Knaapen Paul, van Dockum Willem G, Bondarenko Olga, Kok Wouter E M, Götte Marco J W, Boellaard Ronald, Beek Aernout M, Visser Cees A, van Rossum Albert C, Lammertsma Adriaan A, Visser Frans C
Department of Cardiology, 6D 120 VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands.
J Nucl Med. 2005 Jun;46(6):923-9.
Delayed contrast enhancement (DCE) visualized by cardiac MRI (CMR) is a common feature in patients with hypertrophic cardiomyopathy (HCM), presumed to be related to myocardial fibrosis. The pathophysiologic basis of hyperenhancement in this patient group, however, remains unclear as limited histologic comparisons are available. The present study compares the perfusable tissue index (PTI), an alternative marker of myocardial fibrosis obtained by PET, with DCE-CMR in HCM.
Twenty-one patients with asymmetric septal HCM, 12 chronic myocardial infarction (MI) patients, and 6 age-matched healthy control subjects were studied with DCE-CMR and PET. PET was performed using (15)O-labeled water and carbon monoxide to obtain the PTI.
No hyperenhancement was observed in control subjects and the PTI was within normal limits (1.10 +/- 0.07 [mean +/- SD]). In MI patients, the extent of hyperenhancement (25% +/- 16% [mean +/- SD]) was inversely related to the decrease in the PTI (0.94 +/- 0.12; r = -0.65, P < 0.05). Average hyperenhancement in HCM was 14% +/- 12%, predominantly located in the interventricular septum. The PTI in the hypertrophied interventricular septum, however, was not reduced (1.12 +/- 0.13). Furthermore, in contrast to MI patients, there was a modest positive correlation between the extent of DCE and the PTI in HCM (r = 0.45, P < 0.05).
DCE in the hypertrophied septum of HCM patients is not accompanied by a decline in the PTI, and there is a positive correlation between the extent of DCE and the PTI. These results suggest that hyperenhancement may not be caused solely by fibrotic replacement scarring in this patient group. Other pathologic changes associated with HCM may also cause gadolinium-diethylenetriaminepentaacetic acid hyperenhancement.
心脏磁共振成像（CMR）显示的延迟对比增强（DCE）是肥厚型心肌病（HCM）患者的常见特征，推测与心肌纤维化有关。然而，由于有限的组织学比较资料，该患者群体中强化的病理生理基础仍不清楚。本研究比较了通过PET获得的灌注组织指数（PTI），一种心肌纤维化的替代标志物，与HCM患者的DCE-CMR情况。
对21例不对称性室间隔肥厚型心肌病患者、12例慢性心肌梗死（MI）患者和6例年龄匹配的健康对照者进行了DCE-CMR和PET研究。使用（15）O标记的水和一氧化碳进行PET检查以获得PTI。
对照组未观察到强化，PTI在正常范围内（1.10±0.07[平均值±标准差]）。在MI患者中，强化程度（25%±16%[平均值±标准差]）与PTI的降低（0.94±0.12；r=-0.65，P<0.05）呈负相关。HCM患者的平均强化为14%±12%，主要位于室间隔。然而，肥厚的室间隔中的PTI并未降低（1.12±0.13）。此外，与MI患者不同，HCM患者中DCE程度与PTI之间存在适度的正相关（r=0.45，P<0.05）。
HCM患者肥厚间隔中的DCE并不伴有PTI的下降，且DCE程度与PTI之间存在正相关。这些结果表明，该患者群体中的强化可能并非仅由纤维化替代瘢痕引起。与HCM相关的其他病理变化也可能导致钆喷酸葡胺强化。
