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Cardiac dys-synchronization and arrhythmia in hyperhomocysteinemia
Karni S Moshal1, Clacy K Camel, Ganesh K Kartha
1Department of Physiology and Biophysics, University of Louisville School of Medicine, Kentucky 40202, USA. suresh.tyagi@louisville.edu
Current Neurovascular Research
|November 30, 2007
Summary
Homocysteine (Hcy) accumulation disrupts cardiac synchronization by affecting connexins and extracellular matrix, leading to heart failure and arrhythmias. Hcy also impairs nitric oxide synthase, contributing to cardiac dysfunction.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Biochemistry
Background:
- Cardiac synchronization is crucial for myocardial performance, relying on gap junction proteins (connexins) and extracellular matrix (ECM).
- Myocardial dysfunction and heart failure involve dys-synchronization, but underlying mechanisms remain unclear.
- Systemic factors like homocysteine (Hcy) may influence cardiac synchronization and arrhythmias.
Purpose of the Study:
- To review the role of systemic homocysteine (Hcy) accumulation in cardiac dys-synchronization.
- To explore Hcy's impact on heart failure, hypertension, and cardiac arrhythmias.
- To discuss Hcy-induced alterations in connexin and ECM remodeling and nitric oxide synthase (NOS) pathways.
Main Methods:
- Literature review focusing on homocysteine's effects on cardiac structure and function.
- Analysis of signal transduction pathways involved in Hcy-induced matrix metalloproteinase (MMP) activation.
- Examination of Hcy's attenuation of mitochondrial (mtNOS), endothelial (eNOS), and neuronal (nNOS) nitric oxide synthases.
Main Results:
- Systemic Hcy accumulation is implicated in vasospasm, pressure/volume overload heart failure, and hypertension.
- Hcy contributes to cardiac arrhythmias through attenuation of mtNOS, eNOS, and nNOS.
- Hcy induces matrix metalloproteinase (MMP) activation, leading to cardiac connexin remodeling.
Conclusions:
- Homocysteine accumulation is a significant factor in cardiac dys-synchronization and arrhythmias.
- Hcy-mediated alterations in connexin and ECM remodeling contribute to heart failure pathogenesis.
- Targeting Hcy pathways may offer therapeutic strategies for cardiac arrhythmias and heart failure.
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