Implications of Iron Deficiency in STEMI Patients and in a Murine Model of Myocardial Infarction

Inserte, Javier; Barrabés, José A.; Aluja, David; Otaegui, Imanol; Bañeras, Jordi; Castellote, Laura; Sánchez, Ana M.; Palomares, José F. Rodríguez; Pineda, Víctor; Miró-Casas, Elisabet; Milà, Laia; Lidón, Rosa‐Maria; Sambola, Antonia; Valente, Filipa; Rafecas, Agnès; Ruiz‐Meana, Marisol; Rodríguez‐Sinovas, Antonio; Benito, Begoña; Buera, Irene; Delgado-Tomás, Sara; Benéitez, David; Ferreira‐González, Ignacio

doi:10.1016/j.jacbts.2021.05.004

Cited by 20 publications

(17 citation statements)

References 38 publications

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“…Furthermore, in another rat model of HF, intravenously administering iron resulted in higher tissue activity of the antioxidant superoxide dismutase [ 208 ]. A recent study found similar results in a mice model of myocardial infarction [ 209 ]. Several studies showed that ID participates in the induction of oxidative stress in many organs, including the liver and the kidneys [ 210 , 211 ].…”

Section: Deleterious Biological Consequences Of Iron Deficiencysupporting

confidence: 68%

Iron Deficiency in Heart Failure: Mechanisms and Pathophysiology

Alnuwaysir

Hoes

Veldhuisen

et al. 2021

JCM

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Iron is an essential micronutrient for a myriad of physiological processes in the body beyond erythropoiesis. Iron deficiency (ID) is a common comorbidity in patients with heart failure (HF), with a prevalence reaching up to 59% even in non-anaemic patients. ID impairs exercise capacity, reduces the quality of life, increases hospitalisation rate and mortality risk regardless of anaemia. Intravenously correcting ID has emerged as a promising treatment in HF as it has been shown to alleviate symptoms, improve quality of life and exercise capacity and reduce hospitalisations. However, the pathophysiology of ID in HF remains poorly characterised. Recognition of ID in HF triggered more research with the aim to explain how correcting ID improves HF status as well as the underlying causes of ID in the first place. In the past few years, significant progress has been made in understanding iron homeostasis by characterising the role of the iron-regulating hormone hepcidin, the effects of ID on skeletal and cardiac myocytes, kidneys and the immune system. In this review, we summarise the current knowledge and recent advances in the pathophysiology of ID in heart failure, the deleterious systemic and cellular consequences of ID.

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Section: Deleterious Biological Consequences Of Iron Deficiencysupporting

confidence: 68%

Iron Deficiency in Heart Failure: Mechanisms and Pathophysiology

Alnuwaysir

Hoes

Veldhuisen

et al. 2021

JCM

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“…83 Consistently, in 141 patients with a first anterior ST-elevation myocardial infarction (STEMI) treated by percutaneous coronary intervention (PCI), ID was associated with larger infarct sizes, higher likelihood of adverse left ventricular remodelling and more extensive microvascular obstruction. 78 Conversely, in a different cohort of 420 STEMI patients undergoing primary PCI, those with ID had greater increases in troponin but, surprisingly, no difference in infarct size measured by cardiac magnetic resonance, and reported lower in-hospital mortality/Killip class ≥3 compared with patients without ID. 80 In 39 STEMI patients, those receiving (n = 17) IV ultrasmall superparamagnetic iron-oxide (USPIO)-based iron administration within 4 days following an acute myocardial infarction had a much smaller infarct size, with a decrease in both endocardial extent and transmural infarction, and a smaller left ventricular end-systolic volume.…”

Section: Id In Patients With Cadmentioning

confidence: 96%

“…Only 32% of patients diagnosed with ID also had anaemia. 77 In patients admitted for acute coronary syndrome, ID prevalence has ranged between 29-56% depending on the cohorts' characteristics, [78][79][80] with a meta-analysis estimating an overall prevalence of 43%. 81 In 836 patients with acute coronary syndrome, ID predicted a 50% increased risk of non-fatal myocardial infarction and CV death after extensive adjustments including anaemia.…”

Section: Id In Patients With Cadmentioning

confidence: 99%

Iron deficiency and cardiovascular disease

Savarese

Haehling

Butler

et al. 2022

European Heart Journal

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Iron deficiency (ID) is common in patients with cardiovascular disease. Up to 60% of patients with coronary artery disease, and an even higher proportion of those with heart failure (HF) or pulmonary hypertension have ID; the evidence for cerebrovascular disease, aortic stenosis and atrial fibrillation is less robust. The prevalence of ID increases with the severity of cardiac and renal dysfunction and is probably more common amongst women. Insufficient dietary iron, reduced iron absorption due to increases in hepcidin secondary to the low-grade inflammation associated with atherosclerosis and congestion or reduced gastric acidity, and increased blood loss due to anti-thrombotic therapy or gastro-intestinal or renal disease may all cause ID. For older people in the general population and patients with HF with reduced ejection fraction (HFrEF), both anaemia and ID are associated with a poor prognosis; each may confer independent risk. There is growing evidence that ID is an important therapeutic target for patients with HFrEF, even if they do not have anaemia. Whether this is also true for other HF phenotypes or patients with cardiovascular disease in general is currently unknown. Randomized trials showed that intravenous ferric carboxymaltose improved symptoms, health-related quality of life and exercise capacity and reduced hospitalizations for worsening HF in patients with HFrEF and mildly reduced ejection fraction (<50%). Since ID is easy to treat and is effective for patients with HFrEF, such patients should be investigated for possible ID. This recommendation may extend to other populations in the light of evidence from future trials.

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“…Importantly the NOS triple (n/i/eNOS −/− ) KOs exhibit cardiovascular abnormalities, including hypertension, myocardial infractions, cardiac hypertrophy, bone marrow abnormalities, arteriosclerosis, diastolic heart failure etc., all of which may relate to obstructed heme-maturation of sGC and the globins (Hb and Mb) [ 61 , 67 ]. Moreover conditions of iron deficiency or anemia can cause myocardial infractions or make sGC heme-free as has been demonstrated in a recent study [ 68 ], and such conditions may also exist in the NOS triple (n/i/eNOS −/− ) KO mice.…”

Section: Discussionmentioning

confidence: 91%