Introduction:
The release of cardiac troponin I (cTnI) after reversible ischemia is controversial. It has been hypothesized that elevations in serum cTnI in this scenario reflect selective release from an exchangeable pool rather than cellular necrosis since irreversible injury with sarcolemmal membrane disruption does not begin until ischemia exceeds 15 minutes following a total coronary occlusion.
Objective:
To determine whether cTnI release occurs after a brief coronary occlusion when the duration of ischemia is insufficient to induce myocyte necrosis.
Methods:
Closed-chest propofol-anesthetized swine (n=10) were subjected to a 10 minute LAD occlusion. Blood sampling was performed to measure serum cTnI concentrations before, during and after ischemia. Myocardial tissue was collected either 1 hour (n=5) or 24 hours (n=5) after reperfusion for pathological assessment of infarction (TTC) and apoptosis (TUNEL).
Results:
Regional LAD wall thickening was 60 ± 4% at baseline and became dyskinetic during coronary occlusion (-4 ± 2%, p<0.05). One hour after reperfusion, wall thickening improved but remained depressed relative to baseline, indicative of myocardial stunning (37 ± 4%, p<0.05). It returned to normal after 24 hours (59 ± 2%). Serum cTnI was 0.01 ± 0.01 ng/mL at baseline and remained unchanged at the end of ischemia. A slight increase in cTnI was observed 1 hour after reperfusion (0.06 ± 0.02 ng/mL, p<0.05 vs. baseline), followed by a marked elevation at 24 hours (1.02 ± 0.57 ng/mL, p<0.05 vs. baseline). TTC staining demonstrated no evidence of infarction. Heart tissue collected 1 hour after reperfusion demonstrated a regional increase in apoptotic myocytes (LAD: 17.7 ± 3.7 myocytes/cm
2
vs. Remote: 3.1 ± 2.0 myocytes/cm
2
, p<0.05). Myocyte apoptosis normalized 24 hours after reperfusion (LAD: 5.2 ± 2.3 myocytes/cm
2
vs. Remote: 3.6 ± 1.5 myocytes/cm
2
) when serum cTnI remained elevated.
Conclusion:
A duration of reversible ischemia compatible with angina can lead to cTnI release that is similar in magnitude to that occurring with myocardial infarction. Rather than infarction or release from an exchangeable cTnI pool, the rise in serum cTnI is delayed and appears to reflect focal programmed myocyte death from apoptosis rather than myocardial necrosis.
Can cardiac troponin I measurement help to predict recent coronary occlusion in out-of-hospital cardiac arrest survivors?
