Prodromal angina limits infarct size. A role for ischemic preconditioning
| Autor: | Donatella Ferrini, Patrizia Limonetti, Denis Pantoli, Francesco Sorbello, Marcello Galvani, Filippo Ottani, Franco Rusticali |
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| Rok vydání: | 1995 |
| Předmět: |
Male
medicine.medical_specialty Time Factors medicine.medical_treatment Ischemia Myocardial Infarction Myocardial Ischemia Myocardial Reperfusion Chest pain Coronary Angiography Angina Pectoris Angina Electrocardiography Physiology (medical) Internal medicine Occlusion medicine Humans Thrombolytic Therapy Myocardial infarction Aged Retrospective Studies Vascular disease business.industry Arrhythmias Cardiac Thrombolysis Middle Aged medicine.disease Cardiology Ischemic preconditioning Female medicine.symptom Cardiology and Cardiovascular Medicine business |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 0009-7322 |
| Popis: | 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) 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 prodromal angina, ie, typical chest pain episodes occurring at rest within 24 hours or, alternatively, a complete absence of symptoms before onset of infarction. Therefore, on the basis of their clinical status before infarction, the patients were divided into two groups: group 1, 13 patients without prodromal angina, and group 2, 12 patients with prodromal angina. Despite no difference in time to treatment (81±19 versus 75±21 minutes in group 1 and group 2, respectively; 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 P =NS), the final infarct size (11±7.5 versus 5.6±4 hypokinetic segments, P P 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. |
| Databáze: | OpenAIRE |
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