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THE ROLE OF SURGERY IN HEART FAILURE - part 9 potx

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CABG (see Table 9). This real-world experience
of a huge number of patients arguably provides
a much more reliable and realistic guide for pa-
tient treatment than the super-selected small sub-
set of patients randomized in the AWESOME
trial.
An analysis of the Canadian APPROACH
database (Alberta Provincial Project for
Outcomes Assessment in Coronary Heart Dis-
ease) [57] that began in 1995 and followed patients
for up to 7 years included 4228 patients who had
heart failure who underwent a cardiac catheteriza-
tion: 2538 patients underwent revascularization
by CABG or PCI and 1690 patients were treated
with medical management alone. No direct
comparison between CABG and PCI was made.
Risk-adjusted survival curves for CABG seem
superior to PCI (adjusted hazard ratio for
CABG 0.44, 95% CI 0.38–0.52 versus 0.58 for
PCI, 95% CI 0.49–0.69, both calculated against
medical management group) (Fig. 12).
Surgical revascularization for patients who
have low LVEF remains a challenging procedure
and in general should be attempted in centers able
and willing to provide mechanical assist or heart
transplant services. The oft-cited operative mor-
tality of 5% to 8% is the mortality of centers with
significant experience in handling such patients.
Summary
From the analysis of clinical series presented
above we learn that selected patients who have low


LVEF and CAD clearly benefit from coronary
revascularization with CABG, and that CABG
offers a 5-year survival of 60% to 70% and a life
extension of close to a year at 5 years’ follow-up
compared with a strategy of initial medical man-
agement, with an average perioperative mortality
between 5% to8% in experienced hands (twice that
of patients who have normal ejection fraction).
Clinical improvement should be expected in most
patients who undergo CABG. This is important for
patients who have a limited life span thatthey could
spend with a good functional status rather than
being hospitalized for multiple repeat PCIs or
symptomatic deterioration.
Clinical variables, the use of HAVOC score,
and myocardial viability testing are tools that can
help refine patient selection. The weight the
clinical information available suggests that re-
vascularization by CABG seems to be superior
to PCI in most patients who have low ejection
fraction, particularly in patients who have low
LVEF and symptoms of angina. There are situa-
tions, however, in which PCI may be helpful, such
as in patients who have low ejection fraction and
one or more previous cardiac operations, or in
those whose severe noncardiac comorbidities
preclude major surgery.
References
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225
REVASCULARIZATION FOR HF: CORONARY BYPASS OR PCI?
Revascularization in Heart Failure: The Role
of Percutaneous Coronary Intervention
Ajay J. Kirtane, MD, SM
a,b
, Jeffrey W. Moses, MD
a,
*
a
Columbia University Medical Center, New York, NY, USA
b
Cardiovascular Research Foundation, New York, NY, USA
Ischemic heart disease is the leading cause of
heart failure in North America, accounting for

approximately two thirds of heart failure cases [1].
Patients who have ischemic heart failure suffer
from higher rates of ischemic events, arrhythmic
events, and increased mortality compared with
patients who have normal ventricular function.
Although there are inadequate clinical trial data
in this patient population, coronary revasculariza-
tion, either by way of percutaneous coronary inter-
vention (PCI) or coronary artery bypass grafting
(CABG), has the potential to provide relief of
symptoms, improve ventricular performance, and
possibly improve mortality in patients who have
potentially revascularizable and viable myocar-
dium [2–4]. Although the performance of coronary
revascularization in patients who have depressed
ventricular function is associated with a greater
overall risk for adverse periprocedural events [5–
7] compared with similar patients who have nor-
mal ventricular function, performance of PCI or
CABG in this particular subset of patients may
also be associated with the greatest absolute bene-
fit afforded through revascularization [6,8].
Criteria for revascularization in heart
failure patients
For a patient with heart failure to be consid-
ered a suitable candidate to truly benefit from
coronary revascularization, ischemic heart disease
should be at least a significant cause of the
patient’s depressed ventricular function and clin-
ical heart failure. Although this statement may

seem trite, its importance cannot be overstated.
Because coronary artery disease is so common,
patients who have cardiomyopathy of nonische-
mic origin frequently have coexistent and often
incidental coronary artery disease. Such patients
may derive some benefit from coronary revascu-
larization, but the risks of PCI and CABG,
including periprocedural adverse events and the
requirement for long-term antiplatelet therapies,
are not insignificant. The benefit of revasculariza-
tion in such patients is not likely to be as great as
for a patient who has cardiomyopathy wholly
caused by ischemic coronary artery disease.
Several factors must be present for a patient
who has ischemic cardiomyopathy to be consid-
ered a suitable candidate for improvement
through revascularization. Patient-related factors
include a reasonable life expectancy from other
coexistent disease states and a relative paucity of
other comorbidities (eg, chronic kidney disease,
cerebrovascular disease, pulmonary disease, and
so forth), particularly for patients being consid-
ered for CABG. In general, patients who are good
revascularization candidates have a significant
amount of demonstrably ischemic or hibernating
(ie, viable) myocardium, or anginal symptoms
[2,9,10]. Finally, the ischemic or hibernating
territory should be amenable to revascularization
either through PCI or CABG. For PCI, this im-
plies lesions that can be treated with a percutane-

ous approach with the overall goal of maximal
revascularization of ischemic or hibernating terri-
tories. In the case of CABG, this generally implies
the presence of distal vasculature suitable for
* Corresponding author. Center for Interventional
Vascular Therapy, Columbia University Medical Center
and the Cardiovascular Research Foundation, New
York, NY 10032.
E-mail address: (J.W. Moses).
1551-7136/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.hfc.2007.05.003 heartfailure.theclinics.com
Heart Failure Clin 3 (2007) 229–235
Left Ventricular Restoration: How Important is the
Surgical Treatment of Ischemic Heart Failure Trial?
Lorenzo Menicanti, MD
a,
*
, Marisa Di Donato, MD
b
a
San Donato Hospital, San Donato Milanese, Milano, Italy
b
University of Florence, Firenze, Italy
Chronic ischemic heart failure (CHF) is one of
the major health care issues in the western world
partly because of an aging population and more
effective treatment of acute myocardial infarction
[1,2]. Intensive medical management reduces symp-
toms and improves survival in CHF but patients in
high functional classes (NYHA III-IV) still have

a poor 3-year prognosis despite improved medical
therapy, with high social and economic impact [3].
The increase in left ventricular (LV) volume
following myocardial infarction (MI) is a compo-
nent of the remodeling process characterized by
LV volume increase and geometry abnormalities
with frequently associated mitral regurgitation
that leads to heart failure (HF) progression; this
progression is independent of the neurohormonal
activation, according to the biomechanical model
of HF recently introduced by Mann and Bristow
[4]. The concept of a biomechanical model of HF
reinforces the need for therapies able to reduce LV
volumes and restore geometry; the model also em-
phasizes the need for measuring LV volumes and
geometric parameters and the importance of as-
sessing the presence and the degree of mitral re-
gurgitation in patients who have ischemic dilated
cardiomyopathy and cardiac dysfunction.
Left ventricular shape and function abnormalities
following myocardial infarction
A strict relationship exists between the shape
of the LV and its function. The ellipsoid is the
geometric form that most resembles the shape of
the normal ventricle. It derives from the archi-
tecture of the anatomic distribution of cardiac
muscle fibers. The double spiral that constitutes
the three-dimensional (3-D) architecture of the
heart permits a shortening of 15% of the fibers to
give an ejection fraction of 60% and the different

distribution of the fibers within the wall from the
epicardium to the endocardium accounts for
the twisting effect of the apex that optimizes the
ejection of blood into the aortic vessel. The
elliptic shape enhances blood flow at the inflow
and outflow tract. When disease alters the shape
of the ventricle, the equilibrium of forces and of
spatial orientation of the fibers in the LV is
altered and loses its optimal function. The
extracellular matrix (cardiac interstitium and
collagen) markedly contributes to connect the
myocytes in a complex array of fibers forming
the 3-D architecture of the wall and coordinating
the delivery of forces generated by myocytes.
These forces are important determinants of
diastolic and systolic stiffness and serve to resist
deformation, maintain shape and wall thickness,
and prevent ventricular bulging and rupture [5].
Shape changes after MI (especially if anterior)
mainly consist of a reduction of curvature radius
(the reciprocal of internal radius) at the apical
level that creates a high local tension. The increase
in tension plays a key role in activating complex
neurohormonal mechanisms, including an in-
crease in angiotensin II, collagen deposition, and
degradation through metalloproteinase-1 and -2
activation. This activation may induce apoptosis
launching the complex process called remodeling,
which characterizes ischemic cardiomyopathy
[5–8]. The increase in chamber volume

* Corresponding author. Department of Cardiac Sur-
gery, San Donato Hospital, Via Morandi 30, 20097 San
Donato Milanese, Milano, Italy.
E-mail address: (L. Menicanti).
1551-7136/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.hfc.2007.04.009 heartfailure.theclinics.com
Heart Failure Clin 3 (2007) 237–243

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