Ambrosio G, Betocchi S, Pace L, Losi M A, Perrone-Filardi P, Soricelli A, Piscione F, Taube J, Squame F, Salvatore M, Weiss J L, Chiariello M
Division of Cardiology R, University of Perugia School of Medicine, Italy.
Circulation. 1996 Nov 15;94(10):2455-64. doi: 10.1161/01.cir.94.10.2455.
Delayed recovery of contractile function in spite of normal perfusion (ie, "stunning") has been described in animal models of exercise-induced myocardial ischemia. Therefore, we investigated whether stunning may result from effort angina in patients.
Patients with coronary artery disease underwent exercise testing combined with quantitative measurements of contractile function for up to 240 minutes after exercise determined by either measurement of regional ejection fraction (99mTc radionuclide angiography; n = 17, group A) or computer-assisted measurement of systolic wall thickening (n = 14, group B). In the latter group, myocardial perfusion was also evaluated by 99mTc-sestamibi tomographic imaging. Angina induced marked contractile dysfunction. Hemodynamic and ECG changes brought about by ischemia were promptly normalized. Furthermore, no perfusion defects could be detected in group B patients 30 minutes after exercise, yet contractile function remained impaired well after cessation of exercise. Thirty minutes into recovery, regional ejection fraction of previously ischemic areas was still 82.6 +/- 4.6% of baseline in group A (P < .05). Similarly, in group B patients, systolic thickening of previously ischemic segments was still significantly impaired 60 minutes after exercise, averaging 33.8 +/- 2.8% versus 40.5 +/- 2.7% at baseline (P < .05). Contractile impairment was fully reversible, as the functioning of previously ischemic segments normalized between 60 and 120 minutes of recovery.
Prolonged yet ultimately reversible impairment of regional myocardial function may occur in patients after exercise-induced angina in the absence of perfusion abnormalities. These findings indicate that myocardial stunning may ensue after effort angina in patients with severe coronary artery disease.
在运动诱导的心肌缺血动物模型中,尽管灌注正常,但仍出现收缩功能延迟恢复(即“心肌顿抑”)。因此,我们研究了心肌顿抑是否可能由患者的劳力性心绞痛导致。
冠心病患者接受运动试验,并在运动后长达240分钟内结合收缩功能的定量测量,收缩功能通过测量局部射血分数(99mTc放射性核素血管造影;n = 17,A组)或计算机辅助测量收缩期室壁增厚(n = 14,B组)来确定。在后一组中,还通过99mTc - 甲氧基异丁基异腈断层显像评估心肌灌注。心绞痛引发了明显的收缩功能障碍。缺血引起的血流动力学和心电图变化迅速恢复正常。此外,B组患者运动后30分钟未检测到灌注缺损,但运动停止后收缩功能仍持续受损。恢复30分钟时,A组先前缺血区域的局部射血分数仍为基线的82.6±4.6%(P < 0.05)。同样,在B组患者中,运动后60分钟先前缺血节段的收缩期增厚仍明显受损,平均为33.8±2.8%,而基线时为40.5±2.7%(P < 0.05)。收缩功能损害是完全可逆的,因为先前缺血节段的功能在恢复60至120分钟之间恢复正常。
在无灌注异常的情况下,运动诱发心绞痛后的患者可能出现局部心肌功能的长期但最终可逆的损害。这些发现表明,严重冠心病患者劳力性心绞痛后可能会发生心肌顿抑。