In this case-control study, 208 patients were enrolled and the correlation between the LMR and the occurrence of severe post-calcific stenotic aortic dilatation was analyzed. The results presented the evidence of a lower LMR in the patients with severe post- calcific stenotic aortic dilatation compared to the patients without post-calcific stenotic aortic dilatation. And the incidence of severe post-calcific stenotic aortic dilatation in the high-LMR group was statistically lower than that in the low-LMR group. Finally, the LMR was considered as a novel predictor for severe post-calcific stenotic aortic dilatation after adjusting other possible variables.
The severe post-calcific stenotic aortic dilatation is often clinically silent until its catastrophic complication, acute aortic dissection or rupture, occurs(17). Although Davies and colleagues demonstrated that the ascending aorta with a diameter within 35–39 mm is not associated with aortic rupture or dissection, the risk of rupture or dissection increased dramatically by 27-fold if the diameter of ascending aorta reaches 60 mm or more (18). Thus, it is a clinical priority to identify the predictive biomarkers or modifiable risk factors in the prevention and treatment of severe post-calcific stenotic aortic dilatation.
The associated risk factors for post-calcific stenotic aortic dilatation in the previous reports were mainly male gender, bicuspid aortic valve, hypertension and smoking (19- 21). Aortic dilatation has been recently reported caused by inflammatory diseases such as infectious aortitis, Takayasu arteritis, and giant cell arteritis (7, 8, 22). And levels of several inflammatory biomarkers such as C-reactive protein (CRP) and interleukin (IL)- 6 are elevated in patients with thoracic aortic aneurysms, suggesting the effects of systemic inflammation on the pathophysiology (6). Of note, an increased activity of matrix metalloproteinases (MMPs) has been described in the media of thoracic aortic aneurysm, a characteristic of localized inflammation (9, 23). Recent evidence from basic research has also suggested the role of several canonical inflammatory signaling pathways, AP-1 and the ERK1/2 signaling pathway, in contributing to the inflammation in post-calcific stenotic aortic dilatation (24). However, the detailed mechanisms underlying the inflammatory reaction in post-calcific stenotic aortic dilatation is to still a large extent undetermined. And identifying feasible inflammatory biomarkers will be constructive in predicting the high-risk patients and supportive in early diagnosis and intervention.
LMR is calculated from the exact amounts of lymphocyte and monocyte of peripheral blood and has been uncovered as an independent predictive indicator of clinical outcomes in various cancers(10–14). As an inflammation-related indicator, a lower LMR appears to be associated with decreased survival and increased recurrence in malignancies(15). Our findings demonstrated that the LMR is significantly lower in the patients with severe post-calcific stenotic aortic dilatation compared to the patients without post-calcific stenotic aortic dilatation. And an inverse correlation was observed between the maximal diameter of ascending aorta and the LMR. It indicated that as the maximal diameter of ascending aorta develops from the normal status to dilatation, the LMR might reduce proportionally. Thus, the patients with CAVS having a lower LMR could be potentially categorized into the high-risk population of post-calcific stenotic aortic dilatation. With the aid of risk stratification of post-calcific stenotic aortic dilatation by LMR, early identification of patients at high risk might be realized, which would lead to the close monitoring and early initiation of efficient preventive and therapeutic strategies. And a more accurate cut-off LMR might also be used in early diagnosis of post-calcific stenotic aortic dilatation if more prospective studies with larger sample sizes in multiple ethnicities are available to confirm it.