Division of Pulmonary and Critical Care Medicine, San Diego School of Medicine, University of California, San Diego, CA 92103, USA.
Curr Opin Pulm Med. 2013 Sep;19(5):422-9. doi: 10.1097/MCP.0b013e328364379f.
Chronic thromboembolic pulmonary hypertension (CTEPH) is a life-threatening complication that affects a small but appreciable percentage of patients after acute pulmonary embolism. The cause of CTEPH is under investigation, but no single causative mechanism has yet been identified.
CTEPH is likely a complication of residual thrombotic material in the pulmonary arteries that becomes transformed into intravascular scars. Pulmonary artery residua are relatively common after acute pulmonary embolism, and CTEPH may be an extreme manifestation of this phenomenon. Several intriguing observations have been made in patients with CTEPH that give insights into the mechanisms responsible for its formation. Two general pathways have been investigated: resistance of thromboemboli to lysis and attenuation of cellular processes involved in thrombus resolution. This review discusses the evidence supporting each pathway as a mechanism for CTEPH formation, as well as the interaction between the two.
CTEPH may be due to a complex interaction between thrombotic/thrombolytic processes and angiogenic cellular remodeling of organized thrombi. The factors involved may, in fact, vary among CTEPH patients. An understanding of the interplay between the factors that cause CTEPH may help quantify the risk of its occurrence and provide insights into how it can be prevented.
慢性血栓栓塞性肺动脉高压（CTEPH）是一种危及生命的并发症，在急性肺栓塞后，它会影响一小部分但数量可观的患者。CTEPH 的病因正在研究中，但尚未确定单一的致病机制。
CTEPH 可能是肺动脉内残留血栓物质转化为血管内瘢痕的一种并发症。急性肺栓塞后肺动脉残留物相对常见，而 CTEPH 可能是这种现象的极端表现。在 CTEPH 患者中已经观察到了一些有趣的现象，这些现象为其形成的机制提供了一些见解。已经研究了两种一般途径：血栓栓塞物对溶解的抵抗力和参与血栓溶解的细胞过程的衰减。这篇综述讨论了每种途径作为 CTEPH 形成机制的证据，以及两者之间的相互作用。
CTEPH 可能是由于血栓形成/溶栓过程与血栓机化的血管生成细胞重塑之间的复杂相互作用所致。涉及的因素实际上可能在 CTEPH 患者之间有所不同。了解导致 CTEPH 的因素之间的相互作用可能有助于量化其发生的风险，并深入了解如何预防 CTEPH。
