The intra-aortic balloon pump (IABP) is a mechanical unloading device that is used to decrease myocardial oxygen demand while at the same time increasing cardiac output.^1–3 In patients with acute MI who present with cardiogenic shock intra-aortic balloon counterpulsation (IABC) has been shown to improve survival.^3–9 Mechanical unloading of the ventricle prior to intervention has shown in animal models to reduce infarct size and decrease reperfusion injury.¹⁰ In patients with large acute infarcts, IABC has been shown to improve clinical outcomes.¹¹ Observational data have also suggested that aortic counterpulsation may reduce the rate of re-occlusion of the infarct-related artery after balloon angioplasty.^12,13 However, the use of counterpulsation in patients undergoing emergency cardiac catheterization during acute myocardial infarction (MI) has been associated with both an increase in hemorrhagic complications and a higher rate of vascular complications.^7,14 Hence, it is important to define unequivocal benefit and clarify the mechanisms underlying the beneficial effects of IABC for routine use in high-risk patients.

       In this issue of the journal, Vijayalakshmi et al examined the effects of IABC on coronary flow early after percutaneous coronary intervention in a high-risk group of patients early post- MI.¹⁵ The prophylactic use of IABP in the “high risk” PCI setting is anecdotal and largely observational with no randomized study comparing these strategies. However, the evolution of interventional techniques and the high rate of use of Gp IIb/IIIa inhibitors and thienopyridine anti-platelet therapies have certainly helped improve outcomes. The incremental benefit from IABC in this situation is not known. The authors tested the hypothesis that IABC following PCI in “high risk” patients would acutely improve coronary flow and myocardial perfusion, thereby improving regional cardiac function. They found in their trial no early benefit in TIMI flow grade (TFG), myocardial blush grade (MBG) and TIMI frame count (TFC). In addition, they showed no improvement in function at 30 days using echocardiography. This study is useful because, there were previously very little data available to guide cardiologists with respect to whether IABC is helpful prophylactically in high-risk patients. From their analysis, there is no benefit in using IABC routinely after PCI in high-risk patients early post-MI. However, several potential limitations of their study should be noted.

       Firstly, the small number of patients included in the study and control group makes it difficult to draw firm conclusions as to the net clinical benefit and the generalizability of the results. In addition, the study’s early termination resulted in numerical differences in some of the clinical parameters. This study is hypothesis generating and needs a larger population to define the absolute benefit from IABC in this high-risk population. The applicability of this study to women is called into question as greater than 82% of patients were male in both groups.

       Secondly, given that an IABC changes a number of hemodynamic parameters, it is possible that the use of the angiographic characteristics, including TFC, TFG and MBG only ten minutes after the procedure, being a point estimate of the effects of IABC, is not the ideal way of demonstrating clinical benefit. From a mechanistic point of view, this study does demonstrate lack of improvement in early coronary blood flow. However, in this study, it is not clear how many patients received upstream Gp IIb/IIIa or thienopyridine platelet antagonists, which in previous trials have demonstrated improved outcomes when given upstream in the setting of ST-segment elevation myocardial infarction.^16–19 In addition, it would have been useful to know if IABC actually helped patients with more elevated left ventricular end diastolic pressures as a marker for worse cardiac function in the acute setting. The question arises as to whether there are “higher risk features” in the high-risk group that may benefit from IABC.

       Thirdly, previous animal experiments have shown that using IABC prior to intervention reduces infarct size and decreases reperfusion injury¹⁰ but randomization in this study was after PCI. The benefit of IABC after 24–48 hours was also not determined in this study and perhaps a longer period than just 10 minutes is necessary to gain significant benefit after IABC initiation. In addition, there was a trend towards lower CK levels in the IABC group despite the fact that the average time to PCI was longer in the IABC group, although this was not statistically significant in this study. Future trials addressing these issues will help resolve the late benefit from a mechanistic perspective and the overall clinical benefit.

       Thus, although the results reported by Vijayalakshmi et al are the only data available on the mechanistic effects of IABC early after intervention, we do not believe that it is time to “burst the balloon” for high risk patients. Despite the potential limitations above, we think that this study makes an important contribution to the literature. The results suggest that IABC does not affect the coronary blood flow early after intervention. Future directions will involve determining clinical outcomes in a larger trial involving high-risk patients with pre-intervention IABC implantation.