From the Hospital Angelina Caron, Campina Grande do Sul, Brazil
(R.J.V.B.); and the Divisions of Cardiology (J.G., A.M.F.), Pathology
(A.J.D.), and Cardiothoracic Surgery (R.L.K., W.A.M.), University of
Pittsburgh, Pittsburgh, Pa.
Correspondence to John Gorcsan III, MD, University of Pittsburgh, Department of Cardiology, Scaife Hall Fifth Floor, 200 Lothrop St, Pittsburgh, PA 15213. E-mail gorcsan{at}a1.isd.upmc.edu
Methods and ResultsEight patients, 58±5 years old, with severe
clinical heart failure and EF of 12±3% were studied before and
immediately after PLV. LV performance was assessed by the
predominantly load-insensitive measures of pressure-area relations with
high-fidelity pressure catheters and transesophageal
automated echocardiographic measures of cross-sectional
area as a surrogate for volume. LV end-diastolic volume
decreased from 200±60 to 89±17 mL, EF increased from 12±3% to
41±8%, and right ventricular (RV) fractional area change
increased from 24±12% to 37±16% (all P<.05 versus
before). Changes in pressure-area relations were variable:
end-systolic elastance, 6.5±3.4 to 4.3±2.5
mm Hg/cm2 and preload recruitable stroke work, 33±16 to
34±19 mm Hg (P=NS versus before).
End-diastolic stiffness increased from 0.13±0.06 to
0.19±0.07 mm Hg/cm2 (P<.05 versus
before). Improvement in LV performance was inversely correlated
with semiquantitative histological assessment of
myocardial fibrosis and positively correlated with nuclear enlargement
and hyperchromasia, indicative of myocyte hypertrophy. No
long-term follow-up data were available.
ConclusionsPLV resulted in reductions in LV volumes, increases
in EF and RV ejection, but increases in LV stiffness. Estimates of LV
performance revealed variable results associated with the
degree of myocardial fibrosis. Further study of these effects in
relation to patient outcome is warranted.
The world's largest experience with partial left ventriculectomy has
been the Hospital Angelina Caron in Brazil, with >400
cases.1 4 Improvement in functional class occurs
in the majority of patient survivors.1 The 30-day
mortality is
A potential hypothesis is that patients who have LV dysfunction related
to overstretched myocytes, rather than structural damage, are most
likely to benefit from this immediate reduction in wall stress and
improvement of the mass-volume relationship by
PLV.16 This hypothesis is supported by the
inverse relationship of immediate improvement in LV performance
with degree of fibrosis. Factors such as myocyte apoptosis may
possibly predict outcome; however, this hypothesis remains to be
tested.17 An important future challenge is to
define clinical or morphological features that would be predictive of
long-term patient outcome and aid in patient selection for this
surgical treatment of severe heart failure.
Limitations
Received December 2, 1997;
revision received January 7, 1998;
accepted January 12, 1998.
2.
Bocchi EA, Bellotti G, de Moraes AV, Bacal F, Moreia
LF, Esteves-Filho A, Fukushima T, Guimaraes G, Stolf N, Jantene A,
Pileggi F. Clinical outcome after left ventricular
remodeling in patients with idiopathic dilated
cardiomyopathy referred to heart transplantation:
short-term results. Circulation. 1997;96(suppl
II):II-165II-172. Comment.
3.
Kawaguchi AT, Sugimachi M, Sunagawa K, Takeshita N,
Koide S, Verde JL, Batista RJV. Intraoperative left
ventricular pressure-volume relationship in patients
undergoing left ventricular diameter reduction.
Circulation. 1997;96(suppl I):I-198. Abstract.
4.
Replogie RL, Kaiser GC. Left ventricular
reduction surgery. Ann Thorac Surg. 1997;63:909910.
5.
McCarthy PM. Ventricular remodeling: hype
or hope? Nat Med. 1996;2:859860.[Medline]
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6.
Starling RC, Young JB, Scalia GM, Thomas JD, Vargo
RL, Buda TM, Smedira NG, McCarthy PM. Preliminary observations with
ventricular remodeling surgery for refractory heart
failure. J Am Coll Cardiol. 1997;29:64A. Abstract.
7.
Pashkow FJ, ed. Partial left ventriculectomy a viable
alternative to cardiac transplant. Cardiac Consult.. 1997;8:4.
8.
Gorcsan J, Morita S, Mandarino WA, Deneault LG, Kawai
A, Kormos RL, Griffith BP, Pinsky MR. Two-dimensional
echocardiographic automated border detection accurately
reflects changes in left ventricular volume. J
Am Soc Echocardiogr. 1993;6:482489.[Medline]
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9.
Gorcsan J, Romand J, Mandarino WA, Deneault LG, Pinsky
MR. Assessment of left ventricular performance by
on-line pressure-area relations using echocardiographic
automated border detection. J Am Coll Cardiol. 1994;23:242252.[Abstract]
10.
Gorcsan J, Gasior TA, Mandarino WA, Deneault LG,
Hattler BG, Pinsky MR. Assessment of the immediate effects of
cardiopulmonary bypass on left ventricular
performance by on-line pressure-area relations.
Circulation. 1994;89:180190.
11.
Suga H, Sagawa K, Shoukas AA. Load independence of the
instantaneous pressure-volume ratio of the canine left ventricle and
effects of epinephrine and heart rate on the ratio. Circ
Res. 1973;32:314322.
12.
Glower DD, Spratt JA, Snow ND, Kabas JS, Davis JW,
Olsen CO, Tyson GS, Sabiston DC, Rankin JS. Linearity of the
Frank-Starling relationship in the intact heart: the concept of preload
recruitable stroke work. Circulation. 1985;5:9941009.
13.
Mirsky I, Cohn PF, Levine JA, Gorlin R, Herman MV,
Kreulen TH, Sonnenblick EH. Assessment of left ventricular
stiffness in primary myocardial and coronary artery disease.
Circulation. 1974;50:128136.
14.
Morita S, Kormos RL, Mandarino WA, Eishi K, Kawai A,
Gasior TA, Deneault LG, Armitage JM, Hardesty RL, Griffith BG. Right
ventricular/arterial coupling in the patient
with left ventricular assistance. Circulation.
1992;86(suppl II):II-316-II-325.
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Dickstein ML, Spotnitz HM, Rose EA, Burkhoff DB. Heart
reduction surgery: an analysis of the impact on cardiac
function. J Thorac Cardiovasc Surg. 1997;113:10321040.
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approach to assess myocyte remodeling in cardiac
hypertrophy and failure. J Cardiac Failure. 1997;3:6368.[Medline]
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Nitahara JA, Quaini E, Di Loreto C, Beltrami CA, Krajewski S, Reed J,
Anversa P. Apoptosis in the failing human heart. N
Engl J Med. 1997;336:11311141.
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Nakano K, Sugawara M, Ishihara K, Kanazawa S, Corin WJ,
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© 1998 American Heart Association, Inc.
Brief Rapid Communications
Heterogeneous Immediate Effects of Partial Left Ventriculectomy on Cardiac Performance
![]()
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
BackgroundPartial left
ventriculectomy (PLV) is a novel surgical treatment for severe heart
failure consisting of resection of a large wedge of
myocardium to reduce wall stress and restore the normal
mass-volume ratio. Although ejection fraction (EF) has been shown to
improve after PLV, few other physiological data
describing its immediate effects on left ventricular (LV)
performance are available.
Key Words: ventricles surgery heart failure
![]()
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Partial left
ventriculectomy has been introduced recently as a surgical treatment
for patients with dilated left ventricles and severe heart
failure.1 This novel approach, also referred to
as LV remodeling or reduction surgery, consists of resection of a large
wedge of myocardium from the posterolateral wall and is
often accompanied by mitral valve replacement or repair. PLV markedly
reduces LV volume, with the goal of decreasing wall stress and
restoring the normal mass-volume ratio. Although improvements in EF
have been reported after PLV, its immediate effects on other
parameters of LV performance are
unclear.2 3 Furthermore, patient outcome remains
variable, and details concerning patient selection, the surgical
technique itself, and long-term outcome are just beginning to
emerge.1 2 3 4 5 6 7 The objectives of this study were (1)
to enhance understanding of the immediate effects of PLV on LV
performance in patients with severe heart failure by use of
relatively load-independent measures and (2) to identify potential
clinical or histological variables that may be
associated with improvements in LV performance.
![]()
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Eight consecutive patients with severe heart failure, 58±5
years old, referred to the Hospital Angelina Caron, Brazil, for PLV
were studied. All patients gave informed consent consistent
with the Institutional Policy of the Hospital Angelina Caron. All
patients had been in NYHA functional class III to IV for >6 months
with LV EF of 12±3% (Table 1
). No
patients were on intravenous inotropic or mechanical
support. After median sternotomy, a high-fidelity LV pressure catheter
(MP-500, Millar Instruments, Inc) was inserted and occluders were
placed around the superior and inferior venae cavae. A
transesophageal probe and an automated border-detection
ultrasound system (Sonos 2500, Hewlett-Packard, Inc) that characterizes
backscatter signals as blood or tissue and calculates LV
cross-sectional area on-line were used.8 9 10
After a standard echocardiographic examination,
automated measures of LV cross-sectional area in the transgastric
short-axis view, which have previously been validated to reflect
changes in LV volume in animal models and in humans, were
recorded.8 9 10 This system was interfaced
with an analog-to-digital converter and a computer for data storage.
Three 10-second bicaval occlusion and release maneuvers were made
during end-expiratory apnea to assess pressure-area relations. This
protocol was repeated after PLV was complete and patients were removed
from cardiopulmonary bypass but before chest closure. All
operations were performed by R.J.V.B. with patients on
cardiopulmonary bypass but without cardioplegia or hypothermia.
A large wedge of LV free wall was resected from base to apex. All
patients also had valvular surgery (Table 1
). Continuous
suturing of the LV was performed without felt
buttressing.1 Ees was
determined as the slope of end-systolic points (maximum
pressure/area) for each loop by an iterative linear regression
technique.9 10 11 Stroke work was estimated as the
integral of the pressure-area loop and PRSW as the slope of the
relation of linear stroke work versus end-diastolic
area.9 10 12 Assessment of LV compliance was made
by use of an exponential curve fit with end-diastolic area
as a surrogate for end-diastolic
volume.13 Routine M-mode measures were made from
short-axis images. Volume and EF measures were made by Simpson's rule,
and RV ejection was assessed as fractional area change
[(end-diastolic area minus end-systolic area)
divided by end-diastolic area] from the four-chamber view.
Portions of excised LV wall were frozen in liquid nitrogen, then
sectioned and stained with hematoxylin-eosin and Masson's trichrome
for semiquantitative assessment of endocardial and
interstitial fibrosis, inflammation, necrosis, and nuclear
enlargement or hyperchromasia consistent with myocyte
hypertrophy. Physiological
variables were compared by a paired Student's t test
from before to after PLV. Least-squares linear regression was used to
assess any associations between clinical or
histological features and postoperative LV
performance.
View this table:
[in a new window]
Table 1. Clinical and Operative Patient Data
![]()
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Individual data appear in Table 2
.
Patient 5 suffered a fatal intraoperative myocardial infarction and was
excluded from analysis. Consistent and significant
reductions in LV dimensions and volumes occurred, associated with
increases in EF and RV fractional area change from 24±12% to 37±16%
(P<.05 versus before). Effects of PLV on LV
performance assessed by load-independent measures were more
variable. Complete pressure-area loop data sets were available from
six patients (Table 2
). Although some patients did not demonstrate an
immediate benefit, other patients had a significant improvement in
Ees and PRSW
(Figure
). The most immediate improvement
in LV performance occurred in a patient with chronic aortic
regurgitation who also underwent aortic valve
replacement. Patients with idiopathic dilated
cardiomyopathy had variable results.
Significant improvement in ventriculoarterial coupling was
observed, with Ea decreasing from 17±6 to
11±3 mm Hg/cm2
(P<.05).14 However, a significant
increase in LV stiffness occurred (Table 2
). Heart rate increased from
84±7 to 109±12 bpm (P<.05). LV end-diastolic
and peak-systolic pressures were unchanged at 17±6 to
22±7 mm Hg and 82±10 to 71±12 mm Hg, respectively.
Cardiac outputs available in four patients were also unchanged, from
3.4±0.9 to 4.5±2.1 L/min. Histological
analysis revealed variable degrees of fibrosis and myocyte
hypertrophy but no cellular infiltration or necrosis,
consistent with end-stage heart failure. Semiquantitative
grading of fibrosis was inversely correlated with changes in
Ees (r=-.59) and PRSW
(r=-.95, P<.01) after surgery. Degrees of
nuclear enlargement and hyperchromasia associated with
hypertrophy were correlated with changes in
Ees (r=.70) and PRSW
(r=.88, P<.05). These data suggest that
improvements in LV performance are inversely related to
myocardial fibrosis, in particular with PSRW, which is a more robust
measure.12 The mechanism for an association with
myocyte hypertrophy is unknown. This sample size was too
small to draw any firm conclusions. No other clinical or surgical
variables were predictive of immediate LV performance, and
no long-term patient outcome data were available.
View this table:
[in a new window]
Table 2. Immediate Effects of PLV on LV Performance

View larger version (46K):
[in a new window]
Figure 1. Examples of pressure-area loops from two patients before and
after PLV demonstrating heterogeneous results in measures
of systolic performance.
![]()
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
PLV for patients with severe heart failure resulted in decreases
in LV volume associated with significant increases in EF and RV
ejection. Increases in EF occurred even though mitral valve replacement
or repair for significant mitral regurgitation was
performed in the majority of patients. When the relatively
load-independent measures of pressure-area relations were examined, PLV
was not consistently associated with an immediate improvement
in LV performance, and an increase in end-diastolic
stiffness was observed. Increases in LV performance were
inversely associated with myocardial fibrosis by semiquantitative
histology. Although mathematical modeling predicts increases in
Ees and LV stiffness with PLV, few data from
patients are available.3 15 LV
performance assessed by pressure-area relations has been shown
to decrease immediately after coronary bypass surgery with
cardioplegia and hypothermic arrest.10 This
decrease is thought to be due to ischemia-reperfusion injury
and/or hypothermia, although a precise mechanism is unknown. PLV is
unique because of concomitant reductions in valvular
regurgitation and the use of cardiopulmonary
bypass without cardioplegia or hypothermic arrest in this series,
although other centers use cardioplegia and core cooling. Variability
in LV performance associated with the degree of myocardial
fibrosis suggests that PLV may be beneficial to patients who lack
advanced structural damage, although this observation requires further
study in a larger series.
20%, and survival is estimated to be
55% at 2
years.1 4 Unfortunately, the outcome of many of
these patients is uncertain because of their socioeconomic problems,
with no means to communicate for follow-up. Indeed, no outcome data
from the patients in the present study are available.
McCarthy,5 Starling et al,6
and Pashkow7 have reported preliminary outcome
data after PLV in a series of 53 patients, with a 1-year mortality rate
of
6%. However, 20% to 30% of their patients had subsequent
worsening of heart failure, with 15% to 20% requiring mechanical
circulatory assistance.6 7 The majority of
survivors had improvement in symptoms and functional class. Bocchi et
al2 reported a survival rate of
90% at 1
month and 60% at 6 months in 24 patients with idiopathic
cardiomyopathies who underwent PLV. Although these
data are preliminary, a pattern of variable outcome appears to be
emerging. The variable results of the load-insensitive measures of
LV performance were consistent with the variable
outcome reported in other patients after PLV. No attempt could be made
to associate immediate LV performance with long-term outcome in
this study.
A major limitation of this study is the small sample size,
including patients with heterogeneous clinical diagnoses.
However, patients were similar with respect to the degree of LV
dysfunction and heart failure. Another limitation is that follow-up
data were not available, and these immediate results may not
necessarily correlate with long-term outcome. A methodological
limitation is the use of LV cross-sectional area as a surrogate for LV
volume. This approach has been validated in animal models and
humans,8 9 10 although the alterations in LV
geometry induced by PLV have not been specifically studied before. In
addition, increases in Ees, which usually signify
improvement in LV performance, may not have the same
physiological meaning after
PLV.15 Also, no attempt was made to normalize
Ees or PRSW to LV volume by use of
stiffness-stress relations.18 Despite these
limitations, the present study extends our
physiological understanding of the potential
immediate effects of PLV on LV performance, and these
observations invite further investigation of this novel surgical
therapy.
![]()
Selected Abbreviations and Acronyms
Ea
=
arterial elastance
Ees
=
end-systolic elastance
EF
=
ejection fraction
LV
=
left ventricular
PLV
=
partial left ventriculectomy
PRSW
=
preload-recruitable stroke work
RV
=
right ventricular
![]()
Acknowledgments
Dr Gorcsan was supported in part by the American Heart
Association, Pennsylvania Affiliate, Camp Hill.
![]()
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
1.
Battista RJ, Verde J, Nery P, Bocchino L,
Takeshita N, Bhayana JN, Bergsland J, Graham S, Houck JP, Salerno TA.
Partial left ventriculectomy to treat end-stage heart disease.
Ann Thorac Surg. 1997;64:634638.
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