Why the study?
Does long-term treatment with ivabradine reverse electrophysiological cardiac remodelling and counteract f-channel overexpression in post-myocardial infarcted rats?
Does long-term treatment with ivabradine reverse electrophysiological cardiac remodelling and counteract f-channel overexpression in post-myocardial infarcted rats?
Ivabradine's beneficial effects in post-MI settings may be mechanistically driven by the reversal of electrophysiological remodeling and reduction of HCN channel overexpression.
Hypothesis-generating for ivabradine in post-MI remodelling; leaves open clinical translation pending human trials.
The beneficial effects of ivabradine may be due to the reversal of electrophysiological cardiac remodelling in post-MI rats by reduction of functional overexpression of HCN channels. This is attributable to transcriptional and post-transcriptional mechanisms.
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Suffredini et al. (2011) studied this question.
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