Dataset related to the article "Iron deficiency in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention"

This record contains raw data related to the article "Iron deficiency in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention"

ABSTRACT Background: Iron deficiency (ID) is a known co-morbidity and a potential therapeutic target in heart failure.
Whether ID is frequent also in ST-segment elevation acute myocardial infarction (STEMI) patients and is associated
with worse in-hospital outcomes has never been evaluated.
Methods: We defined ID as a serum ferritin b 100 μg/L or transferrin saturation b 20% at hospital admission.We
assessed the association between ID and the primary endpoint (a composite of in-hospital mortality and Killip
class ≥ 3). We explored the potential association between ID, circulating cell-free mitochondrial DNA
(mtDNA), and cardiac magnetic resonance (CMR) parameters.
Results: Four-hundred-twenty STEMI patients undergoing primary percutaneous coronary intervention (pPCI)
were included. Of them, 237 (56%) had ID. They had significantly higher admission high-sensitivity troponin
and mtDNA levels as compared to non-ID patients (145 ± 35 vs. 231 ± 66 ng/L, P b 0.001; 917 [404–1748] vs.
1368 [908–4260] copies/μL; P b 0.003, respectively). A lower incidence of the primary endpoint (10% vs. 18%, P
=0.01) was observed in ID patients (adjusted OR 0.50 [95% CI 0.27–0.93]; P=0.02). At CMR (n=192), ID patients
had a similar infarct size (21±18 vs. 21±19 g; P=0.95), but a higher myocardial salvage index (0.56±
0.30 vs. 0.43 ± 0.27; P = 0.002), and a smaller microvascular obstruction extent (3.6 ± 2.2 vs. 6.9 ± 3.9 g; P b
0.001).
Conclusions: Iron deficiency is frequent in STEMI patients, it is coupled with mitochondrial injury, and, paradoxically,
with a better in-hospital outcome. This unexpected clinical result seems to be associated with a smaller
myocardial reperfusion injury. The mechanisms underlying our findings and their potential clinical implications
warrant further investigation.