This study investigated the prognostic value of admission SI in patients with acute AD and IMH and obtained several important findings. First, admission SI is associated with short-term, all-cause in-hospital mortality of acute AD and IMH patients. Second, after multivariate adjustments, admission SI was still an independent risk factor for predicting the 30-day, all-cause in-hospital mortality. Third, for patients with a high risk of mortality (SI≥0.7), timely surgery or TEVAR will improve the unfavorable 30-day, in-hospital outcomes.
AD and IMH are life-threatening aortic diseases with high mortality due to potentially fatal complications. A previous study indicates that the early mortality of acute AD is about 1-2% per hour once symptoms occur [20]. Some studies found that the hospitalization mortality is between 20% and 30% in patients with acute AD [20, 21]. Separately, the inpatient mortality for Stanford B AD, about 10% in a recent Japanese nationwide survey [22], is much lower than that for Stanford A AD (up to 32.5%) [23]. According to the analysis from the International Registry of Acute Aortic Dissection, the in-hospital mortalities of Stanford A AD and IMH patients are 26.5% and 26.6% separately, and that are 11.1% and 4.4% for Stanford B AD and IMH patients [24]. However, the difference of mortality from AD and IMH did not reach statistical significance [24]. And in the present study, the in-hospital mortalities for Stanford A and Stanford B AD and IMH are 23.1% and 4.7% respectively, which are a little bit lower than that publicized by previous studies [22-24]. These improved mortalities might be associated with the increased ability of quick diagnose with AAS and obtaining more effective treatments both medication and surgery or TEVAR. However, the long-term outcomes of Stanford B AD are not necessarily better than that of Stanford A AD [25, 26]. Stanford B AD is also associated with a high mortality rate (~20% at 3 years [26] ) and a high morbidity rate (~30% morbidity at 2 years) in the long term [27, 28]. Thus, quick patients screening is so important for acute AD and IMH that we could provide the optimal interventions as early as possible, including not only medical therapy but also surgery or TEVAR.
In 1967, the concept of SI was first proposed as a simple and effective index to evaluate the degree of hypovolemia in hemorrhage and infectious shock states [6]. A previous study has shown that SI is inversely related to blood loss, cardiac index, stroke volume, left ventricular stroke work and mean blood pressure [8], and it provides a non-invasive means to monitor deterioration or recovery of left ventricular stroke work during acute hypovolemic and normovolemic circulatory failure [8]. Elevated SI predicts hemodynamic instability and has been demonstrated to be associated with many critical diseases, such as ruptured abdominal aortic aneurysm [9], stroke [5, 10], acute myocardial infarction [11-14], pulmonary embolism [15, 16], severe sepsis [17, 18], trauma [29], and pneumonia [30, 31]. As a meaningful indicator of predicting pre-hospital or in-hospital risk [5, 9, 11, 13], SI plays an important role in making decisions for treatment of these emergency conditions.
When acute AD or IMH occurs, effective circulating blood volume may decrease, which proportionally lead to hemodynamic instability reflected by a blood pressure decrease and heart rate increase. In the events of accompanying stabbing pain, malperfusion or renal dysfunction, the situation of hemodynamic instability would further deteriorate, especially with cardiac tamponade and rupture of the aorta. So, as a simple index of representing hemodynamic instability, SI should be associated with the risk of death in acute AD and IMH. And our study confirms this relationship, showing that admission SI predicts the 30-day, all-cause in-hospital mortality in acute AD and IMH. Also, in the subgroup analysis, we found that, for the patients without surgery (Stanford A AD and IMH) or TEVAR (Stanford B AD and IMH), the SI≥0.7 indicated the higher in-hospital mortality. This is a very meaningful finding for guiding clinical practice. According to the strata of SI (<0.7 vs ≥0.7), we can further identify the high-risk patients. Then, to decrease the dying risk, it is necessary to monitor patients much closely and to develop better treatment for them.
Although the sample size of our study is large, some limitations need to be acknowledged. First, this is a retrospective study, which poses a risk of patient selection bias. Second, as a single-center study, our participants cannot represent all patients with acute AD and IMH. In addition, we only investigated the relationship between admission SI and the short-time, in-hospital mortality in acute AD and IMH patients, but we do not know how it arises. Strictly designed multi-center prospective studies are needed to further clarify the pathophysiologic mechanisms.