Sage Journals: Discover world-class research

Abstract

Intraaortic balloon pump (IABP) is the most widely used left ventricular support device in a variety of indications. This review focuses on the current literature and discusses the evidence of IABP in ST-elevation myocardial infarction (STEMI) with and without cardiogenic shock. In high-risk STEMI patients without cardiogenic shock several randomized clinical trials have been performed. The majority of the studies could not demonstrate an efficacy benefit for IABP as adjunctive therapy in comparison to standard treatment alone. Hence, recent meta-analyses could not reveal diverging mortality rates at a higher incidence of stroke and major bleedings with IABP use independent of the type of reperfusion therapy. IABP in STEMI patients with cardiogenic shock is recommended according to current American College of Cardiology/American Heart Association (AHA/ACC) and European Society of Cardiology (ESC) guidelines. In recent meta-analyses, IABP in cardiogenic shock complicated by STEMI has been shown to be associated with decreased mortality. However, these beneficial effects are limited to patients treated with thrombolysis, whereas in patients undergoing mechanical revascularization IABP therapy is associated with an increase in mortality. Nevertheless, these data only arise from prospective and retrospective cohort studies, as up to date only one very small randomized clinical trial has been completed. In summary, in high-risk STEMI patients without cardiogenic shock, current data do not support the use of IABP and should only be considered as a standby and bailout strategy if patients develop haemodynamic instability. Current data on IABP in patients with cardiogenic shock complicated by STEMI are scarce and highly limited due to the nonrandomized design of previous trials. However, according to current AHA/ACC and ESC guidelines its use is recommended. Although recent meta-analyses challenge current AHA/ACC/ESC guidelines, adequately powered randomized studies are needed to elucidate the role of IABP in patients with acute myocardial infarction complicated by cardiogenic shock.

Keywords

Intraaortic balloon pump ST-elevation myocardial infarction cardiogenic shock

Introduction

Intraaortic balloon pump (IABP) has been shown to lead to augmentation of coronary blood flow, unloading of the left ventricle and subsequent increase in myocardial oxygen supply by improving the peak diastolic pressure and lowering the end-systolic pressure by means of diastolic inflation and rapid systolic deflation (Figures 1 and 2) [Kern et al. 1993; Williams et al. 1982]. Despite its favourable haemodynamics, IABP is associated with rare but relevant complications such as major bleedings, stroke, local and systemic infections and vascular complications [Davidson et al. 1998]. Owing to the ease of percutaneous implantation, the relatively low cost and the beneficial haemodynamic effects at a presumably low complication rate, IABP is the most widely used left ventricular assist device since its development in the 1960s. In daily clinical routine IABP is mainly used in patients with acute myocardial infarction complicated by cardiogenic shock. In addition, in patients with acute myocardial infarction at high risk for haemodynamic instability and in elective high-risk patients undergoing percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG), IABP therapy is frequently performed. Apart from a significant variance in indications, previous data on IABP and its outcomes report conflicting results. This review will focus on the current literature on IABP in ST-elevation myocardial infarction (STEMI) patients with and without cardiogenic shock and discuss the existing evidence.

Figure 1.

Schematic drawing of an intraaortic balloon pump: inflated during diastole (A) and deflated during systole (B).

Figure 2.

Haemodynamic effects of intraaortic balloon pumping on the aortic pressure cycle.

IABP in STEMI without cardiogenic shock

Preclinical animal studies observed an association of IABP with smaller infarct size and larger amount of salvaged myocardium mainly if applied before reperfusion [Achour et al. 2005; Azevedo et al. 2005; LeDoux et al. 2008]. Thus, several randomized clinical trials were performed analyzing the effect of IABP in high-risk STEMI patients without cardiogenic shock (Table 1) [Flaherty et al. 1985; Kono et al. 1996; O’Rourke et al. 1981; Ohman et al. 1994; Ohman et al. 2005; Patel et al. 2011; Stone et al. 1997; van ‘t Hof et al. 1999; Vijayalakshmi et al. 2007]. Irrespective of the variety of definitions of high-risk STEMI patients such as patients with suboptimal PCI results, poor ST-segment resolution, failed thrombolysis, Killip-class ≥1 or large area at risk, the majority of these studies could not demonstrate an efficacy benefit for IABP as adjunctive therapy in comparison to standard treatment alone. Evidently, the standard treatment of STEMI evolved from thrombolysis to primary PCI in the last decades. A study by Ohman and colleagues performed in the pre-PCI era did observe a significantly lower rate of reocclusion of the infarct-related artery during follow up compared with control patients (8% versus 21%, p = 0.03) and a significantly lower event rate in patients assigned to the IABP group in terms of a composite clinical endpoint including death, stroke, reinfarction, need for emergency revascularization or recurrent ischaemia (13% versus 24%, p = 0.04) [Ohman et al. 1994]. In contrast, the Primary Angioplasty in Myocardial Infarction (PAMI)-II trial including 437 patients reperfused by primary PCI powered for the analysis of a clinical endpoint defined as the combined incidence of in-hospital death, reinfarction, infarct-related artery reocclusion, stroke, postadmission new onset congestive heart failure, or sustained hypotension could not demonstrate an improved clinical outcome by the use of IABP [Stone et al. 1997]. However, this study was performed from 1993–1995, thus stenting or thrombectomy was only performed in 1.3% and 1.2% of all patients. Recently, the Counterpulsation to Reduce Infarct Size Pre-PCI Acute Myocardial Infarction (CRISP AMI) trial including 337 patients with anterior STEMI treated by primary PCI with successful stent implantation in almost all patients (96.9%) and a relatively high rate of thrombectomy (36.2%) could not observe a reduction of infarct size assessed by cardiac magnetic resonance imaging at a similar mortality rate at 6-month follow up in the IABP group implanted before PCI in comparison with the PCI alone group [Patel et al. 2011]. Although the study was not powered for analysis of clinical outcome, the exploratory endpoint of time to death, shock, or new or worsening heart failure occurred significantly less often in the IABP group (p = 0.03). This is surprising given the trend towards larger infarct size in the IABP group. In summary, in patients reperfused by primary PCI, which represents the current standard revascularization treatment for STEMI patients, up to date no unequivocal beneficial effect of IABP on clinical outcome could be demonstrated.

Table 1.

Randomized controlled trials on IABP in STEMI without cardiogenic shock.

Study	Year	Patients (n)	Type of reperfusion	Inclusion criteria	Primary outcome
O’Rourke et al. [1981]	1981	30	No	<12h, Killip II-IV	Hospital/long-term mortality/infarct size
					→ no beneficial effect of IABP
Flaherty et al. [1985]	1985	20	No	<12h, Thallium defect score ≥ 7, Killip I-II (III)	14 day mortality/infarct size
					→ no beneficial effect of IABP
Kono et al. [1996]	1996	45	Thrombolysis	failed TT on CAG	Patency of IRA at 3-week FUP
					→ beneficial effect of IABP
Ohman et al. [1994]	1994	182	Thrombolysis	emergency CAG <24 h, TIMI-flow 2 or 3 by rescue PCI or intracoronary TT	Re-occlusion of IRA during hospitalization
					→ beneficial effect of IABP
Stone et al. [1997](PAMI II)	1997	437	Primary PCI	<12 h, LVEF↓ and high risk: age >70, 3VD, LVEF ≤45%, SVG occlusion, suboptimal PCI result, malignant VT	Composite of death, re-MI, stroke, hypotension/CHF
					→ no beneficial effect of IABP
van ’t Hof et al. [1999]	1999	238	Primary PCI	<3 h, cumulative ΔSTT > 20 mm	Composite of death, re-MI, stroke, LVEF <30% at 6-month FUP
					→ no beneficial effect of IABP
Ohman et al. [2005] (TACTICS)	2005	57	Primary PCI	<12h, anterior STEMI with sysRR ≤90 mmHg or any STEMI with sysRR ≤ 110 mmHg, HR ≥100 bpm or Killip III-IV	All-cause mortality at 6-month FUP
					→ no beneficial effect of IABP
Vijayalakshmi et al. [2007]	2008	33	Primary PCI	sysRR <100 mmHg, HR >100 bpm, LV failure, persistent ST elevation, TIMI-flow ≤2 post-PCI	In-hospital mortality, angiographic/echocardiographic/ ECG parameters, cardiac enzymes
					→ no beneficial effect of IABP
Patel et al. [2011] (CRISP AMI)	2011	337	Primary PCI	STEMI anterior location,< 6 h significant myocardium at risk, primary PCI planned	Infarct size, mortality, MACE (death, repeat MI and heart failure), major bleedings events, transfusions, and major vascular complications
					→ no beneficial effect of IABP

IABP = intraaortic balloon pump, STEMI = ST-elevation myocardial infarction; PCI = percutaneous coronary intervention, < 12/6 h = less than 12/6 h from symptom onset, ΔSTT = ST-segment deviation, TT = thrombolytic therapy, sysRR = systolic blood pressure (mmHg), HR = heart rate, bpm = beats per minute, CAG = coronary angiography, TIMI = thrombolysis in myocardial infarction, LVEF = left ventricular ejection fraction, IRA = infarct related artery, SVG = saphenous vein graft, VT = ventricular tachycardia, CHF = chronic heart failure, MACE = major cardiac events, FUP = follow up, ECG = electrocardiography.

In line with the results of the individual studies, recent meta-analyses could not demonstrate a significant mortality reduction in high-risk STEMI patients treated with or without IABP independent of the type of reperfusion therapy. In addition, no significant effect could be observed concerning left ventricular ejection fraction (LVEF), recurrent ischaemia or reinfarction. Notably, the use of IABP was associated with a significant increase in stroke rate and higher incidence of major bleedings [Bahekar et al. 2011; Sjauw et al. 2009].

Most importantly, current guidelines of the American College of Cardiology and American Heart Association (ACC/AHA) and the European Society of Cardiology (ESC) do not address the topic of IABP in high-risk STEMI patients. In summary, according to current data routine prophylactic IABP use in stable high-risk STEMI-patients is not supported and should only be considered as a standby strategy if patients develop haemodynamic instability.

IABP in STEMI with cardiogenic shock

Despite advances in treatment strategies including aggressive therapeutic interventions such as early revascularization by PCI and/or CABG, mortality of cardiogenic shock complicating STEMI remains high with mortality rates approaching 50% [Goldberg et al. 2009; Thom et al. 2006; Zahn et al. 2001]. Next to an early revascularization strategy and optimal drug therapy including administration of vasopressors and positive inotropic agents, mechanical support is considered as an additional option to achieve initial haemodynamic stabilization and improve clinical outcome. In this setting, IABP is the most often used left ventricular support device. Currently, IABP use in patients with cardiogenic shock complicating acute myocardial infarction is recommended with a class 1B recommendation according to the AHA/ACC guidelines and a class 1C recommendation according to the ESC guidelines [Antman et al. 2008; Van de Werf et al. 2008]. As indicated by the level of evidence, no randomized clinical trial investigating the impact on outcome of IABP use in patients with STEMI and cardiogenic shock has been completed at the time of guideline publication. Thus, this recommendation is based on prospective and retrospective observational studies (Table 2)[Anderson et al. 1997; Barron et al. 2001; Bengtson et al. 1992; Kovack et al. 1997; Moulopoulos et al. 1986; Sanborn et al. 2000; Stomel et al. 1994; Vis et al. 2007a, 2007b; Waksman et al. 1993; Zeymer et al. 2011].

Table 2.

Observational studies on IABP in cardiogenic shock complicated by STEMI.

Study	Period	Patients (n)	Type of reperfusion	Definition cardiogenic shock	Major outcomes
Moulopoulos et al. [1986]	<1986	49	No	SysRR ≤80, urine output < 20 mL/h, clinical signs of hypoperfusion	In-hospital mortality
					→ beneficial effect of IABP
Stomel et al. [1994]	1985 – 1991	64	Thrombolysis/rescue PCI	SysRR ≤80, unresponsive to fluids CI ≤2.0 L/min/m², PCWP ≤18 mmHg, clinical signs of hypoperfusion	In-hospital mortality
					→ no beneficial effect of IABP
Kovack et al. [1997]	1987 – 1995	46	Thrombolysis/rescue PCI	SysRR ≤90 unresponsive to fluids, CI ≤2.2 L/min/m², clinical signs of hypoperfusion	In-hospital mortality
					→ no beneficial effect of IABP after PCI
					→ beneficial effect of IABP after thrombolysis
Bengtson et al. [1992]	1987 – 1988	200	Thrombolysis/rescue PCI	≥30 min sysRR 90 unless IABP/ pressors, CI ≤2.2 L/min/m² and PCWP ≥18, clinical signs of hypoperfusion	In-hospital mortality
					→ beneficial effect of IABP after PCI and after thrombolysis
Waksman et al. [1993]	1989	41	Thrombolysis/rescue PCI	SysRR ≤90 unresponsive to fluids, clinical signs of hypoperfusion	In-hospital and 1-year mortality
					→ no beneficial effect of IABP after PCI
					→ beneficial effect of IABP after thrombolysis
GUSTO-I [Anderson et al. 1997]	1990 – 1993	310	Thrombolysis	SysRR ≤90 unresponsive to fluids, CI ≤2.2 L/min/m², clinical signs of hypoperfusion	30-day and 1-year mortality
					→ no beneficial effect of IABP
NRMI-2 [Barron et al. 2001]	1994 – 1998	8671	Thrombolysis/rescue PCI or primary PCI	SysRR ≤90 unresponsive to fluids, clinical signs of hypoperfusion	In-hospital mortality
					→ no beneficial effect of IABP after rescue or primary PCI
					→ beneficial effect of IABP after thrombolysis
SHOCK registry [Sanborn et al. 2000]	1995 – 2000	856	Thrombolysis/primary PCI	SysRR ≤90 unresponsive to fluids, CI ≤2.2 L/min/m², clinical signs of hypoperfusion	In-hospital mortality
					→ no beneficial effect of IABP after primary PCI
					→ beneficial effect of IABP after thrombolysis
AMC CS cohort [Vis et al. 2007a, 2007b]	1997 – 2005	292	Primary PCI	SysRR ≤90 unresponsive to fluids, CI ≤2.2 L/min/m², clinical signs of hypoperfusion	1-year mortality
					→ no beneficial effect of IABP
EHS PCI registry [Zeymer et al. 2011]	2005 – 2008	653 (71 STEMI)	Primary PCI	SysRR ≤90 unresponsive to fluids, HR>100 bpm, clinical signs of hypoperfusion	In-hospital mortality
					→ no beneficial effect of IABP
IABP shock [Prondzinsky et al. 2010]	2003 – 2004	45	Primary PCI	signs of organ hypoperfusion plus one of the following: sysRR ≤90 unresponsive to fluids, HR > 60/min or CI ≤2.2 L/min/m²	APACHE II score
					→ no beneficial effect of IABP

IABP = intraaortic balloon pump, STEMI = ST-elevation myocardial infarction; PCI = percutaneous coronary intervention, sysRR = systolic blood pressure (mmHg), PCWP = pulmonary capillary wedge pressure, CI = cardiac index, HR = heart rate, bpm = beats per minute.

Recent meta-analyses including these prospective and retrospective cohort studies could demonstrate a mortality reduction using IABP [Bahekar et al. 2011; Sjauw et al. 2009]. However, the beneficial effects of IABP were strongly dependent on the type of reperfusion therapy. The results were mainly driven by the studies performed in the prethrombolytic and thrombolytic era, i.e. the pre-PCI era: in patients undergoing thrombolysis or no reperfusion IABP use resulted in 18% and 29% mortality risk reduction, whereas IABP support in patients undergoing PCI led to a 6% mortality risk increase [Sjauw et al. 2009].

The mortality reduction of IABP in conjunction with thrombolysis might support the hypothesis that IABP and thrombolytic therapy have synergistic effects as IABP may increase the efficacy of thrombolysis by increasing coronary perfusion [Prewitt et al. 1994]. However, according to the results of these meta-analyses, patients treated with IABP were younger and more often of male gender, both baseline characteristics known to be associated with improved outcome. In addition, rescue-PCI or additional CABG was significantly more frequently performed in patients receiving IABP therapy which is also known to be associated with reduced mortality as previously demonstrated in the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial [Hochman et al. 1999]. Here a significant mortality reduction at 6 and 12 months, as well as in long-term follow up after 6 years, was observed with an early revascularization-based management. Thus, these factors might explain the poor outcome in patients treated without IABP after thrombolysis. However, as recommended by current guidelines of the ACC/AHA and ESC, early mechanical revascularization is of paramount importance in the therapy of cardiogenic shock complicated by STEMI, whereas initial stabilization including thrombolysis with or without additional IABP should play only a secondary role.

The observed increase in mortality in patients treated by IABP in addition to early PCI or CABG was mainly influenced by the National Registry of Myocardial Infarction-2 (NRMI-2) registry results [Barron et al. 2001]. In the NRMI-2 cardiogenic shock cohort, IABP therapy was independently associated with mortality after multivariate adjustment for age, several clinical risk factors and revascularization therapy. Nevertheless, selection bias cannot be ruled out due to the nonrandomized design of the studies. Thus, one might argue that in general IABP might have been more frequently used in patients with extremely poor prognosis. In line with NRMI-2 results, data from the Amsterdam Medical Center Cardiogenic Shock (AMC CS) registry found IABP use to be associated with higher mortality rates [Vis et al. 2007a, 2007b], whereas only one other registry reported mortality rates of 38% with versus 63% without IABP [Bengtson et al. 1992]. However, in this cohort patients treated with IABP were younger than those of the non-IABP group. Finally, analysing data from the Euro Heart Survey Programme (EHS PCI) of the ESC including 653 patients with STEMI and non-STEMI, Zeymer and colleagues reported higher in-hospital mortality in patients treated with IABP in comparison to the non-IABP group (56.9% versus 36.1%, p = 0.0004). In multivariate analysis including parameters such as age, gender, mechanical ventilation, severity of coronary artery disease, diabetes, renal failure and history of prior myocardial infarction, IABP use was not independently associated with mortality, although the corresponding p-value of 0.07 can be interpreted as a trend [Zeymer et al. 2011].

In summary, the body of evidence to support or dismiss IABP in patients with cardiogenic shock complicating STEMI is scarce due to the nonrandomized design of previous studies and their inconclusive results with respect to clinical endpoints. Thus, further properly powered, randomized, clinical trials are needed to analyze the impact of IABP on outcome in patients with cardiogenic shock in the setting of acute myocardial infarction and early revascularization. Based on a small randomized pilot study [Prondzinsky et al. 2010], the prospective, randomized, open-label, multicentre, controlled Intraaortic Balloon Pump in cardiogenic shock 2 (IABP-SHOCK II [ClinicalTrials.gov identifier: NCT00491036]) trial is ongoing and will hopefully give us the answer to whether IABP treatment is beneficial for the treatment of cardiogenic shock in addition to PCI.

Discussion

Since its development in the 1960s, IABP is the most commonly used left ventricular support device in clinical routine. By means of diastolic inflation and rapid systolic deflation in the aorta, the peak diastolic pressure is augmented and end-systolic pressures are lowered. This results in unloading of the left ventricle, augmentation of coronary perfusion and reduction in myocardial oxygen demand [Kern et al. 1993; Williams et al. 1982]. Nevertheless, effects on cardiac output are limited [Scheidt et al. 1973]. Despite the potential beneficial haemodynamic effects, the use of IABP is associated with rare but relevant complications such as major bleedings, stroke, local and systemic infections and vascular complications [Davidson et al. 1998]. To reduce mechanical vascular complications such as limb ischaemia, distal embolization or dissection, techniques for sheathless insertion and catheters with smaller diameters were developed. Nevertheless, the clinical benefit of these new developments could not been demonstrated convincingly so far [Patel et al. 1995]. In addition to these local complications, a higher rate of stroke has been reported in patients treated with IABP. This might be explained in part by haemorrhagic events due to the need of full systemic heparinization, or by ischaemic events induced by peripheral embolization. Apart from intracranial haemorrhagic events, IABP use has been shown to be associated with overall major bleedings which again can in part be attributed to the need for full systemic heparinization and the need for prolonged arterial access. Evidently, the complications of full systemic heparinization might be even more pronounced after administration of glycoprotein IIb/IIIa-inhibitors in the setting of high-risk acute myocardial infarction. Apart from the adverse effect on clinical outcome induced by major bleedings itself, they further trigger transfusion which might increase the mortality risk in patients with acute coronary syndromes [Rao et al. 2004]. Evidently, the use of IABP may also lead to local and systemic infections. Although these infections may often be of minor clinical relevance, in patients with pronounced comorbidities they potentially influence clinical outcome and might lead to a further progress of the systemic disease of cardiogenic shock [Stegman et al. 2012].

Certainly, the potential benefits of IABP have to be weighed against its complications. This is especially important in STEMI patients without cardiogenic shock, since in this setting IABP is used as a prophylactic intervention. Although individual studies did report a beneficial impact of IABP use in high-risk STEMI patients reperfused by thrombolysis [Kono et al. 1996; O’Rourke et al. 1981], trials including patients reperfused by primary PCI could not observe any improvement in outcome due to IABP [Flaherty et al. 1985; Ohman et al. 2005; Patel et al. 2011; Stone et al. 1997; van ‘t Hof et al. 1999; Vijayalakshmi et al. 2007]. In line with these results, recent meta-analyses did not observe a 30-day survival benefit or an improvement in LVEF at increased rates of stroke and major bleedings independent of the type of reperfusion therapy [Bahekar et al. 2011; Sjauw et al. 2009]. Thus, the significant higher complication rates were not outweighed by any clinical benefit. Notably, mortality after STEMI in patients without cardiogenic shock could be reduced to <10% in the last decades [Schiele et al. 2010]. This is mainly attributable to optimal interventional and drug treatment in the acute and subacute phase. Thus, much less invasive procedures such as manual thrombectomy or administration of glycoprotein-IIb/IIIa inhibitors or bivalirudin further challenge invasive therapeutic strategies such as IABP use.

In contrast to the clinical outcome in STEMI patients with haemodynamic stability, mortality of cardiogenic shock complicating STEMI remains high with rates of approximately 50% [Goldberg et al. 2009; Thom et al. 2006; Zahn et al. 2001]. The current concept of cardiogenic shock implies the development of a shock spiral induced by progressive left ventricular dysfunction leading to impaired peripheral perfusion and hypoxemia. Apart from the direct haemodynamic effects, the systemic inflammation response syndrome (SIRS) is further promoted leading to paradoxical reduced systemic vascular resistance [Reynolds and Hochman, 2008; Thiele et al. 2010]. In theory IABP use might beneficially influence haemodynamics and improve myocardial recovery which might translate into more rapid haemodynamic stabilization and disruption of the shock spiral. However, by means of insertion of a foreign body with relatively large intravascular surface area, SIRS and thus the shock spiral may further be promoted. In addition, bleeding complications and subsequent transfusions both also negatively contribute to inflammation and subsequently further trigger the shock spiral [Rao et al. 2004]. Local or systemic infections also negatively influence the complex pathophysiology of cardiogenic shock despite its potential limited relevance in stable patients. Although cardiogenic shock can be understood as a systemic illness, early revascularization is of paramount importance and can be understood as the cornerstone for the treatment of cardiogenic shock complicating acute myocardial infarction: as demonstrated by the SHOCK trial, early mechanical revascularization leads to a significant decrease in mortality in comparison to haemodynamic stabilization and optimal medical therapy including thrombolysis [Hochman et al. 1999]. These findings help to interpret the results of current meta-analyses: in patients undergoing thrombolysis or no reperfusion which represents an inferior treatment strategy, IABP use resulted in a significant mortality risk reduction, whereas IABP support in patients undergoing PCI led to a significant mortality risk increase [Bahekar et al. 2011; Sjauw et al. 2009]. However, these data are solely based on registries as up to date only one small randomized clinical trial investigating the impact of IABP use in patients with STEMI and cardiogenic shock has been completed. Certainly registries suffer from multiple potential sources of bias and confounding, thus data arising from such need to be interpreted with caution. Nevertheless, current guidelines of the AHA/ACC and ESC highly recommend IABP use in patients with cardiogenic shock complicated by STEMI (class 1B and 1C recommendation, respectively) [Antman et al. 2008; Van de Werf et al. 2008]. In line with the international ESC/AHA/ACC guidelines, further national directives such as the German–Austrian guidelines also recommend IABP use in patients treated with thrombolysis and clearly state that IABP may be used in patients treated by primary PCI despite lacking evidence [Werdan et al. 2011]. In spite of these recommendations IABP is currently only used in one quarter of patients with cardiogenic shock complicated by STEMI [Thom et al. 2006; Zeymer et al. 2011], which might be in part explained by the lack of evidence and reimbursement policies. The IABP-SHOCK II trial, the first adequately powered randomized controlled study, will further elucidate the current role of IABP in cardiogenic shock. Finally, if a positive impact of IABP on outcome should eventually be demonstrated further large-scale clinical trials are needed to compare the potential beneficial effects of IABP to other left ventricular assist devices. However, data from several small trials could not indicate superiority of left ventricular assist devices over IABP [Arias et al. 2005; Burkhoff et al. 2006; Seyfarth et al. 2008; Thiele et al. 2005; Unverzagt et al. 2011].

Conclusion

In summary, according to current data IABP use in stable high-risk STEMI patients cannot be recommended and should only be considered as a standby and bailout strategy if patients develop haemodynamic instability. In contrast, in patients with cardiogenic shock complicated by STEMI current guidelines strongly recommend the use of IABP. Although data are scarce, based on registries only and challenged by recent meta-analyses, clinical practice should not be changed until further evidence from randomized, controlled, clinical trials is available.

Footnotes

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Holger Thiele has received research funding and speaker honoraria from Maquet Cardiopulmonary AG, Hirrlingen, Germany and Teleflex Medical, Everett, MA, USA.

References

Achour

Boccalandro

Felli

Amirian

Uthman

Buja

. (2005) Mechanical left ventricular unloading prior to reperfusion reduces infarct size in a canine infarction model. Catheter Cardiovasc Interv 64: 182–192.

Anderson

R.D.

Ohman

E.M.

Holmes

D.R.

Jr Col

Stebbins

A.L.

Bates

E.R.

. (1997) Use of intraaortic balloon counterpulsation in patients presenting with cardiogenic shock: observations from the GUSTO-I Study. Global utilization of streptokinase and TPA for occluded coronary arteries. J Am Coll Cardiol 30: 708–715.

Antman

E.M.

Hand

Armstrong

P.W.

Bates

E.R.

Green

L.A.

Halasyamani

L.K.

. (2008) 2007 Focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to review new evidence and update the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction, writing on behalf of the 2004 Writing Committee. Circulation 117: 296–329.

Arias

E.A.

Gonzalez-Chon

Garcia-Lopez

S.M.

Chacon

M.A.

Noriega-Iriondo

Vega

R.E.

. (2005) [Impact of the intra-aortic balloon pump in the mortality due to cardiogenic shock secondary to acute myocardial infarction]. Arch Cardiol Mex 75(3): 260–266.

Azevedo

C.F.

Amado

L.C.

Kraitchman

D.L.

Gerber

B.L.

Edvardsen

Osman

N.F.

. (2005) The effect of intra-aortic balloon counterpulsation on left ventricular functional recovery early after acute myocardial infarction: a randomized experimental magnetic resonance imaging study. Eur Heart J 26: 1235–1241.

Bahekar

Singh

Bhuriya

Ahmad

Khosla

. (2011) Cardiovascular outcomes using intra-aortic balloon pump in high-risk acute myocardial infarction with or without cardiogenic shock: a meta-analysis. J Cardiovasc Pharmacol Ther 17: 44–56.

Barron

H.V.

Every

N.R.

Parsons

L.S.

Angeja

Goldberg

R.J.

Gore

J.M.

. (2001) The use of intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating acute myocardial infarction: data from the National Registry of Myocardial Infarction 2. Am Heart J 141: 933–939.

Bengtson

J.R.

Kaplan

A.J.

Pieper

K.S.

Wildermann

N.M.

Mark

D.B.

Pryor

D.B.

. (1992) Prognosis in cardiogenic shock after acute myocardial infarction in the interventional era. J Am Coll Cardiol 20: 1482–1489.

Burkhoff

Cohen

Brunckhorst

O’Neill

W.W.

(2006) A randomized multicenter clinical study to evaluate the safety and efficacy of the TandemHeart percutaneous ventricular assist device versus conventional therapy with intraaortic balloon pumping for treatment of cardiogenic shock. Am Heart J 152: 469 e461–468.

10.

Davidson

Baumgartner

Omari

Milliken

(1998) Intra-aortic balloon pump: indications and complications. J Natl Med Assoc 90: 137–140.

11.

Flaherty

J.T.

Becker

L.C.

Weiss

J.L.

Brinker

J.A.

Bulkley

B.H.

Gerstenblith

. (1985) Results of a randomized prospective trial of intraaortic balloon counterpulsation and intravenous nitroglycerin in patients with acute myocardial infarction. J Am Coll Cardiol 6: 434–446.

12.

Goldberg

R.J.

Spencer

F.A.

Gore

J.M.

Lessard

Yarzebski

(2009) Thirty-year trends (1975 to 2005) in the magnitude of, management of, and hospital death rates associated with cardiogenic shock in patients with acute myocardial infarction: a population-based perspective. Circulation 119: 1211–1219.

13.

Hochman

J.S.

Sleeper

L.A.

Webb

J.G.

Sanborn

T.A.

White

H.D.

Talley

J.D.

. (1999) Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med 341: 625–634.

14.

Kern

M.J.

Aguirre

Bach

Donohue

Siegel

Segal

(1993) Augmentation of coronary blood flow by intra-aortic balloon pumping in patients after coronary angioplasty. Circulation 87: 500–511.

15.

Kono

Morita

Nishina

Fujita

Onaka

Hirota

. (1996) Aortic counterpulsation may improve late patency of the occluded coronary artery in patients with early failure of thrombolytic therapy. J Am Coll Cardiol 28: 876–881.

16.

Kovack

P.J.

Rasak

M.A.

Bates

E.R.

Ohman

E.M.

Stomel

R.J.

(1997) Thrombolysis plus aortic counterpulsation: improved survival in patients who present to community hospitals with cardiogenic shock. J Am Coll Cardiol 29: 1454–1458.

17.

LeDoux

J.F.

Tamareille

Felli

P.R.

Amirian

Smalling

R.W.

(2008) Left ventricular unloading with intra-aortic counter pulsation prior to reperfusion reduces myocardial release of endothelin-1 and decreases infarction size in a porcine ischemia-reperfusion model. Catheter Cardiovasc Interv 72: 513–521.

18.

Moulopoulos

Stamatelopoulos

Petrou

(1986) Intraaortic balloon assistance in intractable cardiogenic shock. Eur Heart J 7: 396–403.

19.

O’Rourke

M.F.

Norris

R.M.

Campbell

T.J.

Chang

V.P.

Sammel

N.L.

(1981) Randomized controlled trial of intraaortic balloon counterpulsation in early myocardial infarction with acute heart failure. Am J Cardiol 47: 815–820.

20.

Ohman

E.M.

George

B.S.

White

C.J.

Kern

M.J.

Gurbel

P.A.

Freedman

R.J.

. (1994) Use of aortic counterpulsation to improve sustained coronary artery patency during acute myocardial infarction. Results of a randomized trial. The Randomized IABP Study Group. Circulation 90: 792–799.

21.

Ohman

E.M.

Nanas

Stomel

R.J.

Leesar

M.A.

Nielsen

D.W.

O’Dea

. (2005) Thrombolysis and counterpulsation to improve survival in myocardial infarction complicated by hypotension and suspected cardiogenic shock or heart failure: results of the TACTICS Trial. J Thromb Thrombolysis 19: 33–39.

22.

Patel

J.J.

Kopisyansky

Boston

Kuretu

M.L.

McBride

Cohen

(1995) Prospective evaluation of complications associated with percutaneous intraaortic balloon counterpulsation. Am J Cardiol 76: 1205–1207.

23.

Patel

M.R.

Smalling

R.W.

Thiele

Barnhart

H.X.

Zhou

Chandra

. (2011) Intra-aortic balloon counterpulsation and infarct size in patients with acute anterior myocardial infarction without shock: the CRISP AMI randomized trial. JAMA 306: 1329–1337.

24.

Prewitt

R.M.

Schick

Ducas

(1994) Intraaortic balloon counterpulsation enhances coronary thrombolysis induced by intravenous administration of a thrombolytic agent. J Am Coll Cardiol 23: 794–798.

25.

Prondzinsky

Lemm

Swyter

Wegener

Unverzagt

Carter

J.M.

. (2010) Intra-aortic balloon counterpulsation in patients with acute myocardial infarction complicated by cardiogenic shock: the prospective, randomized IABP SHOCK Trial for attenuation of multiorgan dysfunction syndrome. Crit Care Med 38: 152–160.

26.

Rao

S.V.

Jollis

J.G.

Harrington

R.A.

Granger

C.B.

Newby

L.K.

Armstrong

P.W.

. (2004) Relationship of blood transfusion and clinical outcomes in patients with acute coronary syndromes. JAMA 292: 1555–1562.

27.

Reynolds

H.R.

Hochman

J.S.

(2008) Cardiogenic shock: current concepts and improving outcomes. Circulation 117: 686–697.

28.

Sanborn

T.A.

Sleeper

L.A.

Bates

E.R.

Jacobs

A.K.

Boland

French

J.K.

. (2000) Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol 36(3 Suppl. A): 1123–1129.

29.

Scheidt

Wilner

Mueller

Summers

Lesch

Wolff

. (1973) Intra-aortic balloon counterpulsation in cardiogenic shock. Report of a co-operative clinical trial. N Engl J Med 288: 979–984.

30.

Schiele

Hochadel

Tubaro

Meneveau

Wojakowski

Gierlotka

. (2010) Reperfusion strategy in Europe: temporal trends in performance measures for reperfusion therapy in ST-elevation myocardial infarction. Eur Heart J 31: 2614–2624.

31.

Seyfarth

Sibbing

Bauer

Frohlich

Bott-Flugel

Byrne

. (2008) A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction. J Am Coll Cardiol 52: 1584–1588.

32.

Sjauw

K.D.

Engstrom

A.E.

Vis

M.M.

van der Schaaf

R.J.

Baan

Jr. Koch

K.T.

. (2009) A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? Eur Heart J 30: 459–468.

33.

Stegman

B.M.

Newby

L.K.

Hochman

J.S.

Ohman

E.M.

(2012) Post-myocardial infarction cardiogenic shock is a systemic illness in need of systemic treatment is therapeutic hypothermia one possibility? J Am Coll Cardiol 59: 644–647.

34.

Stomel

R.J.

Rasak

Bates

E.R.

(1994) Treatment strategies for acute myocardial infarction complicated by cardiogenic shock in a community hospital. Chest 105: 997–1002.

35.

Stone

G.W.

Marsalese

Brodie

B.R.

Griffin

J.J.

Donohue

Costantini

. (1997) A prospective, randomized evaluation of prophylactic intraaortic balloon counterpulsation in high risk patients with acute myocardial infarction treated with primary angioplasty. Second Primary Angioplasty in Myocardial Infarction (PAMI-II) Trial Investigators. J Am Coll Cardiol 29: 1459–1467.

36.

Thiele

Allam

Chatellier

Schuler

Lafont

(2010) Shock in acute myocardial infarction: the Cape Horn for trials? Eur Heart J 31: 1828–1835.

37.

Thiele

Sick

Boudriot

Diederich

K.W.

Hambrecht

Niebauer

. (2005) Randomized comparison of intra-aortic balloon support with a percutaneous left ventricular assist device in patients with revascularized acute myocardial infarction complicated by cardiogenic shock. Eur Heart J 26: 1276–1283.

38.

Thom

Haase

Rosamond

Howard

V.J.

Rumsfeld

Manolio

. (2006) Heart disease and stroke statistics - 2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 113: e85–e151.

39.

Unverzagt

Machemer

M.T.

Solms

Thiele

Burkhoff

Seyfarth

. (2011) Intra-aortic balloon pump counterpulsation (IABP) for myocardial infarction complicated by cardiogenic shock. Cochrane Database Syst Rev 7: CD007398.

40.

van ‘t Hof

A.W.

Liem

A.L.

de Boer

M.J.

Hoorntje

J.C.

Suryapranata

Zijlstra

(1999) A randomized comparison of intra-aortic balloon pumping after primary coronary angioplasty in high risk patients with acute myocardial infarction. Eur Heart J 20: 659–665.

41.

Van de Werf

Bax

Betriu

Blomstrom-Lundqvist

Crea

Falk

. (2008) Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. Eur Heart J 29: 2909–2945.

42.

Vijayalakshmi

Kunadian

Whittaker

V.J.

Wright

R.A.

Hall

J.A.

Sutton

. (2007) Intra-aortic counterpulsation does not improve coronary flow early after PCI in a high-risk group of patients: observations from a randomized trial to explore its mode of action. J Invasive Cardiol 19: 339–346.

43.

Vis

M.M.

Sjauw

K.D.

van der Schaaf

R.J.

Baan

Jr. Koch

K.T.

DeVries

J.H.

. (2007a) In patients with ST-segment elevation myocardial infarction with cardiogenic shock treated with percutaneous coronary intervention, admission glucose level is a strong independent predictor for 1-year mortality in patients without a prior diagnosis of diabetes. Am Heart J 154: 1184–1190.

44.

Vis

M.M.

Sjauw

K.D.

van der Schaaf

R.J.

Koch

K.T.

Baan

Jr. Tijssen

J.G.

. (2007b) Prognostic value of admission hemoglobin levels in ST-segment elevation myocardial infarction patients presenting with cardiogenic shock. Am J Cardiol 99: 1201–1202.

45.

Waksman

Weiss

A.T.

Gotsman

M.S.

Hasin

(1993) Intra-aortic balloon counterpulsation improves survival in cardiogenic shock complicating acute myocardial infarction. Eur Heart J 14: 71–74.

46.

Werdan

Ruß

Buerke

Engelmann

Ferrari

Friedrich

. (2011) Deutsch-österreichische S3-Leitlinie ‘Infarktbedingter kardiogener Schock – Diagnose, Monitoring und Therapie’. Intensivmedizin und Notfallmedizin 48: 291–344.

47.

Williams

D.O.

Korr

K.S.

Gewirtz

Most

A.S.

(1982) The effect of intraaortic balloon counterpulsation on regional myocardial blood flow and oxygen consumption in the presence of coronary artery stenosis in patients with unstable angina. Circulation 66: 593–597.

48.

Zahn

Schiele

Schneider

Gitt

A.K.

Wienbergen

Seidl

. (2001) Primary angioplasty versus intravenous thrombolysis in acute myocardial infarction: can we define subgroups of patients benefiting most from primary angioplasty? Results from the pooled data of the Maximal Individual Therapy in Acute Myocardial Infarction Registry and the Myocardial Infarction Registry. J Am Coll Cardiol 37: 1827–1835.

49.

Zeymer

Bauer

Hamm

Zahn

Weidinger

Seabra-Gomes

. (2011) Use and impact of intra-aortic balloon pump on mortality in patients with acute myocardial infarction complicated by cardiogenic shock: results of the Euro Heart Survey on PCI. EuroIntervention 7: 437–441.

What is the evidence for IABP in STEMI with and without cardiogenic shock?

Abstract

Keywords

Introduction

IABP in STEMI without cardiogenic shock

IABP in STEMI with cardiogenic shock

Discussion

Conclusion

Footnotes

References