Atrial Fibrillation in β-Thalassemia: Overview of Mechanism, Significance and Clinical Management

Malagù, Michele; Marchini, Federico; Fiorio, Alessio; Sirugo, Paolo; Clò, Stefano; Mari, E; Gamberini, Maria Rita; Rapezzi, Claudio; Bertini, Matteo

doi:10.3390/biology11010148

Cited by 13 publications

(17 citation statements)

References 56 publications

(96 reference statements)

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“…A variety of stressors, including aging, obesity, hypertension, and diabetes, have been identified as AF risk factors [ 6 , 42 ]. Although these stressors all show metabolic abnormalities, they exhibit different metabolic characteristics (summarized in Table 1 ).…”

Section: Metabolic Heterogeneity Among Af Stressorsmentioning

confidence: 99%

Metabolic Inflexibility as a Pathogenic Basis for Atrial Fibrillation

Qin

Zhang

Zheng

2022

IJMS

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Atrial fibrillation (AF), the most common sustained arrhythmia, is closely intertwined with metabolic abnormalities. Recently, a metabolic paradox in AF pathogenesis has been suggested: under different forms of pathogenesis, the metabolic balance shifts either towards (e.g., obesity and diabetes) or away from (e.g., aging, heart failure, and hypertension) fatty acid oxidation, yet they all increase the risk of AF. This has raised the urgent need for a general consensus regarding the metabolic changes that predispose patients to AF. “Metabolic flexibility” aptly describes switches between substrates (fatty acids, glucose, amino acids, and ketones) in response to various energy stresses depending on availability and requirements. AF, characterized by irregular high-frequency excitation and the contraction of the atria, is an energy challenge and triggers a metabolic switch from preferential fatty acid utilization to glucose metabolism to increase the efficiency of ATP produced in relation to oxygen consumed. Therefore, the heart needs metabolic flexibility. In this review, we will briefly discuss (1) the current understanding of cardiac metabolic flexibility with an emphasis on the specificity of atrial metabolic characteristics; (2) metabolic heterogeneity among AF pathogenesis and metabolic inflexibility as a common pathological basis for AF; and (3) the substrate-metabolism mechanism underlying metabolic inflexibility in AF pathogenesis.

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Section: Metabolic Heterogeneity Among Af Stressorsmentioning

confidence: 99%

Metabolic Inflexibility as a Pathogenic Basis for Atrial Fibrillation

Qin

Zhang

Zheng

2022

IJMS

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“…The shortening of the action potential duration may result from a decrease in the late fast Na + current in the plateau phase due to an imbalance between small currents. 33 Significantly, the study of ion channels in ventricular muscle seems to indicate the effect of iron overload on ion channels. The current activity of cardiac myocytes was further elaborated in a study with Mongolian gerbil ventricular myocytes.…”

Section: Calcium Handling Ion Channels Iron Disturbancementioning

confidence: 99%

Iron and atrial fibrillation: A review

Liu

Yang

et al. 2023

Pacing Clinical Electrophis

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Atrial fibrillation (AF), one of the most common arrhythmias in clinical practice, is classified into paroxysmal, persistent, and permanent AF according to its duration. The development of AF is associated with increased cardiovascular morbidity and mortality. However, the exact etiology of this disease remains poorly understood. Recent studies found disorders of iron metabolism might be involved in the progression of AF. Abnormal iron metabolism in cardiomyocytes provides arrhythmogenic substrates through a variety of mechanisms, including calcium mishandling, ion channel remodeling, and oxidative stress overaction. Interestingly, in AF patients with iron overload, interventions on iron metabolism, such as iron chelators and ferroptosis inhibitors, has been shown to prevent AF via reducing ferroptosis. Herein, we review the possible mechanisms, consequences, and therapeutic implications of altered atrial iron handling for AF pathophysiology.

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“…The ferritin test is a non-specific test providing different sensitivities and specificities at dissimilar cutoff points for evaluating cardiac and liver hemosiderosis in multiple studies. Clinical sequelae, such as heart failure, cardiac dysrhythmia, and pulmonary hypertension from transfusional iron overload, still prevail in β-thalassemia patients 6 , 13 , 14 . In contrast, no consensus exists on the optimum cutoff of ferritin to screen for cardiac and liver hemosiderosis.…”

Section: Introductionmentioning

confidence: 99%

Ferritin thresholds for cardiac and liver hemosiderosis in β-thalassemia patients: a diagnostic accuracy study

Darvishi‐Khezri

Aliasgharian

Naderisorki

et al. 2022

Sci Rep

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Ferritin is frequently used to screen some dire consequences of iron overload in β-thalassemia patients. The study aimed to define the best cutoff point of ferritin to screen for cardiac and liver hemosiderosis in these cases. This was a registry-based study on β-thalassemia patients living throughout Mazandaran province, Iran (n = 1959). In this diagnostic research, the index test was ferritin levels measured by a chemiluminescent immunoassay. As a reference test, T2*-weighted magnetic resonance imaging (T2*-weighted MRI) was applied to determine cardiac and liver hemosiderosis. A cutoff point of 2027 ng/mL for ferritin showed a sensitivity of 50%, specificity 77.4%, PPV 42.1%, and NPV 82.5% for cardiac hemosiderosis (area under curve [AUC] 0.66, 95% CI 0.60–0.71, adjusted odds ratio [OR] 2.05, 95% CI 1.05–4.01). At an optimum cutoff point of 1090 ng/mL, sensitivity 66.7%, specificity 68%, PPV 82.9%, and NPV 46.8% for liver hemosiderosis were estimated (AUC 0.68, 95% CI 0.63–0.73, adjusted OR 3.93, 95% CI 2.02–7.64. The likelihood of cardiac hemosiderosis serum ferritin levels below 2027 ng/mL is 17.5%. Moreover, 82.9% of β-thalassemia patients with serum ferritin levels above 1090 ng/mL may suffer from liver hemosiderosis, regardless of the grades.

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Atrial Fibrillation in β-Thalassemia: Overview of Mechanism, Significance and Clinical Management

Cited by 13 publications

References 56 publications

Metabolic Inflexibility as a Pathogenic Basis for Atrial Fibrillation

Metabolic Inflexibility as a Pathogenic Basis for Atrial Fibrillation

Iron and atrial fibrillation: A review

Ferritin thresholds for cardiac and liver hemosiderosis in β-thalassemia patients: a diagnostic accuracy study

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