Progress in the management of arrhythmias: risk scores, ablation, and anticoagulation

Lüscher, Thomas F.

doi:10.1093/eurheartj/ehy059

Cited by 1 publication

(1 citation statement)

References 27 publications

(19 reference statements)

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“…Indeed, over the last two decades, there has been a great deal of progress in arrhythmia management. However, most antiarrhythmic drugs proved ineffective or dangerous in patients with ventricular arrhythmias [40], demonstrating the need for new therapeutic strategies.…”

Section: Discussionmentioning

confidence: 99%

Redox-Active Drug, MnTE-2-PyP⁵⁺, Prevents and Treats Cardiac Arrhythmias Preserving Heart Contractile Function

Barbosa

Sarmento-Neto

Menezes-Filho

et al. 2020

Oxidative Medicine and Cellular Longevity

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Background. Cardiomyopathies remain among the leading causes of death worldwide, despite all efforts and important advances in the development of cardiovascular therapeutics, demonstrating the need for new solutions. Herein, we describe the effects of the redox-active therapeutic Mn(III) meso-tetrakis(N-ethylpyridinium-2-yl)porphyrin, AEOL10113, BMX-010 (MnTE-2-PyP5+), on rat heart as an entry to new strategies to circumvent cardiomyopathies. Methods. Wistar rats weighing 250-300 g were used in both in vitro and in vivo experiments, to analyze intracellular Ca2+ dynamics, L-type Ca2+ currents, Ca2+ spark frequency, intracellular reactive oxygen species (ROS) levels, and cardiomyocyte and cardiac contractility, in control and MnTE-2-PyP5+-treated cells, hearts, or animals. Cells and hearts were treated with 20 μM MnTE-2-PyP5+ and animals with 1 mg/kg, i.p. daily. Additionally, we performed electrocardiographic and echocardiographic analysis. Results. Using isolated rat cardiomyocytes, we observed that MnTE-2-PyP5+ reduced intracellular Ca2+ transient amplitude, without altering cell contractility. Whereas MnTE-2-PyP5+ did not alter basal ROS levels, it was efficient in modulating cardiomyocyte redox state under stress conditions; MnTE-2-PyP5+ reduced Ca2+ spark frequency and increased sarcoplasmic reticulum (SR) Ca2+ load. Accordingly, analysis of isolated perfused rat hearts showed that MnTE-2-PyP5+ preserves cardiac function, increases SR Ca2+ load, and reduces arrhythmia index, indicating an antiarrhythmic effect. In vivo experiments showed that MnTE-2-PyP5+ treatment increased Ca2+ transient, preserved cardiac ejection fraction, and reduced arrhythmia index and duration. MnTE-2-PyP5+ was effective both to prevent and to treat cardiac arrhythmias. Conclusion. MnTE-2-PyP5+ prevents and treats cardiac arrhythmias in rats. In contrast to most antiarrhythmic drugs, MnTE-2-PyP5+ preserves cardiac contractile function, arising, thus, as a prospective therapeutic for improvement of cardiac arrhythmia treatment.

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Section: Discussionmentioning

confidence: 99%

Redox-Active Drug, MnTE-2-PyP⁵⁺, Prevents and Treats Cardiac Arrhythmias Preserving Heart Contractile Function

Barbosa

Sarmento-Neto

Menezes-Filho

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

Progress in the management of arrhythmias: risk scores, ablation, and anticoagulation

Cited by 1 publication

References 27 publications

Redox-Active Drug, MnTE-2-PyP⁵⁺, Prevents and Treats Cardiac Arrhythmias Preserving Heart Contractile Function

Redox-Active Drug, MnTE-2-PyP⁵⁺, Prevents and Treats Cardiac Arrhythmias Preserving Heart Contractile Function

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Progress in the management of arrhythmias: risk scores, ablation, and anticoagulation

Cited by 1 publication

References 27 publications

Redox-Active Drug, MnTE-2-PyP5+, Prevents and Treats Cardiac Arrhythmias Preserving Heart Contractile Function

Redox-Active Drug, MnTE-2-PyP5+, Prevents and Treats Cardiac Arrhythmias Preserving Heart Contractile Function

Contact Info

Product

Resources

About

Redox-Active Drug, MnTE-2-PyP⁵⁺, Prevents and Treats Cardiac Arrhythmias Preserving Heart Contractile Function

Redox-Active Drug, MnTE-2-PyP⁵⁺, Prevents and Treats Cardiac Arrhythmias Preserving Heart Contractile Function