Preinfarction angina does not alter infarct size and in hospital outcome after acute myocardial infarction with ST elevation.

BACKGROUND

Preinfarction angina has been reported to limit infarct size, in a manner analogous to experimental preconditioning. However, other studies have reported inconsistent results. We aimed to investigate prospectively the role of preinfarction angina on infarct size and in hospital outcome.

METHODS

Ninety-nine patients were divided into three groups according to the timing of angina: the group "< 48 h" reported angina within the last 48 h, the group "> 48 h" earlier than 48 h and the group "acute" no angina before infarction. Myocardial injury was estimated by creatine kinase, creatine kinase-MB, troponin I and C-reactive protein. In hospital events included death, recurrent ischemia, congestive heart failure and atrioventricular block.

RESULTS

Clinical characteristics, thrombolysis administration and the magnitude of enzymes released were not statistically different among the three groups: peak creatine kinase was 2139+/-1714 U/l for the >48 h group, vs. 2344+/-1634 U/l for the acute group, vs. 2209+/-1384 U/l for the <48 h group (p=0.88). Peak creatine kinase-MB was 124+/-104 U/l for the >48 h group, vs. 168+/-182 U/l for the acute group, vs. 154+/-108 U/l for the <48 h group (p=0.62). Peak troponin I, peak C-reactive protein and in hospital outcome also did not differ statistically in the three groups; p=0.5, p=0.45.

CONCLUSIONS

Infarct size estimated by cardiac enzymes and by the marker of C-reactive protein, as well as in hospital clinical prognosis are not different in patients with and without preinfarction angina. It seems, therefore, that preinfarction angina confers ischemic conditions inadequate to mimic preconditioning.