High thoracic epidural anesthesia and coronary artery disease
in surgical and non-surgical patients
Julian Alvareza, Beatriz Hernándeza and Peter G. Atanassoff b
Purpose of review
Even though high thoracic epidural anesthesia has been
shown to be highly efficacious in the control of symptoms in
refractory angina, its general use is still restricted. In
patients who undergo coronary revascularization, however,
the technique is becoming more and more popular. The
present review outlines the use of high thoracic epidural
anesthesia in patients with ischemic heart disease who
underwent coronary revascularization in order to further
reveal high thoracic epidural anesthesia’s low complication
rate and to analyze why physicians still refrain from using it
more frequently.
Recent findings
The incidence of severe hemodynamic complications after
high thoracic epidural anesthesia is low in patients with
coronary artery disease. The main advantage would be a
myocardial sympathectomy leading to an improvement in
the oxygen input–demand relationship. Likewise, a
decrease in mortality due to respiratory complications could
not be shown. In patients undergoing myocardial
revascularization with full anticoagulation there is an
increased risk of epidural hematoma formation. Its precise
risk is difficult to evaluate. There is an overall low rate of
epidural hematomas as a result of high thoracic epidural
anesthesia. With the available data, the incidence has been
estimated at between 1/1500 and 1/10 000.
Summary
Epidural anesthesia does not decrease mortality or the
incidence of myocardial infarction after coronary artery
bypass grafting. It reduces the incidence of arrhythmias and
respiratory complications and improves the quality of
analgesia. High thoracic epidural anesthesia has been
shown to be a safe and efficient technique for refractory
angina that reduces the frequency of ischemic events and
improves the clinical condition of patients.
Keywords
coronary artery bypass grafting, coronary artery disease,
high thoracic epidural anesthesia, refractory angina
Curr Opin Anaesthesiol 18:501–506. ß 2005 Lippincott Williams & Wilkins.
a
Department of Anesthesia, University Hospital, Santiago de Compostela, Spain
and bDepartment of Anesthesiology, Yale University School of Medicine,
New Haven, Connecticut, USA
Correspondence to Julian Alvarez, Professor and Head, Department of Anesthesia,
University Hospital, Avda. Choupana s/n 15706 Santiago de Compostela, Spain
Tel: +34 981 950 674; fax: +34 981 950 634;
e-mail: julian.alvarez.escudero@sergas.es
Current Opinion in Anaesthesiology 2005, 18:501–506
Abbreviations
CABG coronary artery bypass grafting
HTEA high thoracic epidural anesthesia
ß 2005 Lippincott Williams & Wilkins
0952-7907
Introduction
Treatment of angina pectoris in patients with coronary
artery disease includes medical therapy or revasculari-
zation, coronary artery bypass grafting (CABG) surgery or
percutaneous coronary intervention [1]. Patients with
refractory unstable angina present a problem [2], in that
they are refractory to conventional medical therapy.
High thoracic epidural anesthesia (HTEA) may be an
interesting technique for the management of these
patients due to its well-known analgesic and hemody-
namic effects. So far, the technique has been adminis-
tered in patients with ischemic heart disease under two
different sets of circumstances: when angina pectoris
does not respond to any other kind of treatment, neither
medical nor surgical, or when the patient undergoes a
coronary revascularization, in which case the HTEA
significantly improves pain relief and the postoperative
complication rate, primarily respiratory ones [3].
Anatomy and physiology of cardiac
innervation: functional significance of high
neuraxial blockade
The myocardium receives sympathetic and parasym-
pathetic fibers. Preganglionic sympathetic fibers that
innervate the myocardium originate from C8 to T4. They
cross over the cervical and upper thoracic ganglia, from
where the superior, medium, and inferior cardiac sym-
pathetic fibers are released. The parasympathetic fibers
originate in the medulla oblongata and course down
within the vagal nerve. Its three branches (superior,
medium and inferior) carry preganglionic fibers that
originate in the ambiguous and in the dorsal vagal
nucleus. They join sympathetic fibers eventually creating
the cardiac plexus. This plexus envelops the aortic root
and arch near the tracheal bifurcation [4]. It is divided
into two segments: an anterior and a posterior one. In
between them, ganglions are located. The Wrissberg
ganglion is responsible for the anterior plexus and the
Pernan ganglion for the posterior one. The auricles of
the myocardium receive a sympathetic (adrenergic) and a
501
502 Regional anaesthesia
parasympathetic (cholinergic) innervation also. In con-
trast, the ventricles may not receive cholinergic inner-
vation, or it is very poor [5,6].
The cardiac performance is regulated by three funda-
mental systems [5,6]: an intrinsic regulation is based on
the Frank–Starling mechanism; a humoral regulation
enables the myocardium to respond to increased plasma
levels of catecolamines; autonomic sympathethic and
parasympathetic fibers impact cardiac performance.
HTEA basically leads to cardiac denervation. Cardiac
fibers that undergo this type of blockade lose their third
control mechanism whereas the first two remain intact.
Therefore, HTEA is usually well tolerated from a cardiac
point of view [7,8].
Sympathetic stimulation produces an increase in the dis-
charge rate of the sinus node, raises the conduction velocity
and the excitation level and increases cardiac contractility.
A full sympathetic stimulation may triple the normal
heart rate and double its contractility, thereby increasing
cardiac output accompanied by a substantial increase in
oxygen consumption. In contrast, a powerful parasympath-
etic stimulation may completely arrest the sinus node and
may block conduction through the auriculo-ventricular
node. The ventricles would then come to an arrest too.
Purkinje fibers located in the ventricular septum, however,
would then autonomically take over generating a rhythm
of 15–40 beats per minute. Parasympathetic stimulation
decreases cardiac output through decreases in cardiac
contractility (20–30%) and heart rate to 50% [9,10,11].
HTEA from T1 to T4 has been shown to reduce the heart
rate, decrease cardiac contractility and produce coronary
vasodilatation owing to a primarily sympathetic but not
parasympathetic blockade [10].
Respiratory and circulatory effects of high thoracic
epidural anesthesia
The most striking effect of HTEA is an improved pain
relief. Yet sympathetic blockade produces important car-
dio-respiratory changes, recently reviewed by Kozian et al.
[11]. Selective blockade of cardiac sympathetic fibers
may result in control of tachycardia, a contributing factor
to cardiac morbidity after surgery. HTEA provides
relief of angina, can attenuate myocardial stunning
and improves left ventricular performance by increasing
myocardial oxygen supply as well as a decrease in myo-
cardial oxygen demand.
The primary control of the heart rate is the balance
between the sympathetic and parasympathetic nervous
system. HTEA includes blockade of T1 to T4, and,
therefore, with the block fully working, a parasympa-
thetic dominance produces bradycardia. A decrease in the
sympathetic output lowers the risk of arrhythmia [12].
This was shown in pulmonary surgery [13] and in animal
models [14], in which HTEA led to a reduction of
ventricular and supra-ventricular arrhythmias due to pro-
longation of the refractory period.
Cardiac sympathetic blockade dilates stenotic coronary
arteries [15]. HTEA has no effect, however, on the
luminal diameter of normal coronary vessels [15]. This
suggests that HTEA, by not increasing myocardial blood
flow in normal coronary arteries, will not shunt blood
away from diseased vessels causing ‘coronary steal’ and
will not increase coronary artery disease related ischemia.
Furthermore, HTEA may increase myocardial blood flow
by decreasing the progressive sympathetic vasoconstric-
tion reflex, which often exists distal to a coronary stenosis
and which may exacerbate the myocardial ischemia
caused by the stenosis.
As previously outlined, HTEA lowers myocardial oxygen
demand by causing a decrease in systolic arterial pressure,
heart rate, and pulmonary capillary wedge pressure
[11]. These hemodynamic alterations do not adversely
affect coronary perfusion pressure or cardiac output, both
of which were not significantly modified by HTEA [11].
The beneficial effects of HTEA may result from altera-
tions in the myocardial oxygen supply/demand ratio by
increasing transmural myocardial coronary blood flow and
by decreasing oxygen demand. The improved myocardial
oxygen supply/demand ratio may not only decrease
ischemic events, but may also attenuate and preserve
global and regional left ventricular function as shown in
patients with coronary artery disease undergoing stress
induced myocardial ischemia [15].
An adequate postoperative analgesia is also essential to
minimize postoperative respiratory complications [11].
Pain free patients may overcome respiratory dysfunction
more easily, but many studies have demonstrated that in
postoperative pulmonary dysfunction there are other
important factors. Surgery and general anesthesia have
several effects on diaphragmatic function not directly
related to pain. Recent studies suggested a reflex inhi-
bition of phrenic nerve or diaphragmatic activation
[11,16]. On the other hand, changes in thorax wall
compliance may result in pulmonary dysfunction.
HTEA may block this inhibition reflex and improve
pulmonary function. Studies showed that epidural
analgesia improves the overall diaphragmatic function
and increases lung volumes by reversing the dia-
phragmatic dysfunction. HTEA decrease pulmonary
morbidity [16]: decreased atelectasias, pulmonary infec-
tions and increased arterial oxygen tension.
The hypoxic pulmonary vasoconstriction reflex may be
influenced by sympathetic neural blockade. Hypoxic

pulmonary vasoconstriction inhibition may increase the
degree of hypoxia. Although results of investigations are
not conclusive, it had not been clearly proven that HTEA
inhibits this reflex [11].
High thoracic epidural analgesia in ischemic
heart disease
Despite improvements in the treatment of coronary
artery disease, there continues to be a subset of patients
refractory to medical treatment and without possibilities
of surgical treatment.
Epidural analgesia for refractory angina pectoris
in non-surgical patients
These patients are usually markedly debilitated, require
frequent hospitalizations and consume significant
amounts of economic resources. A variety of treatments
such as spinal opioids, left sided stellate ganglion
blocks, surgical sympathectomy, transmyocardial laser
revascularization, enhanced external counter pulsation,
transcutaneous electrical nerve stimulator therapy, and
direct spinal cord stimulation were all administered to
improve the patients’ quality of life. Many of these
procedures, however, have significant limitations and
associated complications [17].
A number of articles exist on the use of HTEA in stable
angina [18], unstable angina and acute myocardial ische-
mia [19]. The experience with the technique for these
indications is excellent [19], and HTEA has meanwhile
become an alternative treatment for unstable angina
when conventional strategies have failed. The American
College of Cardiology and American Heart Association
have formally recognized the value of the technique and
included it in the 2002 consensus guidelines for the
management of chronic stable angina [18]. For long-term
administration, the method appears cumbersome, owing
to practical drawbacks for the patients, such as carrying an
infusion pump or administering injections [17]. There is
not much information in the scientific literature on this
issue [17].
In non-surgical patients with unstable angina, HTEA has
been shown to have favorable effects on hemodynamics
(heart rate and mean blood pressure), to induce adequate
symptom relief and thereby a reduction in frequency of
myocardial ischemic events. Stress-induced myocardial
ischemia and left ventricular function were also both
favorably influenced by thoracic epidural anesthesia
treatment [17]. The dilation of stenotic coronary arteries
induced by HTEA and its relieving effects have been
used to control pain in patients with unstable angina
[19]. Exercise tolerance improved with accompanying
reduction in ST segment depression [20]. These patients
in particular displayed a real benefit from HTEA treat-
ment improving their quality of life without worsening
High thoracic epidural anesthesia Alvarez et al. 503
their coronary artery disease [21]. A 1-year survey reported
excellent relief of unstable angina, but the method was
hampered with complications, such as infections, epidural
fibrosis, and paraspinous muscle spasms [8].
High thoracic epidural anesthesia and coronary artery
bypass grafting
There are some randomized controlled trials showing
efficacy of perioperative HTEA in CABG patients, but
the number of patients enrolled in these trials is limited.
Intense postoperative analgesia is the most evident
benefit of HTEA [15,22–35].
High central neuraxial analgesia may offer potential
benefits for patients undergoing CABG and its use com-
bined with general anesthesia has been extensively stu-
died. Results regarding outcome and possible benefits,
however, are still conflicting [3,36]. Potential benefits of
HTEA for this patient group include a favorable control of
the perioperative stress response due to an improved
analgesia with resultant improved myocardial oxygen bal-
ance and fewer arrhythmic events [3,11]. Analgesia
with HTEA reduced intravenous opioid consumption,
time to tracheal extubation, and pulmonary complications
by improving the patients’ ability to cough. There were
fewer incidents of acute renal failure and less postoperative
confusion [32]. Patients could be discharged at an earlier
time point and morbidity and mortality rates were reduced
[27]. In comparison with HTEA, intrathecal opioids offer
fewer benefits with less reduction of the stress response
and shorter duration of analgesia [3,30,32,34–39].
As is so frequently the case, the literature is conflicting.
Fillinger et al. [33] reported no differences in the inci-
dence of atrial fibrillation, in extubation times, or inten-
sive care unit stay. Berendes et al. [15] concluded that
HTEA improves regional left ventricular function and
reduced postoperative ischemia in a trial including 73
patients, in which 36 of them received general anesthesia
and HTEA. Liu et al. [3] reviewed 15 trials enrolling
1178 patients. He concluded that there were no differ-
ences in mortality or myocardial infarction rates after
coronary artery bypass grafting with central neuraxial
analgesia. HTEA did not significantly affect incidences
of mortality or myocardial infarction but reduced dys-
rhythmias, pulmonary complications, time to tracheal
extubation, and pain scores. No study currently exists
to definitively determine whether the potential benefits
of high centroneuraxis blockade outweigh the risks of
serious side effects such as epidural hematoma formation
in context with the perioperative anticoagulation of
CABG patients [40].
Mortality and myocardial infarction
Following CABG surgery, mortality (1.7%) and myo-
cardial infarction (2.4%) are relatively infrequent [41].
504 Regional anaesthesia
As previously outlined, the use of local anesthetics in
HTEA may reduce myocardial oxygen demand by
decreasing heart rate and systemic vascular resistance
[42] and improving myocardial oxygen supply by dilating
stenotic coronary arteries [43]. As such, myocardial
oxygen balance is improved thereby reducing attacks
of angina and the infarct size. Current publications
frequently lack enough power, however, to prove a
reduction in mortality and infarct incidences [3].
Dysrhythmias
Atrial fibrillation and tachycardia are frequent events
after CABG surgery. HTEA was associated with a
decreased risk of postoperative dysrhythmias [11] but
not all studies found this reduction [31]. HTEA with local
anesthetics reduces sympathetic output and blocks
cardiac sympathetic fibers as well as the stress response
to surgery. Postoperative arrhythmias were less frequent
with HTEA than with placebo [32], beta-blockers [44],
and amiodarone [45].
Pulmonary complications and tracheal extubation
HTEA was associated with a reduced risk of pneumonia
and atelectasis formation following cardiac and non-
cardiac interventions [16,25,27,35,37,46–48]. These find-
ings may result from faster tracheal extubation times as
well as reduced pain on respiration permitting near-
normal thorax extensions. Tracheal extubation time after
CABG was found to be dependent on various factors such
as adequate analgesia and the patient’s volume status.
Clinically, however, a few hours of faster extubation time
were of no major advantage [49–54].
Complications and contraindications
The most serious complication of HTEA is epidural
hematoma formation in anticoagulated patients. A further
adverse effect is hypotension due to a decreased preload
if sympathectomy extends beyond a T1–T5 dermatomal
level. For this reason, some authors make sure with the
help of an epidurogram that the position of the epidural
catheter tip is at the T1–T3 level [2]. There is also a
report of ischemia with ST segment elevation during
thoracic surgery under HTEA, which was attributed to
coronary vasospasm as a result of unopposed vagal tone
[2]. An acute abdomen masked by the epidural analgesic
was described in the literature but this is a rather rare
event [55].
Epidural hematoma
Epidural hematoma is an uncommon but serious com-
plication following epidural catheter placement in
patients undergoing antiplatelet or systemic anticoagula-
tion therapy. Spinal cord ischemia with subsequent para-
plegia may result from spinal cord compression. The risk
of epidural hematoma is different in patients with full
anticoagulation for cardiopulmonary bypass compared
with those with refractory angina under antiplate-
let drugs. The risks and benefits of central neuraxial
analgesia in the fully anticoagulated patient for cardio-
pulmonary bypass remains unclear and the guidelines
from the American Society of Regional Anesthesia and
Pain Medicine (ASRA) do not offer any recommenda-
tions [56]. A predicted probability may range between
1:1528 for epidural and 1:3610 for spinal anesthetic
techniques [40] or less than one in 10 000 procedures
[57]. In their current guidelines, ASRA estimates the risk
of epidural hematoma in non-cardiac surgery to be
1:150 000 with epidural anesthesia and 1:220 000 with
spinal anesthesia.
In patients with refractory angina, the contribution of
antiplatelet drugs to the risk of epidural hematoma for-
mation appears minimal [58]. When these non-surgical
patients receive intravenous anticoagulation, intravenous
heparin must be stopped 24 h before catheter insertion.
An increased risk of myocardial infarction, however, in
patients with unstable angina following the removal of
the heparin infusion, albeit temporarily, needs to be
taken into consideration [2].
Conclusion
Continuous blockade of cardiac sympathetic fibers by
epidural infusion of local anesthetics in patients with
unstable angina reduced the incidence of myocardial
ischemia, decreased the number and duration of ischemic
episodes, and reduced the number of anginal attacks
when compared with those with conventional medical
treatment. In addition, HTEA further decreased
the heart rate in patients with b-adrenergic receptor
blockade, while no effect on arterial blood pressure
was seen.
HTEA has shown to be an accepted method for the
treatment of patients with unstable angina. Following
CABG surgery it did not affect significantly incidences of
myocardial infarction or mortality rates. HTEA reduced
the risk of postoperative dysrhythmias owing to a favor-
able impact on the myocardial oxygen consumption.
Time to extubation was shown to be similar with HTEA
as conventional cardiac anesthesia techniques. With full
systemic anticoagulation, the risk of epidural hematoma
may be near to one in 10 000 patients.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
 of special interest
 of outstanding interest
1 Fihn SD, Williams SW, Daley J, et al. Guidelines for the management of
patients with chronic stable angina: treatment. Ann Intern Med 2001;
135:616–632.
2 Overdyk FJ, Gramling-Babb P, Handy J, et al. Thoracic epidural anesthesia as
the last option for treating angina in a patient before coronary artery bypass
surgery. Anesth Analg 1997; 84:213–215.

3 Liu SS, Block BM, Wu LW. Effects of perioperative central neuraxial analgesia
 on outcome after coronary artery bypass surgery. A meta-analysis. Anesthe-
siology 2004; 101:153–161.
Reading of this meta-analysis is highly recommended because it is a review of
randomized trials about epidural anesthesia in myocardial revascularization. It
provides a surprising result as it shows that so far there is no change in mortality
and ischemic events.
4 Riedel BJ, Wright IG. Epidural anesthesia in coronary artery bypass grafting
surgery. Curr Opin Cardiol 1997; 12:515–521.
5 Eckberg DL. Sympathovagal balance: a critical appraisal. Circulation 1997;
96:3224–3232.
6 Malliani A, Pagani M, Ontano N, Mela S. Sympathovagal balance: a
reappraisal. Circulation 1998; 98:2640–2643.
7 Fawcett WJ, Edwards RE, Quinn AC, et al. Thoracic epidural analgesia
started after cardiopulmonary bypass. Adrenergic; cardiovascular and res-
piratory sequelae. Anaesthesia 1997; 52:294–299.
8 Gramling-Babb PM, Miller MJ, Reeves ST, et al. Treatment of medically and
surgically refractory angina pectoris with high thoracic epidural analgesia:
Initial clinical experience. Am Heart J 1997; 134:648–655.
9 Kaufman H. Primary autonomic failure: three clinical presentations of one
disease? Ann Intern Med 2000; 133:382–384.
10 Magnusdottir H, Kirno K, Ricksten SE, et al. High thoracic epidural anesthesia
does not inhibit sympathetic nerve activity in the lower extremities. Anes-
thesiology 1999; 91:1299–1304.
11 Kozian A, Schilling T, Hachenberg T. Non analgesic effects of thoracic
 epidural anaesthesia. Curr Opin Anesth 2005; 18:29–34.
This is a very recommendable review, in which the non-analgesic effects of thoracic
epidural anesthesia are analyzed.
12 Scout NB, Turfrey DJ, Ray DA, et al. A prospective randomized study of the
potential benefits of thoracic epidural anesthesia on outcome after coronary
artery bypass grafting. Anesth Analg 2001; 93:528–535.
13 Oka T, Ozawa Y, Ohkubo Y. Thoracic epidural bupivacaine attenuates
supraventricular tachyarrhythmias after pulmonary resection. Anesth Analg
2001; 93:253–259.
14 Meissner A, Eckardt L, Kirchhof P, et al. Effects of thoracic epidural anesthesia
with and without autonomic nervous system blockade on cardiac monophasic
action potentials and effective refractoriness in awake dogs. Anesthesiology
2001; 95:132–138.
15 Berendes E, Schidt C, Van Aken H, et al. Reversible cardiac sympathectomy
by high epidural anesthesia improves regional left ventricular function in
patients undergoing coronary artery bypass grafting: a randomized trial.
Arch Surg 2003; 138:1283–1290.
16 Ballantyne JC, Carr DB, deFerranti S, et al. The comparative effects of
postoperative analgesic therapies on pulmonary outcome: Cumulative
meta-analyses of randomized controlled trials. Anesth Analg 1998; 86:
598–612.
17 Mannheimer C, Camici P, Chester MR, et al. The problem of chronic refractory
angina. Report from the ESC Joint Study Group on the Treatment of
Refractory Angina. Eur Heart J 2002; 23:355–370.
18 Gibbons RJ, Abrams J, Chatterjee K, et al. ACC/AHA 2002 guideline update
for the management of patients with chronic stable angina: summary article: a
report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines (Committee on the Management of
Patients With Chronic Stable Angina). Circulation 2003; 107:149–158.
19 Olausson K, Magnusdottir H, Lurje L, et al. Anti-ischemic and anti-anginal
effects of thoracic epidural anesthesia versus those of conventional medical
therapy in the treatment of severe refractory unstable angina pectoris.
Circulation 1997; 96:2178–2182.
20 Kock M, Blomberg S, Emanuelsson H, et al. Thoracic epidural anesthesia
improves global and regional left ventricular function during stress-induced
myocardial ischemia in patients with coronary artery disease. Anesth Analg
1990; 71:625–630.
21 Richter A, Cederholm I, Jonasson L, et al. Effect of thoracic epidural analgesia
on refractory angina pectoris: long-term home self-treatment. J Cardiothorac
Vasc Anesth 2002; 16:679–684.
22 El-Baz N, Goldin M. Continuous epidural infusion of morphine for pain relief
after cardiac operations. J Thorac Cardiovasc Surg 1987; 93:878–883.
23 Rein KA, Stenseth R, Myhre HO, et al. The influence of thoracic epidural
analgesia on transcapillary fluid balance in subcutaneous tissue: A study in
patients undergoing aortocoronary bypass surgery. Acta Anaesthesiol Scand
1989; 33:79–83.
24 Liem TH, Hasenbos MA, Booij LH, et al. Coronary artery bypass grafting using
two different anesthetic techniques: II. Postoperative outcome. J Cardiothorac
Vasc Anesth 1992; 6:156–161.
High thoracic epidural anesthesia Alvarez et al. 505
25 Stenseth R, Bjella L, Berg EM, et al. Thoracic epidural analgesia in aortocor-
onary bypass surgery: I. Haemodynamic effects. Acta Anaesthesiol Scand
1994; 38:826–833.
26 Moore CM, Cross MH, Desborough JP, et al. Hormonal effects of thoracic
extradural analgesia for cardiac surgery. Br J Anaesth 1995; 75:387–
393.
27 Stenseth R, Bjella L, Berg EM, et al. Effects of thoracic epidural analgesia on
pulmonary function after coronary artery bypass surgery. Eur J Cardiothorac
Surg 1996; 10:859–865.
28 Brix-Christensen V, Tonnesen E, Sorensen IJ, et al. Effects of anaesthesia
based on high versus low doses of opioids on the cytokine and acute-phase
protein responses in patients undergoing cardiac surgery. Acta Anaesthesiol
Scand 1998; 42:63–70.
29 Loick HM, Schmidt C, Van Aken H, et al. High thoracic epidural anesthesia,
but not clonidine, attenuates the perioperative stress response via sympatho-
lysis and reduces the release of troponin T in patients undergoing coronary
artery bypass grafting. Anesth Analg 1999; 88:701–709.
30 Tenling A, Joachimsson PO, Tyden H, et al. Thoracic epidural anesthesia
as an adjunct to general anesthesia for cardiac surgery: Effects on
ventilation-perfusion relationships. J Cardiothorac Vasc Anesth 1999; 13:
258–264.
31 Jideus L, Joachimsson PO, Stridsberg M, et al. Thoracic epidural anesthesia
does not influence the occurrence of postoperative sustained atrial fibrillation.
Ann Thorac Surg 2001; 72:65–71.
32 Scott NB, Turfrey DJ, Ray DA, et al. A prospective randomized study of the
potential benefits of thoracic epidural anesthesia and analgesia in patients
undergoing coronary artery bypass grafting. Anesth Analg 2001; 93:528–
535.
33 Fillinger MP, Yeager MP, Dodds TM, et al. Epidural anesthesia and analgesia:
Effects on recovery from cardiac surgery. J Cardiothorac Vasc Anesth 2002;
16:15–20.
34 Priestley MC, Cope L, Halliwell R, et al. Thoracic epidural anesthesia for
cardiac surgery: The effects on tracheal intubation time and length of hospital
stay. Anesth Analg 2002; 94:275–282.
35 Royse C, Royse A, Soeding P, et al. Prospective randomized trial of high
thoracic epidural analgesia for coronary artery bypass surgery. Ann Thorac
Surg 2003; 75:93–100.
36 Luca Salvi L, Sisillo E, Brambillasca C, et al. High thoracic epidural anesthesia
for off-pump coronary artery bypass surgery. J Cardiothor Vasc Anesth 2004;
18:256–262.
37 Canto-Pastor M, Sanchez J, Casas MA, et al. Thoracic epidural analgesia in
coronary artery bypass graft surgery: seven years’ experience. J Cardiothor
Vasc Anesth 2003; 17:154–159.
38 Barrington MJ, Kluger R, Watson R, et al. Epidural anesthesia for coronary
artery bypass surgery compared with general anesthesia alone does not
reduce biochemical markers of myocardial damage. Anesth Analg 2005;
100:921–928.
39 Kendall JB, Russell GN, Scawn ND, et al. A prospective randomised single-
blind pilot study to determine the effects of anesthetic technique on troponina
T release after after off-pump coronary artery surgery. Anaesthesia 2004;
59:545–549.
40 Ho AM, Chung DC, Joynt GM. Neuraxial blockade and hematoma in cardiac
surgery: Estimating the risk of a rare adverse event that has not (yet) occurred.
Chest 2000; 117:551–555.
41 Nalysnyk L, Fahrbach K, Reynolds MW, et al. Adverse events in coronary
artery bypass graft (CABG) trials: A systematic review and analysis. Heart
2003; 89:767–772.
42 Gramling-Babb PM, Zile MR, Reeves ST. Preliminary report on high thoracic
epidural analgesia: Relationship between its therapeutic effects and myocar-
dial blood flow as assessed by stress thallium distribution. J Cardiovasc Vasc
Anesth 2000; 14:657–661.
43 Meissner A, Rolf N, Van Aken H. Thoracic epidural anesthesia and the patient
with heart disease: Benefits, risks, and controversies. Anesth Analg 1997;
85:517–528.
44 Connolly SJ, Cybulsky I, Lamy A, et al. Doubleblind, placebo-controlled,
randomized trial of prophylactic metoprolol for reduction of hospital length
of stay after heart surgery: The beta-blocker length of stay (BLOS) study.
Am Heart J 2003; 145:226–232.
45 Yazigi A, Rahbani P, Zeid HA, et al. Postoperative oral amiodarone as
prophylaxis against atrial fibrillation after coronary artery surgery. J Cardio-
thorac Vasc Anesth 2002; 16:603–606.
46 Rodgers A, Walker N, Schug S, et al. Reduction of postoperative mortality
and morbidity with epidural or spinal anaesthesia: Results from overview of
randomised trials. BMJ 2000; 321:1493–1505.
506 Regional anaesthesia
47 Straka Z, Brucek P, Vanek T, et al. Routine immediate extubation for off-pump
coronary artery bypass grafting without thoracic epidural analgesia. Ann
Thorac Surg 2002; 74:1544–1547.
48 Hemmerling TM, Prieto I, Choiniere JL, et al. Ultra-fast-track anesthesia in
off-pump coronary artery bypass grafting: a prospective audit comparing
opioid-based anesthesia vs thoracic epidural-based anesthesia. Can J
Anaesth 2004; 51:163–168.
49 Myles PS, Daly DJD, Djaiani G, et al. A systematic review of the safety and
effectiveness of fast-track cardiac anesthesia. Anesthesiology 2003;
99:982–987.
50 Brucek PJ, Straka Z, Vanek T, Jares M. Less invasive cardiac anesthesia: an
ultra-fast-track procedure avoiding thoracic epidural analgesia. Heart Surg
Forum 2003; 6:E107–E110.
51 Nierich AP, Diephuis J, Jansen EW, et al. Embracing the heart: perioperative
management of patients undergoing off-pump coronary artery bypass grafting
using the Octopus Tissue Stabilizer. J Cardiothorac Vasc Anesth 1999;
13:123–129.
52 Djaiani GN, Ali M, Heinrich L, et al. Ultra-fast-track anesthetic technique faci-
litates operating room extubation in patients undergoing off-pump coronary
revascularization surgery. J Cardiothorac Vasc Anesth 2001; 15:152–157.
53 Aybek T, Kessler P, Dogan S, et al. Awake coronary artery bypass grafting:
utopia or reality? Ann Thorac Surg 2003; 75:1165–1170.
54 Karagoz H, Sonmez B, Bakkaloglu B, et al. Coronary artery bypass grafting in
the conscious patient without endotracheal general anesthesia. Ann Thorac
Surg 2000; 70:91–96.
55 Jankovic Z, Radojevic C, Neskovic V, Stamenkovic D. Acute abdomen after
coronary artery bypass surgery masked by thoracic epidural analgesia. Eur J
Anaesthesiol 2002; 19:526–528.
56 Horlocker TT, Wedel DJ, Benzon H, et al. Regional anestesia in the anti-
coagulated patient: Defining the risks (the second ASRA Consensus
Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain
Med 2003; 28:172–197.
57 Horlocker T, Wedel D, Schroeder D, et al. Preoperative antiplatelet therapy
does not increase the risk of spinal hematoma associated with regional
anesthesia. Anesth Analg 1995; 80:303–309.
58 Horlocker T, Wedel D, Schroeder D, et al. Preoperative platelet therapy does
not increase the risk of spinal hematoma associated with regional anesthesia.
Anesth Analg 1995; 80:303–309.