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Long-term protection and mechanism of pacing-induced postconditioning in the heart

Fawzi A Babiker1, Ilka Lorenzen-Schmidt, Eric Mokelke

  • 1Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands.

Basic Research in Cardiology
|March 26, 2010
PubMed

Insights

Pacing-induced postconditioning (PPC) permanently reduces heart attack size by applying abnormal mechanical load during reperfusion. This cardioprotective effect involves cytoskeletal and mitochondrial pathways, highlighting a novel therapeutic strategy.

Area of Science:

  • Cardiovascular Research
  • Myocardial Infarction
  • Cardioprotection

Background:

  • Brief ventricular pacing during reperfusion (pacing-induced postconditioning, PPC) shows promise in reducing infarct size.
  • The long-term efficacy and underlying mechanisms of PPC require further investigation.

Purpose of the Study:

  • To determine if PPC provides a sustained reduction in myocardial infarct size.
  • To investigate whether abnormal mechanical load from asynchronous activation triggers PPC.
  • To elucidate the signaling pathways involved in PPC-mediated cardioprotection.

Main Methods:

  • Rabbit hearts underwent coronary occlusion followed by reperfusion with or without PPC (10x30s LV pacing intervals).
  • Studies in isolated ejecting rabbit hearts compared LV pacing, biventricular pacing, and high preload.
  • Pharmacological agents targeting adenosine receptors, angiotensin II receptors, microtubules, mitochondrial K(ATP) channels, PKC, PI3-kinase, and stretch-activated channels were used.
  • In situ pig hearts were used to confirm findings and assess timing sensitivity.

Main Results:

  • PPC significantly reduced infarct size normalized to area at risk in rabbits (49.0% to 22.9%) and pigs (35% to 16%), with sustained protection after 6 weeks.
  • Biventricular pacing abolished PPC's effect, while high preload mimicked it, suggesting mechanical load is the trigger.
  • PPC's protective effect was abrogated by colchicine, 5-hydroxydecanoate (5HD), chelerythrine, wortmannin, and gadolinium, implicating cytoskeletal, mitochondrial K(ATP), PKC, PI3-kinase, and stretch-activated channels.
  • Delayed PPC application or reduced pacing cycles abolished the protective effect.

Conclusions:

  • Pacing-induced postconditioning offers permanent reduction in myocardial injury.
  • Abnormal mechanical loading, rather than electrical stimulation, is the likely trigger for PPC.
  • PPC shares downstream signaling pathways with other cardioprotective interventions.

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