Transmural , haemorrhagic myocardial infarction after intracoronary streptokinase
نویسندگان
چکیده
Six of 101 patients with acute myocardial infarction whose coronary arteries were successfully recanalised died in cardiogenic shock one to 18 days after intracoronary thrombolysis. In one patient, cardiogenic shock was preceded by coronary artery reocclusion. On admission, serum creatine kinase was still normal in all six patients and there was significant ST elevation but no changes in the QRS coimplexes. Four of the six patients had an old infarct. The time between the onset of symptoms and coronary artery recanalisation was approximately 2-9 hours. The total dosage of intracoronary streptokinase averaged 200 000 units. Necropsy disclosed a patent vessel supplying the infarct in five patients and thrombotic reocclusion in the one patient with reinfarction. All six patients had a transmural acute myocardial infarction, which was typically anaemic in the two patients with inferior infarction. In one of these two patients, whose artery was recanalised within 1 7 hours, the anaemic infarct was only 4 cm2 in area, whereas in the other (the patient who died after reocclusion) it was 30 cm2. In three patients with an acute occlusion of the left anterior descending coronary artery, whose vessels were recanalised within 3 5 hours, the infarct was haemorrhagic and large, averaging 32 cm2. Haemorrhage was always confined to the area of necrosis and there was no evidence of cardiac rupture. One other patient had both types ofinfarction-a large haemorrhagic infarct in the area ofthe recanalised circumflex coronary artery and an anaemic infarct in the area supplied by the severely stenosed left anterior descending coronary artery. In this patient, who died 18 days after recanalisation, the speed of infarct healing was much delayed in the haemorrhagic but not in the anaemic infarct area. Despite coronary artery recanalisation within three and a half hours, a fatal transmural acute myocardial infarction with reperfusion haemorrhage into the area of necrosis may occur. Myocardial haemorrhage probably delays infarct healing.
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