REVIEW METHODIST DEBAKEY CARDIOVASC J | 16 (1) 2020

Cardiogenic Shock in the Setting of Acute Myocardial Infarction

Navin K. Kapur, MD; Katherine L. Thayer, MPH; Elric Zweck

TUFTS MEDICAL CENTER, BOSTON, MASSACHUSETTS

ABSTRACT: Cardiogenic shock in the setting of acute myocardial infarction remains a major cause of morbidity and mortality. In fact, acute
myocardial infarction accounts for 81% of patients in cardiogenic shock. Despite advances in pharmacologic and device-based approaches to
support patients with cardiogenic shock, no significant improvement in mortality has been observed over the past 20 years, although multiple
registries are providing new insight into this complex syndrome. Key elements for optimal treatment include integration of hemodynamic and
metabolic data for diagnosis and risk stratification, early evaluation and appropriate initiation of acute mechanical circulatory support devices,
and an organized algorithmic approach to decision making.

INTRODUCTION infarction (STEMI).2 Electrocardiographic criteria for STEMI

have been well defined by the American College of Cardiology,
Approximately every 40 seconds, someone in the United States American Heart Association, European Society of Cardiology,
experiences a myocardial infarction. Acute myocardial infarction and World Heart Federation (Table 1).3,4 STEMI is associated
(AMI) accounts for roughly 80% of patients in cardiogenic shock with a 2-fold increased risk for developing CS.5
(CS).1 In this scenario, CS commonly manifests with left ventricular
failure. However, in 20% of cases, CS is due to a complication Due to the high mortality associated with CS and the high
associated with AMI, such as acute mitral regurgitation, ventricular incidence of CS in STEMI patients, it is imperative that we
septal defect, or subacute or acute free wall rupture. Right fully understand the progression of STEMI to CS and how
heart failure may also contribute to CS and is more commonly best to treat patients with this complex syndrome. The lack
associated with right ventricular myocardial infarction. of conclusive research on these patients has resulted in
potentially uninformed approaches to treatment and inconsistent
Of the 805,000 heart attacks that occur each year in the United reporting of outcomes. New registries that take an observational
States, an estimated 38% are due to ST-elevation myocardial approach to classifying CS patients, particularly those with

ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)

The American College of Cardiology, American Heart Association, European Society of Cardiology, and World Heart Federation committee established the
following electrocardiogram (ECG) criteria for STEMI:
• New ST-segment elevation at the J point in two contiguous leads, with the cutoff point as > 0.1 mV in all leads other than V2 or V3
• In leads V2-V3, the cutoff point is > 0.2 mV in men older than 40 years and > 0.25 mV in men younger than 40 years, and > 0.15 mV in women
A new left bundle branch block is considered a STEMI equivalent. Patients with a pre-existing left bundle branch block can be further evaluated using
Scarbossa’s criteria:
• ST-segment elevation of 1 mm or more that is concordant with (in the same direction as) the QRS complex
• ST-segment depression of 1 mm or more in lead V1, V2, or V3
• ST-segment elevation of 5 mm or more that is discordant with (in the opposite direction) the QRS complex

NON–ST-ELEVATION MYOCARDIAL INFARCTION (NSTEMI)

NSTEMI is diagnosed in patients who have symptoms consistent with acute cardiogenic shock and troponin elevation but without ECG changes consistent
with STEMI. Unstable angina and NSTEMI differ primarily in the presence or absence of detectable troponin leak. Myocardial injury is expected at troponin
levels exceeding the 99th percentile upper reference limit, which is specified for each individual assay. Specific cutoffs can be found in manufacturers’
package inserts, in peer-reviewed publications, and on the International Federation of Clinical Chemistry and Laboratory Medicine website.

Table 1.
Definition of myocardial infarction.3,4

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PATIENT PRIMARY END

TRIAL YEAR PATIENTS TREATMENT ARMS RESULTS
POPULATION POINT(S)

SHOCK 1999 302 Shock due to left Emergency 30-day all-cause No significant difference
ventricular failure revascularization mortality in mortality between
complicating or initial medical treatment groups (46.7%
myocardial infarction stabilization vs 56.0%; P = .11)

IABP – SHOCK II 2012 600 Shock complicating Intra-aortic balloon 30-day all-cause No significant difference
acute myocardial counterpulsation mortality in mortality between
infarction or no intra- treatment groups (39.7%
aortic balloon vs 41.3%; P = .69)
counterpulsation

IMPRESS 2016 48 Severe shock Impella CP or intra- 30-day all-cause No significant different in
complicating acute aortic balloon pump mortality mortality between Impella
myocardial infarction CP and IABP (46% vs 50%,
P = .96)

CULPRIT SHOCK 2017 706 Shock presenting Culprit-lesion-only 30-day mortality Culprit-lesion-only PCI was
with multivessel PCI or immediate and renal failure associated with slightly
disease and acute multivessel PCI requiring RRT decreased risk of mortality
myocardial infarction (OR: 0.84, P = .03)
compared to multivessel
PCI, but the risk of RRT did
not differ (OR: 0.71, P = .07)

DCSI 2018 41 Acute myocardial Single treatment Survival to explant Survival to explant was
infarction arm of invasive and change in CPO 85% vs 51% in historical
complicated by hemodynamic controls (P < .001), and
cardiogenic shock monitoring and post-procedure CPO
rapid initiation of increased 67% compared
non-IABP MCS to pre-procedure CPO
(P < .001)

Table 2.
Recent clinical trials evaluating treatment options in cardiogenic shock. IABP: intra-aortic balloon pump; PCI: percutaneous coronary intervention; RRT: renal
replacement therapy; SHOCK: Should we Emergently Revascularize Occluded Coronaries for Cardiogenic Shock trial; IABP-SHOCK II: Intra-Aortic Balloon
Pump Support for Myocardial Infarction with Cardiogenic Shock trial; IMPRESS: Impella Versus IABP Reduces Mortality in STEMI Patients Treated with
Primary PCI in Severe Cardiogenic Shock trial; CULPRIT SHOCK: Culprit Lesion-Only PCI Versus Multivessel PCI in Cardiogenic Shock trial; DCSI: Detroit
Cardiogenic Shock Initiative

cases due to STEMI, could provide the data-driven results in-hospital mortality for these patients decreased from 44.6%
necessary to inform future successful trials. to 33.8% over the same time period.6 Similar findings were
reported in an analysis of the same database from 2003 to
PATIENT OUTCOMES IN CARDIOGENIC SHOCK 2011. In this analysis, the National Cardiovascular Data Registry
(NCDR) reported that 12.2% of STEMI patients experienced
Recent analyses of the National Inpatient Sample report that CS between 2007 and 2011, with an in-hospital mortality rate
the incidence of CS among STEMI patients increased from of 33.1% for STEMI complicated by CS. The authors also
6.5% to 10.1% between 2003 and 2010. It further showed that observed that CS was less prevalent (4.3%) among non-STEMI

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and suggest that mortality due to AMI with CS remains largely

CARDIAC unchanged over the past two decades.
PCWP MORTALITY
CLASS INDEX
(MM HG) (%)
(MM/MIN)
CLASSIFICATION OF CARDIOGENIC SHOCK
I >2 < 18 3
One explanation for varying results for AMI-CS outcomes in
II >2 > 18 9
clinical trials may be the lack of clear definitions for CS severity.
The original Killip and Diamond-Forrester classifications
III <2 < 18 23
for shock severity in AMI used physical exam findings and
hemodynamic data to assess perfusion and congestion. The
IV <2 > 18 51
more recent Diamond-Forrester classification defined four
clinical subsets of shock: (I) no pulmonary congestion or
peripheral hypoperfusion, (II) isolated pulmonary congestion,
Table 3.
(III) isolated peripheral hypoperfusion, and (IV) both pulmonary
The Diamond-Forrester Classification for shock severity in acute
congestion and hypoperfusion. These subsets correlated with
myocardial infarction.12,13
cardiac index and pulmonary capillary wedge pressure and
were associated with increasing mortality (Table 3).12,13 Since
patients but was associated with a higher in-hospital mortality the initial development of this classification system, several
rate of 40.8%.7 consensus statements have highlighted a further need for
improved definitions for diagnosing CS, additional classification
Despite these registry data, randomized clinical trials continue systems to gauge the severity of CS, algorithms for using
to report mortality rates between 40% and 60% for patients acute MCS (AMCS) devices, and a better understanding of
with AMI and shock (Table 2). In 1999, the SHOCK (Should we hemodynamic-guided decision making in CS.
Emergently Revascularize Occluded Coronaries for Cardiogenic
Shock) trial reported 30-day mortality rates of 41% for patients In response to these unmet needs, the Society for
younger than age 75 who received early revascularization and Cardiovascular Angiography and Interventions (SCAI) recently
75% for patients older than 75. While the SHOCK trial failed to proposed a staging system for CS based on expert consensus
show improvement in its primary end point of 30-day mortality, opinion. The purpose of the SCAI classification scheme is to
it was the first trial to report improved 6-month outcomes facilitate patient care and research in CS by providing a uniform
(secondary end point) associated with early revascularization system for identifying patients who have an increased risk of
among the entire patient cohort. However, among patients older dying (Table 4).14 The SCAI system included five classes of
than age 75, both 30-day and 6-month mortality were worse CS: (A) at risk for CS, (B) beginning CS, (C) classic CS, (D)
when receiving early revascularization compared to medical deteriorating CS, and (E) extreme CS. Each stage is defined
therapy alone.8 The long-term benefits of early revascularization by a physical exam along with biochemical and hemodynamic
were confirmed by the same group at 10 years of follow-up.9 findings. These definitions were intentionally left more general
to accommodate the variability of clinical parameters available
More recently, the IABP-SHOCK II (Intra-Aortic Balloon Pump at the time of presentation. Stages C, D, and E include patients
Support for Myocardial Infarction with Cardiogenic Shock) who require inotrope, vasopressor, or short-term MCS therapy
trial reported that the use of an intra-aortic balloon pump for for CS. Stage D patients represent Stage C patients with
AMI (both STEMI and non-STEMI) was not superior to medical clinical deterioration, and Stage E patients are those who
therapy alone in reducing 30-day mortality. Mortality rates in have deteriorated even further.14 The clinical utility of the SCAI
this trial ranged between 39.7% and 41.3% in both treatment staging system is currently under investigation.
arms. In 2017, the CULPRIT SHOCK (Culprit Lesion Only PCI
Versus Multivessel PCI in Cardiogenic Shock) trial reported Several registries have also begun to provide new insight into
that culprit-lesion-only intervention was associated with reduced CS. The Cardiogenic Shock Working Group (CSWG) is a
30-day mortality (43.3%) compared to multivessel intervention national multicenter retrospective registry that uses real-world
(51.6%) for AMI complicated by CS (AMI-CS) (P = .03).10 The experiences of patients with CS. Initiated in 2017, the CSWG
Detroit Cardiogenic Shock Initiative, a single-arm trial, found registry now includes more than 1,500 patients and contains
that early mechanical circulatory support (MCS) intervention hemodynamic data for analysis of more than 1,000 patients.
was associated with improved survival to explant compared This is the largest contemporary US registry for any-cause CS
to historical controls (85% vs 51%, P < .001).11 Despite this and includes experiences with all AMCS device platforms. Due
promising risk reduction, collective trial data are not conclusive to its diverse patient profile and availability of hemodynamic

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PHYSICAL EXAM/ BEDSIDE

STAGE DESCRIPTION BIOCHEMICAL MARKERS HEMODYNAMICS
FINDINGS

A Patient is not currently • Normal JVP • Normal labs Normotensive

experiencing signs or • Lung sounds clear • Normal renal function (SBP ≥ 100 mm Hg or normal)
At risk
symptoms of CS but is at • Warm and well perfused • Normal lactic acid
If hemodynamics done:
risk for its development. • Strong distal pulses
• Cardiac index ≥ 2.5
Patient may have large • Normal mentation
• CVP < 10 mm Hg
acute myocardial infarction
• PA sat ≥ 65%
or prior infarction and/or
acute on chronic heart failure
symptoms.

B Patient has clinical evidence • Elevated JVP • Normal lactate SBP < 90 mm Hg or
of relative hypotension • Rales in lung fields • Minimal renal function MAP < 60 mm Hg or > 30 mm Hg
Beginning CS
or tachycardia without • Warm and well perfused impairment drop from baseline
hypoperfusion. • Strong distal pulses • Elevated BNP
Pulse ≥ 100
• Normal mentation
If hemodynamics done:
• Cardiac index ≥ 2.2
• PA sat ≥ 65%

C Patient manifests with May include: May include: May include:

hypoperfusion that requires • Looks unwell • Lactate ≥ 2 mmol/L
Classic CS SBP < 90 mm Hg or
intervention (inotrope, • Panicked • Creatinine doubling or >
MAP < 60 mm Hg or > 30 mm Hg
pressor, or mechanical • Ashen, mottled, dusky 50% drop in GFR
drop from baseline and
support, including ECMO) • Volume overload • Increased LFTs
drugs/device used to maintain
beyond volume resuscitation • Extensive rales • Elevated BNP
BP above these targets
to restore perfusion. These • Killip class 3 or 4
patients typically present • BiPap or mechanical Hemodynamics:
with relative hypotension. ventilation • Cardiac index < 2.2
• Cold, clammy • PCWP > 15 mm Hg
• Acute alteration in mental • RAP/PCWP ≥ 0.8
status • PAPI < 1.85
• Urine output < 30 mL/h • Cardiac power output
≤ 0.6 W

D Patient is similar to category Any of stage C Any of Stage C and: Any of Stage C and:
C but is getting worse and deteriorating requiring multiple pressors
Deteriorating/
failing to respond to initial or addition of mechanical
doom
interventions. circulatory support devices to
maintain perfusion

E Patient is experiencing • Near pulselessness “Trying to die” • No SBP without

cardiac arrest with ongoing • Cardiac collapse CPR (A-modifier) resuscitation
Extremis
CPR and/or ECMO, being • Mechanical ventilation pH ≤ 7.2 • PEA or refractory VT/VF
supported by multiple • Defibrillator used Lactate ≥ 5 mmol/L • Hypotension despite
interventions. maximal support

Table 4.
The Society for Cardiovascular Angiography and Interventions classification scheme.13 CS: cardiogenic shock; JVP: jugular venous pressure; SBP: systolic blood
pressure; CVP: central venous pressure; PA sat: pulmonary artery saturation; BNP: brain natriuretic peptide; MAP: mean arterial pressure; PCWP: pulmonary
capillary wedge pressure; RAP: right atrial pressure; PAPI: pulmonary artery pulsatility index; GFR: glomerular filtration rate; LFT: liver function test; CPR:
cardiopulmonary resuscitation; ECMO: extracorporeal membrane oxygenation; BiPaP: bilevel positive airway pressure

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data, this registry could provide valuable

insight by stratifying mortality risk by
different etiologies, comorbidities, and
treatments of shock to inform future
randomized clinical trials.15

The National Cardiogenic Shock

Initiative (NCSI) is a prospective registry
that will determine if implementation
of an algorithm to identify CS—using
hemodynamic data and early initiation
of AMCS with the Impella CP device—
improves clinical outcomes among
patients with AMI-CS. A recent analysis
from the NCSI registry involving 171
patients with AMI-CS reported 72%
survival-to-discharge rate; it also
identified predictors of in-hospital
mortality, including age > 70 years,
creatinine > 2.0, lactate > 4.0, and
cardiac power output < 0.6 W.16

More recently, a group of physicians at

the Inova Heart and Vascular Institute
tested whether an algorithm focused
on identification, stratification, and early
initiation of AMCS in CS improves clinical
outcomes (Figure 1).17 One year after
implementing the algorithm, they reported
a significant increase in 30-day survival
(44% to 82%) among patients presenting
with AMI-CS. They further determined
that elevated lactate levels, vasopressor
use, diabetes, dialysis, age, and low
cardiac power output or pulmonary artery
pulsatility index levels were associated
with increased 30-day mortality.

SUMMARY Figure 1.
Cardiogenic Shock Algorithm developed by the INOVA Heart and Vascular Institute. Republished
The relatively minor improvements in CS with permission of Elsevier Science & Technology Journals, from Standardized Team-Based Care for
outcomes over the past decades warrant Cardiogenic Shock, Tehrani et al., 73(13), 2019.17
a more rigorous scientific exploration of
the syndrome. Past studies have helped
identify elements necessary to specify CS treatment protocol may be a barrier to Working Group Registry, the National
and validate the optimal treatment of CS; widespread use of a single classification Cardiogenic Shock Initiative, and the
these include integration of hemodynamic system, but the diversity of classification Inova Heart and Vascular Institute
and metabolic data for diagnosis and systems being developed is no doubt a prospective registry, will provide much
risk stratification, early evaluation and step towards broader implementation needed insight that may improve patient
appropriate initiation of AMCS devices, of CS classification. Recent initiatives, outcomes and the development of
and an organized algorithmic approach to such as the SCAI Shock Classification prospective studies testing the clinical
decision making. The lack of a standard Scheme, the Cardiogenic Shock utility of various treatment approaches.

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cardial infarction in the United States. J Am Heart Assoc. 2014 Jan

KEY POINTS 13;3(1):e000590-e.

• Despite advances in pharmacologic and device-based 7. Anderson ML, Peterson ED, Peng SA, et al. Differences in the profile, treat-
approaches to support patients in cardiogenic shock, no ment, and prognosis of patients with cardiogenic shock by myocardial
significant improvement in mortality has been observed infarction classification: A report from NCDR. Circ Cardiovasc Qual Out-
over the past 20 years. comes. 2013 Nov;6(6):708-15.
• Randomized clinical trials have failed to show clear
superiority of therapeutic strategies. The heterogeneity 8. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute
of trial and registry data is due to an unmet need for myocardial infarction complicated by cardiogenic shock. SHOCK Investiga-
appropriate shock classification criteria. tors. Should We Emergently Revascularize Occluded Coronaries for Cardio-
• Key elements for the optimal treatment of cardiogenic genic Shock. N Engl J Med. 1999 Aug 26;341(9):625-34.
shock include integration of hemodynamic and metabolic
data for diagnosis and risk stratification, early evaluation 9. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization and long-
and appropriate initiation of acute mechanical circulatory term survival in cardiogenic shock complicating acute myocardial infarction.
support devices, and an organized algorithmic approach JAMA. 2006 Jun 7;295(21):2511-5.
to decision making.
10. Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute
Conflict of Interest Disclosure: Myocardial Infarction and Cardiogenic Shock. N Engl J Med. 2017 Dec
Dr. Kapur is a formal advisor for and conducts research on behalf of Abbott, 21;377(25):2419-2432.
Abiomed, Boston Scientific, LivaNova, Medtronic, MD Start, and preCARDIA.
11. Basir MB, Schreiber T, Dixon S, et al. Feasibility of early mechanical circu-
Keywords: latory support in acute myocardial infarction complicated by cardiogenic
cardiogenic shock, acute myocardial infarction, acute mechanical circulatory shock: The Detroit cardiogenic shock initiative. Catheter Cardiovasc Interv.
support, shock classification, early revascularization, risk assessment 2018;91(3):454-61.

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