Download Surgical Ventricular Reconstruction for Heart Failure

The
n e w e ng l a n d j o u r na l
of
m e dic i n e
edi t or i a l
Surgical Ventricular Reconstruction for Heart Failure
Howard J. Eisen, M.D.
Congestive heart failure is one of the leading
causes of death and complications in the developed world, and coronary artery disease is the
major cause of heart failure. Efforts to improve
ventricular function, symptoms, and clinical outcomes in patients with heart failure have included
neurohormonal inhibition with angiotensin-converting–enzyme inhibitors, angiotensin-receptor
blockers, beta-blockers, and aldosterone antagonists, as well as cardiac resynchronization therapy.
All these therapies have been shown in randomized clinical trials to be beneficial.1 However, none
of them specifically address the coronary disease
responsible for ischemic cardiomyopathy and myocardial infarction.
Coronary-artery bypass grafting (CABG), which
was first used to ameliorate symptoms, is now
used to improve survival in selected patients with
ischemic heart disease, although the improved
outcome of percutaneous coronary intervention
(PCI) has resulted in a reduction in the number
of CABG procedures that are performed.2-4 CABG
remains the standard of care for patients with
disease involving at least three vessels or the left
main coronary artery.5 Revascularization with
CABG can improve the perfusion of viable myocardium but does not restore function in areas
of infarction.
The large, aneurysmal myocardial segments
that were seen in the past in patients with myocardial infarction are seldom seen in the current
era of coronary reperfusion. However, regional
zones of myocardial dysfunction are still frequently observed. These areas of regional dysfunction
may result in adverse cardiac remodeling and the
progression of heart failure.6 A surgical procedure to reconstruct dysfunctional myocardial segments and favorably remodel the ventricle, known
as surgical ventricular reconstruction, has been
developed and is performed in selected patients,
usually in conjunction with CABG7,8 (Fig. 1). Previously reported clinical studies of surgical ventricular reconstruction were not randomized and
were conducted either in a single center or in
multiple centers as observational studies.9-11
In this issue of the Journal, Jones et al.12 report the results of the Hypothesis 2 substudy
of the Surgical Treatment for Ischemic Heart
Failure (STICH) trial (ClinicalTrials.gov number,
NCT00023595). This substudy compared CABG
alone with the combined procedure of CABG
with surgical ventricular reconstruction. Patients
were required to have coronary disease amenable to CABG, a left ventricular ejection fraction of
35% or less, and a dominant anterior region of
myocardial akinesia or dyskinesia that was amena­
ble to treatment with surgical ventricular reconstruction. All patients received standard medical
and device therapy for heart failure. The results
of the Hypothesis 1 substudy of the STICH trial,
which compared medical therapy plus CABG
with medical therapy alone, are not reported.
In the Hypothesis 2 substudy, 1000 patients
were recruited from 96 medical centers in 23
countries. The patients in the two study groups
were closely matched in terms of demographic
characteristics, coexisting illnesses, the proportion
who were receiving specific heart-failure medications, the Canadian Cardiovascular Society (CCS)
angina class, the New York Heart Association
(NYHA) heart-failure class, coronary anatomy, and
the extent of anterior myocardial akinesia or dyskinesia. Although Jones et al. indicate that the
use of evidence-based medical therapy (including
heart-failure medications, pacemakers, and cardio­
verter–defibrillators) was monitored throughout
n engl j med 360;17 nejm.org april 23, 2009
Downloaded from www.nejm.org at VANDERBILT UNIVERSITY on May 14, 2009 .
Copyright © 2009 Massachusetts Medical Society. All rights reserved.
1781
The
n e w e ng l a n d j o u r na l
of
m e dic i n e
A
B
Left
atrium
Left
ventricle
Left
ventricle
Damaged
tissue
Right
ventricle
Left
ventricle
Damaged tissue
C
Encircling suture being
placed along the edge of
normal ventricular wall
E
D
Patch
Patch
Ventricular wall sutured over the patch
in order to improve hemostasis and
provide mechanical reinforcement
Figure 1. Surgical Ventricular Reconstruction.
An incision is made through the area of scarring in the left ventricle (Panel A), which is opened to identify the boundary between
damaged and
COLOR FIGURE
healthy myocardium (Panel B). A purse-string suture is placed to encircle the scar, and the healthy portions of the ventricular wall are brought
Rev1
together (Panel C). The suture is tightened or a patch is placed (Panel D), and the scarred sections left outside the
chamber are closed03/24/09
(Panel E).
Author
Dr. Eisen
Fig #
1
1782
n engl j med 360;17 nejm.org april 23, 2009 Title
ME
Downloaded from www.nejm.org at VANDERBILT UNIVERSITY on May
.
DE 14, 2009Jarcho
Copyright © 2009 Massachusetts Medical Society. All rights reserved.
Daniel Muller
Artist
AUTHOR PLEASE NOTE:
editorial
the trial, they have not provided information about
rates of use of these therapies over time.
Both CABG alone and the combined procedure
were equally successful in improving the postoperative CCS angina class and NYHA heart-failure class. The two groups had similar improvements in the 6-minute walk test and similar
reductions in symptoms. There was a greater reduction in the end-systolic volume index with the
combined procedure (16 ml per square meter of
body-surface area), as compared with CABG alone
(5 ml per square meter). Unfortunately, these
data were obtained from only 373 patients at
baseline and at 4 months.
The primary outcome of the trial was a composite of death from any cause or hospitalization
for cardiac causes. There was no difference in the
occurrence of the primary outcome between the
CABG group (59%) and the combined-procedure
group (58%). The 30-day surgical rates of death
for CABG alone (5%) and for the combined procedure (6%) were similar and low overall, and
no difference in the rate of death from any cause
was observed in a median follow-up period of 48
months. Subgroup analyses showed no individual variables interacting significantly with studygroup assignment.
This large clinical trial had many strengths,
including an up-to-date approach to CABG, certification of surgeons and interventionalists in both
PCI and CABG, and an attempt to standardize
heart-failure therapies according to guidelines
throughout the entire study population. The
study also had some limitations, including sparse
data regarding medical or device therapy used in
each study group. The diversity of patients who
were enrolled might have limited the ability of the
investigators to identify particular groups or types
of patients who might benefit from the combined
procedure. Finally, more complete and longitudinal information on the end-systolic volume index
might have provided an indication of whether
ongoing ventricular remodeling occurred, which
might have negated or mitigated the difference
seen in the early postoperative period.
On the basis of this trial, the routine use of
surgical ventricular reconstruction in addition to
CABG cannot be justified. Potential explanations
for the lack of added efficacy of the combined
procedure include the fact that current heartfailure therapies are very effective at limiting adverse remodeling. The addition of CABG may
have enhanced this process, leaving little room
for additional benefit from surgical ventricular
reconstruction. We will have to wait for the results of the Hypothesis 1 substudy of the trial to
know for sure.
It is also apparent that surgical remodeling of
the ventricle is different from remodeling induced
by heart-failure therapies or cardiac resynchronization therapy and that the abrupt geometric reduction in ventricular dimensions with this procedure does not mimic the benefits derived from
neurohormonal inhibition and perhaps revascularization. The extent of volume reduction from
surgical ventricular reconstruction also may not
be consequential. There may be specific subgroups
of patients who might benefit from the combined
procedure, but such an effect is not apparent so
far in the results of the STICH trial and may be
difficult to detect, given the diversity of the study
population.
Dr. Eisen reports receiving consulting and lecture fees from
Medtronic and grant support from Medtronic and St. Jude. No other
potential conflict of interest relevant to this article was reported.
From the Division of Cardiology, Drexel University College of
Medicine, Philadelphia.
This article (10.1056/NEJMe0901815) was published at NEJM.org
on March 29, 2009.
1. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005
guideline update for the diagnosis and management of chronic
heart failure in the adult: a report of the American College of
Cardiology/American Heart Association Task Force on Practice
Guidelines (Writing Committee to Update the 2001 Guidelines
for the Evaluation and Management of Heart Failure): developed
in collaboration with the American College of Chest Physicians
and the International Society for Heart and Lung Transplantation:
endorsed by the Heart Rhythm Society. Circulation 2005;112(12):
e154-e235.
2. Kolessov VI. Mammary artery-coronary artery anastomosis
as method of treatment for angina pectoris. J Thorac Cardiovasc
Surg 1967;54:535-44.
3. Coronary Artery Surgery Study (CASS): a randomized trial of
coronary artery bypass surgery: survival data. Circulation 1983;
68:939-50.
4. Yusuf S, Zucker D, Peduzzi P, et al. Effect of coronary artery
bypass graft surgery on survival: overview of 10-year results from
randomised trials by the Coronary Artery Bypass Graft Surgery
Trialists Collaboration. Lancet 1994;344:563-70. [Erratum, Lancet
1994;344:1446.]
5. Serruys PW, Morice M-C, Kappetein AP, et al. Percutaneous
coronary intervention versus coronary-artery bypass grafting for
severe coronary artery disease. N Engl J Med 2009;360:961-72.
6. Sutton MGS, Sharpe N. Left ventricular remodeling after
myocardial infarction: pathophysiology and therapy. Circulation
2000;101:2981-8.
7. Dor V, Saab M, Coste P, Kornaszewska M, Montiglio F. Left
ventricular aneurysm: a new surgical approach. Thorac Cardiovasc Surg 1989;37:11-9.
8. Ferrazzi P, Matteucci MLS, Merlo M, et al. Surgical ventricular reverse modeling in severe ischemic dilated cardiomyopathy:
the relevance of the left ventricular equator as a prognostic factor. J Thorac Cardiovasc Surg 2006;131:357-63.
9. Menicanti L, Castelvecchio S, Ranucci M, et al. Surgical
n engl j med 360;17 nejm.org april 23, 2009
Downloaded from www.nejm.org at VANDERBILT UNIVERSITY on May 14, 2009 .
Copyright © 2009 Massachusetts Medical Society. All rights reserved.
1783
editorial
therapy for ischemic heart failure: single-center experience with
surgical anterior ventricular restoration. J Thorac Cardiovasc Surg
2007;134:433-41.
10. Athanasuleas CL, Stanley AWH Jr, Buckberg GD, Dor V, DiDonato M, Blackstone EH. Surgical anterior ventricular endocardial restoration (SAVER) in the dilated remodeled ventricle after
anterior myocardial infarction. J Am Coll Cardiol 2001;37:1199209.
1784
11. Athanasuleas CL, Buckberg GD, Stanley AWH Jr, et al. Surgi-
cal ventricular restoration in the treatment of congestive heart
failure due to post-infarction ventricular dilation. J Am Coll Cardiol 2004;44:1439-45.
12. Jones RH, Velazquez EJ, Michler RE, et al. Coronary bypass
surgery with or without surgical ventricular reconstruction.
N Engl J Med 2009;360:1705-17.
Copyright © 2009 Massachusetts Medical Society.
n engl j med 360;17 nejm.org april 23, 2009
Downloaded from www.nejm.org at VANDERBILT UNIVERSITY on May 14, 2009 .
Copyright © 2009 Massachusetts Medical Society. All rights reserved.