Alterations in cardiac sarcoplasmic reticulum Ca2+ regulatory proteins in the atrial tissue of patients with chronic atrial fibrillation
Identifieur interne : 003969 ( Main/Exploration ); précédent : 003968; suivant : 003970Alterations in cardiac sarcoplasmic reticulum Ca2+ regulatory proteins in the atrial tissue of patients with chronic atrial fibrillation
Auteurs : Tomoko Ohkusa [Japon] ; Takeshi Ueyama [Japon] ; Jutaro Yamada [Japon] ; Masafumi Yano [Japon] ; Yoshihiko Fujumura [Japon] ; Kensuke Esato [Japon] ; Masunori Matsuzaki [Japon]Source :
- Journal of the American College of Cardiology [ 0735-1097 ] ; 1999.
English descriptors
- KwdEn :
- Teeft :
- Abnormality, American college, Antisense primer, Atrial, Atrial diameter, Atrial fibrillation, Atrial fibrillation jacc, Atrial myocardium, Atrial tissue, Atrium, Binding sites, Bmax, Brillation, Cardiac, Cardiac sarcoplasmic reticulum, Cardiac surgery, Cdna, Circ, Direct evidence, Electrophysiological, Expression level, Expression levels, Fibrillation, Heart failure, Hemodynamic, Hemodynamic data, Higher levels, Internal control, Internal medicine, Intracellular, Intracellular calcium, Jacc, July, Maximum number, Mitral valvular disease, Mpap, Mrna, Myocardium, Normal sinus rhythm, Ohkusa, Pcwp, Present study, Primer, Pulmonary capillary wedge pressure, Reaction mixture, Receptor, Regulatory proteins, Reticulum, Right atrial pressure, Right atrium, Ryanodine, Ryanodine receptor, Sarcoplasmic, Sarcoplasmic reticulum, Second department, Sense primer, Sinus, Such changes, Uptake functions, Ventricular, Ventricular ejection fraction, Yamaguchi, Yamaguchi university school.
Abstract
Abstract: OBJECTIVESOur purpose was to determine whether atrial fibrillation (AF) patients have alterations in sarcoplasmic reticulum (SR) Ca2+ regulatory proteins in the atrial myocardium.BACKGROUNDClinically, AF is the most frequently encountered arrhythmia. Recent studies indicate that an inability to maintain intracellular Ca2+ homeostasis with a consequent increase in membrane-triggered activity could be the primary initiating factor in some circumstances, and that cytosolic Ca2+ abnormalities are an important mediator of sustained AF.METHODSWe measured the maximum number of [3H]ryanodine binding sites (Bmax) and the expression levels of ryanodine receptor (RyR) mRNA and calcium-adenosine triphosphatase (Ca2+-ATPase) mRNA in atrial myocardial tissue from 13 patients with AF due to mitral valvular disease (MVD) and 9 patients with normal sinus rhythm (NSR).RESULTSIn AF patients, 1) Bmax was significantly lower in each atrium (0.21 ± 0.03 pmol/mg [right], 0.16 ± 0.04 pmol/mg [left]) than in the right atrium (0.26 ± 0.08 pmol/mg) of NSR patients; 2) Bmax was significantly lower in the left atrium than in the right atrium; 3) Bmax in the left atrium was significantly lower at higher levels of pulmonary capillary wedge pressure; 4) the expression level of RyR mRNA was significantly lower in both the left (1.24 × 10−2 ± 1.28 × 10−2) and right (1.70 × 10−2 ± 1.78 × 10−2) atrium than in the right atrium of NSR patients (6.11 × 10−2 ± 2.79 × 10−2); and 5) the expression level of Ca2+-ATPase mRNA was significantly lower in both the left (5.67 × 10−2 ± 4.01 × 10−2) and right (7.71 × 10−2 ± 3.56 × 10−2) atrium than in the right atrium (12.60 × 10−2 ± 3.92 × 10−2) of NSR patients.CONCLUSIONSThese results provide the first direct evidence of abnormalities in the Ca2+ regulatory proteins of the atrial myocardium in chronic AF patients. Conceivably, such abnormalities may be involved in the initiation and/or perpetuation of AF.
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DOI: 10.1016/S0735-1097(99)00169-2
Affiliations:
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<term>RyR</term>
<term>SR</term>
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<term>Atrial diameter</term>
<term>Atrial fibrillation</term>
<term>Atrial fibrillation jacc</term>
<term>Atrial myocardium</term>
<term>Atrial tissue</term>
<term>Atrium</term>
<term>Binding sites</term>
<term>Bmax</term>
<term>Brillation</term>
<term>Cardiac</term>
<term>Cardiac sarcoplasmic reticulum</term>
<term>Cardiac surgery</term>
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<term>Direct evidence</term>
<term>Electrophysiological</term>
<term>Expression level</term>
<term>Expression levels</term>
<term>Fibrillation</term>
<term>Heart failure</term>
<term>Hemodynamic</term>
<term>Hemodynamic data</term>
<term>Higher levels</term>
<term>Internal control</term>
<term>Internal medicine</term>
<term>Intracellular</term>
<term>Intracellular calcium</term>
<term>Jacc</term>
<term>July</term>
<term>Maximum number</term>
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<term>Mrna</term>
<term>Myocardium</term>
<term>Normal sinus rhythm</term>
<term>Ohkusa</term>
<term>Pcwp</term>
<term>Present study</term>
<term>Primer</term>
<term>Pulmonary capillary wedge pressure</term>
<term>Reaction mixture</term>
<term>Receptor</term>
<term>Regulatory proteins</term>
<term>Reticulum</term>
<term>Right atrial pressure</term>
<term>Right atrium</term>
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<term>Sarcoplasmic reticulum</term>
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<front><div type="abstract" xml:lang="en">Abstract: OBJECTIVESOur purpose was to determine whether atrial fibrillation (AF) patients have alterations in sarcoplasmic reticulum (SR) Ca2+ regulatory proteins in the atrial myocardium.BACKGROUNDClinically, AF is the most frequently encountered arrhythmia. Recent studies indicate that an inability to maintain intracellular Ca2+ homeostasis with a consequent increase in membrane-triggered activity could be the primary initiating factor in some circumstances, and that cytosolic Ca2+ abnormalities are an important mediator of sustained AF.METHODSWe measured the maximum number of [3H]ryanodine binding sites (Bmax) and the expression levels of ryanodine receptor (RyR) mRNA and calcium-adenosine triphosphatase (Ca2+-ATPase) mRNA in atrial myocardial tissue from 13 patients with AF due to mitral valvular disease (MVD) and 9 patients with normal sinus rhythm (NSR).RESULTSIn AF patients, 1) Bmax was significantly lower in each atrium (0.21 ± 0.03 pmol/mg [right], 0.16 ± 0.04 pmol/mg [left]) than in the right atrium (0.26 ± 0.08 pmol/mg) of NSR patients; 2) Bmax was significantly lower in the left atrium than in the right atrium; 3) Bmax in the left atrium was significantly lower at higher levels of pulmonary capillary wedge pressure; 4) the expression level of RyR mRNA was significantly lower in both the left (1.24 × 10−2 ± 1.28 × 10−2) and right (1.70 × 10−2 ± 1.78 × 10−2) atrium than in the right atrium of NSR patients (6.11 × 10−2 ± 2.79 × 10−2); and 5) the expression level of Ca2+-ATPase mRNA was significantly lower in both the left (5.67 × 10−2 ± 4.01 × 10−2) and right (7.71 × 10−2 ± 3.56 × 10−2) atrium than in the right atrium (12.60 × 10−2 ± 3.92 × 10−2) of NSR patients.CONCLUSIONSThese results provide the first direct evidence of abnormalities in the Ca2+ regulatory proteins of the atrial myocardium in chronic AF patients. Conceivably, such abnormalities may be involved in the initiation and/or perpetuation of AF.</div>
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