Intra-Aortic Balloon Counterpulsation

Jeffrey C. Trost, MDa,*, and L. David Hillis, MDb

Intra-aortic balloon counterpulsation (IABP) is sometimes used in critically ill pa-
tients with cardiac disease. By increasing diastolic arterial pressure and decreasing
systolic pressure, it reduces left ventricular afterload. IABP may be beneficial in
subjects with cardiogenic shock, mechanical complications of myocardial infarction,
intractable ventricular arrhythmias, or advanced heart failure or those who undergo
“high-risk” surgical or percutaneous revascularization, but the evidence to support its
use in these patient groups is largely observational. Contraindications to IABP
include severe peripheral vascular disease as well as aortic regurgitation, dissection,
or aneurysm. The potential benefits of IABP must be weighed against its possible
complications (bleeding, systemic thromboembolism, limb ischemia, and, rarely,
death). © 2006 Elsevier Inc. All rights reserved. (Am J Cardiol 2006;97:
1391–1398)

For several decades, intra-aortic balloon counterpulsation insertion, which is the predominant insertion technique used
(IABP) has been used to provide hemodynamic support to today.
critically ill patients with cardiac disease. Although the
exact prevalence of its use is unknown, the National Hos-
pital Discharge Survey estimated that IABP was used in Device Insertion and Operation
42,000 patients in the United States in 2002.1
The IABP device is composed of (1) a double-lumen 8Fr to
9.5Fr catheter with a 25- to 50-ml balloon at its distal end
and (2) a console with a pump to deliver gas to the balloon.
History
Before insertion, an appropriate balloon size is selected (on
the basis of the patient’s height). (Balloon recommendations
The beneficial effects of IABP are based on the principle of
from Datascope Corporation, Montvale, New Jersey, are as
“counterpulsation,” whereby blood is pumped or displaced
follows: for patients ⬍5 ft [152 cm] tall, 25 ml; for those 5
“out of phase” with the normal cardiac cycle (i.e., during
ft to 5 ft 4 in [152 to 163 cm] tall, 34 ml; for those 5 ft 4 in
left ventricular [LV] diastole). The application of this prin-
to 5 ft 6 in [163 to 183 cm] tall, 40 ml; and for those ⬎6 ft
ciple was first described (in experimental animals) by Ad-
[183 cm] tall, 50 ml.) The balloon diameter, when fully
rian and Arthur Kantrowitz2 in 1952. In 1958, Harken pro-
expanded, should not exceed 80% to 90% of the diameter of
posed an extracorporeal pump that would remove blood
the patient’s descending thoracic aorta. The IABP catheter
during LV systole, then return it during diastole, and in
is inserted percutaneously in the femoral artery through an
1962, he and his colleagues described the use of such a
introducer sheath using an over-the-wire technique; percu-
device in experimental animals.3,4 That same year, Moulo-
taneous insertion through the brachial artery also is possi-
poulos et al5 developed an intra-aortic device, with which a
ble.8 Alternatively, the catheter can be inserted surgically
balloon mounted on a catheter and positioned in the aorta
using a transthoracic or translumbar approach or through the
was inflated during LV diastole and deflated during systole.5
iliac, subclavian, or axillary artery.9 –11 In comparison with
In 1968, Kantrowitz et al6 reported that IABP in 2 sub-
percutaneous placement, surgical insertion is associated
jects with cardiogenic shock improved systemic arterial and
with increased periprocedural mortality.12,13 Once vascular
central venous pressures as well as urine output, although
access is obtained, the balloon catheter is inserted and ad-
only 1 survived to hospital discharge. These early intra-
vanced, usually under fluoroscopic guidance, to the de-
aortic balloons were inserted through a femoral arterial
scending thoracic aorta, where its tip is positioned 2 to 3 cm
cutdown. In 1980, Bregman et al7 described percutaneous
distal to the origin of the left subclavian artery (at the level
of the carina).
a
Department of Internal Medicine (Cardiology Division), Johns Hop- After the catheter is positioned in the descending tho-
kins University School of Medicine, Baltimore, Maryland; and bDepart- racic aorta, its inner lumen can be used to monitor systemic
ment of Internal Medicine (Cardiology Division), University of Texas arterial pressure, and the outer lumen is used for the delivery
Southwestern Medical School, Dallas, Texas. Manuscript received Sep- of gas from the console to the balloon. Helium is most often
tember 14, 2005; revised manuscript received and accepted November 8,
2005. used because of its low density, which facilitates rapid
* Corresponding author: Tel: 410-550-2463; fax: 410-550-1183. transmission from console to balloon. Once balloon infla-
E-mail address: jtrost2@jhmi.edu (J.C. Trost). tion is initiated, the complete expansion of the balloon

0002-9149/06/$ – see front matter © 2006 Elsevier Inc. All rights reserved. www.AJConline.org
doi:10.1016/j.amjcard.2005.11.070
1392 The American Journal of Cardiology (www.AJConline.org)
 Review/Intra-Aortic Balloon Counterpulsation 1393

should be confirmed fluoroscopically. In addition, the pa-
tient’s peripheral pulses should be assessed to ensure that
the balloon is not compromising perfusion of the aortic arch
vessels or the affected limb. Urine output should be moni-
tored, and serum creatinine concentration should be mea-
sured periodically.
The console is programmed to identify a trigger for
balloon inflation and deflation. The most commonly used
triggers are (1) the electrocardiographic (ECG) waveform
and (2) the systemic arterial pressure waveform. With the
use of the ECG waveform, the peak of the R wave corre-
sponds to the beginning of LV systole; the balloon deflates
at this time. Balloon inflation begins with the onset of
diastole, which corresponds to the middle of the T wave.
Poor ECG quality or electrical interference may cause in-
consistent ECG triggering. Cardiac dysrhythmias, such as
atrial fibrillation, may result in inconsistent balloon infla-
tion, thereby potentially diminishing the benefits of IABP.
Although the ECG signal is often used as an IABP
trigger, it is only an approximation of the onset and termi-
nation of LV systole and diastole, and adjustments in the
precise timing of balloon inflation and deflation may be re-
quired. For this purpose, the systemic arterial pressure wave-
form may be used: the IABP device is set to inflate after aortic
valve closure (which corresponds to the waveform’s dicrotic
notch) and to deflate immediately before aortic valve opening
(which corresponds to the point just before the systolic arterial
upstroke).
The optimal arterial waveforms with IABP are displayed
in Figure 1. When the timing of balloon inflation or defla-
tion is suboptimal, adverse hemodynamic consequences
may result (Figure 1). The pressure waveform should be
examined at least daily by personnel trained to recognize
these abnormal patterns, after which appropriate adjust-
ments, if necessary, can be made.
Depending on the patient’s hemodynamic status, the
IABP device may be programmed to cycle more (1:1, or
1 inflation for every cardiac cycle) or less (1:4, 1:8) often.
The IABP device is often initially set at a frequency of
1:2, thereby enabling the operator to determine the he-
modynamic efficacy of IABP by comparing assisted and
unassisted beats. If the patient’s systemic arterial pres-
sure, cardiac output, and pulmonary arterial wedge pres-
sure fail to improve, more frequent IABP device infla-
tions (1:1) may be used. Conversely, with hemodynamic
improvement, the IABP device can be “weaned” to less
frequent cycling.
Concomitant Medications
Intravenous unfractionated heparin sufficient in amount to
prolong an activated partial thromboplastin time to 50 to 70
seconds is considered to be standard therapy during IABP.
Although heparin may prevent catheter-related thrombotic
events, no data exist to support this belief. In fact, 1 study
that randomly assigned 153 patients to receive heparin (or
no heparin) during IABP found no difference in the inci-
dence of limb ischemia.14
A nonfunctioning balloon should be removed promptly,
or thrombosis may occur. In nonheparinized experimental
animals, an immobile, deflated balloon is subject to throm-
bosis within 20 minutes.15 The largest IABP device manu-
facturer recommends that an immobile IABP device be re-
moved within 30 minutes.16 Occasionally, a balloon may
rupture, leading to extensive thrombus formation; therefore,
any evidence of balloon rupture necessitates the immediate
discontinuation of heparin and prompt IABP device removal.
In preparation for the elective removal of a functioning bal-
loon, we discontinue heparin ⱖ2 hours before removal. During
the time interval from heparin discontinuation to IABP device
removal, the IABP device is inflated periodically (no less
frequently than 1:8) to prevent hemostasis and thrombosis.
Adequate patient sedation and analgesia are essential
before and during IABP. Any movement of the involved leg
or change in patient position may lead to IABP device
migration, which may compromise aortic branch vessels or
produce aortic injury. If a patient with an IABP device
requires extubation, the IABP device should first be re-
moved, at a time when the patient is still sedated. After
IABP device removal, the patient should be immobile for
ⱖ6 hours, after which sedation can be discontinued in
preparation for attempted extubation.

Figure 1. (A) Systemic arterial pressure waveform from a patient with a normally functioning IABP device in whom the IABP device is programmed to inflate
during every other cardiac cycle (commonly referred to as “1:2,” or 1 inflation for every 2 cardiac cycles). With the first beat, aortic systolic and end-diastolic
pressures are shown without IABP support and are therefore unassisted. With the second beat, the balloon inflates with the appearance of the dicrotic notch,
and peak-augmented diastolic pressure is inscribed. With balloon deflation, assisted end-diastolic pressure and assisted systolic pressure are observed. To
confirm that IABP is producing maximal hemodynamic benefit, the peak diastolic augmentation should be greater than the unassisted systolic pressure, and
the 2 assisted pressures should be less than the unassisted values. (B) Systemic arterial pressure waveform from a subject in whom balloon inflation occurs
too early, before aortic valve closure. Consequently, the left ventricle is forced to empty against an inflated balloon; the corresponding increase in afterload
may increase myocardial oxygen demands and worsen systolic function. (C) Systemic arterial pressure waveform from a patient in whom balloon inflation occurs
too late, well after the beginning of diastole, thereby minimizing diastolic pressure augmentation. (D) Systemic arterial pressure waveform from a patient in whom
balloon deflation occurs too early, before the end of diastole. This may shorten the period of diastolic pressure augmentation. A corresponding transient decrease
in aortic pressure may promote retrograde arterial flow from the carotid or coronary arteries, possibly inducing cerebral or myocardial ischemia. (E) Systemic arterial
pressure waveform from a subject in whom balloon deflation occurs too late, after the end of diastole, thereby producing the same deleterious consequences as early
balloon inflation (increased LV afterload, with a resultant increase in myocardial oxygen demands and a worsening of systolic function).
1394 The American Journal of Cardiology (www.AJConline.org)
Hematologic Effects
With IABP, hemoglobin and hematocrit often decrease
modestly because of hemolysis from mechanical damage to
erythrocytes as well as bleeding at the vascular access site.
In 1 nonrandomized analysis of patients with myocardial
infarctions (MIs), the 37 subjects in whom IABP was used
had average decreases in hemoglobin and hematocrit of 2.3
g/dl and 5.7%, respectively, whereas the 13 patients without
IABP device placement manifested decreases of 1.5 g/dl
and 3.9%, respectively (p ⬍0.05).17 Thrombocytopenia may
occur with IABP because of (1) the mechanical destruction
of platelets and/or (2) heparin administration.18 Serum he-
moglobin and hematocrit and the platelet count should be
measured daily during IABP.
Hemodynamic Effects
Effects on systemic arterial pressure and LV perfor-
mance: By increasing diastolic arterial pressure and de-
creasing systolic pressure, IABP reduces LV afterload. The
magnitude of these effects varies among subjects and is
dependent on (1) balloon volume, (2) heart rate, and (3)
aortic compliance. The balloon volume is proportional to
the volume of blood displaced: as balloon volume increases,
the displaced blood volume increases commensurately. As
heart rate increases, LV and aortic diastolic filling times
decrease, producing less balloon augmentation per unit of
time. Finally, as aortic compliance increases (or systemic
vascular resistance decreases), the magnitude of diastolic
augmentation diminishes.
In most patients with systemic arterial hypotension,
IABP increases arterial pressure, because the magnitude of
diastolic pressure augmentation exceeds the decrease in sys-
tolic pressure. In contrast, in normotensive patients, IABP
usually produces little or no change in mean arterial pressure,
because these subjects maintain stable arterial pressure through
circulatory autoregulation. In patients with severe heart failure
and/or cardiogenic shock, IABP reduces systolic arterial pres-
sure, thereby “unloading” the failing heart. By reducing LV
afterload, IABP reduces LV wall tension and oxygen demands.
Subsequently, preload, as reflected by left atrial and/or LV
end-diastolic pressures, decreases. These favorable effects
cause increases in stroke volume and cardiac output.
Effects on coronary arterial blood flow: The augmen-
tation of diastolic aortic pressure during balloon inflation, in
theory, should increase coronary arterial blood flow, partic-
ularly in subjects with coronary arterial hypoperfusion, be-
cause most coronary arterial flow occurs during LV diastole.
However, studies in experimental animals and humans have
yielded conflicting results: several have reported increases in
coronary blood flow with IABP,19 –27 whereas others have
reported no change28 –31 or even decreases.32,33 These studies
vary with respect to (1) the subjects studied (animals or hu-
mans), (2) their hemodynamic conditions at the time of study,
and (3) the methods used to quantify coronary blood flow.
These differences may explain the heterogeneity of results.
Several studies in critically ill patients suggest that IABP
may be beneficial in those with impaired coronary arterial
autoregulation.21,23 Across a wide range of perfusion pres-
sures (from 45 to 125 mm Hg), coronary blood flow remains
constant by autoregulation; within this range of perfusion
pressures, coronary blood flow is relatively pressure inde-
pendent. At extremely large or small perfusion pressures,
however, autoregulation is insufficient to preserve coronary
arterial blood flow. For example, in a subject with profound
hypotension, the effect of autoregulation is lost; in such a
situation, IABP may augment coronary arterial flow by
increasing aortic diastolic pressure. However, in the setting
of a fixed, severe coronary arterial stenosis (⬎90% luminal
diameter narrowing), the IABP-induced increase in aortic
diastolic pressure is not transmitted to the vessel’s postste-
notic segment; as a result, poststenotic coronary blood flow
is unchanged.34
Indications for Use
Cardiogenic shock: Registry data suggest that cardio-
genic shock is 1 of the most common conditions for which
IABP is used, accounting for about 20% of all insertions in
the United States.35,36 In 15 subjects with cardiogenic shock,
Weiss et al37 showed that IABP was associated with (1)
decreases in LV end-diastolic and end-systolic volumes and
pulmonary arterial wedge pressure and (2) increases in
cardiac output, stroke volume, and the LV ejection fraction.
Unfortunately, although hemodynamic and clinical im-
provement was noted in all patients, only 4 survived to
hospital discharge.
In the era of pharmacologic or mechanical reperfusion in
patients with acute MIs, the efficacy of IABP in subjects
with cardiogenic shock has not been evaluated in a ran-
domized, controlled trial. The evidence in support of
IABP in conjunction with reperfusion comes from (1)
canine data, which suggest that IABP facilitates pharma-
cologic reperfusion by improving the speed and com-
pleteness of clot lysis38; (2) observational data from pa-
tients with cardiogenic shock treated with pharmacologic
or mechanical reperfusion; and (3) retrospective analyses
of randomized trials examining reperfusion strategies in
patients with acute MIs.
In the Should We Emergently Revascularize Occluded
Coronaries for Cardiogenic Shock registry, an observational
analysis of patients with acute MIs and cardiogenic shock,
patients who received IABP and thrombolytic therapy had
lower in-hospital mortality (47%) than those receiving
IABP alone (52%), thrombolytic therapy alone (63%), or
neither (77%) (p ⬍0.0001). In this series, however, those
who received IABP were more likely to undergo percuta-
neous or surgical revascularization, which may have con-
tributed to their improved outcomes.39
 Review/Intra-Aortic Balloon Counterpulsation
A retrospective analysis of the data from the Global
Utilization of Streptokinase and Tissue Plasminogen Acti-
vator for Occluded Coronary Arteries study, which random-
ized patients with acute MIs to 1 of 4 thrombolytic regi-
mens, identified 310 patients with cardiogenic shock. IABP
was used in 68 and not used in the other 242; the decision
regarding IABP use was made by each patient’s personal
physician (i.e., the assignment to IABP use was not ran-
dom). One-year mortality was lower in those receiving early
IABP support (57% vs 67%, p ⫽ 0.04). Again, however,
those in whom IABP was used ⬍24 hours after hospital-
ization were more likely to receive other therapies, includ-
ing inotropic agents, pacemakers, assisted ventilation, and
surgical and/or percutaneous revascularization. Those in
whom IABP was used had higher rates of major bleeding
(47% vs 12%, p ⫽ 0.0001).40
Recently, the National Registry of Myocardial Infarc-
tion-2 investigators reported outcomes of patients with
acute MI and cardiogenic shock stratified according to (1)
IABP use and (2) reperfusion therapy (pharmacologic or
mechanical). Among 23,180 subjects with cardiogenic
shock, IABP was used in 7,268. Again, the decision regard-
ing IABP use was made by the subject’s personal physician
(i.e., the assignment was not random). In those who re-
ceived thrombolytic therapy and IABP, in-hospital mortal-
ity was 49%, whereas it was 67% in patients who did not
receive IABP (p ⬍0.001). In contrast, among patients who
received primary percutaneous revascularization, no sur-
vival benefit was observed with IABP (in-hospital mortality
45% vs 47%, p ⫽ NS).41
In summary, patients with cardiogenic shock often man-
ifest hemodynamic improvement with IABP, but it is un-
clear if this translates into reduced morbidity or mortality in
the absence of concomitant revascularization.
Cardiogenic shock due to ventricular septal rupture
(VSR) or papillary muscle rupture, with resultant mitral
regurgitation (MR): In 1% to 2% of patients with acute
MIs, VSR or papillary muscle rupture with resultant severe
MR may occur; either may produce cardiogenic shock.
About 5% of subjects in whom IABP is used have VSR or
acute MR.36 The evidence to support IABP in these patients
comes from several small observational studies. In 1 report
of 5 patients with VSR and 1 with acute MR, IABP was
associated with substantial clinical and hemodynamic im-
provement.42 Similarly, other studies demonstrated short-
term (24-hour) clinical and hemodynamic improvement
with IABP in patients with VSR,43,44 and 1 reported an
improvement in the magnitudes of intracardiac shunting,
systemic arterial pressure, and pulmonary arterial wedge
pressure with IABP therapy.45
Intractable ventricular arrhythmias: IABP is used on
occasion in subjects with ventricular tachyarrhythmias re-
fractory to pharmacologic therapy.36,46 – 49 Fotopoulos et al50
used IABP in 21 patients with medically refractory ventric-
ular arrhythmias, 4 of whom failed to respond to 1 antiar-
1395
rhythmic agent and 17 of whom failed to respond to mul-
tiple drugs. During IABP support, 18 manifested reductions
in or completed the abolition of arrhythmias.
Post-MI angina or unstable angina refractory to med-
ical therapy: About 12% of IABP is performed in subjects
with post-MI angina or unstable angina refractory to med-
ical therapy.36 The data in support of IABP in these patients
are observational. In 1 report, IABP use was accompanied by
symptomatic reduction and electrocardiographic improvement
in 15 of 16 patients with severe unstable angina,51 and another
series reported similar improvement with IABP in 21 patients
with postinfarction angina.52
Heart failure refractory to medical therapy: In sub-
jects with refractory LV failure, IABP is used only as a
temporary supportive measure in those awaiting cardiac
transplantation.36
Hemodynamic support for “high-risk” catheteriza-
tion and angioplasty: IABP is often used in patients who
undergo so-called high-risk catheterization and angio-
plasty.36 Because patients with (1) age ⱖ70 years, (2) left
main coronary artery disease (CAD), and/or (3) poor LV
systolic function are at increased risk during these proce-
dures, it has been hypothesized that IABP may reduce the
probability or magnitude of hemodynamic deterioration or
collapse that is sometimes caused by procedure-induced
myocardial ischemia. No randomized data exist to support
this practice before diagnostic catheterization or percutane-
ous coronary intervention (PCI).
The efficacy of routine postprocedural IABP in high-risk
patients who undergo primary PCI for acute MIs was eval-
uated in a randomized trial. In this study, 437 patients with
acute MIs who were considered to be at high risk (age ⬎70
years, 3-vessel CAD, LV ejection fractions ⬍0.45, saphe-
nous vein graft occlusions, persistent ventricular tachyar-
rhythmias, or suboptimal PCI results) were randomly as-
signed to (1) 36 to 48 hours of postprocedural IABP or (2)
traditional postprocedural care. The 2 groups had similar
rates of death, reinfarction, and infarct-related artery reoc-
clusion.53 Thus, routine IABP after primary PCI appears not
to be indicated.
Hemodynamic support for high-risk coronary artery
bypass grafting (CABG): Many of the aforementioned
variables that predispose patients to periprocedural compli-
cations during angiography and percutaneous revasculariza-
tion may increase the risk for perioperative complications in
patients who undergo CABG. Surgical revascularization
may be complicated by worsening ischemia and/or LV
systolic dysfunction, with resultant hemodynamic instabil-
ity, inability to wean off cardiopulmonary bypass, and
death. In patients at risk for these complications, IABP
support may have beneficial hemodynamic and anti-isch-
emic effects.
Two nonrandomized series (describing data from 251
patients) compared the outcomes of high-risk patients who
1396 The American Journal of Cardiology (www.AJConline.org)
underwent CABG (defined as those who underwent repeat
or nonelective CABG as well as those with left main CAD,
severe LV systolic dysfunction, symptomatic heart failure,
recent MIs, or unstable angina refractory to medical ther-
apy) who received preoperative IABP with those who re-
ceived IABP only intra- or postoperatively.54 In the 2 studies,
the in-hospital mortality rates were lower in those receiving
preoperative IABP. In another series of 163 patients with
preoperative LV ejection fractions ⬍0.25 who underwent
CABG, those with preoperative IABP had lower in-hospital
mortality compared with those not receiving preoperative
IABP (2.7% vs 11.9%, respectively, p ⬍0.005).55
One small randomized trial examined the role of preop-
erative IABP support in patients who underwent CABG. In
this study, 52 patients with ⱖ2 high-risk features (LV ejec-
tion fraction ⬍0.40, left main CAD, reoperation, or medi-
cally refractory angina) were randomly assigned to (1) pre-
operative IABP for 24 hours, (2) preoperative IABP for 1 to
2 hours, or (3) no preoperative IABP. Those who underwent
preoperative IABP, regardless of its duration, had shorter
durations on cardiopulmonary bypass, shorter durations of
postoperative IABP support, greater cardiac indexes, shorter
intensive care unit stays, and reduced mortality (6% vs 25%,
p ⬍0.05).56
In summary, patients with ongoing ischemia, decompen-
sated heart failure, and/or hemodynamic instability who
require urgent CABG may benefit from preoperative IABP.
In contrast, routine IABP is not recommended in those with
left main CAD but without ongoing ischemia as well as in
those with poor LV systolic function but without overt heart
failure.
Septic shock: Profound myocardial dysfunction may oc-
cur in subjects with septic shock, prompting some physi-
cians to consider IABP device insertion. Two small studies
in experimental animals with septic shock provided con-
flicting results.57,58 No data exist for IABP in humans with
septic shock.
Contraindications to Intra-Aortic
Balloon Counterpulsation
IABP is contraindicated in patients with aortic regurgitation
because it worsens the magnitude of regurgitation. IABP
device insertion should not be attempted in a patient with
suspected or known aortic dissection, because inadvertent
balloon placement in the false lumen may result in exten-
sion of the dissection or even aortic rupture. Similarly,
aortic rupture is a potential consequence of IABP device
insertion in patients with sizable abdominal aortic aneu-
rysms.
Percutaneous IABP device placement should be avoided
in patients with severe peripheral vascular disease uncor-
rectable by angioplasty and/or surgery. The presence of
bilateral femoral-popliteal bypass grafts is a contraindica-
tion to percutaneous femoral IABP device insertion, but
patients with aortobifemoral bypass grafts are generally
considered reasonable candidates for percutaneous femoral
IABP device placement. Finally, IABP is contraindicated in
patients with uncontrolled septicemia or a bleeding diathesis.
Complications of Intra-Aortic Balloon Counterpulsation
IABP may be associated with vascular complications, in-
cluding bleeding, systemic embolization, limb ischemia,
and amputation. In addition, as with any indwelling cathe-
ter, IABP may result in infection. We believe that the
presence of a fever in a patient who undergoes IABP, in the
absence of another clear source, requires balloon removal.
IABP may be accompanied by mechanical complications,
including balloon rupture, inadequate inflation, and inade-
quate diastolic augmentation. Rarely does a patient die as a
result of IABP device insertion, usually from aortic dissec-
tion and/or rupture.
In the largest multinational registry to date, 7% of 16,909
IABP recipients experienced ⱖ1 IABP-related complica-
tion. Of these, 2.6% had major complications, including
major bleeding in 0.8%, limb-threatening ischemia in 0.9%,
limb amputation in 0.1%, and IABP-related death in
0.05%.59 Several variables were identified as predictors for
major IABP-related complications: (1) age ⱖ75 years, (2)
peripheral vascular disease, (3) diabetes mellitus, (4) female
gender, and (5) small body surface area (⬍1.65 m2).60,61
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