Chapter 7 Coronary Artery Bypass Graft Surgery
CABG for acute MI or unstable angina. (Level of
Evidence: B) [1,36].
Myocardial protection for chronically
dysfunctional myocardium
Class IIa
Blood cardioplegia is probably indicated in patients
undergoing CPB accompanying CABG in the pres-
ence of a chronically dysfunctional left ventricle.
(Level of Evidence: B) [1].
Cardiac biomarker elevation and outcome
Class IIb
Assessment of cardiac biomarkers in the fi rst 24
hours after CABG may be considered, and patients
with the highest elevations of creatine kinase-MB
(greater than fi ve times upper limits of normal) are
at increased risk of subsequent events. (Level of Evi-
dence: B)
Up to 90% of patients after CABG have some
elevation of CK-MB [37], however marked elevation
of CK-MB (5–10 times the upper limit of normal)
is associated with an adverse prognosis [1]. The
prognostic value of troponins after CABG is not as
clearly defi ned, but some data show that Troponin
T is more discriminatory than CK-MB [38]. Specifi c
attention to optimal medical therapy with antiplate-
let agents, beta-blockers, angiotensin converting
enzyme (ACE) inhibitors, and statins should be
given to the postoperative CABG patient with ele-
vated biomarkers [1].
Adjuncts to myocardial protection
Class IIa
The use of prophylactic intra-aortic balloon pump
as an adjunct to myocardial protection is probably
indicated in patients with evidence of ongoing myo-
cardial ischemia and/or patients with a subnormal
cardiac index. (Level of Evidence: B)
The benefi t of preoperative IABP placement in
high-risk patients has been demonstrated [9], and
the insertion of the IABP immediately prior to
surgery in these patients afforded similar protection
to that accompanying placement the day before
CABG [39,40].
In addition to the long-term survival benefi t
offered by use of the IMA as a conduit in CABG,
reduction in immediate operative mortality is also
achieved by its use in all subgroups analyzed in the
STS database, including the acutely ischemic patient
and the elderly [1,7,42,43]. The only subgroup
found to have similar outcomes between use/nonuse
of the IMA is the patient older than 70 undergoing
reoperative elective or nonelective CABG [1].
Reoperative patients
The use of retrograde cardioplegia techniques may
allow for reduction in atheroembolism from patent/
stenotic vein grafts encountered in reoperative
cases [1].
Inferior infarct with right ventricular (RV)
involvement
Class IIa
After infarction that leads to clinically signifi cant RV
dysfunction, it is reasonable to delay surgery for 4
weeks to allow recovery. (Level of Evidence: C)
RV failure secondary to ischemia, infarction, or
stunning, presents a hazardous situation [7]. This
patient typically has an occluded right coronary
artery proximal to major RV branches and presents
with an acute inferior infarction [1]. RV failure may
or may not be immediately recognized. In this situa-
tion, a high index of suspicion for RV dysfunction
must be raised. Physical examination of the neck
veins, monitoring of the central venous pressure
(CVP), electrocardiographic RV lead placement, or
echocardiography should be employed [1,44,45].
There is substantial risk in operating on a patient
after 4–6 hours of the onset of myocardial infarction
in a patient with RV dysfunction [1]. Recovery of
RV function usually occurs at 4 weeks after injury
[46]. The nonsurgical postinfarction patient can
most often be supported with pacing, volume
loading, and judicious inotropic administration
[47]. In the surgical setting, the RV is more diffi cult
to manage, largely secondary to loss of pericardial
constraint which allows acute dilatation of the RV
[48]. In this situation, the RV often fails to recover
despite revascularization, state-of-art myocardial
protection, and ventricular assistance [1,48]. If early
PCI of the right coronary is indicated, it should be
performed [9].
Attenuation of the systemic sequelae of CPB
Glucocorticoid administration has demonstrated
benefi t in reducing the impact of the diffuse infl am-
matory response induced by CPB [1,49]. Although