PRODROMAL ANGINA LIMITS INFARCT SIZE - A ROLE FOR ISCHEMIC PRECONDITIONING

Background In the experimental setting, it has been demonstrated that preconditioning myocardium before prolonged occlusion with brief ische mic episodes affords substantial protection to the cells by delaying l ethal injury, thereby limiting infarct size. Whether the same occurs i n humans remains unknown. Methods and Results This study was undertake n to determine whether new-onset prodromal angina, defined as chest pa in episodes limited to the 24 hours before myocardial infarction, is t he clinical correlate of the ischemic preconditioning phenomenon. Twen ty-five patients with their first anterior myocardial infarction treat ed with thrombolysis (recombinant tissue plasminogen activator [r-TPA] , 100 mg/3 hours) were retrospectively included in the study because,t hey met the following criteria: (1) <120 minutes from onset of symptom s to reperfusion therapy, (2) <90 minutes from the beginning of thromb olytic therapy to reperfusion (defined as rapid ST elevation reduction >50%), (3) a patent infarct-related coronary artery with TIMI 3 flow and complete absence of collateral circulation to the infarct related artery (assessed at 24+/-5 days), and (4) the presence of new-onset pr odromal angina, ie, typical chest pain episodes occurring at rest with in 24 hours or, alternatively, a complete absence of symptoms before o nset of infarction. Therefore, on the basis of their clinical status b efore infarction, the patients were divided into two groups: group 1, 13 patients without prodromal angina, and group 2, 12 patients with pr odromal angina. Despite no difference in time to treatment (81+/-19 ve rsus 75+/-21 minutes in group 1 and group 2, respectively; P=NS) and t ime to reperfusion (58+/-34 Versus 46+/-24 minutes; P=NS), the peak of CKMB release was markedly lower in group 2 (86.3+/-66 versus 192.3+/- 108.3 IU/L; P<.01). In addition, although both groups were comparable in terms of area at risk (amount of myocardium beyond the infarct-rela ted stenosis; 15.1+/-4.6 versus 13.7+/-4.6 hypokinetic segments in gro up 1 and group 2, respectively, P=NS), the final infarct size (11+/-7. 5 versus 5.6+/-4 hypokinetic segments, P<.04) was smaller in group 2. Thus, the limitation of the infarct size was significantly greater in group 2 (69% versus 36%; P<.05), and this represents an additional 33% reduction (95% confidence intervals, 7.1% to 58.9%; P=.01) in the gro up of patients with prodromal angina. Also, the third index, that is, the ECG, showed a favorable trend toward a lesser number of Q waves an d a higher Sigma R waves, although the values did not reach statistica l significance. Conclusions Despite a similar area at risk, patients w ith new-onset prodromal angina showed a significantly smaller infarct size compared with patients without prodromal symptoms. Since the two groups had similar times to reperfusion and no evidence of collateral circulation to the infarct related artery, the protection afforded by angina in group 2 patients might be explained by the occurrence of isc hemic preconditioning.