Calcium channel blockers for preventing cardiomyopathy due to iron overload in people with transfusion-dependent beta thalassaemia

Sadaf, Alina; Nisar, Muhammad Imran; Hasan, Babar; Das, Jai K; Colan, Steven D.

doi:10.1002/14651858.cd011626

Cited by 7 publications

(10 citation statements)

References 53 publications

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“…In our study, myocardial MRI T2* improved in both sequences, although no significant difference was observed totally in amlodipine group in comparison with standard chelation therapy group at the end of the study. A meta‐analysis 14 comprising two randomised controlled trials (RCT) with an overall sample size of 74 TDT patients demonstrated the potential role of amlodipine in a significant decrease of myocardial iron concentration (MIC). Overall pooled mean difference for MIC changes from baseline were −0.23 95% CI −0.07 to −0.39 and −0.25 95% CI −0.44 to −0.05 after subsequent to 6‐ and 12‐months follow‐up, respectively.…”

Section: Discussionmentioning

confidence: 99%

A double‐blind, controlled, crossover trial of amlodipine on iron overload status in transfusion dependent β‐thalassemia patients

et al. 2021

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Background and aim: This study examined whether administration of amlodipine could improve myocardial iron loading status in patients with transfusion dependent β-thalassemia (TDT), through a placebo-controlled, crossover study. Methods: Amlodipine (5 mg, daily) or placebo were prescribed to all patients (n = 19) for 6 months, and after a 2-week washout period, patients were crossed over to the other group. The efficacy of amlodipine on iron loading was assessed by measuring myocardial T2*-weighted magnetic resonance imaging (MRI T2*, millisecond [ms]) and serum ferritin (ng/mL).Results: Seventeen patients completed the study. The mean ± standard deviation[SD] of myocardial MRI T2* at baseline was 9.83 ± 2.67 ms Myocardial MRI T2* value rose to 11.44 ± 4.14 ms post amlodipine treatment in all patients. After placebo, myocardial MRI T2* value reached 10.29 ± 4.01 ms After controlling the baseline measures, Hedges's g for ferritin and myocardial MRI T2* outcomes were estimated 3.84 (95% confidence interval [CI] 2.68 to 4.97) and −1.80 (95% CI −2.58 to −0.10), respectively. Conclusion:Amlodipine might improve myocardial MRI T2* and serum ferritin level compared to placebo. However, larger clinical studies are needed to confirm the results.

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Section: Discussionmentioning

confidence: 99%

A double‐blind, controlled, crossover trial of amlodipine on iron overload status in transfusion dependent β‐thalassemia patients

et al. 2021

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“…Small randomized trials have shown that the use of calcium channel blockers such as amlodipine can attenuate the beneficial effects of iron chelation . A systematic review of these trials shows that these results should be taken with caution because of the small number of patients included, differences in subgroups analysis and lack of data concerning the type of chelation therapy . Dilemmas concerning the use of calcium channel blockade as a useful strategy in TM should be resolved by future clinical trials which will address these shortcomings.…”

Section: Role Of Iron In Heart Diseasementioning

confidence: 99%

Keeping heart homeostasis in check through the balance of iron metabolism

Vela

2019

Acta Physiologica

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Highly active cardiomyocytes need iron for their metabolic activity. In physiological conditions, iron turnover is a delicate process which is dependent on global iron supply and local autonomous regulatory mechanisms. Though less is known about the autonomous regulatory mechanisms, data suggest that these mechanisms can preserve cellular iron turnover even in the presence of systemic iron disturbance.Therefore, activity of local iron protein machinery and its relationship with global iron metabolism is important to understand cardiac iron metabolism in physiological conditions and in cardiac disease. Our knowledge in this respect has helped in designing therapeutic strategies for different cardiac diseases. This review is a synthesis of our current knowledge concerning the regulation of cardiac iron metabolism. In addition, different models of cardiac iron dysmetabolism will be discussed through the examples of heart failure (cardiomyocyte iron deficiency), myocardial infarction (acute changes in cardiac iron turnover), doxorubicin-induced cardiotoxicity (cardiomyocyte iron overload in mitochondria), thalassaemia (cardiomyocyte cytosolic and mitochondrial iron overload) and Friedreich ataxia (asymmetric cytosolic/mitochondrial cardiac iron dysmetabolism). Finally, future perspectives will be discussed in order to resolve actual gaps in knowledge, which should be helpful in finding new treatment possibilities in different cardiac diseases. K E Y W O R D Scardiomyocyte, heart failure, iron chelation, iron metabolism, mitochondria, transferrin receptor 1

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“…Use of a calcium channel blocker is advocated because it can block non‐transferrin‐bound iron uptake from L‐type Ca 2+ channel in isolated cell and animal models . However, convincing clinical data to support its use in RCT's is lacking . In fact, the available evidence does not suggest that the use of calcium channel blockers is associated with a reduction in myocardial iron in patients with transfusion‐dependent β‐thalassemia .…”

Section: Managementmentioning

confidence: 99%

“…However, convincing clinical data to support its use in RCT's is lacking . In fact, the available evidence does not suggest that the use of calcium channel blockers is associated with a reduction in myocardial iron in patients with transfusion‐dependent β‐thalassemia . In addition, use of β‐adrenergic blocker has been long advocated for tachyarrhythmias which are more frequent in patients with β‐thalassemia .…”

Section: Managementmentioning

confidence: 99%

Iron overload and arrhythmias: Influence of confounding factors

Shizukuda

Rosing

2019

Journal of Arrhythmia

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Arrhythmias as a cardiac complication of iron overload (IO) have been well described for decades in the clinical literature. They are assumed to be directly associated with the myocardial accumulation of iron. However, the influence of heart failure and elevated oxidative stress, which are major arrhythmogenic confounding factors associated with IO on arrhythmias, has not been critically reviewed in the published literature. A comprehensive narrative review of published articles in PubMed was conducted to address the influence of confounding factors of IO on arrhythmias. The previous data may have been largely confounded by the other cardiac complications of IO, particularly heart failure. The previous studies on IO‐related arrhythmias lack proper age‐gender–matched control subjects and/or comparison groups with properly controlled confounding factors to assess accurately their etiology and clinical significance. Given the above considerations, further mechanistic investigations to clarify the etiology and clinical relevance of IO‐induced arrhythmias are needed. In addition, investigations to develop arrhythmia management strategy specific to IO, are warranted.

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Calcium channel blockers for preventing cardiomyopathy due to iron overload in people with transfusion-dependent beta thalassaemia

Cited by 7 publications

References 53 publications

A double‐blind, controlled, crossover trial of amlodipine on iron overload status in transfusion dependent β‐thalassemia patients

A double‐blind, controlled, crossover trial of amlodipine on iron overload status in transfusion dependent β‐thalassemia patients

Keeping heart homeostasis in check through the balance of iron metabolism

Iron overload and arrhythmias: Influence of confounding factors

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