Modulation of Cardiac Potassium Current by Neural Tone and Ischemia

Tomson, Todd T.; Arora, Rishi

doi:10.1016/j.ccep.2016.01.007

Cited by 8 publications

(4 citation statements)

References 69 publications

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“…Parasympathetic effects, on the other hand, caused by the interaction between ACh and muscarinic receptors, generally counterbalance these sympathetic effects and, amongst other effects, result in a slower heart rate, decrease the L-type calcium channel current and activate the acetylcholine-activated potassium current (I K,Ach ) [ 42 ].…”

Section: Cardiac Neuraxismentioning

confidence: 99%

Autonomic modulation of ventricular electrical activity: recent developments and clinical implications

2021

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Purpose This review aimed to provide a complete overview of the current stance and recent developments in antiarrhythmic neuromodulatory interventions, focusing on lifethreatening vetricular arrhythmias. Methods Both preclinical studies and clinical studies were assessed to highlight the gaps in knowledge that remain to be answered and the necessary steps required to properly translate these strategies to the clinical setting. Results Cardiac autonomic imbalance, characterized by chronic sympathoexcitation and parasympathetic withdrawal, destabilizes cardiac electrophysiology and promotes ventricular arrhythmogenesis. Therefore, neuromodulatory interventions that target the sympatho-vagal imbalance have emerged as promising antiarrhythmic strategies. These strategies are aimed at different parts of the cardiac neuraxis and directly or indirectly restore cardiac autonomic tone. These interventions include pharmacological blockade of sympathetic neurotransmitters and neuropeptides, cardiac sympathetic denervation, thoracic epidural anesthesia, and spinal cord and vagal nerve stimulation. Conclusion Neuromodulatory strategies have repeatedly been demonstrated to be highly effective and very promising anti-arrhythmic therapies. Nevertheless, there is still much room to gain in our understanding of neurocardiac physiology, refining the current neuromodulatory strategic options and elucidating the chronic effects of many of these strategic options.

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Section: Cardiac Neuraxismentioning

confidence: 99%

Autonomic modulation of ventricular electrical activity: recent developments and clinical implications

2021

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“…ANS is a major modulator of cardiac electrophysiology and particularly potassium current. 3 Autonomic, cardiovascular, neuronal, psychological factors, and pathological states do affect HRV. Depression and anxiety disorders have low HRV and an increased risk of future cardiovascular disease and mortality, which can be identified by HRV and HRT (heart rate turbulence).…”

Section: Introductionmentioning

confidence: 99%

“…Impaired vagal function and various potassium channels stimulated by sympathetic activity affecting the HRV are possibly the mechanisms linking to brain disorders. 2, 3 HRV is a classical biomarker, an informative indicator of the brain–body integration, pathological states, or concomitant health. 4 By the neurovisceral integration (NVI) model, a reduction in activation of the central autonomic network (CAN) may affect the decreased level of HRV.…”

Section: Introductionmentioning

confidence: 99%

Effect of Fluoxetine and Escitalopram on Heart Rate Variability (HRV) and Serum Potassium Level in Patients of Depression and Anxiety Disorders

Machhi,

Patel,

Pandya

et al. 2023

Journal of Pharmacology and Pharmacotherapeutics

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Background The present study was conducted to generate data regarding the effect of fluoxetine as an anti-depressant and escitalopram as an antianxiety agent on heart rate variability (HRV). There is a scarcity of data regarding the correlation between selective serotonin reuptake inhibitors (SSRIs) and serum potassium levels. Purpose To find out the effect of SSRIs on HRV, and whether it is either dependent or independent of serum potassium level. Methods In this prospective, open-label, observational study, 70 participants were enrolled and divided into two groups, the fluoxetine group ( n = 35) and the escitalopram group ( n = 35) suffering from depression and anxiety, respectively. Parameters, like HRV, serum potassium level, heart rate, respiratory rate, and blood pressure, were measured baseline and after the first, second, and third months of treatment. HRV was calculated by root mean square deviation of successive differences between adjacent RR intervals (RMSSD). ECG (electrocardiogram) was recorded by Physio Pac Digital Polygraph software. All values were expressed as mean ± SD, and statistical analysis was done by using the repeated measure analysis of variance (ANOVA) test with Greenhouse–Geisser correction, post-hoc analysis with Bonferroni correction, and SPSS 20.0 software. Results Among a total of 70 participants, post-hoc tests using the Bonferroni correction showed a statistically significant difference between the HRV of the pretreatment group and after the second, and third month of fluoxetine therapy ( p < .05). In the escitalopram group, the Bonferroni correction showed a significant difference between the HRV of the pretreatment and third-month value ( p < .05). Repeated measure ANOVA with Greenhouse–Geisser correction showed no statistical significance of serum potassium at different time points ( p > .05). There were also no significant changes in heart rate, respiratory rate, and blood pressure at different points of time in both groups. Pearson’s correlation coefficient test for a relationship between HRV and serum potassium was negative at different time points. Conclusion Fluoxetine significantly increased HRV from the pretreatment value to the second and third months of treatment, whereas in the escitalopram group of participants, the third-month value of HRV was increased compared to the first month. The effect of SSRIs on HRV was independent of serum potassium levels at different time points suggesting that the effect of SSRIs on HRV was independent of serum potassium level.

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“…Contractions are caused by electrical conduction/propagation and the mechanical behavior of myocardial cells [ 1 ]. The action potential (AP) of ventricular myocardial cells leads to the contraction of myofilaments through the transmembrane passage of various electrical ions (especially Ca 2+ ions) [ 2 ]. The AP may cause secretion or excretion of these ions, as well as myocardial contractility.…”

Section: Introductionmentioning

confidence: 99%

The effect of myocardial action potential duration on cardiac pumping efficacy: a computational study

Jeong

Lim

2018

BioMed Eng OnLine

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Background and aimsAlthough studies on the relation between arrhythmias and the action potential duration (APD) have been carried out, most of them are based only on electrophysiological factors of the heart and lack experiments that consider cardiac mechanical and electromechanical characteristics. Therefore, we conducted this study to clarify the relevance of the shortening of APD of a cell in relation to the mechanical contraction activity of the heart and the associated risk of arrhythmia.MethodsThe human ventricular model used in this study has two dynamic characteristics: electrophysiological conduction and mechanical contraction. The model simulating electrophysiological characteristics was consisted of lumped parameter circuit that can mimic the phenomenon of ion exchange through the cell membrane of myocyte and consisted of 214,319 tetrahedral finite elements. In contrast, the model simulating mechanical contraction characteristics was constructed to mimic cardiac contraction by means of the crossbridge of a myofilament and consisted of 14,720 hermite-based finite elements to represent a natural 3D curve of the cardiac surface. First, we performed a single cell simulation and the electrophysiological simulation according to the change of the APD by changing the electrical conductivity of the IKs channel. Thus, we confirmed the correlation between APD and intracellular Ca2+ concentration. Then, we compared mechanical response through mechanical simulation using Ca2+ data from electrical simulation.ResultsThe APD and the sum of the intracellular Ca2+ concentrations showed a positive correlation. The shortened APD reduced the conduction wavelength of ventricular cells by shortening the plateau and early repolarization in myocardial cells. The decrease in APD reduced ventricular pumping efficiency by more than 60% as compared with the normal group (normal conditions). This change is caused by the decline of ventricular output owing to reduced ATP consumption during the crossbridge of myofilaments and decreased tension.ConclusionThe shortening of APD owing to increased electrical conductivity of a protein channel on myocardial cells likely decreases the wavelength and the pumping efficiency of the ventricles. Additionally, it may increase tissue sensitivity to ventricular fibrillation, including reentry, and cause symptoms such as dyspnea and dizziness.

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Modulation of Cardiac Potassium Current by Neural Tone and Ischemia

Cited by 8 publications

References 69 publications

Autonomic modulation of ventricular electrical activity: recent developments and clinical implications

Autonomic modulation of ventricular electrical activity: recent developments and clinical implications

Effect of Fluoxetine and Escitalopram on Heart Rate Variability (HRV) and Serum Potassium Level in Patients of Depression and Anxiety Disorders

The effect of myocardial action potential duration on cardiac pumping efficacy: a computational study

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