Cardiac Ion Channels

Grant, Augustus O.

doi:10.1161/circep.108.789081

Cited by 359 publications

(309 citation statements)

References 49 publications

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“…The ability of the heart to beat relies on the conversion of electrical to mechanical energy (1). The electrical basis for heart beats are action potentials that start in the specialized pacemaker cells of the heart, and are then transmitted to the atrial and ventricular heart muscle cells, cardiac myocytes, via the passage of ions between cells through gap junctions.…”

Section: Action Potentials Drive Heart Beatmentioning

confidence: 99%

“…During cardiac action potentials, there is a flux of sodium (Na + ) into the cell, along with an inward flux of calcium (Ca + ), that leads to the depolarization, followed by outward potassium (K + ) currents that repolarize the cell (1,(8)(9)(10)(11)). …”

Section: Action Potentials Drive Heart Beatmentioning

confidence: 99%

“…An action potential is divided into several phases (1,(9)(10)(11)(12). In phase 4, the resting phase, the membrane potential of a ventricular cardiomyocyte is about −90 mV because, like most cells, ventricular cardiomyocytes have a more negative charge inside than outside of the cell.…”

Section: Action Potentials Drive Heart Beatmentioning

confidence: 99%

“…Voltage-gated channels are composed of alpha pore-forming subunits and accessory subunits (1,15). The pore-forming alpha subunits contain multiple t r a n s m e m b r a n e d o m a i n s .…”

Section: Action Potentials Drive Heart Beatmentioning

confidence: 99%

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RNAs that make a heart beat

Mitra

Coller²

2016

Ann. Transl. Med.

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An increase in stress-associated microRNAs has been observed in the heart after an induced myocardial infarction. Liu and colleagues now demonstrate that one of these stress-associated microRNAs, miR-223-3p, can regulate a component of the voltage-gated channel that mediates rapid outward efflux of potassium during an action potential. Aberrations in the potassium current have been associated with ventricular arrhythmia and heart disease. Strikingly, introducing a small RNA antagonist directed against miR-223-3p into rat hearts, while also inducing a myocardial infarction, resulted in a reduction in arrhythmias. We place these studies in the larger context of the field and discuss the potential of anti-miR-223-3p molecules as new therapeutics for myocardial infarction.

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Section: Action Potentials Drive Heart Beatmentioning

confidence: 99%

Section: Action Potentials Drive Heart Beatmentioning

confidence: 99%

Section: Action Potentials Drive Heart Beatmentioning

confidence: 99%

Section: Action Potentials Drive Heart Beatmentioning

confidence: 99%

See 2 more Smart Citations

RNAs that make a heart beat

Mitra

Coller²

2016

Ann. Transl. Med.

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“…4 The activity of Na + channels has 3 modes: transient mode, burst mode, and late-scattered mode. 5 The transient mode is responsible for the peak Na + current (I Na ) during phase 0 and lasts for about 1 ms. 5,6 After the peak I Na , Na + channels quickly become inactivated, resulting in the burst and late-scattered modes responsible for a sustained current component that lasts up to 100 ms during the plateau phase of action potential and is referred to as ''late I Na '' (Figure 1).…”

Section: Biology Of the Sodium Channelsmentioning

confidence: 99%

Ranolazine in Cardiac Arrhythmia

Saad

Mahmoud

Elgendy

et al. 2015

Clinical Cardiology

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Ranolazine utilization in the management of refractory angina has been established by multiple randomized clinical studies. However, there is growing evidence showing an evolving role in the field of cardiac arrhythmias. Multiple experimental and clinical studies have evaluated the role of ranolazine in prevention and management of atrial fibrillation, with ongoing studies on its role in ventricular arrhythmias. In this review, we will discuss the pharmacological, experimental, and clinical evidence behind ranolazine use in the management of various cardiac arrhythmias.

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Pathologic U Waves Secondary to Severe Hypophosphatemia During Refeeding Syndrome

Weatherall

Jardine

2021

JAMA Intern Med

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A patient in their early 20s was admitted to the hospital's acute medical unit complaining of palpitations and weakness. During the previous 3 months, the patient had experienced depression and suicidal ideations. Four days prior to admission, the patient had stopped eating and drinking but had eaten a banana on the way to the hospital. Initial observations of the patient were: weight, 62 kg (7 kg less than baseline); body mass index (calculated as weight in kilograms divided by height in meters squared), 20; heart rate, 110 beats/ min; blood pressure, 122/66 mm Hg; jugular venous pressure, 0 cm H 2 O; respiratory rate, 18 breaths/min; and oxygen saturation, 99%. An electrocardiogram (ECG) performed on admission demonstrated sinus tachycardia with inverted T waves and pathologic U waves (upward deflection >2 mm immediately after the T wave), most prominent in V 2 through V 4 (Figure , A).

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Cardiac Ion Channels

Cited by 359 publications

References 49 publications

RNAs that make a heart beat

RNAs that make a heart beat

Ranolazine in Cardiac Arrhythmia

Pathologic U Waves Secondary to Severe Hypophosphatemia During Refeeding Syndrome

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