Cardiogenic shock (CS) remains one of the most challenging clinical syndromes in modern medicine and is defined by insufficient cardiac output to maintain multi-organ perfusion. CS is the most common cause of in-hospital mortality in the setting of acute myocardial infarction (AMI). An analysis of the Nationwide Inpatient Sample Database between 2003 and 2010 reported an increase in the prevalence of CS among patients presenting with ST-segment elevation myocardial infarction (STEMI) from 6 to 10%.¹ Among patients with STEMI over the age of 75, CS increased from 7 to 12%. A more contemporary and consistently sobering analysis of patients with AMI with CS undergoing percutaneous coronary intervention (PCI) reported that despite an overall increase in the use of PCI for AMI with CS, in-hospital mortality increased from 27 to 30%, and deaths occurring in the catheterization laboratory increased from 15 to 20% between 2005 and 2013.² Despite increasing rates of early revascularization, the prognosis for patients with AMI with CS who survive to hospital discharge is poor. Several recent analyses confirm increases rates of mortality and heart failure within the first year after discharge. An analysis of patients with AMI with CS identified a 22% 1-year mortality rate and 59% re-hospitalization rate compared with 16 and 52%, respectively, for AMI without CS.³ Heart failure-specific readmission rates were 24% for all patients with AMI and 32% for patients with AMI with CS. These data further support the need for new approaches to improve outcomes for patients with AMI with CS.

In the setting of AMI with CS, three primary treatment objectives must be achieved (Figure 1). First, circulatory support to maintain an adequate mean arterial pressure and vital organ perfusion must be achieved. Second, ventricular unloading—defined as a reduction in left ventricular (LV) pressure and volume—to reduce myocardial oxygen demand in the face of limited myocardial oxygen supply is required. Third, augmenting myocardial perfusion by recanalizing an occluded coronary vessel and sustaining coronary arterial pressure while reducing LV diastolic pressure will further reduce the burden of myocardial ischemia and injury. In addition to balloon angioplasty, each of these three components of the hemodynamic support equation (Figure 1) can be achieved with appropriate use of acute mechanical circulatory support (AMCS) pumps.

Figure 1: Solving the Hemodynamic Support Equation in CS

AMCS Device Platforms in 2016

Four primary AMCS device platforms are used in contemporary clinical practice for LV support (Figure 2):

• the intra-aortic balloon pump (IABP)
• centrifugally driven left atrial-to-femoral artery bypass (TandemHeart Percutaneous Ventricular Assist Device [pVAD]; TandemLife)
• centrifugally driven veno-arterial extracorporeal membrane oxygenation (VA-ECMO)
• micro-axial flow catheter (Impella CP; ABIOMED) (HeartMate Percutaneous Heart Pump [PHP]; St. Jude Medical)⁴

At present, the PHP device is approved for clinical use in Europe but is under active investigation in the United States.

Figure 2: Acute Mechanical Circulatory Support Options for the LV

The IABP is a catheter-mounted balloon that augments pulsatile blood flow by inflating during diastole, which displaces blood volume in the descending aorta and increases mean aortic pressure, thereby potentially augmenting coronary perfusion. Because the unloading effect of counterpulsation therapy depends on native LV function, patients with profound LV failure (i.e., CS) may not achieve systolic unloading with IABP therapy. VA-ECMO withdraws deoxygenated venous blood and returns oxygenated blood to the arterial circulation. The net effect of VA-ECMO is to increase mean arterial pressure, load (not unload) the LV, and potentially increase coronary blood flow.⁵ To unload the LV with VA-ECMO, additional LV "venting" strategies are required, which include inotropes, IABP, micro-axial flow catheter, left atrial cannulation, or atrial septostomy.

The pVAD device is an extra-corporeal centrifugal flow pump that reduces LV preload by transferring oxygenated blood from the left atrium (LA) to the descending aorta via two cannulas: a 21-Fr transseptal inflow cannula in the LA and an arterial outflow cannula in the femoral artery. The pVAD device rapidly increases mean arterial pressure, thereby increasing coronary perfusion pressure.⁵ The device unloads the LV primarily by decreasing LV volume. The micro-axial flow catheter is placed into the LV in retrograde fashion across the aortic valve. The pump transfers kinetic energy from a circulating impeller to the blood stream, which results in continuous blood flow from the LV to ascending aorta.⁶ Micro-axial flow catheter activation rapidly increases mean arterial pressure, reduces LV diastolic pressure, and increases trans-myocardial coronary perfusion. Of these four device options, only the Impella CP (ABIOMED) and the TandemHeart pVAD (TandemLife) can achieve all three objectives of the hemodynamic support equation (Figure 1).

What Do the Guidelines Say?

Contemporary North American guidelines for the use of AMCS in the setting of CS are limited. The 2011 PCI guidelines recommend hemodynamic support in patients with CS who do not quickly improve with pharmacologic therapy (Class 1, Level of Evidence [LOE] B).⁷ The guidelines further state that elective insertion of a hemodynamic support device as an adjunct to PCI may be reasonable in patients with CS (Class 2b, LOE C). The 2013 STEMI guidelines suggest that IABP therapy can be useful in CS in patients with STEMI who do not quickly improve with pharmacologic therapy (Class 2a, LOE B) and that alternative LV circulatory support devices may be considered for "refractory" CS (Class 2b, LOE C).⁸ The 2014 European PCI guidelines suggest that AMCS devices may be considered for patients with ACS complicated by CS. The guidelines further indicate that routine use of IABP therapy for CS is not recommended (Class III, LOE A); however, IABP insertion may be considered for patients with CS due to mechanical complications of AMI (Class IIA, LOE C).⁹ The 2012 European STEMI guidelines also suggest that IABP therapy may be considered for CS after STEMI (Class 2b, LOE B).¹⁰ These guidelines state that other LV AMCS devices may be considered for refractory shock after STEMI on an individual basis but are not recommended as first-line treatment (Class 2b, LOE C).

One of the major limitations of these guideline recommendations is the lack of randomized, controlled trials exploring the utility of hemodynamic support in CS. To date, the most rigorously studied device is the IABP, which failed to demonstrate clear benefit in the IABP-SHOCK II (Intraaortic Balloon Pump in Cardiogenic Shock II) trial.¹¹ More recent observational studies have also supported the limited utility and potential harm of IABP therapy in CS.^12,13 These studies have clearly impacted clinical practice; we are now seeing a decline in IABP use accompanied by an increase in Impella CP (ABIOMED) and the TandemHeart pVAD (TandemLife) use.¹⁴ VA-ECMO in the setting of CS also remains controversial, with several conflicting reports recently published.^15,16 Clearly, the lack of randomized, controlled trial data supporting the use of non-IABP AMCS devices (i.e., pVAD, PHP, and VA-ECMO) contributes to the challenge of writing guidelines that more closely mirror clinical practice.

Several small reports demonstrated hemodynamic superiority of the Impella CP (ABIOMED) and the TandemHeart pVAD (TandemLife) when compared with IABP therapy. One large study reported a 60% rate of 30-day survival among 117 patients with CS treated with the pVAD device.¹⁷ The largest dataset supporting the use of the micro-axial flow catheter device in CS was derived from the USpella registry and reported better outcomes with early initiation of device support before PCI in AMI with CS.¹⁸ Based on this report and another analyses of the USpella registry, the Food and Drug Administration recently approved the Impella CP (ABIOMED) as the only device indicated for CS.

The Onus Is On Us

For decades, the SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) trial has been the mainstay of recommendations for the management of CS. However, contemporary management of CS remains nebulous without any uniformity or consensus-driven algorithms. Many uncertainties about shock management remain:

• the need for a pulmonary artery catheter to guide clinical decision-making
• the timing and limitations of vasopressor/inotrope support
• the timing of AMCS device therapy
• correct application of appropriate AMCS device therapy
• the timing of mechanical unloading relative to coronary reperfusion in AMI with CS
• whether subtypes of CS exist such as LV-, right ventricular-, and biventricular-dominant shock

Device companies have accomplished major engineering advances that now allow us to support the left, right, and both ventricles rapidly and effectively. The onus is now on us to answer these questions and come together as a community to address this complex syndrome that continues to grow in prevalence and negatively impacts many of our patients.

References

1. Kolte D, Khera S, Aronow WS, et al. Trends in incidence, management, and outcomes of cardiogenic shock complicating ST-elevation myocardial infarction in the United States. J Am Heart Assoc 2014;13:e000590.
2. Wayangankar SA, Bangalore S, McCoy LA, et al. Temporal Trends and Outcomes of Patients Undergoing Percutaneous Coronary Interventions for Cardiogenic Shock in the Setting of Acute Myocardial Infarction: A Report From the CathPCI Registry. JACC Cardiovasc Interv 2016;9:341-51.
3. Shah RU, de Lemos JA, Wang TY, et al. Post-Hospital Outcomes of Patients With Acute Myocardial Infarction With Cardiogenic Shock: Findings From the NCDR. J Am Coll Cardiol 2016;67:739-47.
4. Rihal CS, Naidu SS, Givertz MM, et al. 2015 SCAI/ACC/HFSA/STS Clinical Expert Consensus Statement on the Use of Percutaneous Mechanical Circulatory Support Devices in Cardiovascular Care: Endorsed by the American Heart Association, the Cardiological Society of India, and Sociedad Latino Americana de Cardiología Intervencionista; Affirmation of Value by the Canadian Association of Interventional Cardiology-Association Canadienne de Cardiologie d'intervention. J Am Coll Cardiol 2015;65:2140-1.
5. Esposito ML, Shah N, Dow S, et al. Distinct Effects of Left or Right Atrial Cannulation on Left Ventricular Hemodynamics in a Swine Model of Acute Myocardial Injury. ASAIO J 2016 Jul 20 [Epub ahead of print].
6. Morine KJ, Kapur NK. Percutaneous Mechanical Circulatory Support for Cardiogenic Shock. Curr Treat Options Cardiovasc Med 2016;18:6.
7. Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. J Am Coll Cardiol 2011;58:e44-122.
8. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:e362-425.
9. Authors/Task Force members, Windecker S, Kolh P, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J 2014;35:2541-619.
10. Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC), Steg PG, James SK, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2012;33:2569-619.
11. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med 2012;367:1287-96.
12. Zheng XY, Wang Y, Chen Y, et al. The effectiveness of intra-aortic balloon pump for myocardial infarction in patients with or without cardiogenic shock: a meta-analysis and systematic review. BMC Cardiovasc Disord 2016;16:148.
13. Iqbal MB, Robinson SD, Ding L, et al. Intra-Aortic Balloon Pump Counterpulsation during Primary Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction and Cardiogenic Shock: Insights from the British Columbia Cardiac Registry. PLoS One 2016;11:e0148931.
14. Stretch R, Sauer CM, Yuh DD, Bonde P. National trends in the utilization of short-term mechanical circulatory support: incidence, outcomes, and cost analysis. J Am Coll Cardiol 2014;64:1407-15.
15. de Waha S, Fuernau G, Desch S, et al. Long-term prognosis after extracorporeal life support in refractory cardiogenic shock: results from a real-world cohort. EuroIntervention 2016;11:1363-71.
16. Sheu JJ, Tsai TH, Lee FY, et al. Early extracorporeal membrane oxygenator-assisted primary percutaneous coronary intervention improved 30-day clinical outcomes in patients with ST-segment elevation myocardial infarction complicated with profound cardiogenic shock. Crit Care Med 2010;38:1810-7
17. Kar B, Gregoric ID, Basra SS, Idelchik GM, Loyalka P. The percutaneous ventricular assist device in severe refractory cardiogenic shock. J Am Coll Cardiol 2011;57:688-96.
18. O'Neill WW, Schreiber T, Wohns DH, et al. The current use of Impella 2.5 in acute myocardial infarction complicated by cardiogenic shock: results from the USpella Registry. J Interv Cardiol 2014;27:1-11.

Keywords: Algorithms, Angioplasty, Balloon, Aorta, Thoracic, Aortic Valve, Arterial Pressure, Biomarkers, Blood Pressure, Blood Volume, Cardiac Output, Consensus, Coronary Vessels, Creatine Kinase, Diastole, Extracorporeal Membrane Oxygenation, Femoral Artery, Heart Atria, Heart Failure, Heart-Assist Devices, Hospital Mortality, Inpatients, Intra-Aortic Balloon Pumping, Lactates, Myocardial Reperfusion, Percutaneous Coronary Intervention, Pulmonary Artery, Pulmonary Wedge Pressure, Shock, Cardiogenic, Ventricular Function, Left

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