The present study is the first time to establish a nomogram for LCOS based on the perioperative risk factors after HVR including BMI, LVEF and GLS. The AUCs for the development and validation groups both exceeded 0.75, indicating the prediction model has statistically significant discriminatory powers. According to the risk factors of LCOS shown in the nomogram model, might be beneficial for predicting outcomes of cardiac function and developing regimens to prevent LCOS.
According to our nomogram (Fig. 2), we can identify the point corresponding to the value of each predictor, and then sum these points together. The total point is associated with a probability that the patient will develop LCOS. For example, a patient underwent MVR with a BMI of 20, LVFE 55%, and GLS − 15. Totaling the points for this patient was 137.5 points in risk of LCOS of nomogram. This results in estimated LCOS rates of 41 % according to the nomogram.
As the most common and the most serious complication after cardiovascular surgery, LCOS affects the prognosis of the patients and increases the rate of death seriously [4]. In our study, the mortality rate (15.2% vs. 1.2%, p < 0.001), ICU stay (4 (3-5.75) vs.2 (2–4), p < 0.001) and the hospital stay (29 (26-33.75) vs. 24 (22–28), p < 0.001) were significantly higher in LCOS patients compared to those without LCOS. The widely accepted characteristics of LCOS included decreased heart pump function and the accompanying tissue hypoperfusion and hypoxia. However, there is no stringent diagnostic criterion of a low cardiac output state. In our study, we used a generally accepted clinical definition of low cardiac output syndrome, including a systolic blood pressure of less than 90 mmHg for at least 30 minutes or postoperative need for IABP and/or prolonged requirement for inotropic support. Low cardiac output syndrome occurs in about 18.4% of patients in our study. This incidence of LCOS is greater than the prevalence of previous reports on isolated mitral and aortic valve surgery (3.9 and 7%, respectively) [3, 6] but lower than the more recent reports (21.5% and 41%, respectively) [7, 8]. The differences in the prevalence of LCOS in our population can be explained by the different type of cardiac disease, demographic characteristics and definition selected.
As World Health Organization BMI classification was not very suitable for Asian, we adopted a China classification and divided patients into the following 3 groups: low weight ≦ 18.5, normal-over weight 18.5–27.9 and obese ≧ 28 [16]. BMI < 18.5 is one option requires defining malnutrition [17]. Malnutrition is associated with a 2-fold increase in the probability of postoperative inotropic support and independently predicts adverse clinical outcomes [14]. Furthermore, low-weight may also be a manifestation of other associated comorbidities, such as cachexia, frailty or severe chronic diseases [18]. In our study, consistent with previous research [19], we found that the risk for LCOS was higher in low weight population. The low-weight patients were older, weaker, more severe impairment of left ventricular ejection, and more complex surgery. We consider these could be the main reason why the LCOS incidence was higher in low-weight patients than that in normal weight. The relationship between obesity and adverse outcomes include LCOS after cardiac surgery were conflicting among previous reports. For instance, some studies concluded that obesity was significantly associated with increased risk of LCOS and other postoperative morbidities [20–22]. Whereas others reported that obesity was a protective factor for postoperative complications [23–25]. Furthermore, multiple studies have suggested a U-shaped relationship between BMI and mortality[26]. However, in the present study, there was no significant correlation between obesity and LCOS risk after HVR.
Left ventricular ejection fraction (LVEF) based on visual analysis of two-dimensional (2D) images or Simpson biplane method is the most widely used parameters to assess the left ventricular systolic function [27]. A decreased LVEF is an independent risk factor for both LCOS and mortality after cardiac surgery, and have been included in risk models such as EUROSCORE [28]. Impaired left ventricular function (LVEF < 50%) as an independent significant risk factor for LCOS has been described in some studies [29, 30]. Consistent with previous research, impaired LVEF was an independent risk factor for LCOS after HVR in our study. However, influence of LVEF is less significant in patients underwent heart valve surgery compared with the CABG [31, 32]. As ejection fraction is highly dependent on loading conditions, heart valve disease such as MR or AR can mask underlying LV dysfunction. Although the measurement of the LV function is normal and without obvious clinical symptoms, LV function is impaired [6, 7, 33]. In addition, this method heavily dependent on image quality and operator experience, and with significant inter-observer variability [34, 35].
Myocardial deformation imaging (Strain imaging) is an echocardiographic technique to directly quantify the extent of myocardial contractility. The most widely used parameter to detect LV systolic function is GLS [27]. Advantages of using GLS to assess LV systolic function compared to LVEF include better reproducibility, ability to identify more subtle alterations in the contractility of the left ventricle, non-reliance on geometric assumptions, and lack of influence by tethering effects [35]. Recent studies suggest that the GLS measured during preoperative transthoracic echocardiogram (TTE) was shown to predict early postoperative mortality and the need for a postoperative inotropic support in patients with LVEF > 50% undergoing HVR [36]. Although the incremental value of GLS over other established risk factors for postoperative LCOS is limited in a study which included all kinds of on-pump cardiac surgery [37], it has been considered as the most significant parameter for LCOS risk in patients with AS without severely depressed LVEF [7]. Consistent with previous studies, the results in our study indicated that GLS was an independent risk factor for LCOS after HVR. If the GLS ≧ -16, the total score of the monogram is more than 100, suggesting that GLS value can increase the LCOS risk of patients by 50% (100/200). In this study, we only included patients without severely depressed LVEF (LVEF < 40%), this result reflected indirectly a higher degree of LV subclinical dysfunction in our patients.
The study has several limitations. First, this is a retrospective cohort with limited cases, which cannot avoid selection bias; thus, prospective study with a larger sample size is needed to further confirm our conclusion. Second, our study is from a single center; although we validated the model by patient samples from different periods, it will be better to validate the model with data from another institution. Finally, we concerned only on patients undergoing valve replacement surgery without severely depressed LVEF and the data on other kinds of on-pump cardiac surgery are lacking; that makes the nomogram validated in this study may not be suitable for all patients. In spite of these drawbacks, this study firstly builds a nomogram of predicting LCOS in HVR patients.