The identification of LVEF after CABG in patients with ischemic cardiomyopathy is considered as a crucial factor to predict the outcome. Improved function and survival following surgical revascularization have been shown in patients with LV dysfunction which is predominantly due to hibernating or stunned myocardium [17]. Our study focused on the effect of CABG on LVEF in patients with baseline impaired systolic function. In this study, a significant improvement in LV systolic function was observed with CABG. This supports the hypothesis that surgical revascularization and restoration of the blood flow to ischemic myocardium preserve already viable and functioning myocardial muscle against later infarction, recruit the hibernating myocardium, and reduce LV remodeling and ischemic burden which all impact LV function recovery.
Because of the lack of routine echocardiographic examination postoperatively, few studies identified the changes in LV systolic function after CABG. Similarly, a recent study was conducted and concluded that successful results of CABG in patients with EF < 50% can be achieved by careful selection of patients and management [18]. Also, another study found that a significant improvement was observed in LV systolic function in patients with preoperative systolic dysfunction [19]. Many factors contributing to the outcome of patients with baseline LV systolic dysfunction after CABG include perioperative care, severity of preoperative LV systolic dysfunction, surgical skills, complete revascularization, type of myocardial protection, cardiac anesthesia management, emergency cardiac facilities, and postoperative intensive care monitoring and management. However, Koene et al. [2] conducted a similar study and concluded that CABG is associated with worse outcome on LV systolic function [20]. A decrease in LV systolic function with CABG surgery could be explained by many factors: significant intraoperative global ischemia which adversely affects the LV function [21] or from myocardial stunning [22] or early postoperative graft failure [23]. In contrast also to our findings, a small study did not find a significant change in LVEF immediately post CABG [24].
Our study demonstrates that in the early mortality, 5.4% is acceptable and in agreement with the current published data [25, 26]. Similarly, Elassy et al. reported higher but insignificant mortality rate in patient with LVEF < 35% (5.6% vs 2.4%) [27]. This is reflecting a marked improvement in the outcome of ischemic cardiomyopathy patients with CABG in highly qualified centers.
Predictors of adverse outcome with CABG
In this study, we classified our patients into two groups with and without severe LV systolic dysfunction and investigated all the predictors that could lead to poor outcome with CABG.
Type II DM was a significant predictor of adverse outcome of our patients.
Although CABG is considered the best revascularization strategy in diabetic patients, a significantly higher rate of mortality was continually observed in patients with type II DM compared to patients without type II DM [28, 29]. Reasons that have been suggested for that are more aggressive disease with advanced stage of DM in these patients, adverse effects of insulin therapy, hyperinflammatory, and hormonal hyperactivation response [30, 31].
The use of intra- or postoperative IABP was a significant predictor of in-hospital mortality in all patients and when EF was < 50%. Although the use IABP is important to support failing circulation during CABG, it is well known as a risk factor for mortality [32, 33]. It can be explained by that patients who are receiving IABP are already at high risk of increased mortality because of unstable hemodynamic status and its complications (stroke, paraplegia, limb ischemia, infection, and hemolysis) that all have an impact on mortality after CAGB [34, 35].
We also demonstrated advanced diastolic dysfunction as a predictor of adverse outcome and mortality in patients with LV dysfunction. Diastolic dysfunction has been reported to be an independent risk predictor of postoperative heart failure, atrial fibrillation, and cardiac death in different studies [36, 37].
Finally, a limited number of patients are included due to the nature of a single center.
Some patients also did not have echocardiography follow-up, hence excluded from our study. Follow-up echocardiography was done few months only post CABG, and thus, our results could not be correlated with long-term outcome after surgery. Like other studies evaluating adverse outcome after CABG in patients with reduced LVEF, data regarding patency of grafts were not applicable in our study. The results of this study are encouraging, and it needs corroboration in multicenter larger population with longer follow-up.