JACC Vol. 15, No.
3 557
March I. 1990:557-63
Long-Term Effects of Excision of the Mitral Apparatus on Global and
Regional Ventricular Function in Humans
CHRISTOS J. PITARYS II, MD, MERVYN B. FORMAN,
HERCULES PANAYIOTOU, MD, DAVID E. HANSEN.
Nashville. Tennessee
To evaluate the long-term sequelae of mitral valve excision
on global and regional wall motion, contrast left ventricu-
lograms from 21 patients with suspected prosthetic mitral
valve dysfunction performed 10.4 + 2.1 years after mitral
valve replacement were analyzed by a computerized radial
shortening method. Patients with significant coronary ar-
tery disease (>30% stenosis in any vessel) were excluded.
In 8 of the 21 patients in whom preoperative ventricu-
lograms were available, regional wall motion was normal
before valve replacement. Although average radial short-
ening (35.6 + 4.8% versus 35.3 + 3.8%, p = NS) and left
ventricular ejection fraction (62.8 + 4.2% versus 57.9 +
2.8%, p = NS) were unchanged in the preoperative and
Mitral valve replacement remains the most common surgical
procedure for restoring valvular competence in patients with
mitral valve dysfunction. Over the last decade refinements in
operative technique have resulted in increasing numbers of
patients undergoing reparative procedures that preserve the
subvalvular apparatus (1). Decreased early operative mor-
tality (l-6) and increased long-term survival after surgery
(2-8) have generally been observed in patients with mitral
valve repair compared with those treated with conventional
valve replacement. Preservation of systolic ventricular func-
tion has been proposed as a mechanism for this beneficial
effect.
Experimental studies (9-l 1) suggest that the mitral valve
apparatus may make an important contribution to global and
From the Department of Medicine, Division of Cardiology, Vanderbilt
University School of Medicine, Nashville, Tennessee. This study was pre-
sented in part at the 61st Annual Scientific Session of the American Heart
Association, Washington. DC., November 1988.Dr. Forman is a recipient of
a First Award from the National Institutes of Health, Bethesda, Maryland.
Dr. Hansen is an Investigator of the American Heart Association, Tennessee
Affiliate, Nashville.
Manuscript received July 31, 1989;revised manuscript received October
4. 1989,accepted October 18, 1989.
Address for reorints: Mervyn B. Forman, MD, PhD, Division of Cardi-
ology, CC-2218Medical Center North. Vanderbilt University Medical Center,
Nashville, Tennessee 37232-2170.
01990 by the American College of Cardiology
MD, PHD, FACC,
MD
postoperative studies of these eight patients, radial short-
ening in the vicinity of insertion of the posteromedial
papillary muscle declined significantly (38.4 f 6.4% to
20.8 f 4.4%, p < 0.04). Postoperative radial shortening
for all 21 patients at the site of insertion of the papillary
muscle was also reduced to a significant degree compared
with the average radial shortening (32.9 + 10.3% versus
17.5 f 2.0%, p < 0.001).
The findings demonstrate significant long-term and pos-
sibly permanent regional ventricular dysfunction after sev-
ering the chordae tendineae during mitral valve replace-
ment.
(J Am Co11Cardiol1990;15:557-63)
regional left ventricular contractile function. However, the
long-term effects of conventional mitral valve replacement
on regional contractile function have not been systematically
studied in humans. Therefore, we used contrast ventriculog-
raphy to examine retrospectively the effects of conventional
mitral valve replacement, including excision of the papillary
muscles, on global and regional ventricular function a mean
of 10.4 years after surgery.
Methods
Patient selection. This study is based on a retrospective
analysis of 56 patients who underwent cardiac catheteriza-
tion between 1985 and 1988 at the Vanderbilt University
Medical Center and the Nashville Veterans Administration
Hospital after conventional mitral valve replacement. The
operative procedure remained unchanged during that period
and included excision of the entire mitral apparatus with
chordae tendineae and papillary muscles. All patients were
referred for suspected prosthetic mitral valve dysfunction.
Exclusion criteria included significant coronary artery
disease (>30% reduction in luminal diameter), other coex-
isting significant valvular disease, moderate or severe left
ventricular contractile dysfunction (ejection fraction ~40%)
0735.1097/90/$3.50
558 PITARYS ET AL. JACC Vol. 15, No. 3
VENTRICULAR FUNCTION AND MITRAL VALVE SURGERY March 1, 1990:557-63

Table 1. Postoperative Clinical and Angiographic Features

in 21 Patients
Age (yr) 56 t 2.4
Gender
Male 7
Female 14
NYHAfunctionalclass
III II
IV IO
Cardiac rhythm 30 12
Sinus 4
Atrial fibrillation I7
Type of prosthesis
Bioprosthetic I5
Mechanical 6
Etiology of valvular disease
Rheumatic 20
Infectious I
Diagnosis
Preoperative*
MR 3 18
MS 5
Postoperative Figure 1. Schematic representation of regional wall motion in 36
MR I9 radii constructed at lo” intervals from the epicenter of the end-
MS I systolic and end-diastolic ventricular silhouettes. Radii 31 to 2
Normal valve function I encompassed the aortic and mitral valves and were excluded from
Time from MVR to cardiac 10.4 + 2.1 analysis. Radii 23 to 28 defined the radial shortening in the region of
catheterization (yr) insertion of the posteromedial papillary muscle (arrow).

*Angiographic and hemodynamic data obtained before mitral valve re-

placement. MR = mitral regurgitation; MS = mitral stenosis; MVR = mitral
valve replacement; age and time from mitral valve replacement to cardiac
catheterization are expressed as mean values k SD.
or prior myocardial infarction. All patients had high quality
angiograms suitable for quantitative analysis.
Twenty-one patients qual$edfor analysis. Of these, both
preoperative and postoperative contrast left ventriculograms
were performed in eight patients.
Clinical features (Table 1). There were 7 women and 14
men, aged 56 ? 2.4 years (mean ? SD) with a range of 22 to
74 years.
All patients had clinical evidence of sign$cant and
progressive congestive heart failure (New York Heart As-
sociation functional class III or IV) after mitral valve re-
placement that prompted referral for diagnostic cardiac
catheterization. Fifteen patients had a bioprosthetic valve
and six had a tilting-disc metallic valve. Most (20 of 21) had
undergone mitral valve replacement for rheumatic mitral
disease. The mean time from mitral valve replacement to
cardiac catheterization was 10.4 ? 2.1 years (range 6 to 1.5).
Cardiac catheterization, Cardiac catheterization and an-
giography were performed by way of the femoral artery and
vein in 8 patients preoperatively and in all 21 postopera-
tively. After measurement of rest intracardiac and ptilmo-
nary hemodynamics with fluid-filled catheters connected to
an external pressure transducer, contrast ventr+ulography
was performed in the 30” right anterior oblique projection
and recorded on 35 mm cinefilm at 60 frames/s. This was
followed by coronary arteriography to exclude significant
coexisting coronary artery disease. Nineteen patients had
chronic mitral regurgitation, one patient had mitral stenosis
and one had a functionally normal prosthetic mitral valve at
the time of cardiac catheterization.
Ventriculographic analysis. Contrast ventriculograms
were reviewed on a frame by frame basis. The earliest well
opacified beat was selected for analysis. Because postoper-
ative ventriculograms were easily identified by the presence
of a mitral valve prosthesis, these studies were analyzed
separately from preoperative studies and without prior
knowledge of the preoperative study. In patients with atria1
fibrillation, a beat with a cycle length approxjmating the
average was chosen. Postextrasystolic beats were excluded
and postextrasystolic potentiation was not assessed. End-
diastolic and end-systolic silhouettes were traced by two
experienced angiographers. Left ventricular ejection frac-
tion was calculated with use of the single plane area-length
method of Sandler and Dodge (12). Regional wall mbtion was
analyzed with a computerized radial shortening program
with customized software as previously described and vali-
dated in our laboratory (13). A longitudinal axis was con-
structed that connected the middle of the aortic valve plane
with the apex of both end-diastolic and end-systolic silhou-
ettes (Fig. 1). A computerized program constructed an array
JACC Vol. 15. No. 3 PITARYS ET AL. 559
March I. 1990:.557-63 VENTRICULAR FIJNCTIONAND MITRAL VAL.VE SURGERY

Table 2. Hemodynamic Data of 21 Patients at the Time of

p=NS
Cardiac Catheterization
n=8
0.80
RAP,,,, (mm Hg) 12 ? 2.4
PAP,,,,, (mm Hg) 43 k 3.x
PCWP,,,, (mm Hg) 24 + I.? GLOBAL o.6o
MAP (mm Hg) 81 ? 2.9
LVEF 0.40
LVEDP (mm Hgl 16 t 2.4
CI (litersiminiper m’) 2.2 + 0.15

Data are mean values SEM. CI = cardiac index: LVEDP = left

2
ventricular end-diastolic MAP = mean arterial pressure; PAP =
pressure;
pulmonaryartery pressure: PCWP = pulmonarycapillarywedgepressure:
RAP = right atrial pressure.
of 36 radii at lo” intervals generated from the midpoint of the
longitudinal axis of the two silhouettes. Radii passing
through the aortic and mitral valve planes were excluded.
The average radial shortening was determined from the
remaining radii. The site of insertion of a posteromedial
papillary muscle encompassed radii 23 to 28 and defined the
radial shortening in this region (Fig. 1). Percent radial
shortening in each radius was computed as end-diastolic
length - end-systolic length/end-diastolic length x 100.
Statistical analysis. Clinical data are expressed as mean
values I SEM unless otherwise stated. Comparison of
means was evaluated with paired Student’s t test for
postoperative angiograms. Because the standard errors of
the mean radial shortening at the posteromedial papillary
muscle insertion sites between the preoperative and postop-
erative angiograms were not normally distributed, nonpara-
metric analysis (Wilcoxon’s matched pairs test) was used for
this comparison. The null hypothesis was rejected at the 5%
level.
0
PREOP POSTOP
Figure 2. Bar graph of left ventricular ejection fraction (LVEF)
preoperatively (PREOP) and postoperatively (POSTOP) in eight
patients. There was no significantchangein ejection fraction before
and 10.4 + 2.1 years after mitral valve replacement. Data are mean
values % SEM.
dial papillary muscle before and after operation in eight
patients. Before operation there was uniform and synchro-
nous wall motion. There was no significant difference in
average radial shortening before and after operation (35.6 *
4.8% versus 35.3 I 3.8%, p = NS). However, in the region
of insertion of the posteromedial papillary muscle, radial
shortening deteriorated significantly (38.4 t 6.4% to 20.8 L
4.4%, p < 0.04). The individual results are summarized in
Figure 4 for the posteromedial papillary muscle region.
Postoperatively, six of the eight patients had varying degrees
of regional hypokinesia confined to the area of posterior
papillary muscle insertion. Two patients manifested im-
proved regional wall motion after valve replacement. A
loose correlation was noted between regional wall motion

Results
Figure 3. Bar graphs illustrating average radial shortening and radial
Hemodynamic features. Rest hemodynamic variables and shortening in the region of insertion of the posteromedial papillary
the nature of the prosthetic dysfunction are summarized in muscle (PPM) both preoperatively (PREOP) and postoperatively
Tables 1 and 2. The moderately elevated right heart and (POSTOP) (mean + SEM) in eight patients. There was no difference
in average radial shortening before and after operation. However, at
pulmonary artery pressures, mildly elevated left ventricular the site of insertion of the posteromedial papillary muscle, radial
filling pressures and markedly reduced cardiac output (by shortening markedly decreased postoperatively. Data are mean
thermodilution method) are consistent with moderate to values + SEM.
severe left ventricular dysfunction in these patients with
class III and IV congestive heart failure. The postoperative AVERAGE PPM
disparity between left ventricular end-diastolic and pulmo- p=NS p<o.o4
nary artery wedge pressure is probably related to the pres- (%) 5Or 1
f
n=8 1 n=8 1
ence of a prominent V wave because the majority of the
patients had moderate valvular incompetence.
Global ventricular function. In the eight patients with
both preoperative and postoperative angiograms, there was RADIAL 30
SHORTENING
no significant difference in ejection fraction (Fig. 2) between 20
the preoperative study and the study performed 10.4 t 2.1
years later (62.8 + 4.2% versus 57.9 + 2.8%, p = NS).
Regional ventricular function. Figure 3 shows the average
radial shortening in the region of insertion of the posterome- PREOP POSTOP PREOP POSTOP
560 PITARYS ET AL.
VENTRICULAR FUNCTION AND MITRAL VALVE SURGERY
p<o.o4
n=8
PPM
RADIAL 4o
SHORTENING
30
”
PREOP POSTOP
Figure 4. Plot showing the change in wall motion for each patient at
the vicinity of insertion of the posteromedial papillary muscle (PPM)
both preoperatively (PREOP) and postoperatively (POSTOP). Six of
the eight patients demonstrated varying degrees of hypokinesia at
the site of insertion of the posteromedial papillary muscle.
and global ejection fraction (r = 0.44; p = 0.05) and time
after mitral valve replacement (r = -0.46; p = 0.07).
The assessment of regional wall motion for all 21 post-
operative left ventriculograms is shown in Figure 5. Regional
wall motion was uniform throughout except in the region of
the posteromedial papillary muscle. Radial shortening in the
region of insertion of the posteromedial papillary muscle was
significantly less than the average value of the remaining
segments (17.5 t 2.0% versus 32.9 ? 2.2%, p < 0.001).
Figure 6 illustrates end-diastolic and end-systolic ventricu-
lographic images in the 30” right anterior oblique projection
before and after mitral valve replacement in a selected
patient. The circumscribed silhouettes of the two images
with the accompanying radii are displayed. Before operation
there was essentially uniform contraction of all regions of the
left ventricle. Hypokinesia in the vicinity of insertion of the
Figure5. Bar graph comparing average (AVG) radial shortening with
that in the region of insertion of the posterior papillary muscle
(PPM) in 21 postoperative contrast ventriculograms. There was a
significant difference in radial shortening at the posterior papillary
muscle insertion site.
(%I
pc0.001
RADIAL
SHORTENING
AVG PPM
JACC Vol. IS, No. 3
March 1, 1990557-63
posteromedial papillary muscle is evident on the postopera-
tive ventriculogram and highlighted on the digitized silhou-
ettes.
Discussion
Effect of excision of mitral apparatus on left ventricular
systolic function. Many studies (14-18) have demonstrated
that conventional mitral valve replacement with excision of
the anterolateral and posteromedial papillary muscles results
in a deterioration in left ventricular systolic function in the
immediate and early postoperative periods. Nevertheless,
the importance of the mitral apparatus and, specifically, the
contribution of the papillary muscles themselves to regional
systolic ventricular function remain controversial. Reasons
for controversy include poorly controlled trials with hetero-
geneous groups of patients and the inherent difficulties in
accurately assessing left ventricular contractile function in
the presence of severe mitral regurgitation.
We examined regional wall motion to gain further insight
into the interaction between the mitral apparatus and the left
ventricle. The present study demonstrates that excision of
the mitral apparatus at the time of surgery for mitral regur-
gitation or mitral stenosis significantly impairs left ventricu-
lar systolic function in the vicinity of insertion of the
posteromedial papillary muscle in the majority of patients
and that this abnormality persists for years or possibly
indefinitely after surgery. In the two patients who manifested
improved regional wall motion, rheumatic involvement of
the mitral subvalvular apparatus may have prohibited dias-
tolic distension in the region of papillary muscle insertion
resulting in poor regional wall motion preoperatively. How-
ever, another four patients with mitral stenosis did not
manifest improved wall motion postoperatively. This dispar-
ity may be due to preserved diastolic properties before
operation because of less severe involvement of subvalvular
structures.
Valvular-ventricular interaction: role of the papillary mus-
cles. Preservation of postoperative left ventricular function
and improved postoperative survival data in patients under-
going mitral valve reconstruction compared with results of
conventional mitral valve replacement may be due to the
influence of the papillary muscles and their continuity with
the mitral valve. Several experimental models (9-11) have
demonstrated that severing the chordae tendineae impairs
intrinsic contractile function of the left ventricle manifested
by a reduction of the maximal elastance of the left ventricle
(a load-independent measure of left ventricular systolic
function) (19-21). Additionally, Hansen et al. (9) have
shown that the ventricular chamber geometry is altered with
systolic bulging in the vicinity of both papillary muscle
insertion sites during systole in the presence of a constant
inotropic state in a well perfused, isovolumetrically contract-
ing left ventricle. Recently, regional left ventricular contrac-
JACC Vol. 15, No. 3
March I, 1990:557-63 VENTRICULAR
POST-m
tile function assessed in a porcine model (22) demonstrated a
reduction in regional left ventricular volume elastance only
at the posteromedial papillary muscle site of insertion. This
suggests that global systolic function may deteriorate after
chordal severing because of abolition of the regional tether-
ing effect.
Lack of this tethering effect by the papillary muscles on
basal regions of the ventricle may be an explanation for the
cause of transverse midventricular rupture, a rare but dev-
astating complication after conventional mitral valve re-
placement (23). The reduction in wall stress provided by the
papillary muscles is believed to be important in this regard.
Comparison with other studies. The absence of a de-
crease in left ventricular ejection fraction noted in the
present study is contrary to that reported in previous studies
(18,24-28), although reported clinical data (14.29) differ with
regard to postoperative left ventricular function after mitral
valve replacement. Impaired postoperative ventricular func-
tion has been observed in patients with pure mitral regurgi-
tation (14,15,18,24-28) as well as those with pure mitral
stenosis (30). However, these studies were conducted either
intraoperatively immediately before and after chordal sever-
ing or up to a mean of 30 months after surgery. This suggests
that there may be adaptive mechanisms over several years to
compensate for the absence of the contribution of the mitral
apparatus to left ventricular systolic performance, including
remodeling, hypertrophy, dilation and a change in loading
conditions.
Regional wall motion abnormalities observed in our study
were consistent with those described by Goldman et al. (28)
in their intraoperative echocardiographic study assessing the
temporal response of ventricular dysfunction after mitral
valve replacement in 18 patients with pure mitral regurgita-
PITARYS ET AL. 561
FUNCTION AND MITRAL VALVE SURGERY
End-svstole
Figure 6. End-diastolic and end-systolic contrast left ventriculo-
grams (LV) in right anterior oblique projection in a patient both
before (PRE-MVR) and after (POST-MVR) mitral valve replace-
ment with accompanyingdigitizedsilhouettes. Note uniform ven-
tricular radial shorteningbefore operation with 3t mitralregurgita-
tion. However. a distinct area of hypokinesia is seen on the
end-systolic frame after valve replacement (arrows).
tion. They noted contractile dysfunction in the anterior and
posterior septum immediately after conventional mitral
valve replacement but not after mitral valve repair. In
patients with pure mitral stenosis, Kazama et al. (30) found
no significant difference in wall motion 3 to 6 weeks after
mitral valve replacement along the posterior and anterior
hemiaxes. but it was decreased significantly along the long
axis (16.3 2 4.9% preoperatively to 11.9 ? 3.8% postoper-
atively; p < 0.001).
Study limitations. This was a retrospective study of a
small heterogeneous group of patients with varying causes of
mitral valve dysfunction. We therefore cannot address the
question of how the underlying etiology of mitral dysfunc-
tion may influence results. Nevertheless, our data support
the general conclusion that surgical excision of the mitral
apparatus has long-term adverse consequences on regional
wall motion.
We were unable to quantitate regional wall motion in the
vicinity of insertion of the anterolateral papillary muscle
because this region is not visualized in the 30”right anterior
oblique projection. Nonetheless, there is no apparent reason
why our findings should not apply to the anterolateral
papillary muscle, because both papillary muscles have been
shown to influence global and regional systolic function in
animal models and humans.
562 PITARYS ET AL.
VENTRICULAR FUNCTION AND MITRAL VALVE SURGERY
Global systolic function was assessed by ejection frac-
tion, a load-sensitive index of contractile function. Despite
potential limitations as shown by Carabello et al. (31), who
suggested that maximal wall stress/volume ratio, rather than
ejection fraction, was more predictive of postoperative out-
come (p < O.OOl),ejection fraction is still used and accepted
in clinical practice as an important measure of ventricular
function and relied on in decisions concerning management
of patients with mitral valve disease. Although various
methods have been proposed to assess left ventricular func-
tion independent of load (19-21), their use in patients with
severe mitral regurgitation needs to be validated.
Conclusions. The present ventriculographic study dem-
onstrates the long-term persistence of regional contractile
abnormalities in the vicinity of insertion of the posteromedial
papillary muscle in patients after conventional mitral valve
replacement. Although left ventricular performance is
known to deteriorate immediately after such replacement,
adaptive mechanisms may come into play over the long term
to compensate for the lack of contribution of the mitral
apparatus to overall ventricular performance. Our study
suggests that these compensatory mechanisms are inade-
quate, resulting in permanent adverse effects on regional left
ventricular mechanics after conventional mitral valve re-
placement.
With the availability of intraoperative echocardiography
to assess residual regurgitation, more aggressive surgical
approaches in an attempt to preserve papillary annular
continuity, even with valve replacement, should be consid-
ered in patients with mitral regurgitation. Likewise, balloon
valvuloplasty or surgical commissurotomy where mitral val-
vular-ventricular interaction is maintained may be beneficial
in selected patients with mitral stenosis. These issues may
especially be applicable to patients with marginal cardiac
reserve. Carefully controlled, prospective, clinical trials
with homogeneous groups of patients are warranted to more
definitively test the potential benefits of mitral valvular-
ventricular interaction in preserving regional and global
ventricular function in patients undergoing mitral valve
surgery.
We gratefully acknowledge the secretarial assistance of Carolyn Coffey in the
preparation of this manuscript.
References
1. Cosgrove DM. Mitral valve reconstruction. Cardiol Clin 1985;3:461-9.
2. Orszulak TA, Schaff HV, Danielson GK, et al. Mitral regurgitation due to
ruptured chordae tendineae. J Thorac Cardiovasc Surg 1985;89:491-8.
3. Duran CG, Pomar JL, Revuelta JM, et al. Conservative operation for
mitral insufficiency: critical analysis supported by postoperative hemody-
namic studies in 72 patients. J Thorac Cardiovasc Surg 1980;79:326-37.
4. Yacoub M, Halim M, Radley-Smith R, McDay R, Nijveld A, Towers M.
JACC Vol. 15, No. 3
March 1. 1990:557-63
Surgical treatment of mitral regurgitation caused by floppy valves: repair
versus replacement. Circulation 1981;64(supplII):II-210-6.
5. Perier P. Deloche A, Chauvaud S, et al. Comparative evaluation of mitral
valve repair and replacement with Starr, Bjork, and porcine valve
prostheses. Circulation 1984;7O(supplI):I-187-92.
6. Adebo OA, Ross JK. Surgical treatment of ruptured mitral valve chordae:
a comparison between valve replacement and valve repair. Thorac
Cardiovasc Surg 1984;32:139-42.
7. Oliveira DBG, Dawkins KD, Day PH, Paneth M. Chordal rupture. II.
Comparison between repair and replacement. Br Heart J 1983;50:318-24.
8. Schmidli J, Rothlin ME, Turina M, Senning A. Langzeitresultate nach
Mitralklappenoperation wegen Mitralinsuffizienz 1972-1982. Schweiz
Med Wochenschr 1985;115:430-9.
9. Hansen DE, Cahill PD, DeCampli WM, et al. Valvular-ventricular
interaction: importance of the mitral apparatus in canine left ventricular
systolic performance. Circulation 1986;73:1310-20.
10. Hansen DE, Cahill PD, Derby GC, Miller DC. Relative contributions of
the anterior and posterior mitral chordae tendineae to canine global left
ventricular systolic function. J Thorac Cardiovasc Surg 1987;93:45-55.
11. Sarris GE, Cahill PD, Hansen DE, Miller DC. Restoration of left
ventricular systolic performance after reattachment of mitral chordae
tendineae: the importance of valvular-ventricular interaction. J Thorac
Cardiovasc Surg 1988;95:969-79.
12. Sandler H. Dodge HT. The use of single plane angiocardiograms for
calculation of left ventricular volume in man. Am Heart J 1%8;75:325-34.
13 Forman MB, Bingham S, Kopelman HA, et al. Reduction of infarct size
with intracoronary perfluorochemical in a canine preparation of repefu-
sion. Circulation 1985;71:1060-8.
I4 Peter CA, Austin EH, Jones RH. Effect of valve replacement for chronic
mitral insufficiency on left ventricular function during rest and exercise.
J Thorac Cardiovasc Surg 1981;82:127-35.
15. David TE, Uden DE, Strauss HD. The importance of the mitral apparatus
in left ventricular function after correction of mitral regurgitation. Circu-
lation 1983;68(suppllI):lI-76-82.
16. Phillips HR, Levine FH, Carter JE, et al. Mitral valve replacement for
isolated mitral regurgitation: analysis of clinical course and late postop-
erative left ventricular ejection fraction. Am J Cardiol 1981;48:647-54.
17. Lessana A, Herreman F, Boffety C. et al. Hemodynamic and cineangio-
graphic study before and after mitral valvuloplasty (Carpenter’s tech-
nique). Circulation 1981;64(supplII):II-195-202.
18. Boucher CA, Bingham JB, Osbakken MD, et al. Early changes in left
ventricular size and function after correction of left ventricular volume
overload. Am J Cardiol 1981;47:991-1004.
19. Suga H, Sagawa K, Shoukas AA. Load independence of the instanta-
neous pressure-volume ratio of the canine left ventricle and effects of
epinephrine and heart rate on the ratio. Circ Res 1973;32:314-22.
20. Suga H, Sagawa K. Instantaneous pressure-volume relationships and
their ratio in the excised, supported canine left ventricle. Circ Res
1974:35:117-26.
21. Sagawa K. The pressure-volume diagram revisited. Circ Res 1978;43:677-
87.
22. Hansen DE, Sarris GE, Niczyporuk MA, Derby GC, Cahill PO, Miller
DC. Physiologic role of the mitral apparatus in left ventricular regional
mechanics, contraction synergy, and global systolic performance.
J Thorac Cardiovasc Surg 1989;97:521-3.
23. Cobbs BW Jr, Hatcher CR Jr, Craver JM, Jones EL, Sewell CW.
Transverse mid-ventricular disruption after mitral valve replacement. Am
Heart J 1980;99:33-50.
24. Duran CG, Pomar JL, Revuelta JM, et al. Conservative operation for
mitral insufficiency: critical analysis supported by postoperative hemody-
namic studies in 72 patients. J Thorac Cardiovasc Surg 1980;79:326-37.
25. Schuler G, Peterson KL, Johnson A, et al. Temporal response of left
ventricular performance to mitral valve surgery. Circulation 1979;59:
1218-31.
JACC Vol. IS. No. 3 PITARYS ET AL. 563
March I. 1990:.557-6.7 VENTRICULAR FUNCTION AND MITRAL VALVE SURGERY

26. Phillips HR, Levine FH, Carter JE, et al. Mitral valve replacement for 29. Miki S, Kusuhara K, Ueda Y, Komeda M. Ohkita Y, Tahata T. Mitral
isolated mitral regurgitation: analysis of clinical course and late postop- valve replacement with preservation of chordae tendineae and papillary
erative left ventricular ejection fraction. Am J Cardiol 1981;48:647-54. muscles. Ann Thorac Surg 1988;45:28-34.

27. Huikuri HV. Effect of mitral valve replacement on left ventricular 30. Kazama S. Katsuhiko N. Sonoda K, et al. Postoperative left ventricular
function in mitral regurgitation. Br Heart J 1983;49:328-33. function in patients with mitral stenosis. Jpn Heart J 1986;27:35-42.

28. Goldman ME, Mora F, Guarino T. Fuster V, Mindich BP. Mitral 31. Carabello BA, Nolan SP, McCuire LB. Assessment of preoperative left
valvuloplasty is superior to valve replacement for preservation of left ventricular function in patients with mitral regurgitation: valve of the
ventricular function: an intraoperative two-dimensional echocardio- end-systolic wall stress-end-systolic volume ratio. Circulation 1981;64:
graphic study. J Am Coll Cardiol 1987:10:568-75. 1212-7.