Roudaut R, Héraudeau A, Gosse P, Aouizerate E, Dequecker J L, Dallocchio M
Arch Mal Coeur Vaiss. 1986 Sep;79(10):1487-94.
In a retrospective series of 960 cases of tricuspid regurgitation studied by two-dimensional echocardiography 6 patients presented a systolic defect of valvular coaptation. The origin of this defect varied: one case was due to carcinoid, two to rheumatic cardiopathy, two to papyraceous right ventricle and one to sclerodermia associated with pulmonary arterial hypertension. The mechanism of the lacking coaptation varies according to the etiology: valvular retraction in carcinoid cardiopathy, right-ventricle dilatation, dilatation of the tricuspid ring and altered kinetics of the right ventricle in the other cases. Changed contractility of the right ventricle is the only element allowing to distinguish tricuspid regurgitation with and without a coaptation defect. Clinically this abnormality always points to an advanced stage of severe tricuspid regurgitation.
在一项通过二维超声心动图研究的960例三尖瓣反流的回顾性系列研究中,6例患者出现瓣膜对合的收缩期缺陷。这种缺陷的起源各不相同:1例是由于类癌,2例是由于风湿性心脏病,2例是由于纸样化右心室,1例是由于与肺动脉高压相关的硬皮病。对合缺乏的机制根据病因而异:类癌性心脏病中的瓣膜回缩,其他病例中的右心室扩张、三尖瓣环扩张以及右心室动力学改变。右心室收缩性改变是区分有和没有对合缺陷的三尖瓣反流的唯一因素。临床上,这种异常总是提示严重三尖瓣反流的晚期阶段。