Ochsenfahrt C, Hemmer W, Oertel F, Hannekum A
Abteilung Herzchirurgie, Universitätsklinikum Ulm.
Z Kardiol. 1999 Nov;88(11):941-7. doi: 10.1007/s003920050372.
There is a significantly higher incidence of cerebral ischemia among patients with an atrial septal aneurysm and/or a patent foramen ovale. According to the information provided by modern diagnostic procedures--and in particular by transesophageal echocardiography--two pathogenic mechanisms should be considered as possible causes of the cerebral ischemia. Thrombi may develop locally in the left atrium or atrial septal aneurysm and lead to embolization or, alternatively, thrombi from the inflow region of the inferior vena cava may become trapped in the atrial septal aneurysm and pass through the patent foramen ovale to bring about embolization in the arterial bloodstream. Current treatment consists of life-long anticoagulation with coumarin derivatives in order to prevent further neurological complications. With this treatment, however, the risk of producing hemorrhages cannot be regarded as trivial, especially in old people. Surgical intervention with the insertion of a button device has so far only been attempted in a few isolated cases, and it is in any case no use if there is only an atrial septal aneurysm without a patent foramen ovale. As an alternative to administering anticoagulants for the rest of the patient's life, we operated on five cases of atrial septal aneurysm with patent foramen ovale followed by the appearance of cerebral ischemia. As with the surgical treatment of atrial septal defects in general, the risk of the operation (or of subsequent complications) is very slight indeed. No such problems arose in any of our patients, no blood transfusions were necessary, and after short postoperative treatment they could all be discharged. For younger patients with little risk from the treatment itself, we regard surgical intervention in cases of atrial septal aneurysm with a patent foramen ovale and cerebral ischemia as an important therapeutic alternative.
房间隔瘤和/或卵圆孔未闭患者发生脑缺血的几率明显更高。根据现代诊断程序——尤其是经食管超声心动图——所提供的信息,应考虑两种致病机制可能是脑缺血的原因。血栓可能在左心房或房间隔瘤局部形成并导致栓塞,或者,来自下腔静脉流入区域的血栓可能被困在房间隔瘤中,并通过卵圆孔未闭进入动脉血流导致栓塞。目前的治疗方法是使用香豆素衍生物进行终身抗凝,以预防进一步的神经并发症。然而,采用这种治疗方法,出血风险不可小觑,尤其是在老年人中。到目前为止,仅在少数孤立病例中尝试过使用纽扣装置进行手术干预,而且如果只有房间隔瘤而没有卵圆孔未闭,这种方法无论如何都不起作用。作为让患者终身服用抗凝剂的替代方法,我们对5例伴有卵圆孔未闭且随后出现脑缺血的房间隔瘤患者进行了手术。与一般房间隔缺损的手术治疗一样,手术风险(或后续并发症)实际上非常小。我们的任何一位患者都没有出现此类问题,无需输血,术后经过短期治疗后他们都可以出院。对于治疗本身风险较小的年轻患者,我们认为对伴有卵圆孔未闭和脑缺血的房间隔瘤患者进行手术干预是一种重要的治疗选择。