• Management of Acute Myocardial Infarction With Cardiogenic Shock: Systematic Care and a Stepwise Intraprocedural Guide

    September 17, 2018

    Rahul Sharma, MD, FSCAI; and Sridevi Pitta, MD, MBA, FSCAI

    Acute myocardial infarction (AMI) is the most common cause of cardiogenic shock (CGS), with a mortality rate as high as 50 percent. 1 There has been a > 2‐fold increase in the incidence of CGS in patients with ST-elevation myocardial infarction (STEMI) from 2003 to 2010, with the increase more marked in women and patients > 75 years.2 Despite recognition of the importance of minimizing time to reperfusion, early revascularization with PCI or CABG was performed in only 51 percent of patients with AMI-CGS in 2010, and mortality rates in these patients have actually increased over time.3 There has been a paradigm shift in the management of CGS, with the focus on earlier and more widespread use of mechanical circulatory devices (MCS) for LV support, RV support, and/or biventricular support. These devices include  Impella (Abiomed in Danvers, MA), TandemHeart (TandemLife in Pittsburgh, PA), and Extracorporeal Membrane Oxygenation (VA ECMO) coupled with LV unloading. The relative inefficacy of intra-aortic balloon counterpulsation (IABP) in the management of AMI-CGS has been recognized.4 Finally, regional systems of care and a team-based algorithmic approach are being implemented to improve outcomes. This SCAI Tip of the Month is aimed at providing a stepwise approach (Figure 1) to the assessment and management of patients presenting with AMI-CGS, incorporating evidence from recently published data.

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    Definition and Evaluation:

    1. CGS is a low-output state due to a primary cardiac condition that results in end-organ hypoperfusion, defined clinically or based on right heart catheterization (RHC) as:
      1. SBP ≤ 90 mmHg for ≥ 30 minutes OR need for pharmacologic and/or IABP support to maintain SBP ≥ 90 mmHg AND signs of end-organ hypoperfusion (oliguria, altered mental status, cool extremities, lactate > 2 mmol/L).5
      2. CI ≤ 2.2 L/min/m2 AND PCWP ≥ 15 mmHg. It is important to understand that tissue hypoperfusion can exist without overt hypotension.
    1. RHC is recommended concurrently with primary PCI to determine the severity and type of cardiac dysfunction (i.e., LV and/or RV failure). Inadditiontousual measurements, the following two indices of LV and RV function should be calculated.
      1. Cardiac power output (CPO) is calculated as []/451. CPO, measured in watts (W), was the strongest hemodynamic predictor of mortality in the SHOCK trial, with a 58 percent probability of in-hospital mortality when CPO < 0.53 W.6
      2. Pulmonary artery pulsatility index (PAPi) is calculated as [PASP-PADP]/RAP.7 In the presence of CGS, PAPi < 0.9, in conjunction with other criteria such as RAP > 15 mmHg and CVP/PCWP > 0.8, indicates severe RV failure.8
    1. Risk stratification: A risk score derived from the IABP-SHOCK II trial incorporated age > 73, lactate > 5 mmol/L, Cr > 1.5 mg/dl, glucose > 191 mg/dL, and prior stroke and TIMI flow < 3 post PCI. Mortality was 20–30 percent in the lowest risk score group and 70–90 percent in the highest risk score group.9 Therefore, lactate, glucose, and creatinine values should be closely monitored.

    Management:

    1. In patients with refractory CGS requiring multiple vasopressors and/or inotropic agents at high doses, a decision to escalate to mechanical circulatory support (MCS) should be made as soon as possible. In the cVAD registry, survival declined from 45 percent with one vasopressor to 35 percent with two to three vasopressors, and 26 percent when four drugs were needed.10
    1. IABP did not lower 30-day or one-year mortality compared with control when placed (mainly post-PCI) in patients with AMI-CGS.4
    1. Although MCS provides superior hemodynamic support, there are no randomized controlled trials that show improved outcomes with a particular MCS device compared with IABP. In the absence of randomized controlled trial (RCT) data, hemodynamic measurements (e.g., MAP, CI, CPO, PAPi), in conjunction with biochemical and clinical markers of tissue perfusion, can be used to make decisions on the timing and choice of MCS.11 Atkinson et al published an interventional perspective on “A Practical Approach to Mechanical Circulatory Support in Patients Undergoing Percutaneous Coronary Intervention,” in which they put forth an illustration outlining an algorithm for percutaneous MCS device selection for different indications.11 Once an MCS device is implanted, vasopressors should be weaned expeditiously.
    1. Door-to-unloading time versus door-to-balloon time: For decades, interventional cardiologists have subscribed to the thinking that time is myocardium, and that the main priority in STEMI is opening the infarct-related artery. Yet, despite timely PCI of the culprit vessel, mortality in CGS continues to be high.5, 12 In addition, there is no benefit of immediate PCI of nonculprit vessels, as shown in the CULPRIT-SHOCK trial.12 On the other hand, research from animal studies has shown a beneficial effect of LV unloading before revascularization.13 Registry data show that pre-PCI LV unloading with Impella was associated with significantly higher in-hospital survival compared with post-PCI placement, despite a longer door-to-balloon time.14 Similar benefits were noted with early (within 90 minutes of the onset of CGS) compared with delayed (> 4 hours) implantation.10

    Escalation vs. De-Escalation of Care and Regional Shock Centers:

    The 2018 American Heart Association (AHA) scientific statement on the “Contemporary Management of Cardiogenic Shock” is an excellent summary of this topic, with a discussion of contemporary data, concepts, and unanswered questions in AMI-CGS. In this scientific statement, a proposal is made for integrated regional hub and shock-care systems with dedicated CS centers.15 In the event that a timely transfer to a regional shock center is not feasible, the initial PCI-capable hospital can prioritize obtaining initial key laboratory values, performing an RHC, implantation of whichever circulatory support device it has readily available (e.g., IABP), primary PCI, and adjunctive critical care support. Once these crucial steps are performed, the invasive right heart hemodynamics can help guide whether the patient ought to remain at the primary hospital versus being transferred to a regional shock center. Hemodynamic and clinical parameters such as CPO, PAPi, serum lactate, and urine output should be monitored closely in order to determine trends in improvement or the need for escalation of support. The critical parameters to follow include:

    1. Escalation: Ongoing presence of a CPO ≤ 0.6 and/or PAPi ≤ 0.9, despite placement of available ventricular support device(s), necessitates escalation to higher forms of support (VA-ECMO; surgically implanted ventricular assist device (VAD); and/or urgent evaluation for cardiac transplantation, if appropriate). In addition, certain clinical scenarios may call for two different forms of MCS to be used concurrently for maximal LV unloading (e.g., VA-ECMO coupled with IABP or LV Impella) or biventricular support.
    2. De-escalation: Once CPO, PAPi, lactate, and other clinical parameters are normalizing, then the timely de-escalation of circulatory support devices is paramount in order to minimize associated hematologic and peripheral vascular complications.

    The integral involvement of several care teams (emergency medical services; interventional cardiologists; cardiac surgeons; heart failure specialists; cardiac anesthesiologists; perfusion; and palliative care, when appropriate) is the linchpin of a successful shock program. Understanding the hemodynamics indices necessary to determine the type of MCS and response to MCS is essential to guide decision-making and the expected response to the selected therapy. Regional cardiogenic shock initiatives have reported significant improvements in survival, with early MCS implementation and decision-making based on systematic protocols.16

    Key Abbreviations

    PCI = percutaneous coronary intervention

    CABG = coronary artery bypass graft surgery

    LV = left ventricle

    RV = right ventricle

    SBP = systolic blood pressure (mmHg)

    CI = cardiac index (L/min/m2)

    PCWP = pulmonary capillary wedge pressure (mmHg)

    CO = cardiac output

    MAP = mean arterial pressure

    PASP = pulmonary artery systolic pressure (mmHg)

    PADP = pulmonary artery diastolic pressure (mmHg)

    CVP = central venous pressure (mmHg)

    RAP = right atrial pressure (mmHg)

     

    References:

    1. Hollenberg SM, Kavinsky CJ, Parrillo JE. Cardiogenic shock. Ann Intern Med. 1999;131:47–59.
    2. Kolte D, Khera S, Aronow WS, Mujib M, Palaniswamy C, Sule S, Jain D, Gotsis W, Ahmed A, Frishman WH, Fonarow GC. Trends in incidence, management, and outcomes of cardiogenic shock complicating ST elevation myocardial infarction in the United States. J Am Heart Assoc. 2014;3:e000590. doi: 10.1161/JAHA.113.000590.
    3. Wayangankar SA, Bangalore S, McCoy LA, Jneid H, Latif F, Karrowni W, Charitakis K, Feldman DN, Dakik HA, Mauri L, Peterson ED, Messenger J, Roe M, Mukherjee D, Klein A. 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 Feb 22;9(4):341–351.
    4. Thiele H, Zeymer U, Neumann FJ, et al. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12-month results of a randomised, open-label trial. Lancet. 2013;382(9905):1638–1645.
    5. Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD, Buller CE, Jacobs AK, Slater JN, Col J, McKinlay SM, LeJemtel TH. 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. 1999;341:625–634. doi: 10.1056/NEJM199908263410901.
    6. Fincke R, Hochman JS, Lowe AM, Menon V, Slater JN, Webb JG, LeJemtel TH, Cotter G; SHOCK Investigators. Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. J Am Coll Cardiol. 2004 July 21;44(2):340.8.
    7. Korabathina R, Heffernan KS, Paruchuri V, Patel AR, Mudd JO, Prutkin JM, Orr NM, Weintraub A, Kimmelstiel CD, Kapur NK. The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv. 2012;80:593–600. doi: 10.1002/ccd.23309.
    8. Lala A, Guo Y, Xu J, Esposito M, Morine K, Karas R, Katz SD, Hochman JS, Burkhoff D, Kapur NK. Right Ventricular Dysfunction in Acute Myocardial Infarction Complicated by Cardiogenic Shock: A Hemodynamic Analysis of the ould We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) Trial and Registry. J Card Fail. 2018 Mar;24(3):148–156.
    9. Poss J, Koster J, Fuernau G, Eitel I, de Waha S, Ouarrak T, Lassus J, Harjola VP, Zeymer U, Thiele H et al. Risk stratification for patients in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol 2017;69(15):1913–1920.
    10. Basir MBSchreiber TLGrines CLDixon SRMoses JWMaini BSKhandelwal AKOhman EMO'Neill WW. Effect of Early Initiation of Mechanical Circulatory Support on Survival in Cardiogenic Shock. Am J Cardiol.2017 Mar 15;119(6):845–851.
    11. Atkinson TM, Ohman EM, O'Neill WW, Rab T, Cigarroa JE. Interventional Scientific Council of the American College of Cardiology. A Practical Approach to Mechanical Circulatory Support in Patients Undergoing Percutaneous Coronary Intervention: An Interventional Perspective. JACC Cardiovasc Interv. 2016 May 9;9(9):871–83.
    12. Thiele H, Akin I, Sandri M, Fuernau G, de Waha S, Meyer-Saraei R, Nordbeck P, Geisler T, Landmesser U, Skurk C, Fach A, Lapp H, Piek JJ, Noc M, Goslar T, Felix SB, Maier LS, Stepinska J, Oldroyd K, Serpytis P, Montalescot G, Barthelemy O, Huber K, Windecker S, Savonitto S, Torremante P, Vrints C, Schneider S, Desch S, Zeymer U; CULPRIT-SHOCK Investigators. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock. N Engl J Med. 2017;377(25):2419–32.
    13. Kapur NK, Paruchuri V, Urbano-Morales JA, et al. Mechanically unloading the left ventricle before coronary reperfusion reduces left ventricular wall stress and myocardial infarct size. Circulation. 2013;128:328–336.
    14. 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.
    15. Diepen SV, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, Kilic A, Memon V, Ohman EM, Sweitzer NK, Thiele H, Washam JB, Cohen MG. American Heart Association Scientific Statement 2018 Contemporary Management of Cardiogenic Shock. 2017;136:e232–e268.
    16. Basir MB, Schreiber T, Dixon S, Alaswad K, Patel K, Almany S, Khandelwal A, Hanson I, George A, Ashbrook M, Blank N, Abdelsalam M, Sareen N, Timmis SBH, O'Neill WW. Feasibility of early mechanical circulatory support in acute myocardial infarction complicated by cardiogenic shock: The Detroit cardiogenic shock initiative. Catheter Cardiovasc Interv. 2018 Feb 15;91(3):454–461.