Galli M, Marcassa C, Bosimini E, Zoccarato O, Comazzi F, Giannuzzi P
Cardiology Division, "Salvatore Maugeri" Foundation IRCCS, Veruno (No), Italy.
Eur J Nucl Med. 1997 Feb;24(2):160-9. doi: 10.1007/BF02439548.
At dipyridamole myocardial scintigraphy, perfusion defects are seldom backed up by significant ECG changes. This would suggest myocardial blood flow heterogeneity, rather than true ischaemia, as the cause of the scintigraphic abnormalities. Electrocardiographic surface mapping has been documented to be more accurate than standard 12-lead ECG in the detection of provoked ischaemia. Thus, to investigate the relationship between ECG changes and perfusion abnormalities, body surface maps were recorded during dipyridamole infusion in 55 subjects (11 normals and 44 patients with ischaemic heart disease) undergoing dipyridamole technetium-99m sestamibi single-photon emission tomography (SPET). All had a normal resting ECG. The extent and severity of the sestamibi defect were quantified. New negative areas in the isointegral maps and rest-dipyridamole map differences >2 SD from normal limits were considered abnormal. After dipyridamole in normals, neither perfusion defects nor >/=1 mm ST segment depression on 12-lead ECG nor new negative areas in isointegral maps occurred. In patients, dipyridamole induced new perfusion defects in 35 (80%) but ST segment depression in only 18 (41%, P<0.001). Of the 35 patients with perfusion defects, 17 (49%, group 1) showed ST segment depression, while the other 18 (51%, group 2) did not. Abnormal body surface maps were found in 100% of group 1 and 88% of group 2 patients (NS). In group 1, the provoked hypoperfusion was of greater extent (P=0.007) and severity (P=0.01) and the onset of map abnormalities was significantly earlier (P<0. 001) than in group 2; time to map abnormalities was also significantly shorter than time to ST segment depression (P=0.01). In the 35 patients with complete scintigraphic, body map and angiographic data, the severity of reversible perfusion defect proved to be the strongest correlate of ST segment depression upon logistic regression analysis. Thus, sestamibi SPET abnormalities after dipyridamole are almost always associated with electrical changes on body surface maps, suggesting myocardial ischaemia as their cause. The much less common 12-lead ECG changes are slower to appear and reflect a more severe hypoperfusion.
在双嘧达莫心肌闪烁显像中，灌注缺损很少伴有明显的心电图改变。这提示心肌血流异质性而非真正的缺血是闪烁显像异常的原因。已有文献证明，在检测激发性缺血方面，心电图体表标测比标准12导联心电图更准确。因此，为了研究心电图改变与灌注异常之间的关系，对55例接受双嘧达莫锝-99m 司他米比单光子发射断层扫描（SPET）的受试者（11例正常人及44例缺血性心脏病患者）在静脉输注双嘧达莫期间记录体表图。所有受试者静息心电图均正常。对司他米比缺损的范围和严重程度进行量化。等积分图中的新负性区域以及静息-双嘧达莫图差异超过正常范围2个标准差被视为异常。在正常人中，静脉输注双嘧达莫后，既未出现灌注缺损，12导联心电图上也未出现≥1mm的ST段压低，等积分图中也未出现新的负性区域。在患者中，双嘧达莫诱发35例（80%）出现新的灌注缺损，但仅18例（41%，P<0.001）出现ST段压低。在35例有灌注缺损的患者中，17例（49%，第1组）出现ST段压低，而另外18例（51%，第2组）未出现。第1组100%的患者和第2组88%的患者体表图异常（无显著性差异）。在第1组中，激发性灌注减低的范围（P=0.007）和严重程度（P=0.01）更大，体表图异常的出现明显早于第2组（P<0.001）；体表图出现异常的时间也明显短于ST段压低出现的时间（P=0.01）。在35例具备完整闪烁显像、体表图和血管造影数据的患者中，经逻辑回归分析，可逆性灌注缺损的严重程度被证明是ST段压低的最强相关因素。因此，双嘧达莫后锝-99m司他米比SPET异常几乎总是与体表图的电变化相关，提示心肌缺血是其原因。12导联心电图改变则少见得多，出现较慢，反映的是更严重的灌注减低。
