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Patent foramen ovale: to close or not to close – still the question

机译:卵圆孔未闭:关闭还是不关闭–仍然是一个问题

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Introduction Patent foramen ovale (PFO) is a physiological remnant of the foramen ovale, a connection between atria which is essential in fetal circulation. It is assumed to be a normal variant, as it is present in 20-27% of the population in autopsy studies but only in 10-15% of patients in contrast transesophageal echocardiography (TEE) [1]. This discrepancy may be due to increase in size of PFO with age. Patent foramen ovale is a flap-like tunnel between atrial septa: primum and secundum in the location of the fossa ovalis. It is potential communication for right-to-left shunt. Patent foramen ovale usually opens during Valsalva manoeuvre and other physiological situations when pressure in the right atrium exceeds the left atrium, that is when negative pressure in the chest (e.g. during deep breath, cough, sneezing) raises systemic venous return. Patent foramen ovale remains unrecognized and silent in most cases. The Mayo Clinic autopsy study showed that the size of a PFO increases from a mean of 3.4 mm in the first decade to 5.8 mm in the 10th decade of life, as the valve of the fossa ovalis stretches with age [1]. The prevalence of PFO presence decreasing with age may be due to shorter life of patients with PFO or spontaneous closure. Recent evidence from surgical data show the opposite, that PFO prevalence is not related to age [2]. Patent foramen ovale (PFO) is associated with cryptogenic strokes, recurrent transient neurological deficits, sleep apnoea, decompression illness, and migraines [3]. Patent foramen ovale and cryptogenic stroke Cryptogenic stroke represents up to 40% of all ischaemic strokes [4]. It is a diagnosis by exclusion, based on thorough investigation of other established causes of stroke. The first paradoxical embolism related to PFO was described by Cohnheim in 1877. The most likely mechanism of cryptogenic stroke is paradoxical embolization through the PFO, but other possible hypotheses, such as the formation and release of thrombus from within the PFO tunnel and the passage of vasoactive humoral substances that are normally degraded in the pulmonary circulation, have also been suggested [5]. It is hard to show clearly, according to evidence-based medicine, that the PFO is worth closing, because there are no randomized positive studies showing a benefit of the closing strategy over... View full text...
机译:引言卵圆孔未闭(PFO)是卵圆孔的生理残余物,卵圆孔之间的连接对胎儿的循环至关重要。它被认为是正常变异,因为在尸检研究中它存在于人口的20-27%中,但在对比经食管超声心动图(TEE)中仅在10-15%的患者中存在[1]。这种差异可能是由于PFO的尺寸随年龄增长而增加。卵圆孔未闭是卵圆窝位置的房间隔:初生和继发膜之间的皮瓣状隧道。这是从右向左分流的潜在沟通方式。当右心房的压力超过左心房时,即当胸部的负压(例如在深呼吸,咳嗽,打喷嚏时)引起全身静脉回流时,卵圆孔未闭通常在Valsalva动作和其他生理情况下打开。在大多数情况下,卵圆孔未被识别并保持沉默。梅奥诊所的尸检研究表明,随着卵圆形窝的瓣膜随着年龄的增长,PFO的大小从生命的最初十年的平均3.4 mm增加到生命的第十个十年的5.8 mm [1]。 PFO的患病率随着年龄的增长而降低,可能是由于PFO患者的寿命缩短或自发性关闭所致。来自外科手术数据的最新证据表明,PFO的患病率与年龄无关[2]。卵圆孔未闭(PFO)与隐源性中风,反复发作的短暂神经功能缺损,睡眠呼吸暂停,减压病和偏头痛有关[3]。卵圆孔未闭和隐源性卒中隐源性卒中占所有缺血性卒中的40%[4]。它是基于对其他确定的中风原因的彻底调查,通过排除诊断。 Cohnheim在1877年首次描述了与PFO相关的悖论性栓塞。隐源性中风的最可能机制是通过PFO的悖论栓塞,但其他可能的假设,例如PFO通道内血栓的形成和释放以及还提出了通常在肺循环中降解的血管活性体液物质[5]。根据循证医学,很难清楚地表明PFO值得关闭,因为没有随机的阳性研究显示关闭策略比...有利。查看全文...

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