Di Carli M F, Asgarzadie F, Schelbert H R, Brunken R C, Rokhsar S, Maddahi J
Department of Medical and Molecular Pharmacology, UCLA School of Medicine, Los Angeles, Calif, USA.
J Nucl Cardiol. 1998 Nov-Dec;5(6):558-66. doi: 10.1016/s1071-3581(98)90109-x.
Stress perfusion imaging can assess effectively the amount of jeopardized myocardium, but its use for identifying underperfused but viable myocardium has yielded variable results. We evaluated the relation between measurements of myocardial perfusion at rest and during pharmacologic stress and the patterns of tissue viability as determined by positron emission tomographic (PET) imaging.
We studied 33 patients with coronary artery disease and left ventricular (LV) dysfunction (LV ejection fraction, 30%+/-8%). PET imaging was used to evaluate regional myocardial perfusion at rest and during pharmacologic stress with [13N]-ammonia as a flow tracer, and to delineate patterns of tissue viability (i.e., perfusion-metabolism mismatch or match) using [18F]-deoxyglucose (FDG). We analyzed 429 myocardial regions, of which 229 were dysfunctional at rest. Of these, 30 had normal perfusion and 199 were hypoperfused. A severe resting defect (deficit >40% below normal) predicted lack of significant tissue viability; 31 of 35 regions (89%) had a PET match pattern denoting transmural fibrosis. Although regions with mild or moderate resting defects (deficit <40% below normal) showed evidence of metabolic activity, perfusion measurements alone failed to identify regions with PET mismatch (reflecting hibernating myocardium). Reversible stress defects were observed with slightly higher frequency in regions with a PET mismatch (10 of 37) than in those with a PET match (36 of 162) pattern of viability. A reversible stress defect was a specific (78%) marker, but was a relatively insensitive marker (27%) of viable myocardium as defined by the PET mismatch pattern.
In patients with LV dysfunction, the severity of regional contractile abnormalities correlates with the severity of flow deficit at rest. Severe reductions in resting blood flow in these dysfunctional regions identify predominantly nonviable myocardium that is unlikely to have improved function after revascularization. Although dysfunctional myocardium with mild to moderate flow reductions contains variable amounts of viable tissue (as assessed by FDG uptake), flow measurements alone do not distinguish between regions with PET mismatch (potentially reversible dysfunction) and PET match (irreversible dysfunction). The presence of an irreversible defect on stress imaging is a relatively specific (78%) marker of PET match, whereas a reversible stress defect is a rather insensitive (27%) marker of viability, as defined by the PET mismatch pattern.
应力灌注成像可有效评估心肌受损量,但其用于识别灌注不足但存活的心肌的结果却不尽相同。我们评估了静息和药物负荷状态下心肌灌注测量值与正电子发射断层扫描(PET)成像所确定的组织存活模式之间的关系。
我们研究了33例冠心病合并左心室(LV)功能障碍(LV射血分数为30%±8%)的患者。PET成像用于评估静息和药物负荷状态下的局部心肌灌注,以[13N] - 氨作为血流示踪剂,并使用[18F] - 脱氧葡萄糖(FDG)描绘组织存活模式(即灌注 - 代谢不匹配或匹配)。我们分析了429个心肌区域,其中229个在静息时功能异常。在这些区域中,30个灌注正常,199个灌注不足。严重的静息缺损(低于正常水平>40%)预示着缺乏显著的组织存活能力;35个区域中的31个(89%)有PET匹配模式,提示透壁性纤维化。尽管静息缺损轻度或中度(低于正常水平<40%)的区域显示有代谢活性,但仅灌注测量无法识别出PET不匹配(反映冬眠心肌)的区域。PET不匹配模式(37个区域中的10个)的区域出现可逆性负荷缺损的频率略高于PET匹配模式(162个区域中的36个)的区域。可逆性负荷缺损是一个特异性(78%)标志物,但作为PET不匹配模式所定义的存活心肌的标志物相对不敏感(27%)。
在LV功能障碍患者中,局部收缩异常的严重程度与静息时血流缺损的严重程度相关。这些功能障碍区域静息血流的严重减少主要识别出非存活心肌,血管重建后其功能不太可能改善。尽管静息血流轻度至中度减少的功能障碍心肌包含不同量的存活组织(通过FDG摄取评估),但仅血流测量无法区分PET不匹配(潜在可逆性功能障碍)和PET匹配(不可逆性功能障碍)的区域。负荷成像上不可逆缺损的存在是PET匹配的相对特异性(78%)标志物,而可逆性负荷缺损作为PET不匹配模式所定义的存活标志物则相当不敏感(27%)。