Prodromal Angina Limits Infarct Size

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Abstract
Background In the experimental setting, it has been demonstrated that preconditioning myocardium before prolonged occlusion with brief ischemic episodes affords substantial protection to the cells by delaying lethal injury, thereby limiting infarct size. Whether the same occurs in humans remains unknown. Methods and Results This study was undertaken to determine whether new-onset prodromal angina, defined as chest pain episodes limited to the 24 hours before myocardial infarction, is the clinical correlate of the ischemic preconditioning phenomenon. Twenty-five patients with their first anterior myocardial infarction treated with thrombolysis (recombinant tissue plasminogen activator [r-TPA], 100 mg/3 hours) were retrospectively included in the study because they met the following criteria: (1) P=NS) and time 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-related stenosis; 15.1±4.6 versus 13.7±4.6 hypokinetic segments in group 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 group of patients with prodromal angina. Also, the third index, that is, the ECG, showed a favorable trend toward a lesser number of Q waves and a higher Σ R waves, although the values did not reach statistical significance. Conclusions Despite a similar area at risk, patients with 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 ischemic preconditioning.

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