Cannon R O, Dilsizian V, O'Gara P T, Udelson J E, Schenke W H, Quyyumi A, Fananapazir L, Bonow R O
Cardiovascular Diagnosis Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md. 20892.
Circulation. 1991 May;83(5):1660-7. doi: 10.1161/01.cir.83.5.1660.
Exercise-induced abnormalities during thallium-201 scintigraphy that normalize at rest frequently occur in patients with hypertrophic cardiomyopathy. However, it is not known whether these abnormalities are indicative of myocardial ischemia.
Fifty patients with hypertrophic cardiomyopathy underwent exercise 201Tl scintigraphy and, during the same week, measurement of myocardial lactate metabolism and hemodynamics during pacing stress. Thirty-seven patients (74%) had one or more 201Tl abnormalities that completely normalized after 3 hours of rest; 26 had regional myocardial 201Tl defects, and 26 had apparent left ventricular cavity dilatation with exercise, with 15 having coexistence of these abnormal findings. Of the 37 patients with reversible 201Tl abnormalities, 27 (73%) had metabolic evidence of myocardial ischemia during rapid atrial pacing (myocardial lactate extraction of 0 mmol/l or less) compared with four of 13 patients (31%) with normal 201Tl scans (p less than 0.01). Eleven patients had apparent cavity dilatation as their only 201Tl abnormality; their mean postpacing left ventricular end-diastolic pressure was significantly higher than that of the 13 patients with normal 201Tl studies (33 +/- 5 versus 21 +/- 10 mm Hg, p less than 0.001). There was no correlation between the angiographic presence of systolic septal or epicardial coronary arterial compression and the presence or distribution of 201Tl abnormalities. Patients with ischemic ST segment responses to exercise had an 80% prevalence rate of reversible 201Tl abnormalities and a 70% prevalence rate of pacing-induced ischemia. However, 69% of patients with nonischemic ST segment responses had reversible 201Tl abnormalities, and 55% had pacing-induced ischemia.
Reversible 201Tl abnormalities during exercise stress are markers of myocardial ischemia in hypertrophic cardiomyopathy and most likely identify relatively underperfused myocardium. In contrast, ST segment changes with exercise and systolic compression of coronary arteries on angiography are unreliable markers of inducible myocardial ischemia in hypertrophic cardiomyopathy. Apparent cavity dilatation during 201Tl scintigraphy may indicate ischemia-related changes in left ventricular filling, with elevation in diastolic pressures and endocardial compression.
肥厚型心肌病患者在铊 - 201闪烁扫描时出现运动诱发异常,而在静息时恢复正常的情况很常见。然而,尚不清楚这些异常是否提示心肌缺血。
50例肥厚型心肌病患者接受了运动铊 - 201闪烁扫描,并在同一周内进行了起搏应激时心肌乳酸代谢和血流动力学测量。37例患者(74%)出现一处或多处铊 - 201异常,在静息3小时后完全恢复正常;26例有局部心肌铊 - 201缺损,26例运动时出现明显左心室腔扩张,其中15例同时存在这些异常表现。在37例铊 - 201异常可逆的患者中,27例(73%)在快速心房起搏时有心肌缺血的代谢证据(心肌乳酸摄取为0 mmol/l或更低),而13例铊 - 201扫描正常的患者中有4例(31%)出现这种情况(p<0.01)。11例患者仅表现为明显的腔扩张作为其唯一的铊 - 201异常;他们起搏后的平均左心室舒张末期压力显著高于13例铊 - 201检查正常的患者(33±5对21±10 mmHg,p<0.001)。收缩期室间隔或心外膜冠状动脉压迫的血管造影表现与铊 - 201异常的存在或分布之间无相关性。运动时出现缺血性ST段反应的患者,铊 - 201异常可逆的患病率为80%,起搏诱发缺血的患病率为70%。然而,69%的非缺血性ST段反应患者有可逆的铊 - 201异常,55%有起搏诱发缺血。
运动应激时可逆的铊 - 201异常是肥厚型心肌病心肌缺血的标志物,很可能识别出灌注相对不足的心肌。相比之下,运动时的ST段改变和血管造影时冠状动脉的收缩压迫是肥厚型心肌病中可诱导心肌缺血的不可靠标志物。铊 - 201闪烁扫描时明显的腔扩张可能提示左心室充盈的缺血相关改变,伴有舒张压升高和心内膜压迫。