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Updated: Jul 13, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Gap junction and Na+-H+ exchanger alternations in fibrillating and failing atrium
Insights
Atrial fibrillation (AF) with congestive heart failure (CHF) alters atrial connexins and NHE1. These molecular changes may worsen cardiac function in patients with AF and CHF.
Area of Science:
- Cardiovascular Medicine
- Molecular Cardiology
Background:
- Atrial fibrillation (AF) often co-occurs with congestive heart failure (CHF).
- Investigating molecular alterations in the atria of patients with both conditions is crucial for understanding disease progression.
Discussion:
- This study analyzed atrial tissue from patients with AF and varying degrees of CHF undergoing mitral valve replacement.
- Connexin 40 (Cx40) and Connexin 43 (Cx43) protein levels, along with Na(+)-H(+) exchanger isoform 1 (NHE1) activity and expression, were assessed.
Key Insights:
- Significant alterations in Cx40 and Cx43 protein expression were observed in relation to AF severity and CHF stage.
- Na(+)-H(+) exchanger activity was notably elevated in patients with AF and severe CHF, correlating with increased NHE1 protein levels.
Outlook:
- These molecular changes, including altered connexin and NHE1 profiles, may directly contribute to the deterioration of cardiac function in the combined AF and CHF state.
- Further research could explore therapeutic strategies targeting these specific molecular pathways to improve outcomes for patients with co-existing AF and CHF.
Abstract:
Atrial fibrillation (AF) frequently complicates congestive heart failure (CHF). The current study examines whether patients with AF and CHF have alternation in atrial connexins (Cxs) and Na(+)-H(+) exchanger isoform 1 (NHE1). Left atrium was obtained from 29 patients of patients undergoing mitral valve replacement. The connexin 40 (Cx40) protein was significantly higher in AF and sever HF, whereas connexin 43 (Cx43) protein were markedly increased in AF and mild HF but downregulated in the patients with AF and sever HF. NHE activity is significantly greater in AF and sever HF with highest level of NHE1 protein. These change may induce a direct effect on the progressive deterioration of cardiac function in the fibrillation and failure heart.
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