Teragaki M, Horio T, Shimada K, Iida H, Itagane H, Tahara A, Toda I, Akioka K, Yasuda M, Oku H
First Department of Internal Medicine, Osaka City University Medical School, Japan.
Jpn Circ J. 1991 Dec;55(12):1200-5. doi: 10.1253/jcj.55.1200.
We described a 37-year-old man with a subaortic "fibrous sac", admitted for congestive heart failure. On 2-dimensional echocardiography a saccular structure was seen to extend from the left coronary cusp of the aortic valve to the outflow tract of the left ventricle. By color Doppler imaging, a grade 3 aortic regurgitation was recognized. Aortic regurgitant flow was recorded from the left coronary cusp to the saccular lesion. When congestive heart failure became exacerbated, the repeat examination showed the regurgitant flow passing through the perforated bottom of this lesion and reaching the left ventricular cavity. On microscopic examination of the excised valve, capillary proliferation and inflammatory changes were recognized near the annular region of the left coronary cusp. The edge of the valve leaflet and the other 2 cusps were intact. It is likely that our patient had a mycotic aneurysm near the aortic ring. We speculate that aortic regurgitation followed inflammation. It dilated the left ventricular cavity and contributed to congestive heart failure. Inflammation also weakened the tissue near the annulus, causing it to protrude into the subaortic region thus forming a small aneurysm. It may have grown to become a large saccular structure under high aortic pressure. That is, it became a "giant" endocardial pocket with inflammatory process. Finally, the rupture of this sac caused a massive aortic regurgitation, exacerbating congestive heart failure.
我们描述了一名37岁患有主动脉下“纤维囊”的男性患者,因充血性心力衰竭入院。二维超声心动图显示一个囊状结构从主动脉瓣左冠状动脉瓣叶延伸至左心室流出道。通过彩色多普勒成像,识别出3级主动脉瓣反流。记录到主动脉反流从左冠状动脉瓣叶流向囊状病变处。当充血性心力衰竭加重时,复查显示反流通过该病变的穿孔底部进入左心室腔。对切除瓣膜进行显微镜检查时,在左冠状动脉瓣叶瓣环区域附近发现毛细血管增生和炎症改变。瓣膜小叶边缘及另外两个瓣叶完整。我们的患者很可能在主动脉环附近患有霉菌性动脉瘤。我们推测主动脉瓣反流继发于炎症。炎症使左心室腔扩张并导致充血性心力衰竭。炎症还削弱了瓣环附近的组织,使其突入主动脉下区域,从而形成一个小动脉瘤。在高主动脉压力下,它可能逐渐增大成为一个大的囊状结构。也就是说,它变成了一个伴有炎症过程的“巨大”心内膜袋。最后,这个囊破裂导致大量主动脉瓣反流,加重了充血性心力衰竭。