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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian, James N. Weiss

Circulation October 2015, 132 (16) 1528-1537; DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.016217

Figure 1.
By Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

Hypokalemia-induced VF in adult isolated Langendorff rabbit (A) and rat (B...
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Hypokalemia-induced VF in adult isolated Langendorff rabbit (A) and rat (B) hearts exposed to 2.7 mmol/L [K]_o. Left, Sinus rhythm during normokalemia, as recorded with a pseudo-ECG, bipolar electrograms from the left atrium (LA) and right ventricle (RV), and an epicardial intracellular microelectrode (ME). Middle and Right, Onset of EAD-mediated triggered activity (*) from sinus rhythm during hypokalemia. Arrows in B indicate DADs. DADs indicates delayed afterdepolarizations; EAD, early afterdepolarization; and VF, ventricular fibrillation.
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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian, James N. Weiss

Circulation October 2015, 132 (16) 1528-1537; DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.016217

Figure 2.
By Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

Optical action potential recordings and activation maps during EAD-mediated triggered activity in an isolate...
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Optical action potential recordings and activation maps during EAD-mediated triggered activity in an isolated-perfused rat heart exposed to hypokalemia (2.7 mmol/L [K]). A, Optical voltage fluorescence (F_V) traces from 4 adjacent sites labeled 1 to 4 in B, illustrating 2 runs of EAD-mediated triggered activity (b1–b13) arising spontaneously from sinus rhythm (beats S1 and S6). B, Optical voltage fluorescence snapshots corresponding to the labeled beats in A. C, Isochronal activation maps of a sinus beat (S6) and the subsequent triggered beat (b7) indicating the different sites of origin. EAD indicates early afterdepolarization.
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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian, James N. Weiss

Circulation October 2015, 132 (16) 1528-1537; DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.016217

Figure 3.
By Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

K dependence of hypokalemia-induced VT/VF in isolated rabbit hearts, in the absence and presence of dofetili...
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K dependence of hypokalemia-induced VT/VF in isolated rabbit hearts, in the absence and presence of dofetilide. A, When extracellular K concentration was lowered from the control value of 5.4 mmol/L to 4.0, 3.5, 2.7, 2.0, or 1.0 mmol/L, the incidence of VT/VF within 90 minutes progressively increased to 100% at 2.0 and 1.0 mmol/L. Data show median and 83% CI for the number of hearts indicated in parentheses, in the absence (black circles) or presence (red circles) of 1 μmol/L dofetilide. The percentage of hearts developing VT/VF at 2.7 mmol/L [K] was significantly increased by dofetilide (P=0.03). Curves are fits to a Hill equation in the absence (black curve) and presence of dofetilide (red curve). B, Kaplan–Meier survival curves comparing time to onset of VT/VF, with 83% CI indicated by shading (solid lines, without dofetilide; dashed line, with dofetilide). Rate of VT/VF onset was significantly faster at 1.0 and 2.0 mmol/L [K] than at higher [K] (P=0.0002–0.002), and significantly faster at 2.7 mmol/L [K] in the presence of dofetilide than in its absence (P=0.02). CI indicates confidence interval; VF, ventricular fibrillation; and VT, ventricular tachycardia.
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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian, James N. Weiss

Circulation October 2015, 132 (16) 1528-1537; DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.016217

Figure 4.
By Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

Suppression of hypokalemia-induced VF by CaMKII inhibition or late I_Na blockade. Represe...
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Suppression of hypokalemia-induced VF by CaMKII inhibition or late I_Na blockade. Representative ECG and RV electrograms from isolated rabbit ventricles at the times indicated after reducing [K]_o from 5.4 to 2.0 mmol/L. A, No drug, illustrating the spontaneous transition from sinus rhythm to VT/VF after 10 minutes. B, KN-93 (1 μmol/L), illustrating maintenance of sinus rhythm after 30 minutes. C, Same heart as in B, 3 minutes after replacing KN-93 with KN-92 (1 μmol/L), illustrating spontaneous onset of VT/VF. D, GS-967 (1 μmol/L), illustrating maintenance of sinus rhythm after 30 minutes. E, Same heart as in D, 38 minutes after washing out GS-967, illustrating onset of spontaneous VT/VF. CaMKII indicates Ca-calmodulin kinase II; RV, right ventricle; VF, ventricular fibrillation; and VT, ventricular tachycardia.
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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian, James N. Weiss

Circulation October 2015, 132 (16) 1528-1537; DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.016217

Figure 5.
By Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

Basal (autophosphorylated) tissue CaMKII activity level, expressed as percentage of maximal Ca/CaM-stimulate...
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Basal (autophosphorylated) tissue CaMKII activity level, expressed as percentage of maximal Ca/CaM-stimulated CaMKII activity, in isolated rabbit ventricular tissue arterially perfused with 5.4 mmol/L or 2.7 mmol [K]_o for 30 minutes. Individual data points, median, 95% confidence intervals, and P value are indicated. For 2.7 mmol/L data, open circles indicate hearts in which no VT/VF occurred during hypokalemia (2 hearts), and open squares indicate hearts in which transient (1- to 2-minute episodes in 2 hearts) or sustained VT/VF developed (1 heart) during hypokalemia. CaMKII indicates Ca-calmodulin kinase II; VF, ventricular fibrillation; and VT, ventricular tachycardia.
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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian, James N. Weiss

Circulation October 2015, 132 (16) 1528-1537; DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.016217

Figure 6.
By Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

Suppression of hypokalemia-induced EADs by CaMKII inhibition and late I_Na blockade in is...
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Suppression of hypokalemia-induced EADs by CaMKII inhibition and late I_Na blockade in isolated patch-clamped rabbit ventricular myocytes. Membrane voltage (V_m) traces during pacing at PCL 6 s. Top to bottom traces: A, [K]_o=5.4 mmol/L; 2.7 mmol/L; 2.7 mmol/L+1 μmol/L KN-92; 2.7 mmol/L+1 μmol/L KN-92. B, [K]_o=5.4 mmol/L+AIP; 2.7 mmol/L+AIP (dialyzed for 30 minutes). C, [K]_o=5.4 mmol/L; 2.7 mmol/L; 2.7 mmol/L; 2.7 mmol/L+1 μmol/L GS-967 (bottom). Right panels show superimposed action potentials under the various conditions for A through C. AIP indicates autocamptide-2–related inhibitor peptide; CaMKII, Ca-calmodulin kinase II; EAD, early afterdepolarization; and PCL, pacing cycle length.
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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian, James N. Weiss

Circulation October 2015, 132 (16) 1528-1537; DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.016217

Figure 7.
By Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

Effects of hypokalemia on membrane voltage (V_m), [Ca]_i, and [Na]_i in the ra...
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Effects of hypokalemia on membrane voltage (V_m), [Ca]_i, and [Na]_i in the rabbit ventricular AP model paced at a CL of 1 s. A, V_m at various times corresponding to B, for [K]_o=5.4 mmol/L (blue traces); [K]_o=2.7 mmol/L (red traces); and [K]_o=2.7 mmol/L with CaMKII signaling disabled (green traces). B and C, Corresponding time course of changes in [Ca]_i (B) and [Na]_i (C). [Ca]_i and [Na]_i accelerate rapidly with the onset of EADs, and systolic [Ca]_i then transiently decreases when EADs transition to repolarization failure. D, Time to onset of the first EAD vs level of [K]_o, with normal I_Kr (black) or I_Kr blocked (red) to simulate the effects of dofetilide. CaMKII indicates Ca-calmodulin kinase II; CL, cycle length; and EAD, early afterdepolarization.
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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian, James N. Weiss

Circulation October 2015, 132 (16) 1528-1537; DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.016217

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Table.
By Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

Effects of Simulated Hypokalemia on [Na]_i, Mean [Ca]_i (averaged throughout the cardiac...
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Effects of Simulated Hypokalemia on [Na]_i, Mean [Ca]_i (averaged throughout the cardiac cycle), Late I_Na (as a surrogate index of CaMKII activity), APD (ms), and EAD Development in the Rabbit Ventricular AP Model Under Various Conditions
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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian, James N. Weiss

Circulation October 2015, 132 (16) 1528-1537; DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.016217

Figure 8.
By Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

Schema of positive feedback loops (red and blue arrows) promoting intracellular Na and Ca overload, CaMKII a...
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Schema of positive feedback loops (red and blue arrows) promoting intracellular Na and Ca overload, CaMKII activation, and EADs during hypokalemia. The potentiation of the blue positive feedback loop by class III antiarrhythmic (AA) drugs such as dofetilide is also shown. APD indicates action potential duration; CaMKII, Ca-calmodulin kinase II; EAD, early afterdepolarization; and I_NaK, Na-K pump current.
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Molecular Basis of Hypokalemia-Induced Ventricular FibrillationCLINICAL PERSPECTIVE
Arash Pezhouman, Neha Singh, Zhen Song, Michael Nivala, Anahita Eskandari, Hong Cao, Aneesh Bapat, Christopher Y. Ko, Thao P. Nguyen, Zhilin Qu, Hrayr S. Karagueuzian and James N. Weiss

Circulation. 2015;132:1528-1537, originally published August 12, 2015
https://doi.org/10.1161/CIRCULATIONAHA.115.016217

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