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Evidence for the delayed effect in human ischemic preconditioning: prospective multicenter study for preconditioning
T Noda1, S Minatoguchi, K Fujii
1Second Department of Internal Medicine, Gifu University School of Medicine, Japan.
Insights
A preinfarction angina attack offers protective benefits against acute myocardial infarction (AMI) in humans. This protective effect, known as preconditioning, is linked to improved left ventricular function and appears to be a delayed response.
Area of Science:
- Cardiology
- Cardiovascular Research
- Myocardial Preconditioning
Background:
- Retrospective and prospective studies suggest a preconditioning (PC) effect in humans, but collaterals were not examined.
- Animal models show classic (short-term) and delayed (24-48h) PC effects on infarct size and stunning.
- The existence of classic and delayed PC effects in human acute myocardial infarction (AMI) remains uninvestigated.
Purpose of the Study:
- To prospectively investigate the protective effect of a first preinfarction angina (PA) attack against AMI in patients without significant coronary collaterals.
- To explore the correlation between the time interval from PA to AMI and left ventricular function and infarct size.
Main Methods:
- 25 patients with first AMI and no/poor collateral circulation underwent percutaneous transluminal coronary angioplasty (PTCA).
- Patients were divided into PA(+) (n=11, angina 2-48h prior) and PA(-) (n=14, no prior angina) groups.
- Left ventricular ejection fraction (LVEF) and regional wall motion (RWM) were assessed acutely and chronically; enzymatic infarct size was measured.
Main Results:
- The increase in RWMI from acute to chronic phases was significantly greater in the PA(+) group compared to the PA(-) group.
- Increases in LVEF and RWMI correlated significantly with the time interval between PA and AMI onset.
- No significant difference in enzymatic infarct size was observed between the groups.
Conclusions:
- Preinfarction angina demonstrates a beneficial effect on left ventricular wall motion, independent of collateral circulation, supporting the PC effect in humans.
- A longer interval between preinfarction angina and AMI suggests a delayed PC effect, enhancing myocardial protection.
- The findings indicate that preinfarction angina can precondition the heart against damage from acute myocardial infarction.
Objectives:
This study aimed to investigate prospectively the protective effect of a first preinfarction angina attack against acute myocardial infarction (AMI) in human hearts without significant collaterals.
Background:
Several retrospective studies and the prospective studies have demonstrated the existence of the preconditioning (PC) effect in humans. However, collaterals were not examined in the prospective studies. In animal models, the PC effect on myocardial infarct size appears soon after PC reperfusion (classic) but disappears within 1 to 2 h. It then reappears 24 to 48 h after reperfusion (the delayed PC effect). Meanwhile, the PC effect on stunning appears 12 h after PC reperfusion (the delayed PC effect). The concept of the classic and delayed PC effects has not been investigated in human AMI studies. If the above concept is also correct in humans, the infarct size and/or impairment of the left ventricular function should be inversely correlated with the time interval between the first preinfarction angina attack and the onset of AMI when that time interval is limited to between 2 and 48 h.
Methods:
The subjects were 25 patients with first AMI of the proximal left anterior descending artery who underwent successful direct percutaneous transluminal coronary angioplasty (PTCA) 2 to 6 h after the onset and with no (or poor) collateral circulation (grade 0 or 1). They were divided into two groups: preinfarction angina (PA)(+) group: 11 patients with new onset preinfarction angina from 2 to 48 h before the onset, PA(-) group: 14 patients without angina before infarction. Peak creatine kinase (CK) and cumulative CK were examined, and the left ventricular ejection fraction (LVEF) and the regional wall motion (RWM) were determined from the left ventriculograms during the acute (immediately after the coronary reperfusion) and chronic (four weeks after the onset of AMI) phases. The RWM index (RWMI) was then calculated as the mean motion of chords (standard deviation [SD]/chord) lying in the area of chords of RWM < or = -2 SD in the acute phase (ischemic risk area). RESULTS The increase in the RWMI between the acute and chronic phases was significantly larger in the PA(+) group than in the PA(-) group (1.55 +/- 1.32 and 0.69 +/- 0.75, p < 0.05, respectively) although no significant difference in the enzymatic infarct size was seen between the two groups. The increases in the LVEF and the RWMI were significantly correlated with the time interval from the first preinfarction angina attack to the onset of AMI (r = 0.622, p < 0.05 and r = 0.646, p < 0.05, respectively), but the enzymatic infarct size was not.
Conclusions:
The beneficial effect of preinfarction angina on left ventricular wall motion, independently of collateral flows, indicates the existence of the PC effect in humans. The greater protective effect of a longer time interval between angina pectoris and AMI suggests that the protection is due to a delayed PC effect.