Olman M A, Auger W R, Fedullo P F, Moser K M
Department of Medicine, University of California, San Diego.
Chest. 1990 Dec;98(6):1430-4. doi: 10.1378/chest.98.6.1430.
After pulmonary thromboendarterectomy, performed for relief of chronic thromboembolic pulmonary hypertension, perfusion lung scans have frequently disclosed new perfusion defects in segments served by undissected pulmonary arteries. Our hypotheses were that these new postoperative defects occurred with great frequency and did not represent postoperative vessel occlusion. We retrospectively reviewed the preoperative and postoperative perfusion scans of 33 consecutive patients undergoing pulmonary thromboendarterectomy. New postoperative perfusion defects were noted in 23 of 33 patients. The incidence of new defects was increased tenfold in segments that had (1) normal preoperative angiographic findings, (2) normal preoperative radionuclide perfusion, and (3) not been entered at the time of surgery. Postoperative angiograms, available in 15 of 33 patients, documented the nonembolic, nonocclusive nature of the new perfusion scan defects. The most plausible alternate explanation for this previously undescribed finding is a redistribution of pulmonary arterial resistance induced by the thromboendarterectomy, namely, a pulmonary vascular "steal."
为缓解慢性血栓栓塞性肺动脉高压而进行肺血栓内膜剥脱术后，灌注肺扫描经常在未解剖肺动脉供血的肺段发现新的灌注缺损。我们的假设是，这些新的术后缺损发生率很高，且并非代表术后血管闭塞。我们回顾性分析了连续33例行肺血栓内膜剥脱术患者的术前和术后灌注扫描结果。33例患者中有23例出现了新的术后灌注缺损。在术前（1）血管造影结果正常、（2）放射性核素灌注正常、（3）手术时未涉及的肺段，新缺损的发生率增加了10倍。33例患者中有15例可获得术后血管造影，证实了新灌注扫描缺损的非栓塞、非闭塞性质。对于这一此前未描述的发现，最合理的另一种解释是肺血栓内膜剥脱术引起的肺动脉阻力重新分布，即肺血管“窃血”。
