Table 1

Consensus Related to Myocardial I/R Concepts and Animal Models

Small animal models (mice, rats) are useful for specific mechanistic evaluations but do not resemble human pathophysiology. It is not recommended to translate results from these models into humans without first testing in large animals (126).
Pig and dog I/R models have similarities and differences with humans but are the closest to human pathophysiology and may be considered complimentary (primates are not considered for ethical reasons) (126).
The post-I/R region (infarcted and salvaged) is not static and exhibits important temporal changes in size and composition (14).
There is greater edema formation in infarcted tissue than in salvaged myocardium (22,70).
After acute MI, the infarct border can be highly irregular with islands and peninsulas of necrosis but with a sharp boundary and no “intermediate zone” at a cellular level (12). “Fuzzy borders” at the edge an acute infarct can arise from partial volume effect due to limited spatial resolution of imaging (13).
In experimental models, edema after I/R is bimodal (70,80,127). There is an initial reperfusion-related wave of edema that significantly attenuates hours after reperfusion. A second healing-related wave of edema initiates days after reperfusion and lasts longer (15,50).
In humans, the dynamics of post-I/R edema is less well established. At least in some patients it might exhibit a 2-wave pattern (45,81–83). Edema appears to be more stable in the time window between days 3 and 7 post-MI (15,45,82,83,90).
MVO precedes IMH in reperfused infarctions (15,128).

IMH = intramyocardial hemorrhage; I/R = ischemia/reperfusion; MI = myocardial infarction; MVO = microvascular obstruction.

  • Controversial topic (majority but not all panelists in agreement).