Key result
Cx43 K258stop mutation increases infarct size ~39% and elevates ventricular arrhythmia susceptibility in mice.
Why the study?
The role of the connexin43 CT domain in regulating infarct size and susceptibility to ventricular arrhythmias after acute myocardial infarction was unclear.
Population
Hearts of mice expressing K258stop mutation or Cx43 allele with one Cx43 knockout allele
Comparison
K258stop/KO hearts vs Cx43/KO control hearts
Design
Ex vivo Langendorff-perfused mouse heart model with induced acute myocardial infarction and arrhythmia testing
Follow-up
1 hour ischaemia and 4 hours reperfusion
Authors
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Mouse model data should not guide MI care; leaves open Cx43 pH regulation in infarct size and arrhythmias.
Absolute Event Rate: 42.2% vs 30.4%
p-value: p=0.004
Maass et al. (2009) studied Acute myocardial infarction (n=16). K258stop mutation (loss of Cx43 regulatory domain) vs. Cx43/KO controls was evaluated on Infarct volume (as per cent of area at risk) (p=0.004). Mice expressing the K258stop mutation in place of Cx43 had significantly larger infarct volumes compared to controls (42.2% vs 30.4%, P=0.004) and increased susceptibility to ventricular arrhythmias.
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