saad

Published in

Annals of hematology. Jul 06, 2026. Epub Jul 06, 2026.

Abstract

In sickle cell anemia (SCA), multiple end-organs are affected by the chronic effects of hemolytic anemia and vaso-occlusive events, with cardiac complications being among the leading causes of death. Cardiac remodeling, including left atrial enlargement, may lead to diastolic dysfunction and increase the risk of atrial arrhythmias. Although hemolysis is an important mechanism in the systemic complications of SCA, the value of lactate dehydrogenase (LDH) as an isolated marker of atrial remodeling remains poorly explored. In this context, we evaluated whether this simple marker could predict left atrial enlargement in patients with SCA in a steady state. In a retrospective cross-sectional study, we reviewed medical records, including echocardiographic examinations, of patients with SCA treated at a referral center. LDH elevation, expressed as multiples of the upper limit of normal (LDH/ULN), was used for comparison. Eighty-one patients were included, with a mean age of 41.7 ± 11.4 years, and 60% were female. The median LDH/ULN was 1.39 (range: 0.45-5.4). Forty-four patients (54%) presented an elevated left atrial volume index (LAVi), and 52 patients (64%) had LDH/ULN > 1.0. Receiver-operating characteristic (ROC) curve analysis identified 1.2 as the optimal LDH/ULN cut-off to detect elevated LAVi, and adjusted logistic regression showed that individuals with LDH/ULN > 1.2 had a 3.70‑fold higher risk of elevated LAVi (confidence interval = 1.33-10.31; p = 0.012). Our study identified an association between LDH and increased LAVi, suggesting a potential role as a simple marker of atrial remodeling, and not solely as a marker of hemolysis.

PMID:
42406107
Bibliographic data and abstract were imported from PubMed on 06 Jul 2026.

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