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Updated: Aug 17, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Preinfarction angina: no interference of coronary microembolization with acute ischemic preconditioning
Andreas Skyschally1, Petra Gres, Philipp Heusch
1Institute of Pathophysiology Center of Internal Medicine, University of Essen Medical School, Essen, Germany.
Insights
Transient episodes of angina can protect or damage the heart. This study found that ischemic preconditioning still protects the heart even when coronary microembolization is present, reducing infarct size.
Area of Science:
- Cardiovascular Physiology
- Myocardial Ischemia Research
- Protective Cardiac Mechanisms
Background:
- Transient angina episodes preceding myocardial infarction may offer protection via ischemic preconditioning or cause damage through coronary microembolization.
- The interaction between ischemic preconditioning and coronary microembolization requires further investigation to understand its impact on myocardial protection.
Purpose of the Study:
- To investigate the potential loss of ischemic preconditioning's protective effects when combined with coronary microembolization.
- To determine if ischemic preconditioning can still protect the myocardium despite the presence of coronary microembolization.
Main Methods:
- Anesthetized pigs were divided into three groups: sustained ischemia alone, coronary microembolization followed by sustained ischemia, and coronary microembolization followed by ischemic preconditioning then sustained ischemia.
- Infarct size was quantified using triphenyl tetrazolium chloride staining after 2 hours of reperfusion.
- Analysis of covariance (ANCOVA) was used to compare the relationship between infarct size and blood flow across groups.
Main Results:
- Sustained ischemia alone resulted in an infarct size of 19.4+/-3.4%.
- Coronary microembolization prior to sustained ischemia slightly increased infarct size to 23.6+/-4.6%.
- When coronary microembolization was followed by ischemic preconditioning, infarct size was significantly reduced to 12.7+/-3.0% (P<0.05 vs. microembolization alone), indicating persistent protection.
Conclusions:
- Coronary microembolization can induce additional infarction when superimposed on sustained ischemia.
- Ischemic preconditioning demonstrates persistent protective effects on microembolized myocardium, despite initial impressions of failed protection.
- The endogenous protective mechanisms of ischemic preconditioning are not interfered with by coronary microembolization.
Abstract:
Transient episodes of angina preceding acute myocardial infarction may both, protect the myocardium by ischemic preconditioning or damage it when associated with coronary microembolization. We now studied the potential loss of ischemic preconditioning with coronary microembolization. Anesthetized pigs (group 1; n=8) were subjected to 90 min sustained low-flow ischemia. Group 2 (n=8) was subjected to coronary microembolization (i.e. microspheres; 42 microm slashed circle; 3000 per ml min-1 inflow) 35 min before sustained ischemia. In group 3, coronary microembolization was followed 10 min later by one cycle of ischemic preconditioning (10 min ischemia/15 min reperfusion) before subsequent sustained ischemia. Infarct size was determined after 2 h reperfusion by triphenyl tetrazolium chloride staining. Infarct size after sustained ischemia alone (group 1) was 19.4+/-3.4% of the area at risk (mean+/-S.E.M.). With coronary microembolization before sustained ischemia (group 2) infarct size was only slightly larger (23.6+/-4.6%, ns). In group 3 with microembolization followed by ischemic preconditioning, infarct size was reduced to 12.7+/-3.0% (P<0.05 vs. group 2). The relationships between infarct size and transmural blood flow in groups 1 and 3 were not different, giving the impression that ischemic preconditioning failed to protect microembolized myocardium. However, additional coronary microembolization shifted the relationship between infarct size and blood flow upwards to a larger infarct size at any given blood flow. Thus when comparing the relationship of group 3 to its true control (group 2), it was shifted downwards (P<0.05; analysis of covariance (ANCOVA)) indicating persistent protection of microembolized myocardium by ischemic preconditioning. Coronary microembolization induces additional infarction when superimposed on sustained ischemia but does not interfere with the endogenous protection by ischemic preconditioning.
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