Berthet K, Lavergne T, Cohen A, Guize L, Bousser M G, Le Heuzey J Y, Amarenco P
Departments of Neurology, Saint-Antoine Hospital, Paris, France.
Stroke. 2000 Feb;31(2):398-403. doi: 10.1161/01.str.31.2.398.
Atrial septal abnormalities have been associated with cryptogenic ischemic stroke in young patients, but the causal link has not yet been established. Paradoxical embolism is considered the most likely mechanism but is rarely proven. It can be hypothesized that, in those patients, paroxysmal atrial arrhythmias, potentially favored by the anatomic abnormalities, can be another cause of thrombus formation and subsequent embolism to the brain. In this study we assessed the relationship between atrial vulnerability, reflecting arrhythmogenic properties of the atria, and atrial septal abnormalities in young patients with cryptogenic ischemic stroke.
We enrolled 62 consecutive patients aged <55 years who had ischemic stroke of unknown cause and transesophageal echocardiography to assess atrial septal aneurysm (ASA) or patent foramen ovale (PFO) (ie, atrial septal abnormalities). These patients underwent electrophysiological study to measure atrial refractoriness and conduction time defining a vulnerability index (ie, latent atrial vulnerability) and to assess the inducibility of sustained (lasting >60 seconds) atrial fibrillation with the use of programmed atrial stimulation. Actual atrial vulnerability was defined by the presence of both latent vulnerability and inducibility of sustained atrial fibrillation lasting >60 seconds.
We found atrial vulnerability in 58% of patients with atrial septal abnormalities and in 25% of patients without (odds ratio=4.1 [95% CI, 1.3 to 12.7; P<0.02]). The difference between patients with and without PFO or between patients with both PFO and ASA and those without were also significant. Patients with inducible sustained atrial fibrillation had more frequent past history of palpitations and syncope than patients without (P<0.02).
Atrial vulnerability is associated with atrial septal abnormalities in patients with cryptogenic stroke. This result raises the question of the potential role of transient atrial arrhythmias in thrombus formation in the presence of PFO or ASA.
房间隔异常与年轻患者的隐源性缺血性卒中相关,但因果关系尚未确立。矛盾栓塞被认为是最可能的机制,但很少得到证实。可以推测,在这些患者中,可能受解剖异常影响的阵发性房性心律失常可能是血栓形成及随后脑栓塞的另一个原因。在本研究中,我们评估了反映心房致心律失常特性的心房易损性与年轻隐源性缺血性卒中患者房间隔异常之间的关系。
我们连续纳入了62例年龄<55岁、患有原因不明缺血性卒中且接受经食管超声心动图检查以评估房间隔瘤(ASA)或卵圆孔未闭(PFO)(即房间隔异常)的患者。这些患者接受电生理研究,以测量心房不应期和传导时间来定义一个易损性指数(即潜在心房易损性),并使用程控心房刺激评估持续性(持续>60秒)心房颤动的诱发情况。实际心房易损性由潜在易损性和持续>60秒的持续性心房颤动的诱发性共同存在来定义。
我们发现,房间隔异常患者中有58%存在心房易损性,无房间隔异常患者中有25%存在心房易损性(比值比=4.1[95%CI,1.3至12.7;P<0.02])。有或无PFO的患者之间,以及同时有PFO和ASA与无PFO和ASA的患者之间的差异也很显著。可诱发持续性心房颤动的患者比无持续性心房颤动的患者有更频繁的心悸和晕厥既往史(P<0.02)。
隐源性卒中患者的心房易损性与房间隔异常相关。这一结果提出了短暂性房性心律失常在存在PFO或ASA时血栓形成中潜在作用的问题。