Kokhabi Pejman, Mollazadeh Reza, Hejazi Seyedeh Fatemeh, Nezhad Aida Hossein, Pazoki-Toroudi Hamidreza
School of Advanced Medical Sciences, Tehran Medical Branch, Islamic Azad University, Tehran, Iran.
Department of Cardiology, School of Medicine, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran.
Curr Cardiol Rev. 2025;21(2):1-18. doi: 10.2174/011573403X299868240904120621.
Current arrhythmia therapies such as ion channel blockers, catheter ablation, or implantable cardioverter defibrillators have limitations and side effects, and given the proarrhythmic risk associated with conventional, ion channel-targeted anti-arrhythmic drug therapies, a new approach to arrhythmias may be warranted. Measuring and adjusting the level of specific ions that impact heart rhythm can be a simple and low-complication strategy for preventing or treating specific arrhythmias. In addition, new medicines targeting these ions may effectively treat arrhythmias. Numerous studies have shown that intracellular and extracellular zinc concentrations impact the heart's electrical activity. Zinc has been observed to affect cardiac rhythm through a range of mechanisms. These mechanisms encompass the modulation of sodium, calcium, and potassium ion channels, as well as the influence on beta-adrenergic receptors and the enzyme adenylate cyclase. Moreover, zinc can either counteract or induce oxidative stress, hinder calmodulin or the enzyme Ca ()/calmodulin-dependent protein kinase II (CaMKII), regulate cellular ATP levels, affect the processes of aging and autophagy, influence calcium ryanodine receptors, and control cellular inflammation. Additionally, zinc has been implicated in the modulation of circadian rhythm. In all the aforementioned cases, the effect of zinc on heart rhythm is largely influenced by its intracellular and extracellular concentrations. Optimal zinc levels are essential for maintaining a normal heart rhythm, while imbalances-whether deficiencies or excesses-can disrupt electrical activity and contribute to arrhythmias.
当前的心律失常治疗方法，如离子通道阻滞剂、导管消融术或植入式心脏复律除颤器，都存在局限性和副作用。鉴于传统的、以离子通道为靶点的抗心律失常药物治疗存在致心律失常风险，或许有必要采用一种新的心律失常治疗方法。测量和调整影响心律的特定离子水平，可能是预防或治疗特定心律失常的一种简单且并发症少的策略。此外，针对这些离子的新药可能有效治疗心律失常。大量研究表明，细胞内和细胞外锌浓度会影响心脏的电活动。锌已被观察到通过一系列机制影响心脏节律。这些机制包括对钠、钙和钾离子通道的调节，以及对β-肾上腺素能受体和腺苷酸环化酶的影响。此外，锌既可以对抗也可以诱导氧化应激，阻碍钙调蛋白或钙（）/钙调蛋白依赖性蛋白激酶II（CaMKII），调节细胞ATP水平，影响衰老和自噬过程，影响钙释放通道受体，并控制细胞炎症。此外，锌还参与昼夜节律的调节。在上述所有情况下，锌对心律的影响在很大程度上受其细胞内和细胞外浓度的影响。最佳的锌水平对于维持正常心律至关重要，而失衡——无论是缺乏还是过量——都可能扰乱电活动并导致心律失常。
