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Diagnosing Paroxysmal Atrial Fibrillation: Are Biomarkers the Solution to This Elusive Arrhythmia?

Howlett PJ, Hatch FS, Alexeenko V, Jabr RI, Leatham EW, Fry CH - Biomed Res Int (2015)

Bottom Line: Atrial fibrillation (AF) is the commonest sustained arrhythmia globally and results in significantly increased morbidity and mortality including a fivefold risk of stroke.Despite these adverse outcomes there have been relatively few diagnostic advances in the field since the introduction of the Holter monitor in 1949.This review aims to establish the available evidence for electrophysiological, molecular, and morphological biomarkers to improve the detection of PAF with reference to the underlying mechanisms for the condition.

View Article: PubMed Central - PubMed

Affiliation: School of Biosciences and Medicine, The University of Surrey, Guildford GU2 7XH, UK.

ABSTRACT
Atrial fibrillation (AF) is the commonest sustained arrhythmia globally and results in significantly increased morbidity and mortality including a fivefold risk of stroke. Paroxysmal atrial fibrillation (PAF) constitutes approximately half of all AF cases and is thought to represent an early stage of the disease. This intermittent form of atrial arrhythmia can be a challenge to identify and as a result many affected individuals are not prescribed appropriate antithrombotic therapy and hence are at risk of stroke and thromboembolism. Despite these adverse outcomes there have been relatively few diagnostic advances in the field since the introduction of the Holter monitor in 1949. This review aims to establish the available evidence for electrophysiological, molecular, and morphological biomarkers to improve the detection of PAF with reference to the underlying mechanisms for the condition.

No MeSH data available.


Related in: MedlinePlus

Illustrative diagram of a typical human left atrial AP with associated currents shown above (a). Electrical remodeling can result in abnormal APs (b). ICaL reactivation (blue) can cause early-after depolarization (EAD) that may result in repetitive EAD. Alternatively spontaneous ryanodine receptor (RYR) release or Na+/Ca2+ exchanger activation (NCX) (red) would result in delayed-after depolarization (DAD) (unpublished).
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fig2: Illustrative diagram of a typical human left atrial AP with associated currents shown above (a). Electrical remodeling can result in abnormal APs (b). ICaL reactivation (blue) can cause early-after depolarization (EAD) that may result in repetitive EAD. Alternatively spontaneous ryanodine receptor (RYR) release or Na+/Ca2+ exchanger activation (NCX) (red) would result in delayed-after depolarization (DAD) (unpublished).

Mentions: The cardiac action potential (AP) is a key determinant of cardiac electrical activity and results from transmembrane ion fluxes through ion channels and transporters. A schematic representation of a human atrial action potential and the principal currents involved is shown in Figure 2(a). The resting potential is maintained at about −80 mV via K+ equilibrium potential. Upon activation, rapid depolarization occurs by a large inward Na+ current (INa) and an inward Ca2+ current via L-type Ca2+ channels (ICaL) resulting in the plateau phase. As the Ca2+ current declines the AP repolarizes to the resting potential.


Diagnosing Paroxysmal Atrial Fibrillation: Are Biomarkers the Solution to This Elusive Arrhythmia?

Howlett PJ, Hatch FS, Alexeenko V, Jabr RI, Leatham EW, Fry CH - Biomed Res Int (2015)

Illustrative diagram of a typical human left atrial AP with associated currents shown above (a). Electrical remodeling can result in abnormal APs (b). ICaL reactivation (blue) can cause early-after depolarization (EAD) that may result in repetitive EAD. Alternatively spontaneous ryanodine receptor (RYR) release or Na+/Ca2+ exchanger activation (NCX) (red) would result in delayed-after depolarization (DAD) (unpublished).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4502272&req=5

fig2: Illustrative diagram of a typical human left atrial AP with associated currents shown above (a). Electrical remodeling can result in abnormal APs (b). ICaL reactivation (blue) can cause early-after depolarization (EAD) that may result in repetitive EAD. Alternatively spontaneous ryanodine receptor (RYR) release or Na+/Ca2+ exchanger activation (NCX) (red) would result in delayed-after depolarization (DAD) (unpublished).
Mentions: The cardiac action potential (AP) is a key determinant of cardiac electrical activity and results from transmembrane ion fluxes through ion channels and transporters. A schematic representation of a human atrial action potential and the principal currents involved is shown in Figure 2(a). The resting potential is maintained at about −80 mV via K+ equilibrium potential. Upon activation, rapid depolarization occurs by a large inward Na+ current (INa) and an inward Ca2+ current via L-type Ca2+ channels (ICaL) resulting in the plateau phase. As the Ca2+ current declines the AP repolarizes to the resting potential.

Bottom Line: Atrial fibrillation (AF) is the commonest sustained arrhythmia globally and results in significantly increased morbidity and mortality including a fivefold risk of stroke.Despite these adverse outcomes there have been relatively few diagnostic advances in the field since the introduction of the Holter monitor in 1949.This review aims to establish the available evidence for electrophysiological, molecular, and morphological biomarkers to improve the detection of PAF with reference to the underlying mechanisms for the condition.

View Article: PubMed Central - PubMed

Affiliation: School of Biosciences and Medicine, The University of Surrey, Guildford GU2 7XH, UK.

ABSTRACT
Atrial fibrillation (AF) is the commonest sustained arrhythmia globally and results in significantly increased morbidity and mortality including a fivefold risk of stroke. Paroxysmal atrial fibrillation (PAF) constitutes approximately half of all AF cases and is thought to represent an early stage of the disease. This intermittent form of atrial arrhythmia can be a challenge to identify and as a result many affected individuals are not prescribed appropriate antithrombotic therapy and hence are at risk of stroke and thromboembolism. Despite these adverse outcomes there have been relatively few diagnostic advances in the field since the introduction of the Holter monitor in 1949. This review aims to establish the available evidence for electrophysiological, molecular, and morphological biomarkers to improve the detection of PAF with reference to the underlying mechanisms for the condition.

No MeSH data available.


Related in: MedlinePlus