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  • Title: Infarct Size Limitation: acute N-acetylcysteine defense (ISLAND trial): preliminary analysis and report after the first 30 patients.
    Author: Sochman J, Vrbská J, Musilová B, Rocek M.
    Journal: Clin Cardiol; 1996 Feb; 19(2):94-100. PubMed ID: 8821417.
    Abstract:
    Our previous experimental research and initial clinical observations regarding the use of N-acetylcysteine in the treatment of ischemic and reperfusion injury in acute myocardial infarction gave rise to a study entitled the Infarct Size Limitation: Acute N-acetylcysteine Defense (ISLAND) trial. Today, this randomized, echocardiographically and angiographically controlled study includes the first 30 patients with a first anterior wall myocardial infarction: Group A (n = 10) consisting of patients with successful recanalization of the infarct-related left anterior descending artery by streptokinase without any further treatment, Group B (n = 10) consisting of patients with failed infarct-related artery recanalization, and Group C (n = 10) comprising patients who had successful streptokinase-induced recanalization of the left anterior descending artery plus N-acetylcysteine administration at a dose of 100 mg/kg body weight. The parameters monitored in our study include changes in global and regional left ventricular ejection fraction of the infarct-related segment using echocardiography and, using electrocardiograms and the Wagner QRS scoring system, the amounts of acutely jeopardized and finally infarcted myocardium. In Group A, global left ventricular ejection fraction rose nonsignificantly within 2 weeks from 37.5 +/- 9.6% to 38.5 +/- 13.8%; it declined significantly in Group B from 36.2 +/- 6.1% to 30.1 +/- 6.7% (p < 0.05), while it considerably improved in Group C from 41.7 +/- 4.1% to 59.6 +/- 8.1% (p < 0.001). Regional left ventricular ejection fraction changed significantly only in Group C: from -4.5 +/- 27.3 to 45.6 +/- 16.3 (p < 0.001). In Group A, in which the amount of acutely jeopardized myocardium was 21.7 +/- 7.2, infarction actually occurred in 20.4 +/- 9.7% (practically no myocardial salvage). In Group B, risk area was 18.1 +/- 4.3%, but infarct size rose to a resulting 29.1 +/- 6.0%. Significant myocardial salvage was accomplished only in Group C: of 26.2 +/- 8.1% of jeopardized myocardium, infarct size was reduced to 10.8 +/- 7.1% (salvage by 58.8%). Also, basic division of patients by therapy showed that, although those with nonidentical findings on their coronary arteries were included into the same groups, patients treated with streptokinase plus N-acetylcysteine had significantly more favorable values of the monitored parameters than those treated with streptokinase alone. We conclude our interim analysis suggests that N-acetylcysteine has a beneficial effect, reducing the functional and structural impacts of myocardial infarction.
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