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冬眠心肌在变力刺激期间的灌注-收缩失匹配

Perfusion-contraction mismatch during inotropic stimulation in hibernating myocardium.

作者信息

Sambuceti G, Giorgetti A, Corsiglia L, Marini C, Schneider-Eicke J, Brunelli C, Marzullo P, L'Abbate A, Capponnetto S, Parodi O

机构信息

Consiglio Nazionale delle Ricerche Institute of Clinical Physiology, Pisa, Italy.

出版信息

J Nucl Med. 1998 Mar;39(3):396-402.

PMID:9529281
Abstract

UNLABELLED

The aims of this study were to assess the value of dobutamine echocardiography in identifying myocardial hibernation versus stunning and to elucidate the underlying pathophysiological mechanism of the contractile impairment.

METHODS

Twenty-one patients with isolated stenosis of the left anterior descending artery were evaluated 1 mo after thrombolysed acute anterior infarction. Regional function and blood flow were measured using echocardiography and PET at rest and during dobutamine administration (10 microg/kg/min).

RESULTS

Defined by [18F]fluorodeoxyglucose uptake, 36 of 102 dyssynergic segments were necrotic, and 66 were viable. The latter segments were subdivided according to their [13N]ammonia flow distribution: 30 hibernating regions with perfusion defects (flow of <80% of maximum) and 36 stunned areas with preserved resting perfusion (flow of > or =80% of maximum). Resting flows were similar in necrosis and hibernation (0.43 +/- 0.18 versus 0.47 +/- 0.16 ml x min(-1) x g(-1); not significant), and both resting values were lower than those seen in stunning (0.79 +/- 0.24; p < 0.05). Flow response to dobutamine was markedly reduced in necrosis (dobutamine/resting flow = 1.16 +/- 0.27), whereas it was maintained in hibernation (1.65 +/- 0.54) and stunning (1.42 +/- 0.57). Dobutamine improved function in a higher number of stunned (55%) than hibernating (16%) or necrotic (11%) segments.

CONCLUSION

Dobutamine improves function mainly in stunned myocardium and does not reliably identify hibernation. The lack of functional response in hibernation is not related to an exhausted vasodilating capacity.

摘要

未标注

本研究的目的是评估多巴酚丁胺超声心动图在鉴别心肌冬眠与心肌顿抑中的价值,并阐明收缩功能障碍的潜在病理生理机制。

方法

对21例急性前壁心肌梗死溶栓治疗1个月后出现单纯左前降支狭窄的患者进行评估。在静息状态及静脉输注多巴酚丁胺(10μg/kg/min)过程中,采用超声心动图和正电子发射断层显像(PET)测量局部心肌功能和血流灌注。

结果

以[18F]氟脱氧葡萄糖摄取为标准,102个运动失调节段中36个为坏死节段,66个为存活节段。存活节段根据[13N]氨血流分布进一步分为:30个冬眠节段伴有灌注缺损(血流<最大血流的80%),36个顿抑节段静息灌注正常(血流≥最大血流的80%)。坏死节段和冬眠节段的静息血流相似(0.43±0.18与0.47±0.16ml·min-1·g-1;无显著性差异),两者的静息值均低于顿抑节段(0.79±0.24;p<0.05)。坏死节段对多巴酚丁胺的血流反应明显降低(多巴酚丁胺/静息血流=1.16±0.27),而冬眠节段(1.65±0.54)和顿抑节段(1.42±0.57)的血流反应得以维持。多巴酚丁胺改善顿抑节段(55%)功能的比例高于冬眠节段(16%)和坏死节段(11%)。

结论

多巴酚丁胺主要改善顿抑心肌的功能,不能可靠地识别心肌冬眠。冬眠心肌缺乏功能反应与血管舒张能力耗竭无关。

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