Intra-aortic balloon pump counterpulsation: are we optimizing the management of cardiogenic shock?

Abstract

Intra-aortic balloon pump counterpulsation (IABPC) has been used in various forms for decades. The change in physiology brought about by their use is conceptually appealing in managing cardiogenic shock and mechanical complications of myocardial infarction. A common myth is that this method of managing acute cardiological emergencies is to be limited to the realms of this specialist field. However, as medical physicians an appreciation and understanding of this novel therapy is essential not only as a lifesaving measure but also as a bridging therapy to more definitive management in the acute medical setting. IABPC is a safe and under-utilized technique despite featuring in all major international guidelines (ESC and ACC) for the management of cardiogenic shock secondary to acute coronary syndromes. Without awareness of this intervention we may be suboptimally managing patients in the first instance. To improve awareness we examine the evidence supporting the use of the IABPC therapy and the contraindications to their use. Complications and advances in technology are also addressed.

Introduction

Intra-aortic balloon pump counterpulsation (IABPC) for the management of cardiogenic shock in acute coronary syndrome is a safe and under-utilized technique despite recommendation in European and American guidelines. It remains shrouded in mystery with many general physicians and secondary care providers unaware of its place in the management of cardiogenic shock.

Raising awareness and understanding of this interventional process is vital for the management of myocardial infarction patients. In critically ill patients IABPC can not only be life saving with timely introduction but can provide haemodynamic stability to patients prior to more definitive measures being put in place. Recognizing the possible need and benefits from such a procedure should be the responsibility of all medical physicians as the onset of cardiac events is one that can occur in any setting.

Here, we examine the evidence around this therapy and address the complications and advances in technology.

Methods

The literature was searched using PUBMED for ‘intra aortic balloon pump’. Relevant papers were appraised and references searched for further information.

Physiology

Cardiogenic shock is an inadequate perfusion of organs as a result of cardiac impairment. This can occur after the sudden occlusion of a large coronary artery, resulting in myocardial ischaemia and necrosis. The resulting hypotension leads to multiorgan failure and death. Early reperfusion of the occluded artery by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) has been shown to improve outcomes in cardiogenic shock.¹ Mechanical circulatory support devices can provide stability until re-vascularization has taken effect which can be particularly lifesaving in the context of acute mitral valve rupture or ventricular septal defect (VSD). The timing of such intervention is vital and early recognition of patients who will need such circulatory support will provide an opportunity for concurrent PCI and IABP insertion, which often yields more favourable outcomes.

Myocardium is supplied by the coronary arteries which carry oxygen-rich blood from the root of the aorta. The large surface epicardial arteries subdivide into smaller subendocardial vessels which supply myocardium. During ventricular contraction, known as systole, the subendocardial coronary vessels are compressed due to high ventricular pressures causing coronary blood flow to stop. As a result most myocardial perfusion occurs during ventricular relaxation, known as diastole. The principle of intra-aortic balloon pump conterpulsation is to improve the ventricular performance of a failing heart by increasing myocardial oxygen supply and reducing myocardial oxygen demand.

Insertion and operation

The catheter is inserted via the femoral artery under fluoroscopic guidance and positioned in the proximal descending aorta, typically a few centimetres distal to the origin of the left subclavian artery. Pumping is dependent on aortic pressure and the electrocardiogram and can be automated by circuitry within the mobile console.

IABPC optimizes coronary perfusion by timing inflation with the diastolic phase of the cardiac cycle. It is within the diastolic phase that coronary perfusion takes place. Therefore, rapid inflation during this period raises the pressure within coronary arteries allowing for improved coronary blood flow and myocardial oxygenation. The deflation of the balloon occurs prior to systole when the aortic valve opens. This reduces cardiac afterload, increases stroke volume and reduces tension in the myocardial muscle, thus reducing myocardial oxygen demand. The outcome is improved overall cardiac function.² Systolic blood pressure reduces by approximately 20% associated with an increase in aortic diastolic pressure by approximately 30%. Subsequently, coronary perfusion may improve the flow beyond critical stenoses.³

The American College of Cardiology has issued guidelines suggesting IABPC use as per Table 1

Table 1.

Indications and contraindications for IABPC insertion

Indications	Relative contraindications	Absolute contraindications
Left ventricular failure or cardiogenic shock	Peripheral vascular disease	Severe aortic valve incompetence
Mechanical complications of acute MI	Bleeding diathesis	Aortic dissection
Support for high risk PCI	Aortic aneurysm	Porcelain aorta
Failure to wean postcoronary artery bypass	Prosthetic aortic vascular grafts
Bridge to transplant

MI, myocardial infarction; PCI, percutaneous coronary intervention

What evidence do we have that IABPC will help in myocardial infarction?

In 1968, Kantrowitz et al.⁴ were the first to report improved blood pressure and urine output in patients stabilized with IABPC before and after surgical re-vascularization. For many the use of IABPC was limited to cardiothoracic surgery due to technical difficulty with catheter size, placements and high risk of complications. Technological advancement has led to the availability of a percutaneous insertable IABP which interventional cardiologists began to test in high-risk PCI patients. In 1980, Michels et al.⁵ conducted a cohort study of 181 patients with either cardiogenic shock post-myocardial infarction (MI) or unstable angina. Of the patients with unstable angina, 42 received haemodynamic stabilization, and despite initially being deemed unfit for surgery, went on to be successfully re-vascularized by CABG. Remarkably, complication rates were not found to be statistically significant. This landmark study demonstrated short-term benefits of IABPC in pump failure and refractory ischaemia, but long-term prognosis essentially unaltered. The improved coronary perfusion and haemodynamic support offered can potentially ‘buy patients time’ and optimize conditions for subsequent re-vascularization.

A randomized controlled study conducted in the late 1990s by Ohman et al.⁶ demonstrated benefit from IABPC to patients receiving re-vascularization through CABG, PCI or thrombolysis, though the difference failed to reach statistical significance. Criticisms of the study included lack of defined clinical endpoints and information regarding haemodynamic compromise were not made available for this study. In contrast, Stanborn et al.⁷ concluded that the treatment of a patient presenting with cardiogenic shock by means of thrombolytic therapy, IABP and then transfer for urgent re-vascularization by means of PCI/CABG was associated with lower in-hospital mortality than standard medical therapy.

In 2009, Sjauw et al.² investigated the use of IABPC in patients with acute ST elevation myocardial infarction (STEMI) leading to cardiogenic shock. Of the seven randomized trials included in one half of this analysis (1009 patients) the 30-day survival benefit was deemed non-significant. This concurred with the observation of no improvement in left ventricular ejection fraction (LVEF). There were 43 deaths recorded in the IABPC group versus 45 in those not receiving and ventricular support. Although the patients included in this study were deemed high-risk this was not standardized throughout the study, which is difficult given the heterogeneity of the patient cohort. The authors concluded there was no clear evidence-base for the use of IABPC in high-risk acute myocardial infarction (AMI) patients. In addition, the risk of bleeding and stroke were also raised (2% and 6% respectively). However, this study does not state that patients in the acute setting do not benefit from IABPC, which is often the drawn conclusion. On the contrary, the aid of haemodynamic stability not only reduces the need for higher dependency care, intubation and reduced inotropic requirements but may also lead to reduced hospital stay.⁸ In addition, those patients with STEMI meeting indications for CABG have a prognostic benefit from surgery.

In the CRISP AMI trial (counterpulsation to reduce infarct size pre-PCI acute myocardial infarction), 337 patients were randomized in a multicentre study to either primary percutaneous coronary intervention (PPCI) therapy and IABP therapy or PPCI alone in patients without cardiogenic shock to assess outcomes on infarct size. Those allocated to the IABPC arm had this initiated pre-PCI and continued for at least 12 hours postprocedure. This study found no significant difference in final infarct size as assessed by cardiac magnetic resonance imaging, between the two arms of the study, 42.1% in the IABPC and PPCI group versus 37.5% in the PCI only group (P = 0.06). This suggested that in patients presenting with acute anterior STEMI without evidence of cardiogenic shock, IABC together with PPCI compared with PPCI alone did not result in reduced infarct size.⁹

Prodzinsky et al.¹⁰ suggested that although IABPC is effective in optimizing haemodynamic support in patients, this is only one element of acute cardiovascular care. Effective destination therapy, i.e. CABG, PCI or cardiac transplant are what alter long-term prognosis. Hence, IABPC use as a bridge, minimizing inotropic demands may be justified until definitive intervention is achieved. This aspect is again vital to the general medical setting. Patients deemed unfit for definitive intervention can arguably be considered for IABPC with the aim to evaluate the clinical status of the patients once cardiac function is optimized. This treatment allows for optimization of medical therapy in the interim.

The indications for the use of IABPC have been supported by international guidelines, including ESC and AHA. These are shown in Table 2.

Table 2.

Clinical indication for IABP use based on international guidelines (AHA Guidelines on IABP Circulation 1996;94:2341–50)

AHAGuidelines	Statement	Level ofevidence
ESC Guidelines	In the setting of an acute coronary syndrome:	I
	(a) Use in STEMI with cardiogenic shock Killip Class IV
	(b) Use in ACS with haemodynamic compromise
	(c) Use in ACS in the setting of mechanical complications of ACS (e.g. acute MR, VSD)
	In the setting of acute heart failure:	IIb
	(a) As a bridge to stabilize patients with heart failure and cardiogenic shock while awaiting treatment response, re-vascularization or alternative destination therapy
AHA Guidelines	In the setting of acute coronary syndromes:	I
	(a) Cardiogenic shock that is not quickly reversed with pharmacological therapy as a stabilizing measure for angiography and prompt re-vascularization
	(b) In acute mitral regurgitation or VSD complications from MI, IABP can be used as a stabilizing therapy for angiography and repair/re-vascularization
	(c) Recurrent intractable ventricular arrhythmias with haemodynamic instability
	(d) Refractory post-MI angina as a bridge to angiography and re-vascularization
	(e) Patients with signs of haemodynamic instability, poor LV function or persistent ischaemia with large areas of myocardium at risk	IIb
	(f) Patients with successful PTCA after failed thrombolysis or in those with three-vessel coronary disease to prevent re-occlusion	IIb
	(g) In patients known to have large areas of myocardium at risk with or without active ischaemia

ACS, acute coronary syndrome; IABP, intra-aortic balloon pump; LV, left ventricular; STEMI, ST elevation myocardial infarction; PTCA, percutaneous transluminal coronary angioplasty; VSD, ventricular septal defect; MR, mitral regurgitation

A very recent trial (IABP-SHOCK II) has been published in the New England Journal of Medicine. This suggested no mortality benefit in patients with cardiogenic shock randomised to IABP compared to those treated with early revascularization and intensive care alone. However, a major criticism was timing of use: 88.6% of IABP were inserted after revascularization. The guidelines remain unchanged with a class I recommendation but may be reviewed in the future. The trial may be repeated in the future with balloon pump insertion at time of presentation and not after definitive therapy.

Complications

IABPC usage is not without complication. The complications can be extremely serious with arterial and aortic damage including dissection.¹¹ These complications are not always evident during the time IABPC is in situ. Some of these complications become apparent when patients return to their general medical ward for further medical treatment and rehabilitation. It is therefore vital that all medical doctors are aware of such possible complications. Embolization, thrombocytopenia, balloon rupture, trapping of gas and infection are all early identified complications.¹² Prolonged use of IABP therapy coincided with a greater risk of serious complication. Incorrect placement by the operator can cause limb ischaemia (a too proximally placed IABP can occlude the origin of the left subclavian and compromise arterial blood flow to the left hand and IABP placed too distally can block the renal arteries and contribute to renal hypoperfusion, low urine output and renal failure). Traditionally, IABPC use was routinely combined with full heparin anticoagulation introducing the risk of heparin induced thrombocytopenia. However, many centres now only load an initial heparin bolus, further minimizing the risk of HIT to an absolute minimum. One of the largest retrospective studies to date, the Benchmark Registry documented that of the 16,909 patients in the study only 2.6% suffered any major complications.¹³

Cohen et al. analysed high-risk features that were associated with increased incidence of IABPC complications. This included female gender, patients known to have peripheral vascular disease, diabetes, stroke/TIA, patients with a body surface area less than 1.8 m² and cardiac index less than 2.2 L/min/m². They found that patients with one or more of the above risk factors had a significantly higher incidence of IABPC-related complications compared with a cohort lacking the above risk factors (15% versus 3%). As such, these authors devised a risk-scoring system to allow clinicians to predict the risk of IABPC-related complications. With this model, they found that the risk of complications significantly increased with the addition of an extra risk factor in the individual patient such that a patient with four risk factors had a 75% risk of complication.¹⁴ Overall, however, the complications seen during the early development of IABPC have markedly decreased. The latest devices can be inserted percutaneously without a sheath, reducing the risk of arterial complications

Can we offer our patients an alternative method of cardiac support?

The lack of high-level evidence supporting the use of IABPC has led to a search for alternative therapies. Left ventricular assist device (LVADs) function by acting as a surrogate pump to support the damaged left ventricle. These devices are usually situated inside or outside the body. A cannula is inserted into the left ventricle and an outflow graft is passed over the diaphragm and joined to the root of the aorta. This drains blood from the left ventricle to the pump, and is subsequently returned to the ascending aorta. LVADs are used far less frequently than IABPC and their use is presently limited to end-stage heart failure as a ‘bridge to recovery’ in those patients awaiting cardiac transplant.⁹

Studies have focused on the use of LVADs in heart failure and patients with impaired cardiac function. In one study (n = 200) the use of LVAD improved New York Heart Association (NYHA) scoring of patients.¹⁵ This was evidenced by nearly 30% of the patients going from class IV to class II. However, the co-morbidities and adjuvant medical therapy were not made apparent for such patients who showed such a significant improvement.

Further data support the fact that LVAD can potentially improve LVEF and functional status.^16,17

Even though these studies do not show evidence base for the use of LVAD in patients post-AMI and impaired LVEF, they do point to the potential benefit upon optimization of alternative therapy in such patients. Possible early consideration of such devices in patients with AMI and possible cardiogenic shock with impaired LVEF may well benefit from early assessment and implantation of such devices. This may lead to earlier discharge from hospital and return to functional status.

Very few individual trial data exist that actively compare LVAD to IABPC. This is mainly due to the fact that at present they are used for varying interim measures. However, Cheng et al. concluded that patients who received LVAD instead of IABPC indeed had no survival benefit and in fact had higher bleeding complications. Any immediate superior haemodynamic superiority provided by LVAD is arguably offset in the long term.¹⁸ This hypothesis was supported by the early termination of the Prospect II trial that aimed to compare the Impella LVAD to that of IABPS in high-risk PCI patients. There was no statistical benefit with regard to adverse events between the two mechanical devices. However, a significant confounding variable of atherectomy was conducted in patients implanted with the Impella device leading to the termination of the study due to futility of the endpoints reached.

Conclusion

Early coronary re-vascularization, be it via PCI or CABG along with supportive care, remains the definitive treatment of cardiogenic shock secondary to acute myocardial infarction.

Despite the recommendations for IABPC use in international guidelines, the literature has led to divided opinion on the true efficacy of using such devices. The use of IABPC lacks robust multiple randomized controlled trial data for long-term survival outcomes in cardiogenic shock. However, observational data suggest that there is a clear role as an adjuvant or ‘bridge’ therapy.

Treating cardiogenic shock is incredibly difficult in the medical setting, especially outside the CCU. The damaged heart needs to be rested, yet without a sufficient mean arterial pressure there is multiorgan under-perfusion. Inotropic support is associated with many complications including arrhythmia, peripheral limb and gastrointestinal tract ischaemia. Although inotropic support has evidence in treating septic shock it is associated with a markedly poorer outcome in managing cardiogenic shock. IABPC can markedly reduce inotropic demands and assist in keeping mean arterial pressures elevated. Although its use and management is yet confined to Coronary Care and Cardiothoracic units, its discussion for use is one that should span the breadth of all medical specialties. Just as dialysis is known to the realms of all medical fields it is also the duty of the caring physician to be aware that IABPC exists to provide patients with a mode of cardiac stabilization that if not leading to PCI or surgery will offer patients a route to minimizing cardiac damage and possibly hospital discharge.

Future studies for IABPC should aim not only to decipher more definitively the role of IABPC in an acute setting but should also look to expand to evaluate whether such use is beneficial in patients with decompensated heart failure and use in other types of shock, e.g. septic shock. Owing to the differing pathophysiology of cases such as septic shock, one must begin with phase one trials in order to gain evidence of the possible beneficial effects that could be applied to a human model.

What we can say with some confidence is that IABPC should be considered in all patients with haemodynamic instability secondary to AMI, leading to cardiogenic shock. This method of cardiac support can be offered to patients in the CCU setting with little risk to the patient and with minimal methods of monitoring. It remains to be seen whether IABPC can be used in patients with acutely unstable cardiac disease with the sole aim to medically stabilize the patient and then treat medically without further intervention. This will be left to the discretion of the treating physician and specialist cardiologist unit.

DECLARATIONS

Competing interests

None declared

Funding

None declared

Ethical approval

Not applicable

Guarantor

CAAC

Contributorship

The original draft was written by FS. FK and MA edited and made revisions to the manuscript. FS and CC conceived the review

Acknowledgements

None