Key result
Lentivirus-mediated delivery of Connexin 43 into myocardial scars reduced the incidence of post-infarction ventricular tachycardia from 80% to 38% compared to control in mice.
Why the study?
Does lentivirus-mediated delivery of Connexin 43 reduce ventricular tachycardia incidence in a mouse model of myocardial infarction?
Does lentivirus-mediated delivery of Connexin 43 reduce ventricular tachycardia incidence in a mouse model of myocardial infarction?
Absolute Event Rate: 38% vs 80%
p-value: p=<0.02
Direct in vivo lentiviral gene therapy with Cx43 in non-cardiomyocytes of the myocardial scar enhances electrical coupling and markedly reduces post-infarction ventricular tachycardia in a mouse model.
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Hypothesis-generating for scar-targeted Cx43 gene therapy in post-MI VT; leaves open translation to larger models or humans.
Roell et al. (2018) studied Post-infarct ventricular tachycardia (n=168). Lentivirus-mediated Connexin 43 (lvCx43) gene therapy vs. Lentivirus-EGFP (lvEGFP) was evaluated on Incidence of ventricular tachycardia (VT) upon burst stimulation (p=<0.02). Lentivirus-mediated delivery of Connexin 43 into myocardial scars reduced the incidence of post-infarction ventricular tachycardia from 80% to 38% compared to control in mice.
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