Endo M, Yamaki S, Ohmi M, Tabayashi K
Department of Thoracic and Cardiovascular Surgery, Tohoku University School of Medicine, Sendai, Japan.
Ann Thorac Surg. 2000 Jan;69(1):193-7. doi: 10.1016/s0003-4975(99)01079-6.
Pulmonary venous obstruction (PVO) induces pulmonary arterial hypertension, as well as pulmonary venous hypertension, and jeopardizes the repair of cardiac lesions.
Four cases of congenital mitral stenosis and 4 cases of cor triatriatum (Lucas type A), ages ranging from 2 months to 16 years, were histologically examined on pulmonary vasculature. Histometrical analysis was performed on medial thickness and intimal changes of both pulmonary arteries and veins. For comparison, the examination of pulmonary vasculature in ventricular septal defect (VSD) cases was also performed.
Medial thickening and intimal fibrosis, in both pulmonary arteries and veins with widespread lymphangiectasia, were characteristic vascular changes of PVO cases. Medial thickness of pulmonary arteries was correlated with preoperative pulmonary arterial pressure (PAP) (r = 0.77, p = 0.03 for systolic PAP), and greater than that of VSD cases. Medial thickness of pulmonary veins was also greater in PVO cases. Intimal fibrosis of pulmonary arteries and veins was seen extensively at the advanced ages, whereas no plexiform lesions or more advanced stages of pulmonary vascular disease were present.
Congenital PVO induced progressive medial thickening and intimal fibrosis in pulmonary arteries and veins accompanied by lymphangiectasia. However, no plexiform lesions or more advanced stages of pulmonary vascular disease were present, which may explain the reversibility of pulmonary hypertension due to congenital PVO.
肺静脉阻塞(PVO)可导致肺动脉高压以及肺静脉高压,并危及心脏病变的修复。
对4例先天性二尖瓣狭窄和4例三房心(卢卡斯A型)患者进行了肺血管组织学检查,患者年龄从2个月至16岁不等。对肺动脉和肺静脉的中膜厚度和内膜变化进行了组织计量学分析。作为对照,还对室间隔缺损(VSD)病例的肺血管进行了检查。
肺动静脉中膜增厚和内膜纤维化伴广泛淋巴管扩张是PVO病例的典型血管变化。肺动脉中膜厚度与术前肺动脉压(PAP)相关(收缩期PAP的r = 0.77,p = 0.03),且大于VSD病例。PVO病例的肺静脉中膜厚度也更大。肺动脉和肺静脉内膜纤维化在年龄较大的患者中广泛存在,而未发现丛状病变或更晚期的肺血管疾病。
先天性PVO可导致肺动脉和肺静脉逐渐出现中膜增厚和内膜纤维化,并伴有淋巴管扩张。然而,未发现丛状病变或更晚期的肺血管疾病,这可能解释了先天性PVO所致肺动脉高压的可逆性。