Comparison of expression of connexin in right atrial myocardium in patients with chronic atrial fibrillation versus those in sinus rhythm

Nao, Tomoko; Ohkusa, Toshifumi; Hisamatsu, Yosuke; Inoue, Noriko; Matsumoto, Tomo; Yamada, Jiro; Shimizu, Akihiko; Yoshiga, Yasuhiro; Yamagata, Toshihiko; Kobayashi, Shigeki; Yano, Masafumi; Hamano, Kimikazu; Matsuzaki, Masunori

doi:10.1016/s0002-9149(02)03403-3

Cited by 99 publications

(73 citation statements)

References 20 publications

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“…23 Whether AF-induced changes in these connexins play a significant role in atrial remodeling remains a subject of debate. 23 AF has been shown to be associated with a net increase 24,25 or decrease 26,27 in connexin 40 expression with redistribution to the lateral borders of the atrial myocytes.This may result in anisotropy and dispersion of atrial conduction, thus favoring an environment vulnerable to AF.…”

Section: Artial Remodelingmentioning

confidence: 99%

Atrial Remodeling And Atrial Fibrillation: Mechanistic Interactions And Clinical Implications

Hassan¹,

Al‐Ghamdi²

2009

J.A.F.I.B

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Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. The prevalence of AF increases dramatically with age and is seen in as high as 9% of individuals by the age of 80 years. In high-risk patients, the thromboembolic stroke risk can be as high as 9% per year and is associated with a 2-fold increase in mortality. Although the pathophysiological mechanism underlying the genesis of AF has been the focus of many studies, it remains only partially understood. Conventional theories focused on the presence of multiple re-entrant circuits originating in the atria that are asynchronous and conducted at various velocities through tissues with various refractory periods. Recently, rapidly firing atrial activity in the muscular sleeves at the pulmonary veins ostia or inside the pulmonary veins have been described as potential mechanism,. AF results from a complex interaction between various initiating triggers and development of abnormal atrial tissue substrate. The development of AF leads to structural and electrical changes in the atria, a process known as remodeling. To have effective surgical or catheter ablation of AF good understanding of the possible mechanism(s) is crucial.Once initiated, AF alters atrial electrical and structural properties that promote its maintenance and recurrence. The role of atrial remodeling (AR) in the development and maintenance of AF has been the subject of many animal and human studies over the past 10-15 years. This review will discuss the mechanisms of AR, the structural, electrophysiologic, and neurohormonal changes associated with AR and it is role in initiating and maintaining AF. We will also discuss briefly the role of inflammation in AR and AF initiation and maintenance, as well as, the possible therapeutic interventions to prevent AR, and hence AF, based on the current understanding of the interaction between AF and AR.

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Section: Artial Remodelingmentioning

confidence: 99%

Atrial Remodeling And Atrial Fibrillation: Mechanistic Interactions And Clinical Implications

Hassan¹,

Al‐Ghamdi²

2009

J.A.F.I.B

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“…Connexin quantification in left atrium has rarely been done [82,83]. Increased Cx40 [47,49,82,84], decreased Cx40 [49,54,85] and no change in Cx40 [54,83] have been reported. A common finding irrespective of quantitative changes in humans or animal models has been an increased heterogeneity in Cx40 distribution manifested as increased regions in which Cx40 containing myocytes are located adjacent to myocytes mostly lacking Cx40 [47,49,54,83,85,86].…”

Section: Remodeling Of Intercellular Connectionsmentioning

confidence: 99%

“…Increased Cx40 [47,49,82,84], decreased Cx40 [49,54,85] and no change in Cx40 [54,83] have been reported. A common finding irrespective of quantitative changes in humans or animal models has been an increased heterogeneity in Cx40 distribution manifested as increased regions in which Cx40 containing myocytes are located adjacent to myocytes mostly lacking Cx40 [47,49,54,83,85,86]. Lateralization of Cx40 where increased Cx40 protein is located on lateral sarcolemmal membranes that are usually devoid of Cx40 has been noted [49,84] along with lateralization of adhesion proteins of the intercalated disk [49].…”

Section: Remodeling Of Intercellular Connectionsmentioning

confidence: 99%

“…In the goat model of AF the appearance of increased heterogeneity without a change in Cx40 quantity paralleled the progression from unsustained to sustained AF [86]. An increase in Cx43 has also been measured [82,87,88], as well as a decrease [49] but the most common finding is no change [47,54,84,85]. Unlike Cx40, Cx43 is uniformly distributed rather than inhomogeneously distributed but like Cx40, lateralization of Cx43 has been observed [49,84].…”

Section: Remodeling Of Intercellular Connectionsmentioning

confidence: 99%

“…The most important is that connexin quantity cannot be equated with structural and/or functional gap junctions. In general, antibodies that have been used have measured both phosphorylated and dephosphorylated isoforms except in one study [85] when only the phosphorylated isoform may be functional. Connexin proteins may also locate in the membrane without forming structural gap junctions [62].…”

Section: Remodeling Of Intercellular Connectionsmentioning

confidence: 99%

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