What does this research mean for the field?

Up-regulation of the inward rectifier K+ current (I_K1) in the heart acts as a substrate for stable and very fast rotors, thereby accelerating and sustaining ventricular tachyarrhythmias. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To test whether cardiac up-regulation of the inward rectifier K+ current (IK1) stabilizes and accelerates reentrant rotors driving ventricular tachycardia and fibrillation.

November 10, 2006The Journal of PhysiologyOpen Access

Up‐regulation of the inward rectifier K+ current (IK1) in the mouse heart accelerates and stabilizes rotors

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Population

Transgenic mice overexpressing Kir 2.1-green fluorescent protein fusion protein in a cardiac-specific…

Comparison

Up-regulation of the inward rectifier K+ current… vs Wild-type (WT) mouse hearts

Design

Preclinical

Authors

SNSami F. NoujaimUniversity of South Florida SPSandeep V. PanditPhoenix Science and Technology (United States)OBOmer BerenfeldElectrophysiology

Discussion

Member takes

Implication

IK1 up-regulation stabilizes rotors in mice; leaves open translation to human VT/VF substrates or therapies.

Key Points

To test whether cardiac up-regulation of the inward rectifier K+ current (IK1) stabilizes and accelerates reentrant rotors driving ventricular tachycardia and fibrillation.
Performed epicardial optical mapping on Langendorff-perfused hearts from transgenic mice overexpressing Kir2.1-GFP and wild-type controls.
Assessed rotor sensitivity to pharmacological IK1 inhibition using 10 µM Ba2+.
Simulated rotor dynamics using a two-dimensional computer model incorporating realistic mouse ionic and action potential parameters with varying IK1 densities.
Transgenic hearts sustained ventricular tachycardia/fibrillation for 350 ± 1181 s with a dominant frequency of 44.6 ± 4.3 Hz, compared to 3 ± 9 s and 26.3 ± 5.2 Hz in wild-type hearts.
Application of 10 µM Ba2+ slowed down and terminated stable, high-frequency reentrant activity in transgenic hearts.
Computational simulations confirmed that doubling IK1 density induced fast, stable rotors (~45 Hz) via increased core outward conductance, shortened core action potential duration, and faster Na+ current recovery.

Structured PICO

Population

Transgenic mice overexpressing Kir 2.1-green fluorescent protein (GFP) fusion protein in a cardiac-specific manner, wild-type mice, and a two-dimensional computer model

Intervention

Up-regulation of the inward rectifier K+ current (IK1) via cardiac-specific overexpression of Kir 2.1

Comparator

Wild-type (WT) mouse hearts

Outcome

Duration and dominant frequency of sustained ventricular tachycardia/fibrillation (VT/VF) rotorssurrogate

Up-regulation of the inward rectifier K+ current (IK1) in the mouse heart provides a substrate for highly stable and fast rotors, accelerating and stabilizing ventricular tachyarrhythmias.

Cite This Study

Noujaim et al. (2006) studied this question.

synapsesocial.com/papers/6a1be90cea84844e355f2acc https://doi.org/10.1113/jphysiol.2006.121475

Topics

Atrial fibrillation Persistent AF management

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Up‐regulation of the inward rectifier K+ current (IK1) in the mouse heart accelerates and stabilizes rotors

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Up‐regulation of the inward rectifier K+ current (IK1) in the mouse heart accelerates and stabilizes rotors

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Topics

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