Supplement to

NOVEMBER/DECEMBER 2017

Treatments, timing
and a tomorrow
for patients
in cardiogenic shock

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sponsored by Getinge Group.
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Introduction
Cardiogenic shock — a life-threatening medical condition — is the leading cause of mortality following acute
myocardial infarction (MI).1 The most widely used treatment for patients in cardiogenic shock following acute MI is the
use of intra-aortic balloon pumps (IABPs).2 Despite advances in treatment technology, the mortality rate remains high
for patients who undergo treatment for cardiogenic shock. Recognizing cardiogenic shock early is key for physicians
to target the best intervention to reduce mortality.
In this Cardiology Today’s Intervention spotlight supplement, leading interventional cardiologists examine
the definition, etiology and diagnosis of cardiogenic shock. Current treatment options, such as IABPs and other
mechanical circulatory support devices, are explored, and a review of the research pertaining to these devices is
discussed. Finally, the cost effectiveness of these treatment options is considered.

1. Glass C, Manthey D. Cardiogenic Shock. In: Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM, eds. Tintinalli’s Emergency
Medicine: A Comprehensive Study Guide. 8th ed. New York, NY: McGraw-Hill; 2016.
2. Thiele H, Allam B, Chatellier G, Schuler G, Lafont A. Shock in acute myocardial infarction: the Cape Horn for trials? Eur Heart J. 2010;31:1828-1835.

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Faculty
Jerry D. Estep, MD, FACC, FASE, is Joseph L. Thomas, MD, FACC, FSCAI,
associate professor of clinical medicine; is an associate health sciences
section head of heart transplant and professor at David Geffen UCLA School
mechanical circulatory support, division of Medicine and director of interven-
of heart failure; and medical director of tional cardiology at Harbor-UCLA
the heart transplant and LVAD program Medical Center. Dr. Thomas reports no
at Houston Methodist Hospital. Dr. Estep relevant financial disclosures.
is a consultant and advisor for Abbott,
Medtronic and Getinge Group.
Atman P. Shah, MD, FSCAI, is an
Steven M. Hollenberg, MD, FACC, FCCM, associate professor of medicine,
FAHA, FCCP, is director of the coronary co-director of the cardiac catheteriza-
care unit at Cooper University Hospital and tion laboratory and clinical director of
professor of medicine at Cooper Medical the section of cardiology at the
School of Rowan University in Camden, University of Chicago. Dr. Shah reports
New Jersey. Dr. Hollenberg reports no no relevant financial disclosures.
relevant financial disclosures.

© Copyright 2017, SLACK Incorporated. All rights reserved. No part of this publication may be reproduced without written permission. The ideas and opinions expressed in this Cardiology Today’s Intervention supplement do
not necessarily reflect those of the editor, the editorial board or the publisher, and in no way imply endorsement by the editor, the editorial board or the publisher.

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Cardiogenic shock: Understanding,

defining and diagnosing
Steven M. Hollenberg, MD, FACC, FCCM, FAHA, FCCP

C
ardiogenic shock is an acute condition defined by in- accounts for up to 80% of all cases of cardiogenic shock.1,2
adequate tissue perfusion resulting from a decrease In the SHOCK trial and registry, 78.5% of all cases of car-
in normal cardiac output in the presence of adequate diogenic shock complicating acute MI were attributable to
intravascular volume.1-3 The resulting tissue hypoxia leads to predominant LV failure (of these MIs, 58.8% were anterior
end-organ dysfunction.2 Spanning a wide clinical spectrum, and 34.4% inferior).5,9
cardiogenic shock ranges from preshock to refractory car- Other causes of cardiogenic shock are shown in Table 1.
diogenic shock (unresponsive to conventional therapies).2,4 Another cause is cardiothoracic surgery — about 2% to 6% of
Risk factors for the development of cardiogenic shock par- patients have a complication of cardiogenic shock.2 The mor-
allel those for left ventricular (LV) function and the severity of tality rate among these patients is particularly high.2,10,11
coronary artery disease, including age, diabetes and previous
cardiac events.1 In general, patients with a greater number of
these risk factors have a larger amount of vulnerable myocar-
dial tissue and, therefore, a higher risk for cardiogenic shock.1 Table 1. Etiologies of
It is essential to recognize acute myocardial infarction (MI)
early and to institute interventions to treat ongoing myocardial
cardiogenic shock
ischemia. Only about 10% of patients with acute MI are in car- Mechanical complications:
diogenic shock when first seen, but cardiogenic shock develops
• Acute mitral regurgitation secondary to
more frequently after initial presentation, with a median time papillary muscle dysfunction or chordal rupture
of onset after arrival of 6 hours.1 Studies have reported that car-
• Ventricular septal defect
diogenic shock occurs within the first 24 hours in 50% to 75%
• Free wall rupture
of patients.2,5,6 Thus, there is a critical window of time during
• Right ventricular infarction
which interventions aimed at minimizing ongoing myocardial
ischemia may be used to prevent cardiogenic shock.1,7,8 • Acute aortic insufficiency (aortic dissection)
Severe depression of cardiac contractility:
Epidemiology of cardiogenic shock • Acute myocardial infarction
Cardiogenic shock occurs in about 4% to 8% of patients
• Sepsis
with ST-elevation myocardial infarction (STEMI) and in about
• Myocarditis
2.5% in patients with non-STEMI.1,2 The overall incidence of
• Myocardial contusion
cardiogenic shock in patients presenting with acute coronary
syndromes in 2014 from an Italian registry was 2.7%.9 • Cardiomyopathy
The incidence of cardiogenic shock seems to be declining, • Pharmacologic toxicity (such as overdose of
beta-blockers or calcium channel blockers)
a trend attributed to the increased usage of revascularization
for patients with acute MI.1 However, despite this trend, the • Unstable dysrhythmia
mortality associated with cardiogenic shock remains high.1 Mechanical obstruction to forward blood flow:
Cardiogenic shock is the primary cause of in-hospital mor-
• Aortic stenosis
tality among patients who experience acute MI.1 The death
• Hypertrophic cardiomyopathy
rate is particularly high — about 50% — in patients with
• Mitral stenosis
refractory cardiogenic shock, defined as ongoing tissue hy-
poperfusion despite intervention.2 Most of these deaths will • Left atrial myxoma
occur within the first 48 hours after presentation.1 • Pericardial tamponade
Reprinted with permission from Tintinalli JE, et al., Tintinalli’s
Etiology of cardiogenic shock Emergency Medicine: A Comprehensive Study Guide. 8th ed.
Several underlying causes have been identified for cardio- New York, NY, 2016.
Table material © McGraw-Hill Education.
genic shock; the most common of these is acute MI, which

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Table 2. Traditional definition
of cardiogenic shock12
Clinical criteria
- Hypotension
• Systolic blood pressure (BP) < 90 mm Hg for > 30 min
or
• Need for supportive measures to maintain systolic
BP ≥ 90 mm Hg
- End-organ hypoperfusion
• Cool extremities
or
• Urine output < 30 cc/hr with heart rate > 60 beats/min
Hemodynamic criteria
- Cardiac index ≤ 2.2 L/min/m2
and
- Pulmonary capillary wedge pressure ≥ 15 mm Hg
Presentation of cardiogenic shock
The definition of cardiogenic shock from the landmark
SHOCK trial is summarized in Table 2. Cardiogenic shock
typically presents with hypoperfusion.1 It is usually — but
not always — accompanied by hypotension (systolic blood
pressure [BP] < 90 mm Hg), but shock may occur at higher
systolic BP in patients with pre-existing hypertension.1 An-
other frequent finding in patients with cardiogenic shock is
low pulse pressure (lower than 20 mm Hg), which indicates
low stroke volume.1 Patients in cardiogenic shock typically
have low cardiac index (< 2.2 L/min/m2) and elevated LV
end diastolic pressure (pulmonary artery occlusion pressure
higher than 15 mm Hg to 18 mm Hg).1
Sinus tachycardia is usually present.1 Patients are dyspneic
and frequently have tachypnea unless they have progressed
to have respiratory fatigue.1 Also common are jugular ve-
nous distention and pulmonary rales. Patients in cardiogenic
shock are typically pale or cyanotic; they may exhibit clini-
cal signs of hypoperfusion such as cool skin and mottled ex-
tremities.1 Peripheral edema may be present, particularly in
cases with pre-existing heart failure.1 An altered mental sta-
tus is a sign of cerebral hypoperfusion, and decreased urine
output indicates renal hypoperfusion.1
Diagnosis of cardiogenic shock
Although there is a traditional definition of cardiogenic
shock, there is currently no consensus on the diagnostic
criteria. During patient assessment, it is important to con-
sider other causes of shock (Table 3).1,2 It is also important
to identify the cause of myocardial dysfunction, as choice
of treatment may differ by cause.1 The most common cause
of cardiogenic shock is acute myocardial ischemia, but oth-
er cardiac causes may include mechanical complications of
MI, end-stage cardiomyopathy, acute myocarditis, acute
mitral or aortic regurgitation, and stress cardiomyopathy.
There are no laboratory markers specific to cardiogenic
shock, but certain biomarkers may aid in the diagnosis.1
Troponin and other cardiac biomarkers may not be initially
elevated just after the acute MI, but eventually rise.1 Elevated
levels of serum lactate typically result from hypoperfusion
and can provide clues when hypotension is not profound.1
End-organ dysfunction is indicated by abnormalities in se-
rum electrolytes and renal and hepatic panels.1 B-type natri-
uretic peptide is an indicator of LV dysfunction with a high
negative predictive value.1
A chest X-ray may reveal pulmonary congestion or ede-
ma, alveolar infiltrates and pleural effusion, although these
findings may not occur for several hours after onset.1 Thus,
their absence cannot be used to rule out cardiogenic shock.1
Pre-existing disease may confound interpretation of the
chest X-ray; for example, pulmonary edema is difficult to
distinguish in patients with severe chronic obstructive lung
disease.1 Patients with a previous history of chronic cardiac
remodeling may already show cardiomegaly.1
Echocardiography is extremely valuable for confirming
the diagnosis of cardiogenic shock and should be done early.
Echocardiography evaluates overall and regional systolic
function, diastolic function and valvular disease, and can be
used to diagnose mechanical causes of shock such as papil-
lary muscle rupture, acute ventricular septal defect, and free
wall rupture and tamponade. An echocardiogram can also
be used to exclude other causes of shock and to guide thera-
peutic decisions.3
If the history, physical examination, chest radiograph and
echocardiogram demonstrate systemic hypoperfusion, low
cardiac output and elevation of venous pressures, then right
heart catheterization may not be necessary for diagnosis. If
there is any uncertainty, however, invasive hemodynamic
monitoring can be quite useful to characterize hemodynamics
and to exclude volume depletion, or right ventricular infarc-
tion. Right heart catheterization is most useful, however, to op-
timize therapy in unstable patients, in whom clinical estimates
of filling pressures can be unreliable. Changes in myocardial
performance or therapeutic interventions, including revascu-
larization, can produce dramatic changes in cardiac output and
filling pressures. Concomitant right ventricular dysfunction is
often underrecognized in patients with cardiogenic shock, and
its importance underappreciated; right heart catheterization
is the best and most expeditious way to assess right-sided he-
modynamics in these patients. Measurement of cardiac output
and mixed venous saturation can speak to the adequacy of car-
diac performance and help select patients for inotropic and/or
mechanical circulatory support.
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Nonhypotensive cardiogenic shock
Some patients may have evidence of hypoperfusion with-
out frank hypotension. Although these patients may not meet
a definition of cardiogenic shock based on BP, the hypoperfu-
sion puts them at very high risk. In fact, data from the SHOCK
trial registry indicate that while patients with classic cardio-
genic shock including hypotension and hypoperfusion had
the highest mortality (66%), those with hypoperfusion had a
higher mortality (43%) than those with hypotension without
hypoperfusion (26%).13
Although some authors have defined this as a group with
preshock, this definition is not entirely adequate, since these
patients meet the definition of shock based on hypoperfusion.
Regardless of terminology, it is clear that identifying patients
with early perfusion failure is important, as these patients are
at high risk. Hypotension is easier to define and measure than
perfusion failure. Developing readily measurable criteria for
early perfusion failure remains an ongoing challenge, but this
is an important challenge, since these patients should be con-
sidered for early hemodynamic support.
Conclusion
Despite relative improvements in the overall outcomes for
patients who develop cardiogenic shock following acute MI,
refractory cardiogenic shock remains an important clinical
challenge. Expeditious coronary revascularization is crucial,
and the randomized multicenter SHOCK trial has provided
important data that help clarify the appropriate role and tim-
ing of revascularization in patients with cardiogenic shock.12
The potential for reversal of myocardial dysfunction with re-
vascularization provides the rationale for supportive therapy
to maintain coronary and tissue perfusion until more defini-
tive revascularization measures can be undertaken. Mechani-
cal support devices improve hemodynamics and have been
associated with good outcomes; widespread use, however, is
limited by a lack of randomized controlled trials showing im-
proved mortality. Application of a thorough understanding of
the essentials of pathophysiology, diagnosis and treatment of
cardiogenic shock can allow for expeditious management and
improved outcomes.
References
1. Glass C, Manthey D. Cardiogenic shock. In: Tintinalli JE, Stapczynski
JS, Ma OJ, Yealy DM, Meckler GD, Cline DM, eds. Tintinalli’s Emergency
Medicine: A Comprehensive Study Guide. 8th ed. New York, NY:
McGraw-Hill; 2016.
2. Reyentovich A, Barghash MH, Hochman JS. Management of refractory
cardiogenic shock. Nat Rev Cardiol. 2016;13(8):481-492.
3. Hollenberg SM. Cardiogenic shock. In: Goldman L, Ausiello D, Drazen
JA, eds. Cecil Textbook of Medicine, 25th ed. New York, NY: Elsevier;
2015:681-685.
4. Atkinson TM, Ohman EM, O’Neil WW, et al. A practical approach to
mechanical circulatory support in patients undergoing percutaneous
coronary intervention: An interventional perspective. JACC: Cardiovasc
Interv. 2016;9(9):871-883.
5
Table 3. Conditions to consider
during differential diagnosis of
cardiogenic shock
Acute pulmonary decompensation:
• Chronic obstructive pulmonary disease exacerbation
• Cor pulmonale
• Massive pulmonary embolism
Distributive shock:
• Sepsis
• Anaphylaxis
• Neurogenic shock (spinal cord injury)
Hypovolemic shock:
• Hemorrhage
• Severe dehydration
Dissociative shock:
• Toxins/drugs of abuse (cyanide)
Reprinted with permission from Tintinalli JE, et al., Tintinalli’s Emergency
Medicine: A Comprehensive Study Guide. 8th ed. New York, NY., 2016.
Table material © McGraw-Hill Education.
5. Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating
acute myocardial infarction — etiologies, management, and outcome:
a report from the SHOCK trial registry. J Am Coll Cardiol. 2000;36(3 Suppl
A):1063-1070.
6. Webb JG, Sleeper LA, Buller CE, et al. Implications of the timing of onset
of cardiogenic shock after acute myocardial infarction: a report from the
SHOCK trial registry. J Am Coll Cardiol. 2000;36(3 Suppl A):1084-1090.
7. 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;57:688-696.
8. Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS; for
NRMI Investigators. Trends in management and outcomes of patients
with acute myocardial infarction complicated by cardiogenic shock.
JAMA. 2005;294(4):448-454.
9. De Luca L, Olivari Z, Farina A, et al. Temporal trends in the
epidemiology, management, and outcome of patients with
cardiogenic shock complicating acute coronary syndromes. Eur J
Heart Fail. 2015;17(11):1124-1132. doi:10.1002/ejhf.339.
10. Goldstein DJ, Oz MC. Mechanical support for postcardiotomy
cardiogenic shock. Semin Thorac Cardiovasc Surg. 2000;12(3):220-228.
11. Deppe AC, Weber C, Liakopolous OJ, et al. Preoperative intra-aortic
balloon pump use in high-risk patients prior to coronary artery bypass
graft surgery decreases the risk for morbidity and mortality – a meta-
analysis of 9,212 patients. J Card Surg. 2017;32(3):177-185. doi:10.1111/
jocs.13114.
12. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute
myocardial infarction complicated by cardiogenic shock. N Engl J Med.
1999;341(9):625-634.
13. Menon V, Slater JN, White HD, et al. Acute myocardial infarction
complicated by systemic hypoperfusion without hypotension: report
of the SHOCK trial registry. Am J Med. 2000;108(5):374-380.
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Treatment and teamwork: Options for

advanced heart failure and cardiogenic shock
Jerry D. Estep, MD, FACC, FASE

D
espite available treatment modalities, the mortal-
ity rates of cardiogenic shock after acute myocar-
dial infarction (MI) still approach 40% to 50%;
those with refractory cardiogenic shock have the worst
prognosis.1 Therefore, early recognition, proper assess-
ment and accurate categorization of each patient’s condi-
tion is critical for the cardiac team to provide the optimal
treatment to patients.
Categorizing severity of cardiogenic shock
In the advanced heart failure (HF) community, physi-
cians often qualify a patient’s presenting profile with the
Interagency Registry for Mechanically Assisted Circula-
tory Support (INTERMACS) profiles, a North American
registry established in 2005 for patients who are receiving
mechanical circulatory support device therapy to treat
advanced HF to help define levels of severity of advanced
HF before device implantation (Figure 1).2
Bridging to recovery
Treatment goals for patients with advanced heart dis-
eases include relieving symptoms by treating the underly-
ing causes of the HF, slowing the progression of the dis-
ease and reducing the need for hospital visits, therefore
improving the patient’s quality of life and survival out-
comes. Temporary mechanical support may be useful as
a bridge when more time is needed to determine whether
an INTERMACS 1 profile patient is a candidate for du-
rable mechanical circulatory support (Figure 2).
Contraindications to implantation of a long-term left
ventricular assist device (LVAD) include severe hemody-
namic instability, irreversible major end-organ failure, major
coagulopathy, significant right HF, uncertain neurologic sta-
tus, prolonged need for mechanical ventilation, and sepsis or
vasodilatory syndrome.3 For example, in an INTERMACS 1
profile patient, unclear neurologic status or unclear revers-
ibility of the end-organ failure are reasons to not take the
patient directly to transplant or LVAD
as they will most likely not have good
outcomes with this intervention.
Many patients become depen-
dent on the device and/or the sup-
port used. In many patients, there is
an evolving experience about using
these temporary support devices as
a bridge to heart transplant directly.
In these patients, end-organ inter-
vention treatment should be consid-
ered. Working in collaboration with
programs that offer these end-organ
interventions is key.

Treatment options for

cardiogenic shock
For 30 years, the intra-aortic bal-
loon pump (IABP) was essentially
*Intravenous inotropic therapy only approved for refractory Class IV symptoms.
the sole option in most centers.
Figure 1. INTERMACS profiles of patients with advanced heart failure. New percutaneous ventricular as-
Abbreviations: A, arrhythmia; ADL, activities of daily living; AMB, ambulatory; CMS, Centers for Medicare and Medicaid sist devices (PVADs) have broad-
Services; DT, destination therapy; FF, frequent flyer; HF, heart failure; INO, inotropes; INTERMACS, Interagency Registry
ened the scope of potential support
for Mechanically Assisted Circulatory Support; IV, intravenous; NYHA, New York Heart Association; TCS, temporary
circulation support; TCA, temporary cardiac assistance; VO2, oxygen consumption (mL/kg/min). options. Currently, the three main
Reprinted from Garrick C. Stewart, Lynne W. Stevenson, Keeping Left Ventricular Assist Device treatment strategies for restoring
Acceleration on Track, Circulation, 2011;123(14):1559-1568. http://circ.ahajournals.org/ organ perfusion and cardiac output
content/123/14/1559. Printed with permission from Wolters Kluwer. in cardiogenic shock after acute MI

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are revascularization, infusion of vasopressors/inotro-

pes and initiation of mechanical circulatory support.
Cardiogenic shock

Revascularization
Restoration of coronary blood flow (revascularization) Co-existing multiorgan failure,
No
Yes unsure neurologic status or unclear
is typically achieved via primary percutaneous coronary LVAD/transplant candidacy

intervention (PCI) or coronary artery bypass grafting

(CABG). However, for patients in whom PCI or CABG Temporary
Durable MCS
MCS
cannot be performed immediately (within 2 hours),
thrombolytic therapy may be considered.4,5 Early revas-
cularization was flagged as the most important treat-
Bridge to
ment strategy for cardiogenic shock after acute MI in Bridge to
Decision
Destination Bridge to
Recovery Therapy Recovery
the SHOCK trial.6,7 A similar benefit of early revascular- (end-organ
intervention or
ization was noted in the Swiss Multicenter Study of An- palliative care)
Heart
gioplasty for Shock.8 Although not widely practiced, the Transplant
current guidelines also encourage PCI of critical stenosis
or unstable lesions in addition to the culprit lesion5; how-
ever, the impact on mortality has not yet been proven. Figure 2. Multiple patient and programmatic factors must be
considered when determining the role of temporary mechanical
Vasopressor and inotropic agents circulatory support.
Irrespective of early revascularization by PCI or Abbreviations: LVAD, left ventricular assist device; MCS, mechanical
circulatory support.
CABG with or without mechanical circulatory support,
Source: Brown J and Estep JD. Heart Failure Clinics 2016.
volume expansion with the use of vasopressors and ino-
tropes remains a cornerstone of hemodynamic support
in cardiogenic shock.4,9 However, excessive increases Mechanical circulatory support: Conventional IABP devices
in volume and systemic vascular resistance may in- Several options are available for percutaneous me-
crease cardiac afterload and worsen cardiac failure.10,11 chanical circulatory support in the setting of cardiogen-
Moreover, inotrope use has been shown to increase the ic shock. These include IABPs, continuous flow pumps
mortality risk by up to 80%.12 Therefore, it appears that Impella (Abiomed) and TandemHeart (CardiacAssist),
these drugs worsen the ischemia-related imbalance of and extracorporeal membrane oxygenation (ECMO)
oxygen supply and demand in acute MI. (Figure 3).13

Figure 3. Percutaneous assist devices in cardiogenic shock. (A) Intra-aortic balloon counterpulsation; (B) Impella pump; (C)
TandemHeart; (D) extracorporeal membrane oxygenation (ECMO).
Reprinted from Werdan K, et al. Mechanical circulatory support in cardiogenic shock. Eur Heart J. 2014;35:156-167, by permission of Oxford University
Press.

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Success With IABP:
A Case Study
For physicians considering how patients with advanced
heart failture (HF) will progress, it is important to high-
light those patients with end-stage HF who may present
with acute-on-chronic HF. These patients are extremely
sick, requiring a permanent left ventricular assist de-
vice (LVAD). Their outcomes are typically not good, with
higher post-LVAD mortality, longer hospitalization and
greater morbidity. This more severe shock, requiring
LVAD, is influenced by that severity and thus, physicians
focus a great deal on trying to optimize the management
of these patients to improve their disease course. The
following case study describes a 59-year-old man who
achieved good outcomes when treated with an intra-
aortic balloon pump (IABP).
Patient history:
• 59-year-old man
• Established history of ischemic cardiomyopathy
- Known left ventricular ejection fraction < 20%
• Comorbidities: atrial fibrillation, hypertension and
dyslipidemia
• Baseline serum creatinine 1.5 mg/dL
• Medications: amiodarone, hydralazine, isosorbide
dinitrate, spironolactone, aspirin and atorvastatin
Current presentation:
• Presents to emergency department (ED) with a 4-week
history of progressive shortness of breath (lying flat
and at rest), mild leg swelling and a cough
• No chest pain
• Alert and attentive
Initial management in ED:
• Started on intravenous diuretics
• Followed by an inotropic agent because of fluid
overload and “exam signs of low perfusion”
Patient workup:
• Lab work:
- Over 2 days, shows an increase in serum creatinine
from 1.5 mg/dL to 2.4 mg/dL
- Total bilirubin and liver function tests normal
- Mildly positive troponin
• Echocardiography highlights overt left ventricular
remodeling and significantly elevated filling pressures
• Mean pulmonary capillary wedge pressure: 34 mm Hg
• Evidence of secondary pulmonary hypertension
• Right atrial pressure in the upper limit of normal
• Patient presentation consistent with cardiogenic
shock, with development of end-stage HF and a poor
prognosis.
Intervention and results:
•  IABP resulted in significant improvement in serum
creatinine, HF symptoms and renal function.
• The patient is currently doing well more than 1 year
after heart transplantation.
IABP counterpulsation systems increase the myocar-
dial oxygen demand ratio by increasing coronary and
systemic circulation via diastolic augmentation while
lowering the afterload to systolic ejection and there-
fore increasing cardiac output.14 Therefore, researchers
anticipated they would reduce mortality by increasing
myocardial oxygen supply while decreasing demand in
patients with cardiogenic shock.
There has been an introduction of new devices and
improvement of existing devices on the market. A key
example is the Mega 8 Fr. 50 cc IABP (Getinge), which
allows greater displacement of blood volume and offers
greater support. These features can be very important
for patients who have a lower stroke volume and a lower
cardiac output, and require greater hemodynamic sup-
port to improve end-organ function. A retrospective
review of real-world patients in clinical practice sup-
ported with a traditional IABP vs. the Mega IABP has
been reported.15 This study showed greater systolic un-
loading, higher diastolic augmentation and a greater
reduction in pulmonary capillary occlusion pressure
among patients who received the Mega IABP compared
with those who received traditional IABP.
Recently, the use of the large-volume 50 cc IABP as a
first-line percutaneous mechanical circulatory support
strategy (with escalation when needed) was retrospec-
tively analyzed in a single-center observational study of
100 patients with cardiogenic shock, with a promising
rate of overall survival to hospital discharge of 66% with
escalation to a PVAD or transplant only in one-quarter
of patients.16 However, a randomized controlled trial is
needed to further validate these findings.
Mechanical circulatory support: Percutaneous LVADs
Percutaneous LVADs represent a newer type of me-
chanical support device. Currently available percutaneous
LVADs include TandemHeart (CardiacAssist); Impella 2.5,
Impella 5.0 and Impella CP systems (Abiomed); and the
paracorporeal pulsatile device iVAC2L (PulseCath BV).17
Both the TandemHeart and Impella systems have shown
improved short-term hemodynamic support; however, no
trials have been conducted using the iVAC2L system.
Thiele and colleagues first examined wheth-
er TandemHeart with active circulatory support
might have positive hemodynamic effects and de-
crease mortality in patients with cardiogenic shock
after acute MI.18 The authors showed that percu-
taneous LVAD improved hemodynamic and meta-
bolic parameters more rapidly than standard treat-
ment with IABP. However, percutaneous LVAD
resulted in more complications, including bleeding/
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vascular complications.18-21
The use of IABP to support patients
with chronic systolic HF in cardiogenic Cardiogenic shock
shock before LVAD implantation has presentation (left +/- right
sided advanced heart failure)
been evaluated.22 Right and left ven-
tricular cardiac power indexes at base-
line were used to identify those patients Advanced heart Team Thoracic surgeon
failure cardiologist
most likely to stabilize. Clinical decom-
pensation after IABP was associated
with worse outcomes after LVAD. This Severe refractory
cardiogenic shock
work showed that more than half of the No with overt hypoxia/
Yes

patients included stabilized with IABP acidemia or severe

Swan Ganz + intra-
right ventricular failure
support as a bridge to LVAD. Swan Ganz Catheter
aortic balloon pump,
arteriorvenous
+ intra-aortic balloon extracorporeal
pump membrane
Tag team: Working together for early oxygenation
recognition of cardiogenic shock Favorable
response based on
One of the most critical aspects for No hemodynamics, urine Yes
output, lactic acid level,
treating patients, regardless of wheth- end-organ function
Maintain same
er it is before or after the onset of se- Impella CP or 5.0 and
remove intra-aortic Short time interval to define response mechanical
vere cardiogenic shock, is to maintain balloon pump (hours, not days) circulatory support
a team approach, as illustrated by Doll
and colleagues.23 Elements of a multi-
disciplinary cardiogenic shock team in- Figure 4. Houston Methodist Hospital team structure approach and cardiogenic
clude the intensive care unit group, the shock algorithm.
cardiac catheterization laboratory, the Source: Brown J and Estep JD. Heart Failure Clinics 2016.
cardiothoracic surgery group and the ad-
vanced HF group. Conclusion
The team structure at Houston Methodist allows A main treatment goal is to bridge patients with non-
for a clear algorithm of what is best practice, includ- ischemic advanced heart failure to clinical stability or
ing the early implementation of IABP (Figure 4). For recovery. Currently, revascularization, vasopressor and
patients with a severe case, the degree of hemody- inotropic agents and mechanical circulatory support de-
namic support is escalated, with attention to the po- vices are all common treatment strategies for patients in
tential risks associated with this approach. For patients cardiogenic shock after acute MI. Despite the decided
with severe refractory cardiogenic shock, manage- course of treatment, the common denominator for a
ment with veno-arterial extracorporeal membrane successful approach, regardless of the institution, is hav-
oxygenation with IABP, anticipating a need for LV ing an organized team in deciding on goals and treat-
venting and hemodynamic monitoring with a Swan- ment options for patients.
Ganz catheter, has been shown to be helpful. For
those patients who are not as severe but show signs of References
cardiogenic shock with hypotension and tachycardia,
1. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon
the protocol is to use an IABP combined with hemo- support for myocardial infarction with cardiogenic shock. N Engl
dynamic monitoring first. A favorable response is de- J Med. 2012;367(14):1287-1296.
2. Stewart GC, Stevenson LW. Keeping left ventricular assist
fined in short time intervals (hours, not days), based on device acceleration on track. Circulation. 2011;123(14):1559-
hemodynamics, urine output, lactic acid and improve- 1568.
ment in end-organ function. 3. Slaughter MS, Pagani FD, Rogers JG, et al; HeartMate II Clinical
Investigators. Clinical management of continuous-flow left
For patients who do not respond, the Impella CP or ventricular assist devices in advanced heart failure. J Heart
Lung Transplant. 2010;29(4 Suppl):S1-S39.
5.0 is considered. In cases of a favorable response with
4. Levy B, Bastien O, Karim B, et al. Experts’ recommendations for
clinical stability on a balloon pump, it is maintained as the management of adult patients with cardiogenic shock. Ann
this is associated with the best benefit/risk profile to Intensive Care. 2015;5(1):52.
curb the adverse events associated with these devices. 5. Windecker S, Kolh P, Alfonso F, et al. 2014 ESC/EACTS guidelines
on myocardial revascularization: The Task Force on Myocardial
Revascularization of the European Society of Cardiology

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(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(37):2541-2619.
6. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization
and long-term survival in cardiogenic shock complicating
acute myocardial infarction. JAMA. 2006;295(21):2511-2515.
7. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization
in acute myocardial infarction complicated by cardiogenic
shock. N Engl J Med. 1999;341(9):625-634.
8. Urban P, Stauffer JC, Bleed D, et al. A randomized evaluation
of early revascularization to treat shock complicating
acute myocardial infarction. The (Swiss) Multicenter Trial of
Angioplasty for Shock-(S)MASH. Eur Heart J. 1999;20(14):1030-
1038.
9. Thiele H, Ohman EM, Desch S, Eitel I, de Waha S. Management
of cardiogenic shock. Eur Heart J. 2015;36(20):1223-1230.
10. Unverzagt S, Wachsmuth L, Hirsch K, et al. Inotropic agents
and vasodilator strategies for acute myocardial infarction
complicated by cardiogenic shock or low cardiac output
syndrome. Cochrane Database Syst Rev. 2014;1:CD009669.
11. Francis GS, Bartos JA, Adatya S. Inotropes. J Am Coll Cardiol.
2014;63(20):2069-2078.
12. Samuels LE, Kaufman MS, Thomas MP, Holmes EC, Brockman
SK, Wechsler AS. Pharmacological criteria for ventricular assist
device insertion following postcardiotomy shock: experience
with the Abiomed BVS system. J Card Surg. 1999;14(4):288-293.
13. Werdan K, Gielen S, Ebelt H, Hochman JS. Mechanical circulatory
support in cardiogenic shock. Eur Heart J. 2014;35(3):156-167.
14. Sanborn TA, Sleeper LA, Bates ER, et al. 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. J
Am Coll Cardiol. 2000;36(3 Suppl A):1123-1129.
15. Kapur NK, Paruchuri V, Majithia A, et al. Hemodynamic
effects of standard versus larger-capacity intraaortic balloon
counterpulsation pumps. J Invasive Cardiol. 2015;27(4):182-188.
16. Visveswaran GK, Cohen M, Seliem A, et al. A single center
tertiary care experience utilizing the large volume Mega 50 cc
intra-aortic balloon pump counterpulsation in contemporary
clinical practice. Catheter Cardiovasc Interv. 2017. doi:10.1002/
ccd.26908.
17. Thiele H, Allam B, Chatellier G, Schuler G, Lafont A. Shock in
acute myocardial infarction: the Cape Horn for trials? Eur Heart
J. 2010;31(15):1828-1835.
18. Thiele H, Sick P, Boudriot E, et al. 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. 2005;26(13):1276-1283.
19. Redfors B, Watson BM, McAndrew T, et al. Mortality, length
of stay, and cost implications of procedural bleeding after
percutaneous interventions using large-bore catheters. JAMA
Cardiol. 2017;2(7):798-802.
20. Badiye AP, Hernandez GA, Novoa I, Chaparro SV. Incidence
of hemolysis in patients with cardiogenic shock treated with
Impella percutaneous left ventricular assist device. ASAIO J.
2016;62(1):11-14.
21. Abaunza M, Kabbani LS, Nypaver T, et al. Incidence and prognosis
of vascular complications after percutaneous placement of left
ventricular assist device. J Vasc Surg. 2015;62(2):417-423.
22. Sintek MA, Gdowski M, Lindman BR, et al. Intra-aortic balloon
counterpulsation in patients with chronic heart failure
and cardiogenic shock: clinical response and predictors of
stabilization. J Card Fail. 2015;21(11):868-876.
23. Doll JA, Ohman EM, Patel MR, et al. A team-based approach
to patients in cardiogenic shock. Catheter Cardiovasc Interv.
2016;88(3):424-433.
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IABP: Workhorse support in a rapidly
changing field
Joseph L. Thomas MD, FACC, FSCAI; and Atman P. Shah, MD, FSCAI
T
reatment of patients in cardiogenic shock is now rou-
tine in cardiac catheterization labs with the expecta-
tion that the shock state is a potentially reversible
and treatable condition. Research into cardiogenic shock is
complicated by the fact that the shock population is incred-
ibly heterogeneous at presentation and throughout treatment.
Extra-cardiac organ dysfunction affects treatment options
and powerfully dictates outcomes, such that the avoidance
of multiorgan failure is paramount. Hemodynamic indices
and laboratory values, such as lactate levels, are often accurate
markers of clinical improvement, though survival remains the
ultimate measurable endpoint for this condition.
In this context, the need for percutaneous support has
grown more obvious. This has been encouraged by matura-
tion in primary percutaneous coronary intervention (PCI)
care, persistently poor outcomes for cardiogenic shock and the
high visibility of novel mechanical support devices. Theoreti-
cally, the best support option would be the one that most in-
creases or maintains tissue perfusion, unloads the injured ven-
tricle and enhances coronary perfusion. Other attributes of an
optimal support device would be ease of use, wide availability
and a clear safety profile. For 30 years, the intra-aortic balloon
pump (IABP) was the sole option in most centers. New percu-
taneous ventricular assist devices (PVADs) have dramatically
altered the landscape and broadened the scope of potential
support options.
Physiologic principles of mechanical support
The mechanism of action of IABP is based on rapid in-
flation and deflation of a low-profile balloon catheter in the
descending aorta during diastole. The primary modes of ef-
fect are augmentation of diastolic blood pressure, increased
coronary perfusion and, with rapid deflation at the onset of
systole, a reduction in afterload. Additional putative physi-
ologic effects are often discussed, but their mechanism of ac-
tion is less clear. Labeled indications include acute coronary
syndrome (ACS), cardiac and noncardiac surgery and com-
plications of heart failure (Table 1).1 Examples falling under
the ACS and complications of heart failure umbrella include
hemodynamic support during diagnostic or PCI procedures
and for complications of myocardial infarction (MI) includ-
ing cardiogenic shock.2
The TandemHeart (CardiacAssist) device utilizes dual ac-
cess cannulae (transseptal venous and arterial) and an extra-
corporeal centrifugal pump. The TandemHeart circuit with-
Produced by SLACK Incorporated and sponsored by Getinge Group
11
draws oxygenated blood directly from the left atrium and
returns blood via a large-bore femoral artery cannula. High
flows (3 L/min to 5 L/min) are possible with this system de-
pending on inflow cannula size. The utility of TandemHeart
is limited by the requirement for transseptal puncture and
large-bore cannulae. Unlike extracorporeal membrane oxy-
genation (ECMO) systems, TandemHeart is only appropriate
for patients with adequate oxygenation. In most published
case series, access-site bleeding and transfusion are frequent.3,4
ECMO utilizes similar large-bore cannulae but also includes
an oxygenator in its external circuitry. ECMO has become
more widely available in recent years with a significant in-
crease in use over the past decade.5
The HeartMate PHP (Abbott) received a CE mark in 2015
for use in patients undergoing high-risk PCI. Specific features
of the device include insertion of the device through a 14-Fr
sheath and then expansion to 24-Fr to allow more than 4 L/
min of mean flow. However, the SHIELD II comparative trial
of the PHP and Impella (Abiomed) in high-risk PCI was re-
cently halted.
The Impella family of percutaneous support devices in-
cludes both fully percutaneous and surgically placed micro-
catheter axial flow systems. The 2.5 and CP models are fully
Table 1. Indications for IABP1,2
Acute coronary syndrome*
• Refractory angina
• Post-MI angina
• Complications of acute MI
• Support for diagnostic/PCI procedures
• Ischemic ventricular arrhythmia
Cardiac and noncardiac surgery*
• Pre- and post-CPB
• Bridge to other assist devices
Complications of heart failure*
• Ischemic and nonischemic
• Cardiogenic shock
*FDA-approved, labeled indication.
Abbreviations: CPB, cardiopulmonary bypass; IABP, intra-aortic balloon pump;
MI, myocardial infarction; PCI, percutaneous coronary intervention.
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Score 100
Variable Points n=480 patients Pairwise log-rank test:
Age >37 years 1 3/4 vs. 0-2 p<0.0001
History of stroke 2 80 5-9 vs. 0-2 p<0.0001
Score 5-9
Glucose >10.6 mmol/L (191 mg/dL)* 1
Creatinine >132.6 μmol/L (1.5 mg/dL)* 1

Mortality (%)
Arterial lactate >5 mmol/l* 2 60
TIMI flow grade <3 after PCI 2 Score 3/4
Maximum 9
40
Score 0-2
20
Risk categories
Category Points 0
Low 0-2 0 5 10 15 20 25 30
Intermediate 3/4
Time (Days)
High 5-9

Figure 1. IABP-SHOCK II trial risk score for patients in cardiogenic shock complicating acute myocardial infarction.

Abbreviations: AMI, acute myocardial infarction; AUC, area under the curve; CABG, coronary artery bypass grafting; CI, confidence interval; CS,
cardiogenic shock; GFR, glomerular filtration rate; HR, hazard ratio; IABP, intra-aortic balloon pump; PCI, percutaneous coronary intervention;
ROC, receiver-operating characteristic.
Reprinted from J Am Coll Cardiol. , Risk stratification for patients in cardiogenic shock after acute myocardial infarction, 69, Pöss J, Köster J, Fuernau G, Eitel I, de
Waha S, Ouarrak T, Lassus J, Harjoa V-P, et al. 1913-1920, 2017, with permission from Elsevier.

percutaneous, and the 5.0 device requires surgical placement.
These devices pull blood from the left ventricular cavity and
expel the blood into the proximal ascending aorta with maxi-
mal flows dependent on specific Impella catheter type and
device power setting.
Data supporting mechanical support during
cardiogenic shock
The original SHOCK trial provided a benchmark for out-
comes from the early primary angioplasty era. In that study,
302 patients with acute MI and cardiogenic shock experienced
a 50% mortality rate at 30 days.6 IABP use was recommended
in the study protocol, and nearly 90% of all participants were
treated with an IABP. Although this trial’s intent was to com-
pare early revascularization with initial medical stabilization,
its legacy has been to set a benchmark for mortality in car-
diogenic shock that has not significantly changed over time;
cardiogenic shock complicating acute MI has an approxi-
mate 50% short-term mortality. Subsequent observational
and randomized data reinforce relatively static outcomes in
cardiogenic shock, even while the larger acute ST-elevation
myocardial infarction (STEMI) population has experienced
considerable improvements in survival over the same period.
The 2012 IABP-SHOCK II study was well-conducted and
remarkable in the field of cardiogenic shock for its relatively
large size (600 patients) and rapid enrollment (completed in
less than 3 years).7 Enrolled patients were critically ill as evi-
denced by their poor short-term survival. The primary end-
point of all-cause mortality at 30 days did not differ between
the control or IABP arms (41% vs. 40%). With the caveats as-
sociated with subgroup analysis, only treatment in younger
patients (age < 50 years) carried a signal for benefit with IABP.
Additional considerations in the study’s execution may have
affected results. There was a 10% crossover rate with IABP us-
age in the control arm, and the timing of IABP insertion was
left to the discretion of the operator. Nearly 90% of patients
had the IABP placed after PCI, and it is now accepted that early
initiation of support may provide additional clinical benefit.
There is a paucity of adequately powered, randomized in-
vestigations in cardiogenic shock. In that context, SHOCK
II added significantly to the field. A predictive risk score has
been developed with data from this trial and can be used to
assist clinical decision-making. Using six clinical variables
(age > 73, history of stroke, post-PCI TIMI flow grade < 3, and
creatinine, glucose and lactate levels) that are readily available,
this score provides substantive prognostic information and
has been validated in multiple cohorts (Figure 1).8
Two well-done meta-analyses have attempted to reconcile
the varying data on IABP support for shock. Compiling 3 de-
cades of randomized and observational experience, neither
analysis could demonstrate a benefit to IABP in acute MI with
or without shock.9,10 The majority of component studies in the
analyses were small, with highly heterogeneous populations
and results. The report by Sjauw and colleagues showed a
mortality benefit but only in STEMI populations with cardio-
genic shock receiving either fibrinolysis or not receiving any
reperfusion therapy at all.8 The applicability of those findings
in the contemporary era of routine primary PCI is not clear.
Comparative studies of IABP and PVADs
A few small studies compare the IABP with novel percuta-
neous support devices (Table 2),11-13 but these studies were all

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Table 2. Mortality at 30 days in randomized
comparisons of IABP with PVAD
IABP
Study No. of patients
Thiele H, et al.11 20
ISAR-SHOCK 12
13
IMPRESS13 24
Abbreviations: IABP, intra-aortic balloon pump; NS, not significant; PVAD, percutaneous ventricular assist device.
underpowered, so the results remain exploratory. Thiele and
colleagues conducted a randomized study comparing IABP
(n = 20) with TandemHeart (n = 21) in cardiogenic shock.11
Half of patients had suffered prior cardiac arrest, and nearly all
were intubated. The primary aim was to quantify the hemo-
dynamic effects of the novel system. As expected, Tandem-
Heart provided a greater improvement in cardiac output, pul-
monary artery pressure, filling pressures and cardiac power
index, though all parameters also improved in the IABP arm.
Despite the difference in device power, the use of inotropes
was similar between groups. Fever, bleeding, transfusion and
coagulopathy were all more common with TandemHeart. At
30 days, mortality was identical.
ISAR-SHOCK compared Impella 2.5 to IABP in a small co-
hort (n = 26) of shock patients with a primary endpoint evalu-
ating immediate hemodynamic changes.12 There was improve-
ment in both groups’ parameters with a significantly greater
immediate increase in cardiac index (0.49 vs. 0.11 L/min/m2,
P = .02) with Impella. Notably, at 4 hours and 30 hours, cardiac
index was identical for both groups. Severity of illness scores
and survival were similar. Transfusion and hemolysis were
more common with Impella.
The most recent comparative IABP study, the IMPRESS
trial, involved the Impella CP catheter in a critically ill cardio-
genic shock population.13 The majority of patients had experi-
enced cardiac arrest, and all were mechanically ventilated. In
that milieu, half of all deaths were related to anoxic brain in-
jury, though one-third of deaths in both groups were due to
refractory cardiogenic shock. Although there was no differ-
ence in short- or midterm survival (50% or 12/24 patients in
each group) between groups, there was numerically superior
survival in those who received either device before PCI rather
than after PCI (25% (6 patients) vs. 53% (19 patients), P = 0.16).
Bleeding occurred more often in Impella-treated patients than
13
PVAD P value
Mortality No. of patients Mortality
45% 21 43% NS
46% 12 46% NS
50% 24 50% NS
in IABP-treated patients (8 patients vs. 2 patients, respectively).
The authors concluded that the PVAD added no additional
benefit over IABP in patients with cardiogenic shock after acute
MI. The same authors conducted a meta-analysis including the
only three randomized comparisons (n = 95) of IABP and Im-
pella that yielded similar findings.14
The limitations inherent to small trials and meta-analyses of
underpowered studies are obvious. However, each study com-
pared first-line use of IABP with more powerful PVADs with-
out even surrogate endpoints suggesting superior efficacy. It is
important to note that serum lactate levels were similar with or
without IABP in the SHOCK II study. In the comparative stud-
ies, lactate levels were also similar regardless of device, suggest-
ing that the generalized physiologic effect of IABP and PVADs
are comparable (Figure 2, page 14).11,13
Registry data with PVADs
In the absence of randomized data, registry data become
more important in clarifying the role of PVADs. Short-term
mortality rates for cardiogenic shock have been benchmarked
around 40% to 50% for 2 decades. In that context, publications
from the USpella, Euroshock and cVAD registries including a
total of 561 patients describe short-term death rates in excess of
50%. While survival may appear worse if centers have reserved
PVADs only for the most critically ill patients, the registries
have not provided a signal for improved outcomes. Only the
recent Detroit cardiogenic shock initiative has reported better
results, with an 84% survival to discharge in a small cohort of
37 patients.15-18
Current state of IABPs
IABP remains the most commonly used support device
and persists as a reasonable first-line approach. The introduc-
tion of larger-displacement balloon catheters is an important
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ISAR-SHOCK IMPRESS
15
IABP (n = 24)
pMCS (n = 24)
12

Lactate (mmol/L)
10
10 Impella (n = 12)
IABP (n = 13)
Serum-Lactate (mmol/L)

8
5

4 0

Before randomization

Day 1 [0-8h]

Day 1 [8-16h]

Day 1 [16-24h]

Day 2 [0-8h]

Day 2 [8-16h]

Day 2 [16-24h]

Day 3

Day 4
2

0
0 1 6 12 24 48 72

Time after Implantation (hours)

Figure 2. Serum lactate in comparative trials of IABP and PVAD.12,13

Abbreviations: IABP, intra-aortic balloon pump; pMCS, percutaneous mechanical circulatory support; PVAD, percutaneous ventricular assist device.
Figures reprinted with permission from Journal of the American College of Cardiology, Percutaneous Mechanical Circulatory Support Versus Intra-Aortic Balloon Pump in Cardiogenic
Shock After Acute Myocardial Infarction, Ouweneel DM, 69, 3, 2017; permission conveyed through Copyright Clearance Center, Inc.; and reprinted from Journal of the American
College of Cardiology, 52, 19, Seyfarth M,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, 1584-1588, 2008, with permission from Elsevier.

Table 3. Bleeding events in Multiple arterial access points and

larger catheter sizes almost exclusively
contemporary randomized trials of IABP translate into more bleeding and vascular
complications. Contemporary safety data
Trial IABP No IABP P value are available for more than 600 patients
randomly assigned to IABP in clinical
BCIS-1 minor bleeding21 15.9% 7.3% .02
trials (Table 3).7,21,22 Supporting its estab-
BCIS-1 major bleeding21 3.3% 4.0% .77 lished safety profile, there was no signifi-
cant increase in either major bleeding or
CRISP AMI major bleeding22 3.1% 1.7% .49
major vascular complications with the
CRISP AMI major vascular22 4.3% 1.1% .09 IABP.

SHOCK II moderate bleeding7
SHOCK II major bleeding7
SHOCK II major vascular7
Trial enrollment: BCIS-1, n = 301; CRISP AMI, n = 337; SHOCK II, n = 600.
Abbreviation: IABP, intra-aortic balloon pump.
enhancement.19,20 As compared with 40-cc catheters, the larg-
er 50-cc catheter has demonstrated greater systolic unloading
and reduction in filling pressures along with up to twice the
relative increase in cardiac output.19 In the near term, ques-
tions of efficacy are likely to remain unanswered both for the
IABP and PVADs. This reality makes device safety and cost
even more critical in determining treatment choices.
17.3% 16.4% .77 Costs of care and guidelines
Additional health care expenses are
3.3% 4.4% .51
both reasonable and justifiable for de-
4.3% 3.4% .53 vices with robust clinical benefit. Novel
PVADs may cost 10 to 30 times more
than the IABP. The implications for
health care costs are dramatic consider-
ing the exponential increase in PVAD
use. Using Medicare data, Shah and col-
leagues demonstrated that a 30% migration from IABP to
PVAD could be associated with an additional $1 billion in ad-
ditional hospital costs. A first-line strategy of IABP with esca-
lation to PVADs could avoid up to $2.5 billion of incremental
costs.23
The neutral results of IABP-SHOCK II weighed heavily on
European Society of Cardiology guidelines. Routine use of the

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IABP in cardiogenic shock was given a Class III recommen-
dation. Importantly, the IABP has retained an endorsement
(Class IIa) for unstable and cardiogenic shock patients with
mechanical complications, and it remains in another recom-
mendation for short-term mechanical support in cardiogenic
shock.24 The IABP is included in recommendations in the latest
U.S. guidelines for post-MI shock patients who do not quickly
stabilize with pharmacotherapy.25,26 In the absence of direc-
tion from randomized data, the 2015 SCAI/ACC/HFSA/STS
Clinical Expert Consensus Statement on mechanical support,
endorsed by the American Heart Association, did not provide
specific guidance on device use.27
Conclusions
The IABP is unique in its safety profile, cost efficiency and
breadth of experience, and retains its position as the most
widely used hemodynamic support device. Although a direct
relationship between device power and improved outcomes
is intuitive, it is, as of yet, unproven. Higher-flow PVADs may
ultimately be best to solve the challenges of hemodynamic
collapse. However, it is most likely that the IABP and PVADs
will each play complementary roles in shock and acute care.
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