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Eur J Vasc Endovasc Surg (2010) xx, 1e8

REVIEW

Perioperative Cardiac Damage in Vascular


Surgery Patients
W.-J. Flu a, O. Schouten b, J.-P. van Kuijk a, D. Poldermans c,*

a
Department of Anesthesiology, Erasmus Medical Center, ‘s-Gravendijkwal 230, 3015 CE, Rotterdam, The Netherlands
b
Department of Surgery, Reinier de Graaf Hospital, Delft, The Netherlands
c
Department of Vascular Surgery, Erasmus Medical Center, Rotterdam, The Netherlands

Submitted 26 November 2009; accepted 11 March 2010


Available online xxx

KEYWORDS Abstract Background: Patients undergoing vascular surgery are at increased risk for devel-
Asymptomatic oping cardiac complications. Majority of patients with perioperative myocardial damage are
myocardial damage; asymptomatic. Our objective is to review the available literature addressing the prevalence
Vascular surgery and prognostic implications of perioperative myocardial damage in vascular surgery patients.
Methods: An Internet-based literature search was performed using MEDLINE to identify all pub-
lished reports on perioperative myocardial damage in vascular surgery patients. Only those
studies published from 2000 to 2010 evaluating myocardial damage using troponin I or T, with
or without symptoms of angina pectoris were included.
Results: Thirteen studies evaluating the prevalence of perioperative myocardial ischaemia or
infarction were included in the study. The incidence of perioperative myocardial ischaemia
ranged from 14% to 47% and the incidence of perioperative myocardial infarction ranged from
1% to 26%. In addition, 10 studies evaluating the prognostic value of perioperative myocardial
ischaemia towards postoperative mortality or the occurrence of major adverse cardiac events
were included. In the retrieved studies, hazard ratios varied from 1.9 to 9.0.
Conclusion: The high prevalence and asymptomatic nature of perioperative myocardial
damage, combined with a substantial influence on postoperative mortality of vascular surgery
patients, underline the importance of early detection and adequate management of perio-
perative myocardial damage.
This article provides an extended overview regarding the prevalence and prognostic value of
perioperative myocardial ischaemia and infarction in vascular surgery patients. In addition,
treatment options to reduce the risk of perioperative myocardial damage are provided based
on the current available literature.
ª 2010 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.

* Corresponding author. Tel.: þ31 10 7034613; fax: þ31 10 7034957.


E-mail address: d.poldermans@erasmusmc.nl (D. Poldermans).

1078-5884/$36 ª 2010 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.ejvs.2010.03.014

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with a concomitant reduction of coronary perfusion,


Introduction leading to perioperative myocardial damage.9
It is estimated that of the 230 million patients under-
In the present article, an extended overview is provided going major surgery annually, approximately 1% (2,300,000
regarding the prevalence and prognostic value of peri- patients) suffer perioperative MI with a cardiovascular
operative myocardial ischemia and infarction in vascular mortality rate around 0.3% (690.000 patients).10 However,
surgery patients. In addition, treatment options in order to cardiac risk imbedded in surgical interventions can differ
reduce the risk of perioperative myocardial damage are depending on the magnitude, duration, location, blood loss
provided based on the current available literature. and fluid shifts related to the specific procedure. In 2005,
Boersma et al. developed a model to risk stratify surgical
procedures, based on the occurrence of 30-day cardiac
Perioperative myocardial damage: ischaemia death and MI.11 Surgical procedures were classified low
and infarction cardiac risk (<1%), intermediate cardiac risk (1e5%) or high
cardiac risk (>5%) for the development of 30-day adverse
The heart is an organ with a high metabolic demand, even at cardiac outcome. High-cardiac-risk surgery is considered to
rest, and requires a continuous high level of oxygen supply to be open lower extremity revascularisation and open
the myocardium. The amount of oxygen supplied to the abdominal aortic surgery. In addition, percutaneous trans-
myocardium is determined by (1) the blood flow in the luminal angioplasty, endovascular aortic aneurysm repair
coronary arteries and (2) the oxygen-carrying capacity of the and carotid surgery are considered as intermediate cardiac
blood. Therefore, an increase of myocardial oxygen demand risk because they are associated with reduced myocardial
must be met by an increase in coronary blood flow. In addi- stress and the need for lower fluid administration compared
tion, an imbalance between oxygen supply and oxygen with open lower extremity revascularisation and open
demand results in myocardial damage, characterised by abdominal aortic surgery.12,13
myocardial ischaemia and myocardial infarction (MI).1
In general, myocardial damage can be subdivided
according to two pathological processes, described as type Methods
1 and 2 by the universal definition of MI.2 Type 1 MI is
defined as an acute coronary syndrome that occurs when A systematic Medline search was undertaken to identify
a coronary plaque ruptures, leading to thrombus formation, studies addressing perioperative cardiac damage, assessed
acute coronary thrombosis, supply ischaemia and MI. A with troponin I or T, in patients undergoing elective
reduction of arterial blood flow is the cause of myocardial peripheral vascular surgery published between 2000 and
damage in type 1 MI. In addition, myocardial damage may 2010. The keywords used were ‘cardiac troponin, vascular
also be caused by a sustained myocardial oxygen supplye surgery’, ‘perioperative ischaemia, vascular surgery’,
demand imbalance, or type 2 MI. In case of type 2 MI, ‘cardiac ischaemia, vascular surgery’ in combination with
myocardial damage is caused by an increased myocardial ‘prevalence’, ‘incidence’, ‘prognostic value’, ‘long term
oxygen demand in response to stress, characterised by outcome’, ‘long-term mortality’ and ‘major adverse
tachycardia and increased myocardial contractility, which cardiac events’. The retrieved articles were also searched
is not met by a sufficient increase of coronary blood flow.3 for any relevant references. The current study included
During surgery, high catecholamine production is solely studies addressing the prognostic value of increased
responsible for vasoconstriction and haemodynamic stress,4 troponin T or I levels when using regression analyses or
associated with an increased oxygen demand of the contingency table analyses.
myocardium. Perioperative myocardial damage may occur
when the increased oxygen demand is not met by an
adequate increase of oxygen supply.5 This is similar to MIs Results
occurring in the non-surgical setting; however, surgery
itself is a significant stress factor leading to an increased Vascular surgery patients are at increased risk for devel-
risk of plaque rupture. Two retrospective studies investi- oping perioperative cardiac complications, especially
gated the coronary pathology of fatal perioperative MI. As patients undergoing open lower extremity revascularisation
demonstrated in the autopsy study by Dawood et al., 55% of and open abdominal aortic surgery. In 1981, Brown et al.
the fatal perioperative MIs have direct evidence of plaque described that about 40% of the patients undergoing elec-
disruption, defined as fissure or rupture of plaque and tive abdominal aortic aneurysm resection had a history of
haemorrhages into the plaque cavity.6 Similar autopsy either MI or angina pectoris.14 In addition, Hertzer et al.
results were found in the study of Cohen and Aretz, who performed routine coronary angiography in more than 1000
observed that plaque rupture was present in 46% of patients patients to detect uncorrected coronary artery disease in
with postoperative MI.7 patients with advanced peripheral vascular disease.15 They
Next to surgical stress, haemodynamic fluctuations found coronary artery disease to be highly present in these
during surgery are an important cause of perioperative patients with a prevalence of severe three-vessel disease in
myocardial damage as well. Perioperative fluid adminis- 18% of the patients and left main disease in 4% of
tration increases the pre- and afterload in the left patients.15 In 1989, Oeyang et al. observed that episodes of
ventricle, making patients susceptible to perioperative perioperative myocardial damage in patients having
myocardial damage.8 Conversely, perioperative preload peripheral vascular surgery are most often silent.16 Utoh
reductions in the left ventricle can result in tachycardia et al. performed routine coronary angiography in patients

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Perioperative Cardiac Damage in Vascular Surgery Patients 3

undergoing abdominal aneurysm repair and demonstrated Abraham et al. report the highest incidence of perioper-
that the incidence of silent ischaemia was 20%. In addition, ative myocardial damage within the first 3 days after
the authors concluded that the number of coronary risk surgery.27
factors and resting electrocardiograms were not worth-
while for predicting silent coronary artery disease.17
Perioperative myocardial damage is difficult to diagnose Prognosis after perioperative myocardial damage
due to its silent nature. In 1994, Adams 3rd et al. demon-
strated that the measurement of cardiac troponin I is In order to put the significance of perioperative myocardial
a sensitive and specific method for the diagnosis of peri- damage into perspective, it is pivotal to address the influ-
operative MI in vascular surgery patients.18 Hereafter, ence of perioperative myocardial damage on long-term
several studies have correlated serial cardiac troponin postoperative outcome. Multiple studies have been per-
measurements with continuous 12-lead ST-segment analysis formed over the years to evaluate this issue. In 1982,
after major vascular surgery.19 Troponin elevations occurred Jamieson et al. were among the first to describe the
after prolonged, transient, postoperative ST-segment influence of ischaemic heart disease on early and late
depression, and peak troponin elevations correlated with mortality after surgery for peripheral occlusive vascular
the duration of ST depression.20 Landesberg et al. demon- disease. The authors concluded that coronary artery
strated that 85% of postoperative cardiac complications were disease is a major determinant of both early and late
preceded by prolonged ST-segment depression.21 In addi- mortality after arterial reconstruction and that selective
tion, Fleisher et al. found that 78% of patients with cardiac myocardial revascularisation may improve survival of these
complications had at least one episode of prolonged patients.28 Because perioperative myocardial damage is
myocardial ischaemia (¡.e., >30 min) either before or during most often silent, the great majority of patients (95%) with
the cardiac event.22 The hypothesis that ST-depression can perioperative myocardial damage remain untreated. This
lead to perioperative MI is further supported by increased might contribute to an increased risk of long-term cardio-
troponin T levels during or shortly after prolonged vascular mortality as well.16,29,30
ST-depression ischaemia.23 Episodes of perioperative From 2000 to 2010, perioperative myocardial damage,
ST-depression, indicating endocardial (non-transmural) defined as postoperative troponin elevations whether or
myocardial ischaemia, has been described in up to 41% of not in combination with ST-segment alterations, has been
vascular surgery patients and mostly occur within the first 2 related to adverse short-, mid- and long-term cardiac
days after surgery.24 ST-elevation-type ischaemia is consid- morbidity and mortality as well in multiple studies, out-
ered relatively uncommon, confirmed by the incidence (12%) lined in Table 2.20,27,31e38 In the current study, hazard
of intra-operative ST-elevation in a study performed by ratios describing the prognostic value of troponin T or I
London et al.25 Recent studies using highly sensitive troponin towards postoperative mortality or the occurrence of major
essays demonstrated that low-level (>0.03 ng ml1) troponin adverse cardiac events varied from 1.9 to 9.0.
elevations postoperatively are common in high-cardiac-risk In patients undergoing vascular surgery, asymptomatic
patients, even with little or no evidence of ischaemia with elevated troponin T levels were associated with an
electrocardiogram monitoring.26 increased risk, of more than four- to six-fold, for cardiac
In the current study, we performed a systematic Medline events during a 6-month follow-up period, as demonstrated
search to evaluate the prevalence of myocardial ischaemia by Kim et al.39 Landesberg et al. and Kertai et al. studied
or infarction in vascular surgery patients detected with the prognostic value of low- and intermediate-to-high cut-
troponin I or T measurement whether or not in combination off levels of troponin T elevations on long-term mortality
with electrocardiogram changes or symptoms of angina after vascular surgery. These studies demonstrated that
pectoris. As demonstrated in Table 1, the incidence of postoperative troponin elevations even at low cut-off levels
perioperative myocardial ischaemia ranged from 14% to 47% are independent and complementary predictors of long-
and that of perioperative MI ranged from 1% to 26%. The term mortality.20,37 In addition, early mortality after peri-
wide range of incidence might be related to (1) different operative MI ranges between 3.5% and 25% and is higher in
cut-off values of troponin I or T used in the study, (2) patients with an intermediate- to high-level troponin
a variety of vascular procedures included in the studies and elevation, compared with patients with a low-level
(3) that patient-specific cardiac risk factors differed troponin elevation.20,32,34.
between the studies. For example, in the study performed Endovascular surgery is associated with a reduced inci-
by Ali et al. the highest incidence of perioperative dence of perioperative myocardial damage, compared with
myocardial damage was found (both ischaemia and infarc- open vascular surgery, possibly explained by reduced
tion), probably related to the fact that this study only myocardial stress during endovascular procedures.13
included patients undergoing open abdominal aortic repair. However, Winkel et al. recently demonstrated that
In addition, Schouten et al. included only included patients asymptomatic perioperative myocardial damage, defined
with three or more cardiac risk factors (age >70 years, as cardiac troponin T elevations in the absence of ischaemic
angina pectoris, MI, congestive heart failure, stroke, renal symptoms or electrocardiogram abnormalities, was associ-
dysfunction and diabetes mellitus). In the study performed ated with an increased mortality risk of patients undergoing
by Abraham et al., about 75% of the patients underwent endovascular abdominal aortic aneurysm repair.40 During
endovascular abdominal aortic aneurysm repair and a 2.9-year follow-up of 220 patients, they found that
patients with increased cardiac troponin T in combination patients with asymptomatic myocardial damage had
with a significant postoperative increase in serum creati- a mortality rate of 49%, compared with 15% for patients
nine (>50%) were excluded from the study. Importantly, without perioperative myocardial damage (P < 0.001).

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Table 1 Prevalence of perioperative myocardial ischaemia or MI in vascular surgery patients.


Study Surgical N Myocardial Myocardial
procedure ischaemia infarction
Bollinger et al.53 AAA 133 cTnI >2.0 14% e
(2009) Lower extremity
Flu et al.54 AAA 627 cTn-T >0.03 17% cTn-T >0.2 þ symptoms or 5%
(2009) Carotid ECG changes
Ali et al. 33 * AAA 43 cTnI >0.54 47% cTnI >0.54 þ symptoms or 26%
(2008) ECG changes
McFalls et al.55 AAA 377 cTnI >0.1 27% cTnI >0.1 þ symptoms or 10%
Lower extremity ECG changes
Schouten et al.56 ** AAA 77 cTn-T >0.03 30% cTn-T >0.2 þ symptoms or 7%
(2007) ECG changes
Barbagallo et al.34 AAA 75 cTnI >0.5 33% cTn-T >0.05 þ symptoms or 12%
(2006) Lower extremity ECG changes
Abraham et al.27 *** AAA 149 cTn-T >0.02 11% [ cTn-T þ ECG changes 1%
(2005)
Manach et al.35 AAA 1136 cTnI >0.2 14% cTnI >1.5 5%
(2005)
Landesberg et al.20 AAA 503 cTnI >0.6 or 23% [ cTnI or [ cTn-T þ 11%
(2003) Lower extremity/ cTn-T >0.03 Symptoms
carotid
Kim et al.39 * AAA 229 cTnI >0.4 43% [ cTnI þ ECG changes 3%
(2002) Lower extremity
Haggart et al.57 AAA 35 cTnI >0.5 29% cTnI >0.5 þ symptoms or 14%
(2001) Lower extremity ECG changes
Andrews et al.36 AAA 100 cTnI >0.8 18% [ CKMB þ Symptoms or 12%
(2001) Lower extremity/carotid ECG changes
Godet et al.58 AAA 316 cTnI >0.5 16% cTnI >1.5 8%
(2000)

Discussion b-Blockers

Prevention of perioperative myocardial damage In the non-surgical setting, b-blockers are widely used for
the prevention and treatment of ischaemic heart disease
In general, the management of perioperative myocardial and heart failure, all major determinants of adverse post-
damage is focussed on (i) coronary plaque stabilisation to operative outcome Proposed mechanisms by which
reduce acute coronary syndromes, with subsequent supply b-blockers exert intra-operative cardioprotective effects
ischaemia (type I MI), that occurs when a coronary plaque include heart rate control, reduction of systolic pressure
ruptures and (2) limiting surgical stress, which is the cause and ventricular contractile force and its anti-arrhythmic
of sustained myocardial oxygen supplyedemand imbalance properties. In the long term, b-blockers reduce mechanical
(type 2 MI). The high incidence of perioperative myocardial stress imposed on coronary plaques preventing plaque
damage reflects the high prevalence of underlying ischae- rupture.37 In addition, the anti-inflammatory properties of
mic heart disease in the vascular surgery population.29 b-blockers exert a beneficial effect towards coronary pla-
Therefore, adequate preoperative evaluation is inevitable que stabilisation as well.38 In addition, b-blockers are
to: (1) identify patients at increased cardiac risk, (2) known to reduce the process of adverse cardiac remodel-
initiate risk reduction therapy and (3) select optimal ling in patients with impaired left ventricular function,
surgical and anaesthesia techniques. In conventional which is highly prevalent in the vascular surgery population,
preoperative cardiac risk indices (Revised Cardiac Risk by inhibiting the sympathetic nervous system and hormone
index and Adapted Lee index), age, heart failure, ischaemic activation (A-type and B-type natriuretic peptides and
heart disease, cerebrovascular disease, renal dysfunction, norepinephrine).41
diabetes mellitus and high-risk surgery (such as vascular In the most recent European Society of Cardiology (ESC)
surgery) have been identified as independent predictors of guidelines, b-blockers are recommended (Class I, Level of
perioperative cardiovascular events.11,30 evidence B) in patients scheduled for high-risk surgery. In
addition, b-blockers should be considered (Class IIa, level
Pharmacological treatment of evidence B) in patients undergoing intermediate-risk
The unpredictable progression of an unstable coronary surgery, such as percutaneous transluminal angioplasty,
plaque during surgical stress is the most important target endovascular aortic aneurysm repair and carotid surgery.42
for systemic pharmacological therapy to reduce the inci- Factors that influence the effectiveness of perioperative
dence of perioperative myocardial damage. b-blockers treatment are the patients with underlying

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Table 2 Prognostic value of increased perioperative troponin T or I levels for cardiac outcome of vascular surgery patients.
Study Surgical procedure N Troponin I or T Cardiac outome
53
Bollinger et al. AAA 133 cTnI >2.0 MACE 1 year: HR 9.0 (3.6e23.2)
(2009) Lower extremity Mortality 1 year: HR 8.5 (2.9e24.9)
Winkel et al40 AAA 220 cTn-T >0.01 Mortality LT HR 2.3 (1.1e5.1)
(2009)
Ali et al. 33* AAA 43 cTnI >0.54 MACE LT OR 5.4 (1.2e24)
(2008)
McFalls et al.55 AAA 377 cTnI >0.1 Mortality 1 year P < 0.01*
(2008) Lower extremity
Barbagallo et al.34 AAA 75 cTnI >0.5 MACE 1 month P < 0.003*
(2006) Lower extremity
Manach et al.35 AAA 1136 cTnI >0.2 In-hospital mortality P < 0.05
(2005)
Kertai et al.59 AAA 393 cTn-T >0.1 Mortality LT HR 1.9 (1.1e3.1)
(2004) Lower extremity
Landesberg et al.20 AAA 447 cTnI >0.6 or Mortality LT OR 2.2 (1.48e3.42)
(2003) Lower extremity/ cTn-T >0.03
carotid
Kim et al.39 * AAA 229 cTnI >0.4 Mortality 6 m OR 4.9 (1.3e19)
(2002) Lower extremity
Andrews et al.36 AAA 100 cTnI >0.8 In-hospital MACE P < 0.001
(2001) Lower extremity/carotid
* Contingency table analyses evaluating increased risk for adverse cardiac outcome associated with perioperative increases of troponin T.

cardiac risk factors and variations in treatment protocols, vasoconstriction.48 Aspirin reduces the risk of non-fatal MI
such as b-blocker type, b-blocker dose and timing of by 34% and, in the setting of secondary prevention, reduces
b-blocker initiation before surgery. As recommended in the cardiovascular events by 27% and cardiovascular deaths by
ESC guidelines, b-blocker treatment should be initiated 18%.49 The most recent ESC guidelines addressing peri-
optimally between 30 days and at least 1 week before operative care state that continuation of aspirin should be
surgery with a target heart rate between 60 and 70 beats considered in the perioperative period of patients previ-
per minute and systolic blood pressure >100 mmHG. ously treated with aspirin (Class IIa, level of evidence B).42
The thienopyridine derivate clopidogrel is an anti-platelet
Statins agent that inhibits the adenosine diphosphate-mediated
platelet aggregation.50 Randomised controlled studies are
Statins are widely used to decrease low-density lipoprotein needed to investigate the role of clopidogrel as a preven-
cholesterol in patients. Furthermore, statins seem to sta- tive treatment in patients with asymptomatic cardiac
bilise atherosclerotic plaques during surgery through damage.
pleiotropic effects and therefore have a beneficial influ-
ence on cardiovascular outcome.43 Multiple studies have Prophylactic revascularisation
not only shown beneficial effects of statins in patients with Preoperative cardiac risk evaluation by means of risk factor
coronary artery disease, but in patients undergoing vascular assessment and non-invasive testing may identify vascular
surgery as well.44e46 In the most recent ESC guidelines, surgery patients with asymptomatic coronary artery
initiation of statins is recommended in patients undergoing disease. Two randomised, controlled trials have evaluated
high-risk surgery, optimally between 30 days and at least 1 the potential benefit that may be expected from preoper-
week before surgery (Class I, Level of evidence B).42 ative revascularisation in these patients. The Coronary
Artery Revascularisation Prophylaxis (CARP) trial rando-
Anti-platelet agents mised 510 patients with significant coronary artery stenosis
to receive either revascularisation or no revascularisation
The perioperative surgical stress results in a hypercoagu- prior to vascular surgery.51 The main finding of the CARP
lable state, which is in combination with atherosclerotic trial was that there was no difference in the primary
plaques, the perfect substrate for the development of outcome of long-term mortality (median follow-up 2.7
perioperative cardiac damage. Anti-platelet drugs are years) in patients who underwent preoperative coronary
established agents in the prevention of cardiovascular and revascularisation compared with patients who received
cerebrovascular ischaemic events. Treatment with aspirin optimised medical therapy (22% vs. 23%, relative risk: 0.98;
or clopidogrel is recommended in patients with stable 95% CI: 0.70e1.37). In the prospectively randomised
coronary artery disease to prevent cardiovascular events.47 DECREASE-V trial,52 mainly including patients with three-
Aspirin irreversibly blocks platelet cyclo-oxygenase-1 vessel coronary artery disease, comparable results to the
known to decrease the tromboxane-A2 synthesis. There- CARP trial were obtained. Although the study population in
fore aspirin reduces platelet activation and the DECREASE-V trial reflected vascular surgery patients at

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highest cardiac risk, revascularisation did not improve Conclusion


cardiovascular outcomes. The incidence of the composite
endpoint of 30-day cardiovascular mortality and MI was 43% The high prevalence and asymptomatic nature of peri-
versus 33% (odds ratio (OR) 1.4, 95% CI: 0.7e2.8). operative myocardial damage, combined with a substantial
Furthermore, no benefit was observed during 1-year follow- influence on postoperative mortality of vascular surgery
up after coronary revascularisation (49 vs. 44%; OR 1.2, 95% patients, underlines the importance of early detection and
CI: 0.7e2.3; P Z 0.48). The results from these trials indi- adequate management of perioperative myocardial
cate that prophylactic coronary revascularisation of damage. With the use of preoperative cardiac risk indices,
cardiac-stable patients provides no benefit for post- high-cardiac-risk patients at risk for developing perioper-
operative outcome, with an exception for patients with left ative myocardial damage during vascular surgery can be
main coronary artery stenosis. The reasoning behind this unveiled. Routine assessment of perioperative cardiac
apparent lack of benefit could be related to the fact that troponin levels and/or continuous electrocardiogram
perioperative myocardial damage is not only caused by monitoring can detect perioperative myocardial damage in
a significant blood-flow-limiting coronary artery stenosis patients at risk. In order to reduce the risk of developing
(Type 1 MI). The perioperative stress response (evoking perioperative myocardial damage, pharmacological treat-
type 2 MI) may cause non-flow-limiting coronary plaques to ment with b-blockers, statins and aspirin has demonstrated
rupture during surgery and to become flow limiting after to exert beneficial effects. In addition, prophylactic coro-
all. This may explain why surgical or percutaneous treat- nary revascularisation does not seem to provide sufficient
ment of flow-limiting coronary plaques apparently provides extra protection in addition to pharmacological treatment.
insufficient extra protection in addition to pharmacological Future randomised, controlled trials are needed to eval-
treatment. In the most recent ESC guidelines addressing uate if remote ischaemic preconditioning or treatment with
perioperative care, it is only recommended to consider clopidogrel may serve as novel preventive treatment
prophylactic revascularisation in patients undergoing high- strategies to reduce asymptomatic myocardial damage
risk surgery, such as lower extremity revascularisation or during vascular surgery.
open abdominal aortic surgery, with proven ischaemic
heart disease (Class IIb, level of evidence B).42
Conflict of Interest/Funding
Future perspective: is there a role for remote ischemic
preconditioning? None
Because prophylactic coronary revascularization had not
proven to be successful, there remains a need for alter-
native strategies to protect the myocardium during vascular
Refrence
surgery. Research performed by Przyklenk et al. in a canine
1 Ardehali A, Ports TA. Myocardial oxygen supply and demand.
heart models demonstrated that brief occlusions of a coro-
Chest 1990;98(3):699e705.
nary artery may protect the myocardial bed supplied by
2 Thygesen K, Alpert JS, White HD. Universal definition of
that coronary artery from prolonged ischemia.56 In addi- myocardial infarction. J Am Coll Cardiol 2007;50(22):2173e95.
tion, Gho et al. demonstrated that brief ischemia in 3 Mangano DT. Perioperative cardiac morbidity. Anesthesiology
‘‘remote’’ organs (i.e. after occlusion of the anterior 1990;72(1):153e84.
mesenteric artery or left renal artery) protects the 4 Mangano DT. Perioperative medicine: NHLBI working group
myocardium against infarction as effectively as myocardial deliberations and recommendations. J Cardiothorac Vasc
preconditioning, described by Przyklenk et al.57 Therefore, Anesth 2004;18(1):1e6.
brief ischemia followed by reperfusion in one organ may 5 Priebe HJ. Perioperative myocardial infarctioneaetiology and
provide systemic protection from prolonged ischemia in prevention. Br J Anaesth 2005;95(1):3e19.
6 Dawood MM, Gutpa DK, Southern J, Walia A, Atkinson JB,
another organ. In the patients undergoing abdominal
Eagle KA. Pathology of fatal perioperative myocardial infarc-
aneurysm repair remote ischemic preconditioning has been
tion: implications regarding pathophysiology and prevention.
evaluated as well. Ali et al. included eighty-two patients International Journal of Cardiology 1996;57(1):37e44.
which were randomized to conventional abdominal aortic 7 Cohen MC, Aretz TH. Histological Analysis of Coronary Artery
aneurysm repair (control) and abdominal aortic aneurysm Lesions in Fatal Postoperative Myocardial Infarction. Cardio-
repair with remote ischemic preconditioning.58 Two cycles vascular Pathology 1999;8(3):133e9.
of intermittent cross clamping of the common iliac artery 8 Schrier RW, Ecder T. Gibbs memorial lecture. Unifying hypoth-
with 10 minutes ischemia followed by 10 minutes reperfu- esis of body fluid volume regulation: implications for cardiac
sion served as the remote ischemic preconditioning stim- failure and cirrhosis. Mt Sinai J Med 2001;68(6):350e61.
ulus. The authors found that remote ischemic 9 Doesch AO, Celik S, Ehlermann P, Frankenstein L, Zehelein J,
Koch A, Katus HA, Dengler TJ. Heart rate reduction after heart
preconditioning reduced the incidence of postoperative
transplantation with beta-blocker versus the selective If channel
myocardial injury, MI, and renal impairment. In addition, in
antagonist ivabradine. Transplantation 2007;84(8):988e96.
a small pilot study, Walsh et al. demonstrated that remote 10 Weiser TG, Regenbogen SE, Thompson KD, Haynes AB,
ischemic preconditioning reduced urinary biomarkers of Lipsitz SR, Berry WR, Gawande AA. An estimation of the global
renal injury in patients undergoing elective endovascular volume of surgery: a modelling strategy based on available
abdominal aneurysm repair.59 However, the authors point data. Lancet 2008;372(9633):139e44.
out that future large scale trials are needed to determine 11 Boersma E, Kertai MD, Schouten O, Bax JJ, Noordzij P,
the effect of remote ischemic preconditioning on the Steyerberg EW, Schinkel AF, van Santen M, Simoons ML,
occurrence of major adverse cardiac events. Thomson IR, Klein J, van Urk H, Poldermans D. Perioperative

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cardiovascular mortality in noncardiac surgery: validation of 27 Flu WJ, van Kuijk JP, Voute MT, Kuiper R, Verhagen HJ, Bax JJ,
the Lee cardiac risk index. Am J Med 2005;118(10):1134e41. Poldermans D. Asymptomatic low ankle-brachial index in
12 Elkouri S, Gloviczki P, McKusick MA, Panneton JM, Andrews J, vascular surgery patients: a predictor of perioperative
Bower TC, Noel AA, Harmsen WS, Hoskin TL, Cherry K. Peri- myocardial damage. Eur J Vasc Endovasc Surg;39(1):62e69.
operative complications and early outcome after endovascular 28 Ali ZA, Callaghan CJ, Ali AA, Sheikh AY, Akhtar A, Pavlovic A,
and open surgical repair of abdominal aortic aneurysms. J Vasc Nouraei SA, Dutka DP, Gaunt ME. Perioperative myocardial
Surg 2004;39(3):497e505. injury after elective open abdominal aortic aneurysm repair
13 Brown OW, Hollier LH, Pairolero PC, Kazmier FJ, McCready RA. predicts outcome. Eur J Vasc Endovasc Surg 2008;35(4):413e9.
Abdominal aortic aneurysm and coronary artery disease. Arch 29 McFalls EO, Ward HB, Moritz TE, Apple FS, Goldman S,
Surg 1981;116(11):1484e8. Pierpont G, Larsen GC, Hattler B, Shunk K, Littooy F, Santilli S,
14 Hertzer NR, Beven EG, Young JR, O’Hara PJ, Ruschhaupt 3rd WF, Rapp J, Thottapurathu L, Krupski W, Reda DJ, Henderson WG.
Graor RA, Dewolfe VG, Maljovec LC. Coronary artery disease in Predictors and outcomes of a perioperative myocardial infarc-
peripheral vascular patients. A classification of 1000 coronary tion following elective vascular surgery in patients with docu-
angiograms and results of surgical management. Ann Surg 1984; mented coronary artery disease: results of the CARP trial. Eur
199(2):223e33. Heart J 2008;29(3):394e401.
15 Ouyang P, Gerstenblith G, Furman WR, Golueke PJ, Gottlieb SO. 30 Schouten O, Dunkelgrun M, Feringa HH, Kok NF, Vidakovic R,
Frequency and significance of early postoperative silent Bax JJ, Poldermans D. Myocardial damage in high-risk patients
myocardial ischemia in patients having peripheral vascular undergoing elective endovascular or open infrarenal abdominal
surgery. Am J Cardiol 1989;64(18):1113e6. aortic aneurysm repair. Eur J Vasc Endovasc Surg 2007;33(5):
16 Utoh J, Goto H, Hirata T, Hara M, Kitamura N. Routine coronary 544e9.
angiography prior to abdominal aortic aneurysm repair: inci- 31 Barbagallo M, Casati A, Spadini E, Bertolizio G, Kepgang L,
dence of silent coronary artery disease. Panminerva Med 1998; Tecchio T, Salcuni P, Rolli A, Orlandelli E, Rossini E, Fanelli G.
40(2):107e9. Early increases in cardiac troponin levels after major vascular
17 Adams 3rd JE, Sicard GA, Allen BT, Bridwell KH, Lenke LG, surgery is associated with an increased frequency of delayed
Davila-Roman VG, Bodor GS, Ladenson JH, Jaffe AS. Diagnosis of cardiac complications. J Clin Anesth 2006;18(4):280e5.
perioperative myocardial infarction with measurement of 32 Abraham N, Lemech L, Sandroussi C, Sullivan D, May J. A
cardiac troponin I. N Engl J Med 1994;330(10):670e4. prospective study of subclinical myocardial damage in endo-
18 Landesberg G, Mosseri M, Zahger D, Wolf Y, Perouansky M, vascular versus open repair of infrarenal abdominal aortic
Anner H, Drenger B, Hasin Y, Berlatzky Y, Weissman C. aneurysms. J Vasc Surg 2005;41(3):377e80. discussion 380e
Myocardial infarction after vascular surgery: the role of pro- 371.
longed stress-induced, ST depression-type ischemia. J Am Coll 33 Le Manach Y, Perel A, Coriat P, Godet G, Bertrand M, Riou B.
Cardiol 2001;37(7):1839e45. Early and delayed myocardial infarction after abdominal aortic
19 Landesberg G, Shatz V, Akopnik I, Wolf YG, Mayer M, Berlatzky Y, surgery. Anesthesiology 2005;102(5):885e91.
Weissman C, Mosseri M. Association of cardiac troponin, CK-MB, 34 Kim LJ, Martinez EA, Faraday N, Dorman T, Fleisher LA,
and postoperative myocardial ischemia with long-term survival Perler BA, Williams GM, Chan D, Pronovost PJ. Cardiac troponin
after major vascular surgery. J Am Coll Cardiol 2003;42(9): I predicts short-term mortality in vascular surgery patients.
1547e54. Circulation 2002;106(18):2366e71.
20 Landesberg G, Luria MH, Cotev S, Eidelman LA, Anner H, 35 Haggart PC, Adam DJ, Ludman PF, Bradbury AW. Comparison of
Mosseri M, Schechter D, Assaf J, Erel J, Berlatzky Y. Importance of cardiac troponin I and creatine kinase ratios in the detection of
long-duration postoperative ST-segment depression in cardiac myocardial injury after aortic surgery. Br J Surg 2001;88(9):
morbidity after vascular surgery. Lancet 1993;341(8847):715e9. 1196e200.
21 Fleisher LA, Nelson AH, Rosenbaum SH. Postoperative myocar- 36 Andrews N, Jenkins J, Andrews G, Walker P. Using postoperative
dial ischemia: etiology of cardiac morbidity or manifestation of cardiac Troponin-I (cTi) levels to detect myocardial ischaemia
underlying disease? J Clin Anesth 1995;7(2):97e102. in patients undergoing vascular surgery. Cardiovasc Surg 2001;
22 Landesberg G, Mosseri M, Shatz V, Akopnik I, Bocher M, Mayer M, 9(3):254e65.
Anner H, Berlatzky Y, Weissman C. Cardiac troponin after major 37 Godet G, Dumerat M, Baillard C. Ben Ayed S, Bernard MA,
vascular surgery: the role of perioperative ischemia, preoper- Bertrand M, Kieffer E, Coriat P. Cardiac troponin I is reliable
ative thallium scanning, and coronary revascularization. J Am with immediate but not medium-term cardiac complications
Coll Cardiol 2004;44(3):569e75. after abdominal aortic repair. Acta Anaesthesiol Scand 2000;
23 Mangano DT, Browner WS, Hollenberg M, London MJ, Tubau JF, 44(5):592e7.
Tateo IM. Association of perioperative myocardial ischemia with 38 Jamieson WR, Janusz MT, Miyagishima RT, Gerein AN. Influence
cardiac morbidity and mortality in men undergoing noncardiac of ischemic heart disease on early and late mortality after
surgery. The Study of Perioperative Ischemia Research Group. N surgery for peripheral occlusive vascular disease. Circulation
Engl J Med 1990;323(26):1781e8. 1982;66(2 Pt 2):I92eI97.
24 London MJ, Hollenberg M, Wong MG, Levenson L, Tubau JF, 39 Raby KE, Goldman L, Cook EF, Rumerman J, Barry J,
Browner W, Mangano DT. Intraoperative myocardial ischemia: Creager MA, Selwyn AP. Long-term prognosis of myocardial
localization by continuous 12-lead electrocardiography. Anes- ischemia detected by Holter monitoring in peripheral vascular
thesiology 1988;69(2):232e41. disease. Am J Cardiol 1990;66(19):1309e13.
25 Bursi F, Babuin L, Barbieri A, Politi L, Zennaro M, Grimaldi T, 40 Pasternack PF, Grossi EA, Baumann FG, Riles TS, Lamparello PJ,
Rumolo A, Gargiulo M, Stella A, Modena MG, Jaffe AS. Vascular Giangola G, Primis LK, Mintzer R, Imparato AM. Beta blockade to
surgery patients: perioperative and long-term risk according to decrease silent myocardial ischemia during peripheral vascular
the ACC/AHA guidelines, the additive role of post-operative surgery. Am J Surg 1989;158(2):113e6.
troponin elevation. Eur Heart J 2005;26(22):2448e56. 41 Kertai MD, Boersma E, Klein J, Van Urk H, Bax JJ, Poldermans D.
26 Bolliger D, Seeberger MD, Lurati Buse GA, Christen P, Rupinski B, Long-term prognostic value of asymptomatic cardiac troponin T
Gurke L, Filipovic M. A preliminary report on the prognostic elevations in patients after major vascular surgery. Eur J Vasc
significance of preoperative brain natriuretic peptide and Endovasc Surg 2004;28(1):59e66.
postoperative cardiac troponin in patients undergoing major 42 Winkel TA, Schouten O, van Kuijk JP, Verhagen HJ, Bax JJ,
vascular surgery. Anesth Analg 2009;108(4):1069e75. Poldermans D. Perioperative asymptomatic cardiac damage

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(2010), doi:10.1016/j.ejvs.2010.03.014
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after endovascular abdominal aneurysm repair is associated 51 Patrono C. Aspirin as an antiplatelet drug. N Engl J Med 1994;
with poor long-term outcome. J Vasc Surg; 2009. 330(18):1287e94.
43 Kannel WB, Abbott RD. Incidence and prognosis of unrecognized 52 Collaborative overview of randomised trials of antiplatelet
myocardial infarction. An update on the Framingham study. N therapyeI. Prevention of death, myocardial infarction, and
Engl J Med 1984;311(18):1144e7. stroke by prolonged antiplatelet therapy in various categories
44 Lopez-Sendon J, Swedberg K, McMurray J, Tamargo J, of patients. Antiplatelet Trialists’ Collaboration. Bmj 1994;
Maggioni AP, Dargie H, Tendera M, Waagstein F, Kjekshus J, 308(6921):81e106.
Lechat P, Torp-Pedersen C. Task ForceOn Beta-Blockers of the 53 Coukell AJ, Markham A. Clopidogrel. Drugs 1997;54(5):745e50.
European Society of C. Expert consensus document on beta- discussion 751.
adrenergic receptor blockers. Eur Heart J 2004;25(15):1341e62. 54 McFalls EO, Ward HB, Moritz TE, Goldman S, Krupski WC,
45 Warltier DC, Pagel PS, Kersten JR. Approaches to the prevention Littooy F, Pierpont G, Santilli S, Rapp J, Hattler B, Shunk K,
of perioperative myocardial ischemia. Anesthesiology 2000; Jaenicke C, Thottapurathu L, Ellis N, Reda DJ, Henderson WG.
92(1):253e9. Coronary-artery revascularization before elective major
46 Kukin ML. Beta-blockers in chronic heart failure: considerations vascular surgery. N Engl J Med 2004;351(27):2795e804.
for selecting an agent. Mayo Clin Proc 2002;77(11):1199e206. 55 Poldermans D, Schouten O, Vidakovic R, Bax JJ, Thomson IR,
47 Poldermans D, Bax JJ, Boersma E, De Hert S, Eeckhout E, Hoeks SE, Feringa HH, Dunkelgrun M, de Jaegere P, Maat A, van
Fowkes G, Gorenek B, Hennerici MG, Iung B, Kelm M, Sambeek MR, Kertai MD, Boersma E, Group DS. A clinical
Kjeldsen KP, Kristensen SD, Lopez-Sendon J, Pelosi P, Philippe F, randomized trial to evaluate the safety of a noninvasive
Pierard L, Ponikowski P, Schmid JP, Sellevold OF, Sicari R, Van approach in high-risk patients undergoing major vascular
den Berghe G, Vermassen F, Hoeks SE, Vanhorebeek I. Task surgery: the DECREASE-V Pilot Study. J Am Coll Cardiol 2007;
Force for Preoperative Cardiac Risk Assessment and Perioper- 49(17):1763e9.
ative Cardiac Management in Non-cardiac Surgery ESoC, Euro- 56 Przyklenk K, Bauer B, Ovize M, Kloner RA, Whittaker P. Regional
pean Society of A. Guidelines for pre-operative cardiac risk ischemic ’preconditioning’ protects remote virgin myocardium
assessment and perioperative cardiac management in non- from subsequent sustained coronary occlusion. Circulation
cardiac surgery: the Task Force for Preoperative Cardiac Risk 1993;87(3):893e9.
Assessment and Perioperative Cardiac Management in Non- 57 Gho BC, Schoemaker RG, van den Doel MA, Duncker DJ,
cardiac Surgery of the European Society of Cardiology (ESC) and Verdouw PD. Myocardial protection by brief ischemia in
endorsed by the European Society of Anaesthesiology (ESA). Eur noncardiac tissue. Circulation 1996;94(9):2193e200.
Heart J 2009;30(22):2769e812. 58 Ali ZA, Callaghan CJ, Lim E, Ali AA, Nouraei SA, Akthar AM,
48 Liao JK. Clinical implications for statin pleiotropy. Curr Opin Boyle JR, Varty K, Kharbanda RK, Dutka DP, Gaunt ME. Remote
Lipidol 2005;16(6):624e9. ischemic preconditioning reduces myocardial and renal injury
49 Kapoor AS, Kanji H, Buckingham J, Devereaux PJ, McAlister FA. after elective abdominal aortic aneurysm repair: a randomized
Strength of evidence for perioperative use of statins to reduce controlled trial. Circulation 2007;116(11 Suppl):I98e105.
cardiovascular risk: systematic review of controlled studies. 59 Walsh SR, Boyle JR, Tang TY, Sadat U, Cooper DG, Lapsley M,
Bmj 2006;333(7579):1149. Norden AG, Varty K, Hayes PD, Gaunt ME. Remote ischemic
50 JBS 2. Joint British Societies’ guidelines on prevention of preconditioning for renal and cardiac protection during endo-
cardiovascular disease in clinical practice. Heart 2005; vascular aneurysm repair: a randomized controlled trial. J
91(Suppl. 5):v1e52. Endovasc Ther 2009;16(6):680e9.

Please cite this article in press as: Flu W, et al., Perioperative Cardiac Damage in Vascular Surgery Patients, Eur J Vasc Endovasc Surg
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