Key result
Reduction in connexin43 content and altered distribution of gap junctions in ischemic heart disease may result in heterogeneous anisotropic conduction and form a proarrhythmic substrate.
Population
Mammalian heart / ischemic heart disease (review of pathophysiology)
Design
Review
Authors
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May guide mechanistic arrhythmia research in ischemia; leaves open connexin43-targeted therapies pending prospective validation.
Reduction and disorganization of connexin43 gap junctions in ischemic heart disease contribute to altered electrophysiology and proarrhythmic substrates.
Nicholas J. Severs (1994) conducted a review in Ischemic heart disease. Reduction in connexin43 content and altered distribution of gap junctions in ischemic heart disease may result in heterogeneous anisotropic conduction and form a proarrhythmic substrate.
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