Cardiac arrhythmias are serious myocardial electrical disturbances that affect the rate and rhythm of heartbeats. Despite the rapidly accumulating data about the pathophysiology and the treatment, new insights are required to improve the overall clinical outcome of patients with cardiac arrhythmias. Three major arrhythmogenic processes can contribute to the pathogenesis of cardiac arrhythmias; 1) enhanced automaticity, 2) afterdepolarization-triggered activity and 3) reentry circuits. The mathematical model of the quantum tunneling of ions is used to investigate these mechanisms from a quantum mechanical perspective. The mathematical model focuses on applying the principle of quantum tunneling to sodium and potassium ions. This implies that these ions have a non-zero probability of passing through the gate, which has an energy that is higher than the kinetic energy of ions. Our mathematical findings indicate that, under pathological conditions, which affect ion channels, the quantum tunneling of sodium and potassium ions is augmented. This augmentation creates a state of hyperexcitability that can explain the enhanced automaticity, after depolarizations that are associated with triggered activity and a reentry circuit. Our mathematical findings stipulate that the augmented and thermally assisted quantum tunneling of sodium and potassium ions can depolarize the membrane potential and trigger spontaneous action potentials, which may explain the automaticity and afterdepolarization. Furthermore, the quantum tunneling of potassium ions during an action potential can provide a new insight regarding the formation of a reentry circuit. Introducing these quantum mechanical aspects may improve our understanding of the pathophysiological mechanisms of cardiac arrhythmias and, thus, contribute to finding more effective anti-arrhythmic drugs.
Citation: Mohammed I. A. Ismail, Abdallah Barjas Qaswal, Mo'ath Bani Ali, Anas Hamdan, Ahmad Alghrabli, Mohamad Harb, Dina Ibrahim, Mohammad Nayel Al-Jbour, Ibrahim Almobaiden, Khadija Alrowwad, Esra'a Jaibat, Mira Alrousan, Mohammad Banifawaz, Mohammed A. M. Aldrini, Aya Daikh, Nour Aldarawish, Ahmad Alabedallat, Ismail M. I. Ismail, Lou'i Al-Husinat. Quantum mechanical aspects of cardiac arrhythmias: A mathematical model and pathophysiological implications[J]. AIMS Biophysics, 2023, 10(3): 401-439. doi: 10.3934/biophy.2023024
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Cardiac arrhythmias are serious myocardial electrical disturbances that affect the rate and rhythm of heartbeats. Despite the rapidly accumulating data about the pathophysiology and the treatment, new insights are required to improve the overall clinical outcome of patients with cardiac arrhythmias. Three major arrhythmogenic processes can contribute to the pathogenesis of cardiac arrhythmias; 1) enhanced automaticity, 2) afterdepolarization-triggered activity and 3) reentry circuits. The mathematical model of the quantum tunneling of ions is used to investigate these mechanisms from a quantum mechanical perspective. The mathematical model focuses on applying the principle of quantum tunneling to sodium and potassium ions. This implies that these ions have a non-zero probability of passing through the gate, which has an energy that is higher than the kinetic energy of ions. Our mathematical findings indicate that, under pathological conditions, which affect ion channels, the quantum tunneling of sodium and potassium ions is augmented. This augmentation creates a state of hyperexcitability that can explain the enhanced automaticity, after depolarizations that are associated with triggered activity and a reentry circuit. Our mathematical findings stipulate that the augmented and thermally assisted quantum tunneling of sodium and potassium ions can depolarize the membrane potential and trigger spontaneous action potentials, which may explain the automaticity and afterdepolarization. Furthermore, the quantum tunneling of potassium ions during an action potential can provide a new insight regarding the formation of a reentry circuit. Introducing these quantum mechanical aspects may improve our understanding of the pathophysiological mechanisms of cardiac arrhythmias and, thus, contribute to finding more effective anti-arrhythmic drugs.
Data-intensive machine learning has become widely used, and as the size of training data increases, distributed methods are becoming increasingly popular. However, the performance of distributed methods is mainly determined by stragglers, i.e., nodes that are slow to respond or are unavailable.
Raviv et al. [11] used coding theory and graph theory to reduce stragglers in distributed synchronous gradient descent. A coding theory framework for straggler mitigation, called gradient coding, was first introduced by Tandon et al. [14]. Gradient coding consists of a system with one master and n worker nodes, where the data are partitioned into k parts, and one or more parts are assigned to each worker. In turn, each worker computes the partial gradients on each given partition, combines the results linearly according to a predefined vector of coefficients, and sends this linear combination back to the primary node. By choosing the coefficients at each node appropriately, it can be guaranteed that the primary node can reconstruct the full gradient even if a machine fails to do its job.
The importance of straggler mitigation is demonstrated in [8,16]. Specifically, it was shown by Tandon et al. [14] that stragglers run up to 5 times slower than the performance of typical workers (8 times in [16]). In [11], for gradient calculations, a cyclic maximum distance separable (MDS) code is used to obtain a better deterministic construction scheme than existing solutions, both in the range of parameters that can be applied and in the complexity of the algorithms involved.
One well-known family of MDS codes is generalized Reed-Solomon (GRS) codes. GRS codes have interesting mathematical structures and many real-world applications, such as mass storage systems, cloud storage systems, and public-key cryptosystems. On the other hand, although more complex than cyclic codes, quasi-cyclic codes satisfy the condition of the Gilbert-Varshamov lower bound at minimum distances, as shown in [6]. Quasi-cyclic codes are also equivalent to linear codes with circulant block generator matrices. This type of matrix has circular blocks of the same size, such as m, which denotes the co-indexes of the associated quasi-cyclic code. From this point of view, one way to generalize quasi-cyclic codes is to let the generator matrix have circular blocks of different sizes. This code is called a generalized quasi-cyclic code with shared indices (m1,m2,…,mk), where m1,m2,…,mk represents the size of the circular block in the generator matrix.
In [10], a generalized quasi-cyclic code without block length limitations is studied. By relaxing the conditions on block length, several new optimal codes with small lengths could be found. In addition, the code decomposition and dimension formulas given by [3,12,13] have been generalized.
In this paper, we describe the construction of generalized quasi-cyclic GRS codes over totally real number fields, as well as their application in exact gradient coding. The construction method is derived by integrating known results from the inverse Galois problem for totally real number fields. Furthermore, methods in [2,4,11,14] will be adapted to generalized quasi-cyclic GRS codes to mitigate stragglers.
Let F be a Galois extension of Q and choose non-zero elements v1,…,vn in F and distinct elements a1,…,an in F. Also, let v=(v1,…,vn) and a=(a1,…,an). For 1≤k≤n, define the GRS codes as follows:
GRSn,k(a,v)={(v1f(a1),…,vnf(an))|f(x)∈F[x]k}, |
where F[x]k is the set of all polynomials over F with degree less than k. The canonical generator of GRSn,k(a,v) is given by the following matrix:
G=(v1v2⋯vj⋯vnv1a1v2a2⋯vjaj⋯vnanv1a21v2a22⋯vja2j⋯vna2n⋮⋮⋱⋮⋱⋮v1ai1v2ai2⋯vjaij⋯vnain⋮⋮⋱⋮⋱⋮v1ak−11v2ak−12⋯vjak−1j⋯vnak−1n) | (2.1) |
Theorem 2.1. [7] Let v∈Fn be a tuple of non-zero elements in F and a∈Fn be a tuple of pairwise distinct elements in F; then,
a) The GRSn,k(a,v) is a [n,k,n−k+1] code, i.e., GRS codes are MDS codes.
b) The dual code of GRSn,k(a,v) is as follows:
GRSn,k(a,v)⊥=GRSn,n−k(a,u), |
where u=(u1,…,un) with
u−1i=vi∏j≠i(ai−aj). |
Proof. (a) See the proof of [7, Theorem 6.3.3]. (b) See the proof of [7, Theorem 6.5.1].
Let ¯F=F∪{∞} and a be an n-tuple of mutually distinct elements of ¯F, and let c be an n-tuple of non-zero elements of F. Also, define
[ai,aj]=ai−aj,[∞,aj]=1[ai,∞]=−1for allai,aj∈F. |
Definition 2.2. ([9]) Let B(a,c) be the k×(n−k) matrix with the following entries:
cj+kci[aj+k,ai],for1≤i≤k,1≤j≤n−k. |
The generalized Cauchy code Ck(a,c) is an [n,k,n−k+1] code defined by the generator matrix (Ik|B(a,c)).
The following proposition shows that the GRS codes are also generalized Cauchy codes.
Proposition 2.3. [9, Proposition C.2] Let a be an n-tuple of mutually distinct elements of ¯F, and let c be an n-tuple of non-zero elements of F. Also, let
ci={bi∏kt=1,t≠i[ai,at],if1≤i≤k;bi∏kt=1[ai,at],ifk+1≤i≤n. |
Then, GRSn,k(a,b)=Ck(a,c).
Let Gal(F/Q) be the Galois group of F over Q and PΓL(2,F) denote the group of semilinear fractional transformations given by
f:¯F⟶¯Fx⟼aγ(x)+bcγ(x)+d, |
where ad−bc≠0 and γ∈Gal(F/Q). Let Sn be the symmetric group on a set of n elements and Per(C)={ξ∈Sn|ξ(C)=C}, where n is the length of the code C. The set Per(C) is called the permutation group of the code C. We have the following theorem that is related to the permutation group of a Cauchy code.
Theorem 2.4. [1, Corollary 2] Let C=Ck(a,y) be a Cauchy code over F, where 2≤k≤n−2 and a=(a1,…,an). Also, let L={a1,…,an}. Then, the map
ω:{f∈PΓL(2,F)|f(L)=L}⟶Per(C)f⟼σ, |
where aσ(i)=f(ai) for i=1,…,n is a surjective group homomorphism.
A number field F is a finite Galois extension of the rational field Q. In this section, we describe a way to construct a number field F with Gal(F/Q)≅⟨σ⟩ for σ∈Sn, where ⟨σ⟩ is a cyclic subgroup generated by σ.
Let σ=σ1σ2⋯σt be a permutation in Sn, where σ1,σ2,…,σt are disjoint cycles. Also, let ⟨σ⟩ be the cyclic group generated by σ. Let l(σj) be the length of the cycle σj, and define a set P={p:pprime and∃j∈{1,…,t}∋p|l(σj)}. Since P is finite, assume that p1<p2<⋯<p|P| are all elements in P. For any j, we have
l(σj)=|P|∏i=1pαiji, | (3.1) |
where αij∈Z≥0. Based on Eq (3.1), we have
ord(σ)=|⟨σ⟩|=|P|∏i=1pmaxj{αij}i, | (3.2) |
where ord(σ) is the order of the permutation σ. Since ⟨σ⟩ contains the element of order pmaxj{αij}i for all i=1,…,|P|, by the structure theorem for finite Abelian groups, we have
⟨σ⟩≅|P|∏i=1Zpmaxj{αij}iZ≅Z∏|P|i=1pmaxj{αij}iZ. | (3.3) |
Let ζp be the primitive p-th root of unity and Q(ζp) be the corresponding cyclotomic extension of Q. The following theorem shows a Galois extension of Q, where its Galois group is isomorphic to ⟨σ⟩. The proof of the theorem is similar to the proof of [5, Theorem 3.1.11]. We write the proof here to give a sense of how to construct the related Galois extension.
Theorem 3.1. There exists a totally real Galois extension K of Q such that Gal(K/Q)≅⟨σ⟩.
Proof. By Eq (3.3), we have
⟨σ⟩≅|P|∏i=1Zpmaxj{αij}iZ≅Z∏|P|i=1pmaxj{αij}iZ. |
Now, choose a prime p such that
p≡1mod2|P|∏i=1pmaxj{αij}i. |
Let ζp be the p-th root of unity. By [5, Theorem C.0.3], Q(ζp) is a Galois extension of Q, with its corresponding Galois group being isomorphic to G=(Z/pZ)×, where (Z/pZ)× is the multiplicative group of Z/pZ−{¯0}. Since p is a prime number, G is a cyclic group. Moreover, we can find a unique subgroup H of G such that
|H|=p−1∏|P|i=1pmaxj{αij}i. |
Let Q(ζp)H be a subset of Q(ζp) which is invariant under the action of H. By the fundamental theorem of Galois theory ([15, Theorem 25]), Q(ζp)H is also a Galois extension of Q, with the corresponding Galois group isomorphic to G/H. Moreover, |G/H|=∏|P|i=1pmaxj{αij}i, and, as a consequence,
G/H≅Z∏|P|i=1pmaxj{αij}iZ≅⟨σ⟩. |
Also, by using a similar argument as in the proof of [5, Theorem 3.1.11], we have that Q(ζp)H is a totally real Galois extension of Q. The following algorithm provides a way to construct Q(ζp)H in the proof of Theorem 3.1. The algorithm is based on Theorem 3.1 and [5, Proposition 3.3.2].
Algorithm 3.2. Suppose that σ∈Sn and G=Gal(Q(ζp)/Q)≅(Z/pZ)×, where p is a prime number such that p≡1mod2⋅ord(σ).
1) Choose H⊆G, where H is the subgroup of G with order p−1ord(σ).
2) Calculate
α=∑λ∈Hλ(ζp). |
3) Find minimal polynomial mα(x) of α over Q.
4) Construct the splitting field F of mα(x) by using Algorithm A.1.
5) Then, F=Q(ζp)H.
In this section, we describe a way to construct an invariant GRS code under a given permutation in Sn. We call this GRS code the GRS generalized quasi-cyclic (GQC) code. Let σ=σ1,σ2,⋯,σt be a permutation in Sn, where σ1,σ2,…,σt are disjoint cycles. Also, let G=⟨σ⟩ be a cyclic group generated by σ.
Theorem 4.1. If σ is a permutation in Sn, then there exists a GQC GRSn,k(¯α,b) over F, with its corresponding permutation being σ for some totally real number field F.
Proof. We can find the number field F and its corresponding minimal polynomial mα(x) with Gal(F/Q)≅⟨σ⟩ by using Algorithm 3.2. Since Gal(F/Q)≅⟨σ⟩, there exists γ∈Gal(F/Q) to be associated with σ∈⟨σ⟩. Let L={α1,…,αn} be the roots of mα(x) and some additional elements from linear combinations of the roots. We can see that γ is a permutation on L, i.e., γ(L)=L. Note that the orbit of L under H can be used to rearrange the elements of L such that
γ(αi)=ασ(i), | (4.1) |
for all i=1,2,…,n. Let ¯α=(α1,α2,…,αn) and b=(b1,b2,…,bn) be an n-tuple of non-zero elements in F. Define a Cauchy code Ck(¯α,c), where c=(c1,c2,…,cn), with
ci={bi∏kt=1,t≠i[αi,αt],if1≤i≤k;bi∏kt=1[αi,αt],ifk+1≤i≤n. | (4.2) |
Then, by Proposition 2.3, Ck(¯α,c) is a GRSn,k(¯α,b) code. Moreover, according to Theorem 2.4 and Eq (4.1), ω(γ)=σ is an element in Per(Ck(¯α,c)).
Consider the following example.
Example 4.2. Let σ=(1,2,3,4)(5,6) in S6. We would like to construct a GRS code of length 6 over a totally real number field that is invariant under the action of σ. We can see that ord(σ)=4 and ⟨σ⟩=Z/4Z. Choose p=17 so that p≡1mod2×4. The corresponding subgroup H of Gal(Q(ζ17)/Q) will have the order equal to 4. Since the unique subgroup of (Z/17Z)× with order 4 is {1,4,13,16}, we have
H={λk|k=1,4,13,16}, |
where λk:ζ17↦ζk17. Then, we have
α=∑λ∈Hλ(ζ17)=ζ17+ζ417+ζ1317+ζ1617. |
From [5, Example 3.3.3], the minimal polynomial of α is as follows:
mα(x)=x4+x3−6x2−x+1. |
The roots of mα(x) given by
r1=14(−1−√17−√34+√17),r2=14(−1−√17+√34+√17), |
r3=14(−1+√17−√34−√17).,r4=14(−1+√17+√34−√17). |
Let γ be a map such that
r1↦r2,r2↦r3,r3↦r4,r4↦r1. |
We can see that ⟨γ⟩=Gal(Q(ζ17)H/Q)≅Z/4Z.
Choose L={α1,…,α6}, where αi=ri for i=1,2,3,4,α5=r1+r3, and α6=r2+r4. We can check that
γ(αi)=ασ(i), |
for all i=1,…,6. Take ¯α=(α1,…,α6), any n-tuple of non-zero elements b (from the set of linear combinations of roots of mα(x)), and c=(c1,…,c6), where ci is as in Eq 4.2. We have that Ck(¯α,c) is a GQC GRS code with corresponding permutation σ.
In Section 4, we described the construction of GRS code, which is invariant under the action of a given permutation in Sn. Moreover, the alphabet for the corresponding codes is a totally real number field, not a complex number field. This feature can be useful for bandwidth reduction in exact gradient coding schemes.
Algorithm 1 describes the process of gradient coding. The algorithm is a slight modification of [11, Algorithm 1].
Algorithm 1 Gradient coding |
Input:
Data S={zi=(xi,yi)}mi=1, number of iterations t>0, learning rate {η}tr=1, straggler tolerance parameter {sr}tr=1, a matrix B∈Cn×n, a function Λ:P(n)→Cn, a vector of non-zero elements ¯β=(β1,…,βn)∈Cn Initialize: w(1)←(0,0,…,0) Partition S=⋃ni=1Si and send {Sj|j∈supp(bi)} to Wi for every i∈[n] for r=1 to t do M broadcasts w(r) to all nodes Each Wj sends ∑i∈supp(bj)bj,i∇LSi(w(r))βi to M M waits until at least n−sr nodes have responded M computes vr=Λ(Kr)⋅C, where the i-th row of C is 1n times the response from Wi if it has responded, and 0 otherwise; also, Kr is the set of non-stragglers in the current iteration r M updates w(r+1)←w(r)−ηrvr end for return 1t∑tr=1w(r+1) |
Algorithm 1 works in the following way. In order to execute the gradient descent process, the master node M distributes a particular partition of the training set S to all worker nodes Wj, where j=1,…,n. In the r-th iteration of the gradient descent process, the master M broadcasts the parameter w(r) to all worker nodes. Using the received parameter w(r), the worker node Wj calculates the partial gradient ∇LSi(w(r)) and sends its linear combination ∑i∈supp(bj)bj,i∇LSi(w(r))βi to M. The linear combination is chosen from the entries bj,i of a particular matrix B. In this work, B is constructed by using GRS codes which are invariant under the action of a particular permutation. After M has received the linear combinations of partial gradients from some number of worker nodes, M updates the parameter w by using the decoding vector Λ(Kr),w(r), and some other additional vectors (mentioned in the algorithm). Note that we will see later that the decoding vector Λ(Kr) can be computed by using Algorithm 2[11, Algorithm 2].
Definition 5.1. A matrix B∈Cn×n and a function Λ:P(n)→Cn satisfy the exact computation (EC) condition with respect to ¯β∈Cn, where ¯β is an n-tuple of non-zero elements in Cn if, for all K⊆[n] such that |K|≥maxr∈[t]sr, we have that Λ(K)⋅B=¯β.
Note that Definition 5.1 is a slight modification of [11, Definition 2]. Let ¯β=(β1,…,βn) be an n-tuple of non-zero elements of Cn and
N¯β(w)=1n(∇LS1(w)β1∇LS2(w)β2⋮∇LSn(w)βn). |
Lemma 5.2. If Λ and B satisfy the EC condition with respect to ¯β, then, for all r∈[t], we have that vr=∇LS(w(r)).
Proof. Given r∈[t], let B′ be the matrix whose i-th row b′i equals to bi if i∈Kr, and 0 otherwise. The matrix C in Algorithm 1 can be written as C=B′⋅N¯β(w(r)). Since supp(Λ(Kr))⊆Kr, we have that Λ(Kr)⋅B′=Λ(Kr)⋅B. Therefore, we have
vr=Λ(Kr)⋅C=Λ(Kr)⋅B⋅Nβ(w(r))=β⋅Nβ(w(r))=1n∑ni=1∇LSi(w(r))=1n∑ni=11m/n∑z∈Si∇l(w(r),z)=1m∑z∈S∇l(w(r),z)=∇LS(w(r)). |
For a given n and s, let C=GRSn,n−s(¯α,¯β) GQC code over a number field F with corresponding permutation π of order n. Clearly, the vector ¯β is in C. Moreover, by [11, Lemma 8], there exists a codeword c1 in C whose support is {1,2,…,s+1}. Let ci=πi−1(c1) for i=2,…,n and B=(cT1,cT2,…,cTn).
Theorem 5.3. The matrix B satisfies the following properties:
a) Each row of B is a codeword in σ(C), where σ is a permutation such that
σ−1=(123⋯i⋯nnπn−1(n)πn−2(n)⋯πn−(i−1)(n)⋯π(n)). | (5.1) |
b) wH(b)=s+1 for each row b in B.
c) The column span of B is the code C.
d) Every set of n−s rows of B are linearly independent over F.
Proof. (a) Let c1=(c1,…,cn). Notice that the i-th row of B is as follows:
(ci,cπn−1(i),cπn−2(i),…,cπ(i)). |
Since ord(π)=n, the i-th row of B is a permutation of c1 for all i=1,…,n. Moreover, by considering the last row of B, we can see that all rows of B constitute a codeword in σ(C), where σ is the permutation as in Eq (5.1).
(b) By part (a), we have that the Hamming weight of every row of B is $ s+1.
(c) Let σ=(1,2,…,n) be a cyclic permutation and G1 be a cyclic group generated by σ. Also, let G2 be a cyclic group generated by π. Define ¯S1=span(G1c1) and ¯S2=span(G2c1), where Gc1={λ(c1)|λ∈G}. Since ord(σ)=ord(π)=n, we have that G1≅G2 by the following group isomorphism:
τ:G1→G2σi↦πi. |
Define the following map:
¯τ:¯S1→¯S2∑ni=1αiσi(c1)↦∑ni=1αiπi(c1). |
The map ¯τ is a linear map. Since it is induced by τ,¯τ is a bijective map. So, ¯S1≅¯S2. By [11, Lemma 12 B3], ¯S1=C. Since ¯S2⊆C and dim¯S2=n−s, we have that ¯S2=C.
(d) Similar to [11, Lemma 12 B4].
Let G be the canonical generator for the C=GRSn,n−s(¯α,¯β) GQC code, as in Eq (2.1). By Theorem 2.1(b), the canonical generator for the dual code C⊥ is G⊥=G⋅D, where D=diag(u1,…,un), with
ui=1β2i∏j≠i(αi−αj) |
for all i=1,…,n. Using this setting, Algorithm 2[11, Algorithm 2] can be used to compute the decoding vector a(K).
The authors declare they have not used Artificial Intelligence (AI) tools in the creation of this article.
This research was funded by Hibah PPMI KK Aljabar Institut Teknologi Bandung 2023.
The authors declare no conflict of interest.
The following algorithm provides a way to construct the unique splitting field of a given polynomial f(x) in Q[x].
Algorithm A.1. Given a polynomial f(x) in Q[x], we will construct the splitting field L of f(x) based on the construction of a chain of number fields:
K0=Q⊂K1⊂K2⊂⋯⊂Ks−1⊂Ks=L |
such that Ki is an extension of Ki−1 containing a new root of f(x).
1) Factorize f(x) over Ki into irreducible factors f1(x)f2(x)⋯ft(x).
2) Choose any non linear irreducible factor g(x)=fj(x) for some j∈{1,…,t}.
3) Construct the field extension Ki+1=Ki[x]⟨g(x)⟩.
4) Repeat the process for Ki+1 until f(x) completely factors.
The following algorithm can be used to compute the decoding vector in the exact gradient coding scheme [11, Algorithm 2].
Algorithm 2 Computing decoding vector Λ(K) |
Data: any vector x′∈Cn such that x′B=β
Input: A set K⊆[n] of n−s non-stragglers Output: a vector Λ(K) such that supp(Λ(K))⊆K and Λ(K)B=β find f∈Cs such that fGKc=−x′KcD−1Kc y←fGD return Λ(K)←y+x′ |
[1] |
Huikuri HV, Castellanos A, Myerburg RJ (2001) Sudden death due to cardiac arrhythmias. New Engl J Med 345: 1473-1482. https://doi.org/10.1056/NEJMra000650 ![]() |
[2] |
Srinivasan NT, Schilling RJ (2018) Sudden cardiac death and arrhythmias. Arrhyth Electrophysi Rev 7: 111. https://doi.org/10.15420/aer.2018:15:2 ![]() |
[3] |
John RM, Tedrow UB, Koplan BA, et al. (2012) Ventricular arrhythmias and sudden cardiac death. Lancet 380: 1520-1529. https://doi.org/10.1016/S0140-6736(12)61413-5 ![]() |
[4] |
Janse MJ, Wit AL (1989) Electrophysiological mechanisms of ventricular arrhythmias resulting from myocardial ischemia and infarction. Physiol Rev 69: 1049-1169. https://doi.org/10.1152/physrev.1989.69.4.1049 ![]() |
[5] |
Peretto G, Sala S, Rizzo S, et al. (2019) Arrhythmias in myocarditis: state of the art. Heart Rhythm 16: 793-801. https://doi.org/10.1016/j.hrthm.2018.11.024 ![]() |
[6] |
Kumar S, Stevenson WG, John RM (2015) Arrhythmias in dilated cardiomyopathy. Card Electrophy Clin 7: 221-233. https://doi.org/10.1016/j.hrthm.2018.11.024 ![]() |
[7] |
Tisdale JE, Chung MK, Campbell KB, et al. (2020) Drug-induced arrhythmias: a scientific statement from the American Heart Association. Circulation 142: e214-233. https://doi.org/10.1161/CIR.0000000000000905 ![]() |
[8] |
Behere SP, Weindling SN (2015) Inherited arrhythmias: The cardiac channelopathies. Ann Pediat Cardiol 8: 210. https://doi.org/10.4103/0974-2069.164695 ![]() |
[9] |
FISCH C (1973) Relation of electrolyte disturbances to cardiac arrhythmias. Circulation 47: 408-419. https://doi.org/10.1161/01.CIR.47.2.408 ![]() |
[10] |
Tse G (2016) Mechanisms of cardiac arrhythmias. J Arrhythm 32: 75-81. https://doi.org/10.1016/j.joa.2015.11.003 ![]() |
[11] |
Antzelevitch C, Burashnikov A (2011) Overview of basic mechanisms of cardiac arrhythmia. Card Electrophy Clin 3: 23-45. https://doi.org/10.1016/j.ccep.2010.10.012 ![]() |
[12] |
Marbán E (2002) Cardiac channelopathies. Nature 415: 213-218. https://doi.org/10.1038/415213a ![]() |
[13] |
Franz MR, Cima R, Wang D, et al. (1992) Electrophysiological effects of myocardial stretch and mechanical determinants of stretch-activated arrhythmias. Circulation 86: 968-978. https://doi.org/10.1161/01.CIR.86.3.968 ![]() |
[14] | Morand J, Arnaud C, Pepin JL, et al. (2018) Chronic intermittent hypoxia promotes myocardial ischemia-related ventricular arrhythmias and sudden cardiac death. Sci Rep 8: 1-8. https://doi.org/10.1038/s41598-018-21064-y |
[15] |
Orchard CH, Cingolani HE (1994) Acidosis and arrhythmias in cardiac muscle. Card Res 28: 1312-1319. https://doi.org/10.1093/cvr/28.9.1312 ![]() |
[16] |
Morris CE (2011) Voltage-gated channel mechanosensitivity: fact or friction?. Front Physiol 2: 25. https://doi.org/10.3389/fphys.2011.00025 ![]() |
[17] | Dehghani-Samani A, Madreseh-Ghahfarokhi S, Dehghani-Samani A (2019) Mutations of voltage-gated ionic channels and risk of severe cardiac arrhythmias. Acta Cardiol Sin 35: 99. https://doi.org/10.6515%2FACS.201903_35(2).20181028A |
[18] |
Li Q, Huang H, Liu G, et al. (2009) Gain-of-function mutation of Nav1. 5 in atrial fibrillation enhances cellular excitability and lowers the threshold for action potential firing. Biochem Biophys Res Commun 380: 132-137. https://doi.org/10.1016/j.bbrc.2009.01.052 ![]() |
[19] | Moskalenko A (2014) Cardiac Arrhythmias Mechanisms, Pathophysiology, and Treatment: 1-162. https://doi.org/10.5772/57008 |
[20] | Cardiac Arrhythmia Suppression Trial (CAST) Investigators.Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med (1989) 321: 406-412. https://doi.org/10.1056/nejm198908103210629 |
[21] |
Brooks MM, Gorkin L, Schron EB, et al. (1994) Moricizine and quality of life in the Cardiac Arrhythmia Suppression Trial II (CAST II). Control Clin Trials 15: 437-449. https://doi.org/10.1016/0197-2456(94)90002-7 ![]() |
[22] |
Kurian TK, Efimov IR (2010) Mechanisms of fibrillation: Neurogenic or myogenic? reentrant or focal? multiple or single?: Still puzzling after 160 years of inquiry. J Card Electrophysiol 21: 1274. https://doi.org/10.1111%2Fj.1540-8167.2010.01820.x ![]() |
[23] |
Calvillo L, Redaelli V, Ludwig N, et al. (2022) Quantum biology research meets pathophysiology and therapeutic mechanisms: a biomedical perspective. Quantum Rep 4: 148-172. https://www.mdpi.com/2624-960X/4/2/11 ![]() |
[24] |
Kim Y, Bertagna F, D'souza EM, et al. (2021) Quantum biology: An update and perspective. Quantum Rep 3: 80-126. https://www.mdpi.com/2624-960X/3/1/6 ![]() |
[25] |
Cao J, Cogdell RJ, Coker DF, et al. (2020) Quantum biology revisited. Sci Adv 6: eaaz4888. https://doi.org/10.1126/sciadv.aaz4888 ![]() |
[26] |
Slocombe L, Sacchi M, Al-Khalili (2022) An open quantum systems approach to proton tunnelling in DNA. Commun Phys 5: 109. https://doi.org/10.1038/s42005-022-00881-8 ![]() |
[27] |
Sutcliffe MJ, Scrutton NS (2002) A new conceptual framework for enzyme catalysis: Hydrogen tunneling coupled to enzyme dynamics in flavoprotein and quinoprotein enzymes. Eur J Biochem 269: 3096-3102. https://doi.org/10.1046/j.1432-1033.2002.03020.x ![]() |
[28] |
Qaswal AB (2019) Quantum tunneling of ions through the closed voltage-gated channels of the biological membrane: A mathematical model and implications. Quantum Rep 1: 219-225. https://www.mdpi.com/2624-960X/1/2/19 ![]() |
[29] | Miller DA (2008). Quantum mechanics for scientists and engineers. Cambridge University Press |
[30] |
Aryal P, Sansom MS, Tucker SJ (2015) Hydrophobic gating in ion channels. J Mol Biol 427: 121-130. https://doi.org/10.1016/j.jmb.2014.07.030 ![]() |
[31] |
Oelstrom K, Goldschen-Ohm MP, Holmgren M, et al. (2014) Evolutionarily conserved intracellular gate of voltage-dependent sodium channels. Nat Commun 5: 3420. https://doi.org/10.1038/ncomms4420 ![]() |
[32] |
Jensen MØ, Borhani DW, Lindorff-Larsen K, et al. (2010) Principles of conduction and hydrophobic gating in K+ channels. Proceedings of the National Academy of Sciences 107: 5833-5838. https://doi.org/10.1073/pnas.0911691107 ![]() |
[33] |
Trick JL, Aryal P, Tucker SJ, et al. (2015) Molecular simulation studies of hydrophobic gating in nanopores and ion channels. Biochem Society Transact 43: 146-150. https://doi.org/10.1042/BST20140256 ![]() |
[34] |
Rao S, Klesse G, Lynch CI, et al. (2021) Molecular simulations of hydrophobic gating of pentameric ligand gated ion channels: insights into water and ions. J Phys Chem B 125: 981-994. https://doi.org/10.1021/acs.jpcb.0c09285 ![]() |
[35] |
Chandra AK (1974). |
[36] |
Miyazaki T (2004). |
[37] | Serway RA, Moses CJ, Moyer CA (2004). Modern physics |
[38] |
Eckart C (1930) The penetration of a potential barrier by electrons. Phys Rev 35: 1303. https://doi.org/10.1103/PhysRev.35.1303 ![]() |
[39] |
Zhu F, Hummer G (2012) Drying transition in the hydrophobic gate of the GLIC channel blocks ion conduction. Biophys J 103: 219-227. http://dx.doi.org/10.1016/j.bpj.2012.06.003 ![]() |
[40] |
Rao S, Lynch CI, Klesse G, et al. (2018) Water and hydrophobic gates in ion channels and nanopores. Faraday Discuss 209: 231-247. https://doi.org/10.1039/C8FD00013A ![]() |
[41] |
Neale C, Chakrabarti N, Pomorski P, et al. (2015) Hydrophobic gating of ion permeation in magnesium channel CorA. PLoS Comput Biol 11: e1004303. https://doi.org/10.1371/journal.pcbi.1004303 ![]() |
[42] |
Khavrutskii IV, Gorfe AA, Lu B, et al. (2009) Free energy for the permeation of Na+ and Cl− ions and their ion-pair through a zwitterionic dimyristoyl phosphatidylcholine lipid bilayer by umbrella integration with harmonic fourier beads. J Am Chem Society 131: 1706-1716. https://doi.org/10.1021/ja8081704 ![]() |
[43] |
Vorobyov I, Olson TE, Kim JH, et al. (2014) Ion-induced defect permeation of lipid membranes. Biophys J 106: 586-597. http://dx.doi.org/10.1016/j.bpj.2013.12.027 ![]() |
[44] |
Leontiadou H, Mark AE, Marrink SJ (2007) Ion transport across transmembrane pores. Biophys J 92: 4209-4215. http://dx.doi.org/10.1529/biophysj.106.101295 ![]() |
[45] |
Zhang HY, Xu Q, Wang YK, et al. (2016) Passive transmembrane permeation mechanisms of monovalent ions explored by molecular dynamics simulations. J Chem Theory Comput 12: 4959-4969. https://doi.org/10.1021/acs.jctc.6b00695 ![]() |
[46] |
Chen F, Hihath J, Huang Z, et al. (2007) Measurement of single-molecule conductance. Annu Rev Phys Chem 58: 535-564. https://doi.org/10.1146/annurev.physchem.58.032806.104523 ![]() |
[47] |
Qaswal AB (2020) Quantum electrochemical equilibrium: Quantum version of the Goldman–Hodgkin–Katz equation. Quantum Rep 2: 266-277. https://www.mdpi.com/2624-960X/2/2/17 ![]() |
[48] |
Qaswal AB (2021) The role of quantum tunneling of ions in the pathogenesis of the cardiac arrhythmias due to channelopathies, ischemia, and mechanical stretch. Biophysics 66: 637-641. https://doi.org/10.1134/S0006350921040072 ![]() |
[49] |
Ababneh O, Qaswal AB, Alelaumi A, et al. (2021) Proton quantum tunneling: Influence and relevance to acidosis-induced cardiac arrhythmias/cardiac arrest. Pathophysiology 28: 400-436. https://www.mdpi.com/1873-149X/28/3/27 ![]() |
[50] |
Zhang XC, Yang H, Liu Z, et al. (2018) Thermodynamics of voltage-gated ion channels. Biophys Rep 4: 300-319. https://doi.org/10.1016/j.celrep.2021.109931 ![]() |
[51] |
Summhammer J, Salari V, Bernroider G (2012) A quantum-mechanical description of ion motion within the confining potentials of voltage-gated ion channels. J Integr Neurosci 11: 123-135. https://doi.org/10.1142/S0219635212500094 ![]() |
[52] |
Summhammer J, Sulyok G, Bernroider G (2018) Quantum dynamics and non-local effects behind ion transition states during permeation in membrane channel proteins. Entropy 20: 558. https://doi.org/10.1142/S0219635212500094 ![]() |
[53] |
Summhammer J, Sulyok G, Bernroider G (2020) Quantum mechanical coherence of K+ ion wave packets increases conduction in the KcsA ion channel. Appl Sci 10: 4250. https://www.mdpi.com/2076-3417/10/12/4250 ![]() |
[54] |
Wang K, Wang S, Yang L, et al. (2021) THz trapped ion model and THz spectroscopy detection of potassium channels. Nano Res 15: 3825-3833. https://doi.org/10.1007/s12274-021-3965-z ![]() |
[55] |
Karandashev K, Xu ZH, Meuwly M, et al. (2017) Kinetic isotope effects and how to describe them. Struct Dynam 4: 061501. https://doi.org/10.1063/1.4996339 ![]() |
[56] |
Sen A, Kohen A (2010) Enzymatic tunneling and kinetic isotope effects: chemistry at the crossroads. J Phys Org Chem 23: 613-619. https://doi.org/10.1002/poc.1633 ![]() |
[57] |
Eckhardt AK, Gerbig D, Schreiner PR (2018) Heavy atom secondary kinetic isotope effect on H-tunneling. J Phys Chem A 122: 1488-1495. https://doi.org/10.1021/acs.jpca.7b12118 ![]() |
[58] |
Nappi P, Miceli F, Soldovieri MV, et al. (2020) Epileptic channelopathies caused by neuronal Kv7 (KCNQ) channel dysfunction. Pflüg Arch-Eur J Phy 472: 881-898. https://doi.org/10.1007/s00424-020-02404-2 ![]() |
[59] | Niday Z, Tzingounis AV (2018) Potassium channel gain of function in epilepsy: an unresolved paradox. Neurosci 24: 368-380. https://doi.org/10.1177/1073858418763752 |
[60] |
Miceli F, Soldovieri MV, Ambrosino P, et al. (2015) Early-onset epileptic encephalopathy caused by gain-of-function mutations in the voltage sensor of Kv7. 2 and Kv7. 3 potassium channel subunits. J Neurosci 35: 3782-3793. https://doi.org/10.1523/JNEUROSCI.4423-14.2015 ![]() |
[61] |
Du W, Bautista JF, Yang H, et al. (2005) Calcium-sensitive potassium channelopathy in human epilepsy and paroxysmal movement disorder. Nat Genet 37: 733-738. https://doi.org/10.1038/ng1585 ![]() |
[62] |
Robinson RB, Siegelbaum SA (2003) Hyperpolarization-activated cation currents: from molecules to physiological function. Annu Rev Physiol 65: 453-480. https://doi.org/10.1146/annurev.physiol.65.092101.142734 ![]() |