Department of Nuclear Medicine, Cardiac Imaging, University Hospital Zurich, Ramistrasse 100, CH-8091, Zurich, Switzerland.
Eur J Nucl Med Mol Imaging. 2019 Oct;46(11):2322-2328. doi: 10.1007/s00259-019-04440-2. Epub 2019 Jul 29.
The human pathophysiology of stunned, hibernating and scarred myocardium in ischemic cardiomyopathy is a subject of controversy. While the "smart heart" theory postulates that reduced myocardial blood flow (MBF) at rest is responsible for myocytes switching to a state of hibernation, other theories suggest that a reduced myocardial flow reserve (MFR) may be the cause.
We included 110 patients with ischemic cardiomyopathy. Based on quantitative myocardial perfusion assessment and viability imaging with N-NH3 and F-FDG positron emission tomography, respectively, as well as wall motion assessment from echocardiography, myocardial tissue was characterized as remote (i.e., normal myocardium), stunned (i.e., dysfunctional but viable myocardium with normal rest perfusion), hibernating (i.e., dysfunctional but viable myocardium with impaired rest perfusion), or scarred myocardium (i.e., non-viable myocardium).
Compared to remote myocardium, dysfunctional but viable myocardium (including stunned and hibernating) had reduced rest MBF (0.89 mL/min/g vs. 0.79 and 0.76 mL/min/g, respectively; p < 0.001) and MFR (1.53 vs. 1.27 and 1.17; p < 0.001). Between stunned and hibernating myocardium, however, rest MBF and MFR did not differ (p = 0.40). In scarred myocardium, rest MBF was lowest (0.66 mL/min/g; p < 0.001) but, in contrast to the other myocardial states, k2 (i.e., tracer washout) was increased (0.199/min vs. 0.178/min to 0.181/min; all p < 0.05 in pairwise comparison).
In patients with ischemic cardiomyopathy, impaired MFR is associated with stunning and hibernation. These states of dysfunctional but viable myocardium have lower rest MBF compared to remote myocardium. At the end of the continuum, rest MBF is lowest in scar tissue and linked to increased rate of tracer washout.
缺血性心肌病中顿抑、冬眠和瘢痕心肌的人体病理生理学是一个有争议的问题。虽然“智能心脏”理论假定静息时心肌血流（MBF）减少导致心肌细胞转变为冬眠状态，但其他理论表明，心肌血流储备（MFR）降低可能是原因。
我们纳入了 110 例缺血性心肌病患者。根据定量心肌灌注评估和正电子发射断层扫描分别用 N-NH3 和 F-FDG 进行的存活力成像，以及超声心动图的壁运动评估，心肌组织被特征化为远程（即正常心肌）、顿抑（即功能障碍但存活的心肌，静息灌注正常）、冬眠（即功能障碍但存活的心肌，静息灌注受损）或瘢痕心肌（即无活力的心肌）。
与远程心肌相比，功能障碍但存活的心肌（包括顿抑和冬眠）的静息 MBF 降低（0.89mL/min/g 比 0.79 和 0.76mL/min/g，p<0.001）和 MFR 降低（1.53 比 1.27 和 1.17；p<0.001）。然而，在顿抑和冬眠心肌之间，静息 MBF 和 MFR 没有差异（p=0.40）。在瘢痕心肌中，静息 MBF 最低（0.66mL/min/g；p<0.001），但与其他心肌状态相反，k2（即示踪剂洗脱）增加（0.199/min 比 0.178/min 至 0.181/min；所有在两两比较中均为 p<0.05）。
在缺血性心肌病患者中，受损的 MFR 与顿抑和冬眠有关。这些功能障碍但存活的心肌状态的静息 MBF 低于远程心肌。在连续体的末端，静息 MBF 在瘢痕组织中最低，并与示踪剂洗脱率增加有关。
