Cardiac adrenergic denervation in patients with non-Q-wave versus Q-wave myocardial infarction

被引:0
作者
Sakari Simula
Timo Lakka
Tomi Laitinen
Jouko Remes
Raimo Kettunen
Jyrki Kuikka
Juha Hartikainen
机构
[1] Department of Medicine,
[2] Kuopio University Hospital,undefined
[3] Kuopio,undefined
[4] Finland,undefined
[5] Department of Clinical Physiology and Nuclear Medicine,undefined
[6] Kuopio University Hospital,undefined
[7] Kuopio,undefined
[8] Finland,undefined
[9] Department of Internal Medicine,undefined
[10] Satakunta Central Hospital,undefined
[11] Pori,undefined
[12] Finland,undefined
来源
European Journal of Nuclear Medicine | 2000年 / 27卷
关键词
Key words: Myocardial adrenergic innervation; Myocardial infarction; Metaiodobenzylguanidine;
D O I
暂无
中图分类号
学科分类号
摘要
In spite of smaller infarct size and better preserved left ventricular function the long-term prognosis after a non-Q-wave infarction is not better than after a Q-wave infarction. In fact, the risk of sudden cardiac death is higher in patients with a non-Q-wave infarction than in patients with a Q-wave infarction. One possible reason for postinfarction arrhythmias is cardiac adrenergic denervation resulting from myocardial infarction. In this study we compared cardiac adrenergic innervation after non-Q-wave and Q-wave infarctions. Single-photon emission tomography using iodine-123 metaiodobentzylguanidine (MIBG) and technetium-99m sestamibi (MIBI) tracers were conducted in order to compare cardiac adrenergic denervation and myocardial perfusion in 12 patients with a non-Q-wave infarction and 15 patients with a Q-wave infarction. MIBG and MIBI defects were determined as regional uptake ≤30% of maximal myocardial activity. The size of MIBI defects calculated as a percentage of left ventricular mass was significantly smaller in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (4%±3% vs 9%±7%, P<0.05, respectively). According to the maximal serum creatine kinase activity, less myocardium was damaged in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (502±436 IU/l vs 1878± 1265 IU/l, P<0.001). In spite of this, the extent of MIBG defects was similar in patients with a non-Q-wave and patients with a Q-wave infarction (21%±18% vs 23%± 12%, respectively). In addition, the size of MIBG defect correlated with the infarct size (maximal creatine kinase activity) (r=0.52, P<0.05) after a Q-wave infarction but not after a non-Q-wave infarction. In conclusion, despite a smaller infarct size in non-Q-wave infarct patients, the extent of cardiac adrenergic denervation was similar in patients with a non-Q-wave and patients with a Q-wave infarction. In addition, the extent of cardiac adrenergic denervation was related to the infarct size in patients with a Q-wave infarction but not in patients with a non-Q-wave infarction.
引用
收藏
页码:816 / 821
页数:5
相关论文
empty
未找到相关数据