Article Text
Abstract
Background: Ischaemic preconditioning results in a reduction in ischaemic-reperfusion injury to the heart. This beneficial effect is seen both with direct local preconditioning of the myocardium and with remote preconditioning of easily accessible distant non-vital limb tissue. Ischaemic postconditioning with a comparable sequence of brief periods of local ischaemia, when applied immediately after the ischaemic insult, confers benefits similar to preconditioning.
Objective: To test the hypothesis that limb ischaemia induces remote postconditioning and hence reduces experimental myocardial infarct size in a validated swine model of acute myocardial infarction.
Methods: Acute myocardial infarction was induced in 24 pigs with 90 min balloon inflations of the left anterior descending coronary artery. Remote ischaemic postconditioning was induced in 12 of the pigs by four 5 min cycles of blood pressure cuff inflation applied to the lower limb immediately after the balloon deflation. Infarct size was assessed by measuring 72 h creatinine kinase release, MRI scan and immunohistochemical analysis.
Results: Area under the curve of creatinine kinase release was significantly reduced in the postconditioning group compared with the control group with a 26% reduction in the infarct size (p<0.05). This was confirmed by MRI scanning and immunohistochemical analysis that revealed a 22% (p<0.05) and a 47.52% (p<0.01) relative reduction in the infarct size, respectively.
Conclusion: Remote ischaemic postconditioning is a simple technique to reduce infarct size without the hazards and logistics of multiple coronary artery balloon inflations. This type of conditioning promises clear clinical potential.
- LAD, left anterior descending artery
- LE, late enhancement
- LV, left ventricule
- PTCA, percutaneous transluminal coronary angioplasty
- STEMI, ST elevation myocardial infarction
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Footnotes
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↵* MPF and PA have contributed equally as the principal investigators of this study and are joint senior authors.
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Published Online First 19 April 2007
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Funding: This work was supported by grants from the OTKA (Grant F43380 to P A), the ETT (Grant 302/2003 to P A), the Gottsegen Hungarian Institute of Cardiology (to P A) and the Semmelweis University (to P A). PA is the recipient of the Hungarian Academy of Sciences Bolyai Postdoctoral Fellowship. G Sz is the recipient of the Research Fellowship of the European Society of Cardiology.
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Competing interests: None.