Key result
Bradykinin infusion suppresses post-MI inducible sustained ventricular tachycardia in ~67% of pigs.
Why the study?
The antiarrhythmic effect of ACE inhibitors may be partly due to elevation of endogenous bradykinin levels, but the in vivo effect of bradykinin on inducible sustained VT after myocardial infarction was unclear.
Does bradykinin infusion reduce the inducibility of sustained ventricular tachycardia in pigs 2 weeks after myocardial infarction?
Comparison
Bradykinin infusion vs control state
Design
Preclinical in vivo study
Follow-up
2 weeks after myocardial infarction
Authors
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May support bradykinin-mediated antiarrhythmic effects of ACE inhibitors; hypothesis-generating in a post-MI animal model and requires clinical translation.
Does bradykinin infusion reduce the inducibility of sustained ventricular tachycardia in pigs 2 weeks after myocardial infarction?
Absolute Event Rate: 33.3% vs 100%
p-value: p=<0.05
Exogenous bradykinin reduced the inducibility of sustained VT in a post-MI pig model, suggesting the antiarrhythmic effect of ACE inhibitors may be partly due to elevated endogenous bradykinin levels.
Tolle et al. (1991) studied Myocardial Infarction (n=6). Bradykinin infusion vs. Control state was evaluated on Inducibility of sustained ventricular tachycardia (p=<0.05). Bradykinin infusion rendered 4 out of 6 pigs with previously inducible sustained ventricular tachycardia noninducible 2 weeks after myocardial infarction (p<0.05).
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