We were able to develop a simple score to predict the detection of PFO in ESUS patients. The AEM score measured with non-contrast TTE could be used to identify high-risk patients for PFO and reduce the use of bubble test. This allows the clinician to easily screen patients at highest risk of PFO for further confirming exams. Moreover, our data addressed the echocardiographic changes of heart structures and functions in PFO patients, which could be useful to explore the potential mechanism of ESUS caused by PFO.
Dilatation of the aortic root may increase the risk of RLS by changing the angulation of the heart in such a way that flow streaming from the inferior vena cava into the right atrium is directed more towards the ostium secundum; thrombotic material is therefore more likely to cross into the systemic circulation, possibly causing a cryptogenic stroke. It has been reported that ARd, marked at the level of the sinuses of Valsalva (34 ± 4 vs 31 ± 3 mm, p < 0.01), is larger in PFO patients with cryptogenic stroke than in healthy people.7 In this study, we compared the ARd in a ESUS patient cohort. All subjects had a homologous profile and our results consisted with previous study, demonstrated a larger median ARd of 34 mm in PFO patients than those without PFO.
E-wave velocity reflects the left atrial (LA)-left ventricle (LV) pressure gradient during early diastole and is affected by alterations in the rate of LV relaxation and LA. Elevated LA pressure is associated with the absence of RLS in AF stroke patients and may prevent opening of a PFO.8 In our study, patients with PFO had lower Em suggest a decreased LA pressure, may associated with a RLS-related stroke.
Mitral regurgitation is the most common valvular heart disorder in high-income countries, and its prevalence increases with age.9 In a large-scale cohort of UK adults with 10 years of follow-up, elevated blood presure was continuously associated with an increased risk of mitral regurgitation.10 Considering that the association between high blood pressure and mitral regurgitation is similar with that of arteriosclerosis stroke. ESUS patients with no mitral regurgitation may have fewer atherosclerotic risk factors, however, higher likelihood of PFO.
Several limitations of the present study need to be underlined. First, it was a single-center retrospective cohort study with a small sample size. Second, PFO was only diagnosed by the bubble test of TCD, not TEE. Although TEE was considered to be the standard technique for identifying a PFO, some patients were intolerant of this method. Finally, all patients in our study had a stroke. Thus, the differences between those with and without stroke in PFO were not examined, which needs to be addressed in further studies.