Extent of cardiac sympathetic neuronal damage is determined by the area of ischemia in patients with acute coronary syndromes

Abstract

Background - Prior studies have demonstrated that acute ischemic injury causes sympathetic neuronal damage exceeding the area of necrosis. The aim of this study was to test the hypothesis that sympathetic neuronal damage measured by 123I-metaiodobenzylguanidine (MIBG) imaging would be determined by the area of ischemia as reflected by area at risk in patients undergoing reperfusion therapy for acute coronary syndromes. Methods and Results - In 12 patients, the myocardium at risk was assessed by 99mTc- sestamibi SPECT before reperfusion, and infarct size was measured by follow- up 99mTc-sestamibi SPECT 1 week later. All patients also underwent 123I-MIBG SPECT within a mean of 11 days after onset. The SPECT image analysis was based on a semiquantitative polar map approach. Defect size on the 123I-MIBG or 99mTc-sestamibi SPECT was measured for the left ventricle (LV) with the use of a threshold of -2.5 SD from the mean value of a normal database and was expressed as %LV. The 123I-MIBG defect size (47 ± 18%LV) was larger than the infarct size (27 ± 23%LV, P < 0.001) but was similar to the risk area (49 ± 18%LV, P = NS). Furthermore, the 123I-MIBG defect size was closely correlated with the risk area (r = 0.905, P < 0.001). Conclusions - Sympathetic neuronal damage measured by 123I-MIBG SPECT is larger than infarct size and is closely related to risk area, suggesting high sensitivity of neuronal structures to ischemia compared with myocardial cells.