This is the first study to investigate the effect of pIABP in STEMI patients undergoing urgent CABG, including those with CS and cardiac arrest. The key findings of this study were that patients undergoing urgent CABG with pIABP had (1) still high 30-day and 1‑year mortality, (2) similar 30-day and 1‑year mortality to the non-pIABP group despite being at higher risk at baseline, (3) similar postoperative complications to those without pIABP, (4) no particular subgroups with a significantly different treatment effect.
Despite the significant differences in clinical presentation at baseline in favour of the non-pIABP group, both groups had similar unadjusted 30-day and 1‑year mortality. However, after adjusting for relevant confounders such as age, gender, comorbidity, CS, poor LVEF and PI, using IPTW, patients in the pIABP group had a significant survival benefit.
It has previously been demonstrated that an IABP increases coronary blood flow, decreases the workload of the myocardium and increases the cardiac output by 0.5–1 l/min [13, 14]. The rationale of pIABP is that these haemodynamic improvements can precondition the ischaemic heart so that the risk of postoperative low-cardiac output syndrome, postoperative CS and mortality is reduced. There is conflicting evidence regarding pIABP in elective patients. In the first randomised clinical trials (RCTs) by Christenson et al., pIABP use reduced in-hospital mortality in high-risk patients, generally defined as patients with left main disease or LVEF < 40% undergoing elective CABG [3,4,5]. A meta-analysis of 10 RCTs on pIABP in high-risk surgery patients also suggests a mortality benefit [15].
However, in two more recent RCTs with larger study populations, pIABP use did not improve outcome in high-risk cardiac bypass surgery patients [7, 16]. The primary outcome in these studies was a composite endpoint of major morbidity and mortality. Rocha Ferreira et al. suggest that in the case of optimal preoperative treatment, an IABP has little additive value [16]. These results are in line with the findings of the BCIS-1 trial, demonstrating that IABP insertion prior to complex PCI does not reduce mortality [17]. Thus, the value of pIABP in elective patients is still questionable.
In patients with STEMI, whether complicated by CS or not, the balance between myocardial oxygen demand and supply is even more disturbed than in elective high-risk patients. Therefore, haemodynamic support in these patients could be of more importance.
In a previous study in patients with non-STEMI and STEMI, the authors concluded that pIABP was associated with reduced in-hospital mortality [8]. Patients were included in this study if CABG was performed within 5 days of admission. Time to surgery is not reported; however, this time interval may have increased selection bias. Patients with persisting complaints or deteriorating haemodynamics were likely to have had surgery sooner than relatively stable patients who could wait until day 5. To avoid this risk of selection bias, we included only patients who underwent CABG within 2 days in this study and used the factor ‘CABG after 24 h’ in our analysis and propensity score. Furthermore, the authors excluded CS patients based on the IABP SHOCK-II trial findings. In this landmark trial, IABP use did not reduce mortality in STEMI complicated by CS [11]. However, in this study, most patients were treated with primary PCI, with only 3.5% undergoing immediate CABG. Therefore, the results of this study cannot be extrapolated to patients with STEMI and CS undergoing urgent CABG. In our study, all patients with STEMI, as well as those with CS and cardiac arrest, were included.
In patients with persisting or ongoing ischaemia, an IABP can be inserted as a bridge-to-CABG, although robust evidence is lacking. Unsuccessful PCI in STEMI is associated with higher mortality than STEMI with successful PCI, especially in patients with CS [18, 19]. In previous retrospective studies, IABP use in patients with PI after primary PCI was associated with reduced mortality [19, 20]. However, more recently, IABP insertion did not reduce mortality in patients with large anterior STEMI and PI [21]. In our study, subgroup analysis did not demonstrate reduced mortality in patients with PI treated with a pIABP.
A possible explanation for previous failure to demonstrate the benefit of a pIABP could be an increased complication risk counterbalancing the positive effect of IABP use. An IABP is inserted via the femoral artery through a 7 French sheath and is associated with an increased bleeding risk and higher mortality [17]. Adequate positioning, just below the aortic arch on a chest X‑ray, is imperative for good functioning, whereas malpositioning is associated with a 4- to 13-fold increase in life-threatening complications [22]. Furthermore, thromboembolic or ischaemic events may occur due to blocking major abdominal vessels or dislodging of atheromatous debris from the aortic vessel wall [23]. Unfortunately, our study did not have sufficient data to investigate these complications.
As an IABP can improve cardiac output, coronary flow and afterload, we found an improved clinical outcome in our study. Perhaps a device generating more haemodynamic support, such as Impella (Abiomed, Danvers, MA, USA), could further improve the clinical outcome. The Impella is a catheter-based microaxial flow pump placed across the aortic valve into the left ventricle (LV). It unloads the LV and increases the cardiac output and coronary blood flow [24,25,26]. It also increases the cardiac power output, which was previously shown to be the strongest haemodynamic predictor of mortality in patients with STEMI complicated by CS [27, 28]. Impella use in elective high-risk PCI does not reduce mortality compared to an IABP but does improve procedural success [29]. However, there are only limited data on Impella use in high-risk CABG, moreover related only to postoperative Impella use [30]. Until now, there has been no study on the effect of preoperative Impella use in urgent CABG.
LimitationsThere are several limitations to this study. First, this is a single-centre study with an observational design. Second, the small sample size, especially the non-pIABP group, limits subgroup analysis. Third, implantation of a pIABP was not dictated by a protocol, increasing the potential for selection bias. We partially tried to overcome this by performing a propensity score analysis. Finally, we did not have data on several variables, such as lactate and haemodynamic parameters during hospital stay. Given the above-mentioned limitations, the findings of our study should be interpreted as hypothesis generating.
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