Key result
Pre-treatment with the selective K(ATP) blocking agent HMR 1883 significantly increased postarrhythmic action potential duration compared with control hearts (118 vs 100 ms, P=0.0013).
Why the study?
Does the selective K(ATP) blocking agent HMR 1883 prevent postarrhythmic action potential shortening and reduce ventricular fibrillation inducibility in Langendorff-perfused rabbit hearts?
Does the selective K(ATP) blocking agent HMR 1883 prevent postarrhythmic action potential shortening and reduce ventricular fibrillation inducibility in Langendorff-perfused rabbit hearts?
Absolute Event Rate: 118% vs 100%
p-value: p=0.0013
Blocking K(ATP) channels with HMR 1883 prevents postarrhythmic action potential shortening and reduces the inducibility of ventricular fibrillation in a preclinical rabbit heart model.
K(ATP) involvement in post-VF MAP changes is hypothesis-generating; leaves open relevance to human VF storms.
AIM: Patients with sustained ventricular tachyarrhythmias are at high risk for sudden cardiac death. The mechanisms leading to multiple temporally related episodes of ventricular fibrillation (VF) are not yet fully elucidated, and treatment options are limited. We investigated whether K(ATP)-channels could be involved in triggering VF. METHODS: We determined postarrhythmic changes of monophasic action potentials (MAP) after repetitive induction of VF in 32 Langendorff-perfused rabbit hearts. RESULTS: Postarrhythmic action potential duration (APD) was significantly shorter compared with baseline (100 +/- 12 ms vs. 140 +/- 8 ms, P < 0.05). With increasing numbers of VF and shortening of recovery intervals between VF episodes (2 min) inducibility of VF increased, and abbreviation of APD became more prominent (90 +/- 5 ms vs. 130 +/- 4 ms, P < 0.05). Pre-treatment with the selective K(ATP) blocking agent HMR 1883 led to a significant increase of postarrhythmic APDs compared with control hearts (100 +/- 12 ms vs. 118 +/- 3 ms, P = 0.0013). Moreover, HMR 1883 significantly reduced inducibility of VF and increased the rate of successful defibrillation. CONCLUSIONS: Repetitive episodes of VF result in postarrhythmic abbreviation of APDs, a phenomenon thought to be of potential relevance for incessant tachyarrhythmias in patients. Prevention of postarrhythmic MAP-shortening by HMR 1883 might be useful in suppressing VF.
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Bauer et al. (2007) studied Ventricular fibrillation (n=32). HMR 1883 vs. Control hearts was evaluated on Postarrhythmic action potential duration (APD) (p=0.0013). Pre-treatment with the selective K(ATP) blocking agent HMR 1883 significantly increased postarrhythmic action potential duration compared with control hearts (118 vs 100 ms, P=0.0013).