Download Surgical Ventricular Reconstruction for Ischemic or Idiopathic

Aus der
Chirurgischen Universitätsklinik
Abteilung für Herz- und Gefäßchirurgie
der Albert-Ludwigs-Universität Freiburg i. Br.
Ärztlicher Direktor: Prof. Dr. F. Beyersdorf
Surgical Ventricular Reconstruction for Ischemic
or Idiopathic Dilated Cardiomyopathy
INAUGURALDISSERTATION
zur
Erlangung des Medizinischen Doktorgrades
der Medizinischen Fakultät
der Albert-Ludwigs-Universität
Freiburg i. Br.
Vorgelegt 2004
von Lynda Ahn-Veelken
geboren in New York City, U.S.A.
Dekan:
Prof. Dr. med. Josef Zentner
1. Gutachter:
Prof. Dr. med. Friedhelm Beyersdorf
2. Gutachter:
Prof. Dr. med. Martin Werner
Jahr der Promotion:
2004
2
Table of Contents
1
1.1
1.2
1.2.1
1.2.1.1
1.2.1.2
1.3
1.3.1.
Introduction .......................................................................................................4
Functional Anatomy of the Ventricular Wall......................................................4
Myocardial Infarction..........................................................................................6
Treatment ............................................................................................................9
Medical Treatment ..............................................................................................9
Surgical Treatment ............................................................................................10
Dilated Cardiomyopathy ...................................................................................11
Treatment of DCM ............................................................................................12
2
2.1
2.2
2.2.1
2.3.2
2.3.3
2.4
2.5
Methods ............................................................................................................13
Patient Population..............................................................................................13
Preoperative Assessment...................................................................................13
Assessment of Ejection Fraction, Mitral Regurgitation, Left
Ventricular End Diastolic Diameter and Dyskinesia or Akinesia.....................13
Cardiac Catheterization or Arteriography .........................................................14
Surgical Procedures...........................................................................................14
Dor Surgical Ventricular Reconstruction (SVR) procedure and the
Modified Dor Procedure....................................................................................14
Batista Partial Left Ventriculectomy (PLV) procedure.....................................15
Concomitant Procedures ...................................................................................15
Telephone Interview..........................................................................................16
Data Analysis ....................................................................................................17
3
3.1
3.2
3.2.1
3.2.2
3.2.3
3.2.4
3.3
3.3.1
3.3.2
3.3.3
Results...............................................................................................................18
Preoperative Clinical Data and Surgical Procedures.........................................18
Dor SVR Procedure...........................................................................................19
New York Heart Association (NYHA) Status ..................................................20
Echocardiographic Results to Determine Effect of Operation..........................22
Survival under Dor SVR Procedure ..................................................................23
Hospital Mortality and Late Deaths ..................................................................25
Batista PLV Procedure ......................................................................................27
NYHA Status.....................................................................................................27
Echocardiographic Results to Determine Effect of Operation..........................27
Hospital Mortality and Late Deaths under Batista PLV Procedure ..................28
4
Discussion .........................................................................................................29
5
Summary ..........................................................................................................40
Zusammenfassung ...........................................................................................41
6
References ........................................................................................................42
2.2.2
2.3
2.3.1
Curriculum Vitae ............................................................................................55
Acknowledgements..........................................................................................56
3
1
INTRODUCTION
1.1
Functional Anatomy of the Ventricular Wall
In 1660, Lower described clockwise and counterclockwise spiral patterns of the myocardium at
the apex of the heart. These helical structures appeared to be the basis for the elliptical shape of
the heart. According to Torrent-Guasp (99), the myocardial fibers actually originate and end at
the basis of the heart and form long, intertwined loops. The final orientation of the loops is
circumferential around the heart base and helical at the apex (Figure 1).
Figure 1. Two views of the spiral patterns at the apical vortex of the heart. (Cook
TA. The curves of life, 1979. Dover publications, Inc.).
This difference in orientation is the anatomical basis for an efficient cardiac ejection fraction:
During systole, contraction of the basal region of the ventricle first results in constriction,
followed by contraction of the apical loop which shortens the ventricle and ejects the
intraventricular volume directionally towards the base. The overall motion pattern thus
resembles the wringing of water out of a wet cloth, an observation made first by Borelli, a
student of Galileo in 1680 (De Motu Animalium, Rome. 1681) (Figure 2).
Ejection
Suction
Figure 2. At the beginning of
systole, a clockwise and counterclockwise twisting similar to the
wringing of a rag leads to ejection.
During diastole, the upper part of
the ventricle twists in the opposite
direction to produce lengthening
and filling (99)
4
This anatomical arrangement and physiological coordination is the fundamental mechanism how
a systolic shortening of an individual myocardial fiber of 15% can be translated into a 60%
ventricular ejection fraction (16).
Any alteration of the functional cardiac anatomy, also referred to as "ventricular remodeling",
will therefore severely impair ventricular function and cardiac output (Figure 3). When structural
disorder changes the physiological elliptical geometry of the myocardium (top) to that of dilated
enlarged ventricle (bottom), the result is a transverse fiber orientation. The same 15% fiber
shortening will therefore result only in a 30% ejection fraction as opposed to the normal 60%
(16) (Figure 4). When these structural alterations of the ventricle impair the functional capacity
of the ventricle to fill with and to eject blood, the result is progressive cardiac failure. Important
pathological conditions that alter the heart shape are myocardial infarction and dilated
cardiomyopathy of any etiology.
Figure 3. Top figure is
of a normal elliptical
ventricle. When the
chamber dilates and
the ventricle becomes
enlarged
(bottom
figure), the result is a
transverse
fiber
orientation, and the
loss of contraction
efficiency (18).
Figure 4. Normal fiber shortening of 15% results in a
60% ejection fraction (left). The same 15% fiber
shortening results in a 30% ejection fraction in a
remodeled, spherical ventricle (19).
5
1.2
Myocardial Infarction
Myocardial infarction is defined as regional necrosis of cardiac tissue due to acute ischemia.
Shortly after myocyte necrosis, edema and inflammation occur in the infarcted area. Eventually,
a scar develops and is characterized by fibroblast proliferation and collagen deposition. Before
definite scar formation, however, the infarcted area can thin and dilate. Eaton and Sutton define
this process infarct expansion (46, 93). Within 72 hours, serine proteases such as plasmin and
matrix metalloproteinases released from neutrophils degrade the intermyocyte collagen that acts
as structural frame (93). Histologically, the thinning of the infarcted area is characterized by
slippage between muscle bundles caused by collagen degradation (93). This results in a
decreased myocyte density across the infarcted region (81).
This vulnerable period for developing an expansion has been demonstrated to begin as early as
24 hours after myocardial infarction and continues before scar formation is completed (72).
Structural changes as a result of expansion may lead to the formation of a left ventricular
aneurysm which has been associated with an approximately 60% one-year mortality (72). Eaton
et al. reported a 50% mortality within eight weeks after development of regional expansion and
ventricular dilatation (46).
Anatomically, aneurysms are composed of fibrotic tissue that replace the myocardium in the
infarcted zone. Functionally, ventricular aneurysms are characterized by a local expansile or
paradoxical wall motion. Complications associated with an aneurysm are arterial embolism,
ventricular arrhythmias and congestive heart failure that often occur within weeks to months.
The 1-year mortality rate is much higher in patients who have developed an aneurysm shortly
after an anterior infarct than in those patients without an aneurysm (46, 71, 81). When the
noncontractile area involves more than 20-25% of the surface area of the left ventricle, the result
is a noncompensatory ventricular enlargement and mycardial decompensation (62), defined as an
impaired contractile function due to the distortion of the ventricle and its structural
configuration.
The development of an infarct expansion and aneurysm formation has been characterized as the
early postinfarction remodeling phase (93). The late remodeling phase involves myocyte
hypertrophy and a global alteration in the ventricular shape.
The process of cardiac structural and functional disorder is initated by myocyte injury. In the
case of an infarction, the acute loss of myocardium leads to a diminished cardiac output,
increased end-systolic volume, and a secondary increase in end-diastolic pressure caused by the
increase in ventricular volume. The increase in radius leads to the elevation of diastolic and
systolic wall stresses. The wall tension can be calculated according to Laplace's law, K = P x
r/2d [N x m-2] and rises proportionally to the ventricular diameter r when the same
6
intraventricular pressure P is maintained and the wall thickness d does not increase.
Simultaneously, infarct expansion occurs in response to elevated wall stresses, particularly since
the necrotic myocardium predominates and scar tissue has not yet formed. Infarct expansion
would increase systolic and diastolic volumes with resultant increase in wall tension. The
increase in wall tension leads to a higher strain and oxygen requirement on the remote
noninfarcted myocardium.
To maintain a normal cardiac output, activation of the adrenergic system, with secretion of
catecholamines by the adrenal glands and the renin-angiotensin-aldosterone system (RAAS) are
invoked. This neurohormonal activation then leads to two pathways, one that leads to molecular
and phenotypic changes that have direct effects on cardiac myocyte growth (77, 93) and a second
pathway that leads to an increasing afterload due to vasoconstriction. The increases in preload
and ventricular afterload lead to an increased ventricular radius and diastolic pressure that result
in greater wall tension.
When adaptive responses are no longer able to counteract these distending forces, volumeoverload hypertrophy in the remote noninfarcted myocardium develops which leads to
progressive cavity enlargement and global dilatation. This process is known as ventricular
remodeling (52, 71, 93). Cardiac hypertrophy occurs, however, not only in response to RAAS
but also to increasing wall tension (93). Mechanical strains induced by rising wall tension
activate a range of intracellular signals, including secretion of angiotensin II, that lead to protein
synthesis and myocyte hypertrophy (77, 93).
The complex process of ventricular remodeling with its various contributing factors is described
in the diagram on the next page.
7
Myocyte injury
Loss of
contractile function
Decreased
cardiac output
Increased enddiastolic pressure
Infarct expansion
Increased wall stress
Further ventricular
dilatation
Hypertrophy of remote
noninfarcted tissue with
pathological phenotype
of cardiomyocytes
VENTRICULAR
REMODELING
Neurohormonal
activation
Increased afterload
Water and NaCl
retention
Figure 5. A schematic illustration of interactive forces and components that lead to
ventricular remodeling after regional infarction.
Since elevated wall stresses are a major stimulus for ventricular remodeling (71, 81), it is
important to decrease wall stress by limiting the radius. In patients studied for 3 years after first
myocardial infarction, development of progressive dilatation and severe ventricular dysfunction
was found in 20% of patients (52). The consequence is an increase in left ventricular volume, the
development of chronic heart failure and an adverse prognosis.
8
1.2.1
Treatment
Therapeutic options that exist for patients with ventricular remodeling include pharmacotherapy,
cardiac transplantation for heart failure, the surgical ventricular reconstruction according to Dor
and aneurysmectomy for patients who develop a left ventricular aneurysm during the early
remodeling phase. Understanding the pathophysiology, the goal of therapy is to alleviate
symptoms and to improve survival by preventing the progression of the remodeling process by
minimizing risk factors.
1.2.1.1
Medical Treatment
Pharmacological intervention include the use of angiotensin-converting enzyme inhibitors (ACEI), beta blockers (b-blockers) and digitalis glycosides.
ACE-I are used to inhibit the activation of the renin-angiotensin-aldosterone system which
become activated in heart failure. Indeed, the Studies of Left Ventricular Dysfunction (SOLVD)
trial has shown that ACE-I may reverse the remodeling process (53, 64, 90, 93). However, the
incidence of sudden death has not been reduced with the use of ACE-I (24). Randomized trials
have hitherto failed to define the optimal dose of ACE-I (59). Moreover, the side effects of ACEI, which include hyperkalemia, azotemia, angioedema or severe coughing may also prevent their
long-term use in individual patients.
B-blockers are used to decrease sympathetic stimulation due to ventricular failure and are
indicated for patients after a heart attack. However, for patients with reactive airway disease,
diabetes, bradyarrhythmias and heart block without a pacemaker, the use of b-blockers is
contraindicated.
Digitalis glycosides (primarily digoxin) are used for symptomatic patients with heart failure who
have a low ejection fraction. Recently, a randomized placebo-controlled study of digoxin showed
that the rate of a deteriorating heart and hospitalization decreased with the digoxin group.
However, there was no difference in mortality between the two groups (35). Furthermore, for
patients with renal failure, there are contraindications for the use of digoxin and potentially life
threatening side effects. Ventricular tachycardia or fibrillation, supraventricular arrhythmia, and
atrioventricular block also continue to pose significant problems with the use of digoxin.
Although medical treatment has prolonged the life expectancy in which 50% of patients with
heart failure now live 8 years (17), the number of deaths has increased steadily despite the
advances in treatment (55). For patients categorized in NYHA III or IV status, there remains an
adverse 3-year prognosis, despite the improvement of symptoms (74, 103). Past and recent
clinical trials have demonstrated that intervention with ACE-I and b-blockers may attenuate
remodeling (15, 53, 93), however the overall mortality rate is higher than surgical intervention
9
(17, 23, 24, 90). Furthermore, Sutton et al. (94) have reported that treatment beyond 1 year with
captopril (ACE-I) for patients from the SAVE trial (Surgical and Ventricular Enlargement trial)
had no affect on progressive ventricular dilatation and declining ventricular function.
1.2.1.2
Surgical Treatment
Surgical intervention offers an additional option for treatment for patients with chronic heart
failure and/or a remodeled ventricle. Surgical methods such as an implantable left ventricular
assist device (LVAD), coronary revascularization, heart transplantation for end-stage cardiac
failure, conventional aneurysmectomy and the Dor surgical ventricular reconstruction procedure
are discussed below.
LVAD is a mechanical device that serves to support patients with circulatory failure and
ventricular arrythmias. This device, however, is a temporary and not a permanent solution.
Disadvantages include high initial costs, substantial monitoring and complications such as
bleeding, infection and the risk of thromboembolism, since most devices do not have an
endothelial covering (98).
Myocardial reperfusion may modify ventricular enlargement by restoring the remaining viable
myocardium in the infarcted zone. Maintaining a patent vessel would salvage the vulnerable area
of myocardium that is most open to damage and thereby limit infarct expansion. Pfeffer et al.
observed a progressive ventricular enlargement over a period of one year in patients with an
occluded artery in the infarct area and attributed the increase in ventricular volume of 21 +/- 8 ml
to late effects on the viable myocardium at the border between infarcted and noninfarcted
myocardium (82). Reperfusion has also been demonstrated to reduce infarct size and improve
cardiac performance (9, 88). As a result, coronary revascularization has been used as a treatment
to possibly attenuate remodeling. However, despite the benefits of myocardial reperfusion, one
study noted higher mortality and the development of congestive heart failure when LVESV
index was 100ml/min/m2 or greater after revascularization alone (109). Among patients with a
low ejection fraction (EF) (EF<30%), the eight-year survival rate for revascularization alone was
58% (100). Furthermore, the value of revascularization in patients with left ventricular
dysfunction but no detectable ischemia is unclear.
Heart transplantation offers an additional therapeutic option for patients, particularly for those
with end-stage heart failure. However, organ availability continues to be a limiting factor, and
approximately 20% of patients on the waiting list die (69). In addition, rejection of the donor
organ remains a problem. Vasculopathy of the allograft after heart transplantation is the main
cause of illness and death after the first year (47).
10
In 1984, Dor et al. recognized the importance of excluding the noncontracting segment (either of
akinetic or dyskinetic nature) in the left ventricle in order to enhance cardiac function. He
postulated an improvement in ventricular function when nonfunctioning myocardium is resected
and replaced with an endoventricular patch which would restore the remodeled ventricle to its
normal elliptical form. This geometric approach, which is usually combined with CABG,
modified the first simple resection of a left ventricular aneurysm in 1958 by Cooley and later by
Jatene in 1962. Conventional aneurysmectomy involves resection of the aneurysm on a nonbeating heart followed by a longitudinal suturing of the opening (25) or a circular suture of the
orifice with or without a Dacron patch (57). The failure to address volume reduction and
ventricular reconstruction are the main disadvantages of traditional surgical methods. Dor's
procedure however, should be more advantageous in the long term because the physiological
distribution and pattern of the muscle fibers are taken into consideration by suturing a
intraventricular patch in place of the excluded dysfunctional myocardium. The ventricular size
and volume is subsequently reduced and concomitantly a CABG or repair of mitral valve is
performed when necessary.
CABG is an integral procedure in Dor's operation when patients present with ischemic
conditions, particularly since coronary artery stenosis is an underlying disease in patients with an
aneurysm and angina pectoris is a frequent indication for surgery (8, 20, 27, 34, 41, 80).
Furthermore, compared to revascularization alone for patients with an EF<30%, survival at eight
years was higher at a rate of 69% under the Dor SVR procedure (40).
1.3
Dilated Cardiomyopathy
The theory that cardiac reconstruction prevents progressive remodeling may also pertain to other
conditions of a pathologically enlarged heart, such as dilated cardiomyopathy (DCM).
Ventricular remodeling in DCM is progressive global dilatation, a decrease in systolic function
and a distortion of the mitral valve. The concept of reducing chamber diameter and subsequently
wall tension was therefore not only limited to ventricular remodeling after a myocardial
infarction, but was also performed on DCM.
By etiology, there are two fundamental forms of DCM (1) a primary myocardial involvement
which include idiopathic, familial; and (2) a secondary myocardial involvement which includes
infective DCM as a result of viral, bacterial, fungal, protozoal myocarditis; metabolic disease;
neuromuscular disease such as Duchenne's progressive muscular dystrophy; connective tissue
disorders such as systemic lupus erythematosus, rheumatoid arthritis, polyarthritis nodosa,
progressive systemic sclerosis and dermatomyositis; alcohol and drug toxicity, for example with
11
anthracycline derivatives, particularly doxorubicin; peripartum associated nutritional deficiency,
just to name a few.
Characteristic of DCM is the four chamber dilatation of the heart. In spite of the various causes,
the eventual result is cardiac muscle damage, myocardial degeneration and interstitial and
perivascular fibrosis leading to congestive heart failure which manifests in common clinical
symptoms. Patients diagnosed with dilated cardiomyopathy present with dyspnea, fatigue,
orthopnea, peripheral edema, palpitation, and paroxysmal nocturnal dyspnea (105).
Complications due to the poor cardiac contraction and the stasis of blood in the heart include
thrombus formation, systemic embolization, and ventricular arrhythmias which is closely
associated with sudden death (105). Two-year survival after the onset of heart failure is 35%, and
5-year survival is 10% (55). Because of the poor prognosis, particularly in patients with endstage cardiac disease, heart transplantation is recommended.
1.3.1
Treatment of DCM
The various options for treatment of DCM are maximal medical management for symptoms of
cardiac failure which overlaps with ICM, cardiac transplantation (which remains the standard
treatment), or surgical options which include dynamic cardiomyoplasty, LVAD or partial left
ventriculectomy (PLV). Initially proposed by Batista in Brazil in 1996, the Batista procedure, or
PLV, was developed for patients with end-stage dilated cardiomyopathy of various etiologies.
The principle behind PLV is to improve ventricular performance for patients with end-stage
cardiomyopathy by resecting viable cardiac muscle inorder to reduce the ventricular volume and
mass. Large segments of the left ventricular wall are resected from the lateral wall beginning at
the apex, extending between the papillary muscles, and ending proximal to the mitral annulus.
The wound is then closed by direct suture. Reduction of the end-diastolic diameter of the heart
thereby decreases wall tension and improves cardiac performance.
The objective of this study was to assess the effect of surgical ventricular reconstruction on
patients with left ventricular ischemia and idiopathic dilated cardiomyopathy and to evalute the
clinical outcome and long-term prognosis.
12
2
METHODS
2.1
Patient Population
Between February 1996 to July 1999, 47 patients underwent the Dor left ventricular surgical
reconstruction and 3 patients underwent the Batista partial left ventriculectomy at the
Department of Cardiovascular Surgery of Freiburg University Hospital. The Dor procedure or
the Batista procedure was offered on an individual basis to patients with presence of an
aneurysm or scar after a myocardial infarction, or to patients diagnosed with DCM. Candidate
selection was based on the decision of the attending surgeon performing the operation. Often the
decision to reconstruct the left ventricle in this study was made by the surgeon on the operating
table based on the size of the ventricle and appearance of the anterior wall.
2.2
Preoperative Assessment
2.2.1
Assessment of Ejection Fraction, Mitral Regurgitation, Left Ventricular EndDiastolic Diameter and Dyskinesia or Akinesia
Transthoracic echocardiography was performed preoperatively and postoperatively within the
first 48 hours in all patients to assess mitral regurgitation, ejection fraction, the presence of an
aneurysm or regional hypokinesia, and the left ventricular end-diastolic diameter (LVEDD).
The degree of mitral valve regurgitation was determined by standard color flow Doppler
ultrasonography. The severity of mitral valve inefficiency was assessed according to an
approximation of the flow velocity and spatial relationship to the left atrium. If the height of the
blood flow was shortly above the mitral valve, mitral valve regurgitation (MR) was considered
first degree. Second degree MR was determined when back flow of blood filled 1/3 of the left
atrium. When greater than 2/3 of the left atrium was filled with blood, MR was of third degree.
The ejection fraction was estimated by two-dimensional echography.
Akinesia and/or dyskinesia was determined not only with echocardiography, but in a fraction of
patients also by ventriculography, and magnetic resonance imaging.
The diastolic diameter of the left ventricle was measured before the start of cardiac muscle
contraction through M-mode echocardiography. M-mode echocardiography refers to a single
transducer that emits 1000-2000 pulses per second along a single line and is widely used to
measure left ventricular size and wall thickness. Not all measurements were available in every
patient. The LVEDD was not recorded in 19 patients due to suboptimal quality of images,
inability to obtain measurement or due to death one day after operation.
13
2.2.2
Cardiac Catheterization or Arteriography
All patients came with standard left heart catheterization and coronary angiography reports. For
patients with recurrence of clinical symptoms (unstable angina, postinfarction angina), repeat
coronary angiography was performed.
2.3
Surgical Procedures
2.3.1
Dor Surgical Ventricular Reconstruction (SVR) Procedure and the Modified
Dor Procedure
The surgical approach in the Dor SVR procedure and modified Dor procedure is to exclude the
apical and septal noncontractile area of the left ventricle, replace it with a patch and restore the
left ventricular shape to its original elliptical form (Figure 6). The main difference between the
two procedures is the "open-beating heart" technique in the modified Dor procedure. The beating
heart technique is used for myocardial protection inorder to limit the amount of ischemia and to
better evaluate the border between contracting and noncontracting myocardium in postinfarction
left ventricular akinesia.
Figure 6. The Dor SVR procedure.
An anteroseptal incision is made at
the
apical
segment
of
the
myocardium. The aneurysm or
noncontracting scarred segment is
excised. In the modified Dor
procedure, palpation of the beating
heart allows the surgeon to make a
clearer
distinction
between
contracting
and
noncontracting
muscle. Inclusion of a Fontan stitch
systematically
narrows
the
aneurysmal neck, helps to restore the
physiological
geometry
of
the
ventricle and allows a more tailored
insertion of the Dacron patch. An
appropriate reconstruction of the
ventricle is achieved (36).
14
The Dor surgical ventricular reconstruction was conducted with the use of a cardiopulmonary
bypass machine under total cardiac arrest with aortic cross clamping. In the case of the modified
Dor procedure, the aortic cross-clamp is removed to restore the beating state. Palpation and
inspection allowed the surgeon to determine the border between contracting and noncontracting
myocardium. Preoperative dynamic assessment of the left ventricle through ventriculogram or
echocardiogram enabled the surgeon to prepare in advance the location of the nonfunctioning
myocardium to be excised. A ventricular anteroseptal incision was made, the visible scar or
aneurysm was located and calcified or fibrous endocardium or in the case of an aneurysm, the
dyskinetic myocardium was resected. In large anterior infarctions, the scarred septum was also
resected since it is frequently affected as a result of an occluded anterior descending artery. A
circumferential Fontan stitch (2-0 monofilament suture) was placed in the inner wall of the
muscle to reduce cavity size and create a "surgical neck" for the exclusion of
noncontracting/nonfunctioning sections of the muscle. The "Fontan-Neck Suture" was then
pulled closer together to build the more physiological ventricle volume and to help measure the
dimensions of the patch. Depending on the size of the opening, the remaining aperture was
directly closed or if the endocardium was fibrous or resistent, the aperture was closed with an
oval Dacron patch which was fixed on the Fontan Neck suture. The excluded segment was either
sutured directly above the patch or folded or glued over the patch for hemostasis.
2.3.2
Batista Partial Left Ventriculectomy (PLV) Procedure
The surgical approach in the Batista procedure is to reduce the end-diastolic diameter of the LV
for patients with end-stage dilated cardiomyopathy. Under conventional blood cardioplegic
arrest, viable muscle section was resected from the lateral wall beginning at the apex, extending
between the papillary muscles and ending proximal to the mitral annulus. The left ventricle was
then closed by direct suture.
2.3.3
Concomitant Procedures
The Dor operation was combined with CABG if the segment to be resected was associated with
coronary artery disease and a distally graftable vessel was available. The Dor procedure also
included mitral valve (MV) repair for patients with moderate-to-severe mitral regurgitation
(Grade 3-4). Both associated coronary grafting and MV repair were performed before left
ventricular reconstruction. In the case of severe aortic valve inefficiency, replacement or
reconstruction was performed. Intraaortic balloon counterpulsation (IABP) and epicardial
defibrillator implantation were available for mechanical support after the operation.
15
2.4
Telephone Interview
The NYHA functional classification of heart disease is used as a means of quantifying the
limitation on activity imposed by the symptoms of patients with cardiac failure. It is grouped in
four classes as follows; NYHA Class I: No limitation on physical activity. Normal, everyday
activity does not cause dyspnea, fatigue or anginal pain. Class II: Slight limitation of physical
activity, or more specifically, symptoms are present upon more strenuous physical activity. Class
III: Marked limitation of physical activity. (Symptoms are present upon less than ordinary
activity and already by trivial physical activity.) Class IV: Symptoms may be present even at
rest. (Unable to conduct any physical activity without feeling discomfort.)
Postoperative NYHA functional class was obtained by a follow-up personal interview by
telephone and was conducted from March - September 1999. In most cases there was direct
contact with the patient. For those patients who could not be reached for the telephone interview,
NYHA status was extrapolated through hospital records, interview with the patients' physician,
and/or with immediate family members.
Patients were asked how their overall condition was at the time of the interview. Did they find
themselves in excellent condition, in good condition, or were they impaired within the last
month. The following specific questions were asked:
¾
Are you working?
¾
Do you have shortness of breath, are you fatigued, and do you have anginal pain by daily
routine such as grocery shopping, cooking, cleaning around the house? If so, at what point,
at 10 minutes, 30 minutes or 1 hour;
¾
Do you have shortness of breath, are you fatigued, and do you have anginal pain when
walking on an even level? If so, at what point, at 10 minutes, 30 minutes or 1 hour;
¾
Do you have shortness of breath, are you fatigued, and do you have anginal pain when
walking on an inclined level? If so, at what point, at 10 minutes, 30 minutes or 1 hour;
¾
Do you have shortness of breath, are you fatigued, and do you have anginal pain when
climbing stairs?
¾
How many stair cases can you climb before feeling shortness of breath?
With respect to exertional dyspnea, patients were asked to rate their shortness of breath from a
scale of 0 - 10 , 0 being no shortness of breath and 10 being extreme shortness of breath.
16
Data Analysis
Statistical assessment of the NYHA functional class for the ICM and DCM groups was
performed with the Wilcoxon signed rank test, using Prism Graph software. The paired T-test
was used for EF and LVEDD assuming Gaussian distribution. Univariate analysis of survival
was performed by Kaplan-Meier statistics with the help of Prism Graph software. Data are
expressed as means + SD. P < 0.05 is considered significant.
17
3
RESULTS
3.1
Preoperative Clinical Data (Table I) and Surgical Procedures (Figure 7)
Forty-three patients were diagnosed with ischemic cardiomyopathy with extensive ventricular
anterior akinesia (scar) or dyskinesia (aneurysm). The age ranged between 52 and 80 years with
a median age of 67. There were 24 male and 19 women in the ICM group. Risk factors included
diabetes in 15 patients (35%), hypertension in 27 patients (63%), hypercholesterolemia in 35
patients (81%) and smoking in 18 patients (42%). Coronary angiography showed single vessel
disease in 7 patients (16%), double vessel disease in 9 patients (20%), and triple vessel disease in
19 patients (43%). 36 (84%) patients presented with ventricular aneurysm and 7 (16%) with
ventricular scar as a result of ICM. There were 5 patients in NYHA class II, 27 in NYHA class
III and 10 in NYHA class IV.
There was a total of 7 patients, all male who were diagnosed with DCM. The age ranged from 15
to 67 years, with a median age of 47.5 years. Co-morbidities for 3 out of the 6 patients included
1 patient with ventricular arrhythmia Lown IVb; 1 patient with COPD, alcohol toxic hepatitis
and ventricular arrhythmia Lown III; and 1 patient with Kiener-Becker type muscle dystrophia
and ventricular arrhythmia Lown III. There were 4 patients classified in NYHA III and 3 patients
in NYHA class IV. Mean LVEDD was 77 mm.
Table I. Preoperative characteristics of patients before reconstruction surgery
No. of Patients
Age
Male/Female
Risk Factors:
Coronary artery disease:
Mitral valve regurgitation:
Type of lesion:
EF % (mean + SD)
LVEDD [mm] (mean + SD)
NYHA
Diabetes
Hypertension
Hypercholesterolemia
Smoking
1 vessel
2 vessels
3 vessels
Grade 1
Grade 2
Grade 3
Dyskinesia
Akinesia
I
II
III
IV
ICM
43
52-80
24/19
15
27
35
18
7
9
19
15
4
1
36
7
31 (+ 8.4)
61 (+ 7.3)
0
5
27
10
DCM
7
15-72
7/0
0
3
1
2
2
2
18 (+ 7.5)
77 (+ 4.2 )
0
0
4
3
18
Figure 7 presents the two surgical techniques and the number of patients in the ICM and DCM
group. It also categorizes the associated surgical procedures performed and the number of
patients who received the additional surgical procedures. The results for each subgroup are
described in the following sections.
50 Patients
Total
Procedure
Dor SVR: 47
Batista: 3
Indication
DCM: 5
Concomitant
CABG?
+MR: 1
Dyskinesia: 36
+CABG: 25
-MR: 4
-CABG: 11
+MR: 1
-MR: 10
Akinesia: 6
+CABG: 5
DCM: 2
-CABG: 1
Concomitant
MR?
+MR: 1
+CABG: 1
Akinesia: 1
-CABG: 0
-MR: 1
Figure 7. Surgical Techniques and Concomitant Procedures.
SVR: Surgical ventricular reconstruction. DCM: Dilated cardiomyopathy. CABG:
Coronary Artery Bypass Grafting. MR: Mitral Valve Replacement.
3.2
Dor SVR Procedure
Thirty-six patients were operated on for the presence of ventricular dyskinesia (aneurysm). 25
patients out of the 36 underwent concomitant CABG with a mean number of 2.4 distal
anastomoses per patient. The remaining 11 patients did not receive CABG. Additional surgical
procedures included one mitral valve reconstruction for a patient in the non-CABG group. There
were 6 patients with ventricular akinesia (scar) who also underwent the Dor procedure with 5
receiving concomitant CABG. The mean number of distal anastomoses per patient for this group
was 2.8. In addition to the dyskinesia/akinesia group, there were 5 patients diagnosed with DCM
who underwent the Dor procedure. Out of the 5 patients, 1 patient, who also received a mitral
and aortic valve reconstruction, experienced severe ventricular arrhythmias after 4 months and
was subsequently transplanted on a emergency basis.
19
Other associated surgical procedures to the Dor operation included 1 patient who underwent
closure of a ventricular and atrial septal defect; 1 patient who underwent a pericardectomy for
pericarditis constrictiva; 1 patient who underwent an atrio-ventricular fistula closure; 1 patient
who underwent a papillary muscle plastic and 2 patients who received an aortic valve
replacement due to severe stenosis.
The mean durations of aortic cross clamping and cardiopulmonary bypass were 66.9 minutes and
114.2 minutes, respectively.
A total of 4 patients who underwent the Dor procedure required postoperative mechanical
support: The condition of 1 of the 31 patients with preoperative NYHA status III disease steadily
deteriorated, requiring an IABP, as with 3 of the patients in preoperative NYHA status IV
disease. An epicardial defibrillator implantation was also required for 1 patient diagnosed with
idiopathic DCM.
3.2.1
New York Heart Association (NYHA) Status
Figure 8 depicts the change in NYHA status before and after the Dor SVR procedure for patients
with a left ventricular aneurysm (dyskinesia) who received concomitant CABG and for those
who did not. NYHA functional class was recorded for 35 patients at a median follow-up of 19
months (2-36 months). In a range of NYHA class I - IV, a significant improvement in NYHA
functional class was demonstrated for the aneurysm group as a whole (p = 0.003).
Post
operatively, 6 (17%) were in NYHA I, 16 (46%) were in NYHA II, 8 (23%) were in NYHA III,
and 5 (14%) in NYHA class IV. When subgroups broken down to CABG and non-CABG
patients were analyzed, the subgroup consisting of 25 patients with associated coronary grafting
demonstrated a significant improvement in NYHA (p = 0.0008). The non-CABG group
consisting of 11 patients demonstrated no significant improvement in NYHA functional class (p
= 0.1953).
For the 6 patients with left ventricular akinesia and the 5 DCM patients who also underwent the
Dor SVR procedure, Figure 9 and Figure 10 depicts respectively the NYHA status pre- and post
operation. No significance could be demonstrated due to the small number of patients. However,
an overall improvement was evident for both groups. In the ventricular akinesia group,
postoperational NYHA functional class was recorded for 5 patients: 2 (40%) were in NYHA
class I and 3 (60%) were in NYHA II (Figure 9). Postoperational NYHA functional class was
recorded for 4 patients in the DCM group. 3 (75%) were in NYHA class II and 1 (25%) were in
NYHA III (Figure 10).
20
+ CABG
- CABG
I
II
III
IV
Death
Pre-Op
Post-Op
Pre-Op
Post-Op
Figure 8. Change in New York Heart Association functional class in patients with
postinfarction left ventricular aneurysm. Pre and Post (before and after) Dor surgical
ventricular reconstruction.
I
I
II
II
III
III
IV
IV
Death
Death
Pre-Op
Post-Op
Figure 9. Change in New York Heart
Association functional class in patients
with
postinfarction
left
ventricular
akinesia. Pre and Post (before and after)
Dor surgical ventricular reconstruction
Pre-Op
Post-Op
Figure 10. Change in New York Heart
Association functional class in patients
with idiopathic DCM. Pre and Post
(before and after) Dor surgical
ventricular reconstruction.
21
3.2.2
Echocardiographic Results to Determine Effect of Operation
Transthoracic echocardiographic measurements of ejection fraction and left ventricular enddiastolic diameter before and after the Dor SVR procedure are shown in Table II. A significant
increase in ejection fraction was demonstrated for the ventricular aneurysm group (p = 0.001).
Mean preoperative EF was 31% increasing postoperatively to 35%. When CABG and nonCABG patients within the aneurysm group were separately analyzed, the patients with
concomitant CABG did not demonstrate a significant increase in EF (p = 0.1360), whereas the
patients without concomitant CABG did demonstrate a significant increase in EF (p = 0.011)
(Table II). EF improvement for patients with ventricular akinesia and patients with DCM was not
statistically significant, although they did demonstrate an increase: Patients with ventricular
akinesia went from a mean preoperative EF of 31.0% to postoperative 32.5%. For the 5 DCM
patients, mean preoperative EF was 19.0% and increased postoperative to 22.0%. Preoperative
LVEDD for patients with ventricular aneurysm measured 61mm and decreased significantly to
58mm (p = 0.0002). LVEDD for patients with ventricular akinesia decreased from 66mm to
62mm and LVEDD for the DCM patients decreased from a mean of 77 mm to 75 mm (Table II).
Table II. Echocardiographic changes in patients before and after Dor surgical
reconstruction
Ejection Fraction (%)
LVEDD (mm)
Pre-Op
Post-Op
P
Pre-Op
Post-Op
p
Dyskinesia
30.9 (+8.3)
34.5 (+6.9)
0.001
61 (+8.0)
58 (+8.0)
0.0002
+ CABG
31.4 (+9.2)
34.1 (+7.2)
0.136
- CABG
30.0 (+5.7)
35.5 (+6.1)
0.011
Akinesia
31.0 (+8.6)
32.5 (+10.0)
n.s.
66 (+4.0)
62 (+3.0)
n.s.
DCM
19.0 (+8.0)
22.0 (+7.5)
n.s.
77 (+1.2)
75 (+3.3)
n.s.
Mean (+SD) Ejection Fraction and Left Ventricular End-Diastolic Diameter (LVEDD)
n.s.: not significant
22
3.2.3
Survival under Dor SVR Procedure
Overall survival for both ICM and DCM patients who underwent the Dor surgical ventricular
reconstruction was 85% at a median follow-up of 19 months (2-36 months) (Figure 11).
Proportion alive
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0.0
Figure 11. Kaplan-Meier survival
curve with 95% confidence
intervals for all 47 patients who
underwent the Dor surgical
ventricular reconstruction. Median
follow-up was 81.5 weeks (range
from 4-160 weeks).
0
20
40
60
80
100 120 140 160 180
Weeks
For the 36 patients with left ventricular aneurysm, overall survival was 89% at a median followup of 19 months (2-36 months). Figure 12 shows a comparison of the overall survival for
patients who underwent associated CABG and non-CABG patients. There was a significantly
better survival rate of 96% for the CABG group in comparison to a 73% survival rate for the
non-CABG group (Figure 12). When age, ejection fraction and NYHA functional class were
compared, there were no alternative explanations for the different outcome between both groups
(Table III).
Proportion alive
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0.0
Figure 12. Kaplan-Meier survival
curve comparison with 95%
confidence intervals between Dor
surgical ventricular reconstruction with associated coronary
artery bypass grafting and
without. Survival for patients with
CABG was 96% over a threewith CABG
year period as opposed to 73%
without CABG
when concomitant CABG was not
performed. Median follow-up was
81.5 weeks (range from 4-160
100 120 140 160 180 weeks).
p = 0.0455
0
20
40
60
80
Weeks
23
Table III. Patients with left ventricular aneurysm: Characteristics between patients
who underwent the Dor procedure with associated CABG and those without CABG.
n.s.: not significant
+ CABG
- CABG
25
11
Mean Age (years) + SD
66.8
68.9
n.s.
Male/Female
17/8
4/7
n.s. (p= 0.345)
Preoperative EF (mean) + SD
31.4 (9.2)
30.0 (5.7)
n.s.
Postoperative EF (mean) + SD
34.1 (7.2)
35.5 (6.1)
n.s.
Preoperative NYHA
3.0
3.1
n.s.
Postoperative NYHA
2.1
2.5
n.s.
+2
3 (12%)
1 (9%)
n.s.
+1
14 (56%)
5 (45%)
+0
5 (20%)
3 (27%)
-1
1 (4%)
1 (9%)
No. of patients
NYHA change
p values
Out of the 6 patients with left ventricular scar (akinesia), overall survival was 67% at a median
follow-up of 10.5 months (1-20 months) (Figure 13). When all patients with associated coronary
grafting in the ventricular aneurysm (dyskinesia) and ventricular scar (akinesia) groups were
compared, there was a trend for superior outcome (p = 0.0587) for the dykinesia group (Figure
14). The difference, however does not reach statistical significance perhaps due to the small
number of a patients in the ventricular scar group. The overall survival for the 5 DCM patients
was 80% at a median follow up of 5.5 months (1-10 months). One of the surviving patients,
however, did receive a heart transplantation approximately 4 months after the Dor procedure due
to severe ventricular arrhythmia.
Proportion alive
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0.0
Figure
13.
Kaplan-Meier
survival curve with 95%
confidence intervals for 6
patients with Dor surgical
ventricular reconstruction for
ventricular akinesia. Survival
was 67% at a median followup of 42.5 weeks (range from
6-79 weeks).
0
20
40
60
80 100 120 140 160 180
Weeks
24
Proportion alive
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0.0
Figure 14. Kaplan-Meier
survival curve comparison
with 95% confidence intervals
between
the
ventricular
aneurysm and ventricular
scar groups for patients who
underwent the Dor surgical
ventricular reconstruction with
CABG.
p = 0.0587
Dyskinesia
Akinesia
0
20
40
60
80
100 120 140 160 180
Weeks
3.2.4
Hospital Mortality and Late Deaths
Overall hospital mortality after the Dor SVR procedure was 4% (2/47) (Table IV). Both patients
died within one day after the operation. One of the patients had constrictive pericarditis as
comorbidity, the other patient died of cardiac complications. There was a total of 5 late deaths (>
4 weeks) after the Dor SVR procedure. Left ventricular decompensation was the cause of 3 of
the late deaths five, nine and fifty-nine weeks after the operation. The other 2 late deaths could
not be determined (Table IV).
Table IV. In-hospital and late deaths for patients after Dor procedure with LV aneurysm
Procedures
Patients
Hospital deaths
Late deaths (>4 weeks)
SVR
12
1
3
SVR + CABG
28
1
2
SVR + CABG + VSD
1
0
0
SVR + MVR
2
0
0
SVR + AVR
2
0
0
SVR + CABG + AVR
1
0
0
SVR + AVFC
1
0
0
Total
47
2
5
SVR: surgical ventricular reconstruction; CABG: coronary artery bypass grafting; VSD:
ventricular septal defect repair; MVR: mitral valve repair; AVR: aortic valve repair;
AVFC: atrio-ventricular fistula closure.
25
The other 2 out of 5 late deaths were patients with a left ventricular scar (Table V). Both
underwent associated coronary grafting for 3 diseased coronary arteries. One of the patients died
59 weeks after the Dor procedure due to cardiac failure, the other patient died 6 weeks after the
operation of unknown cause. The last of the five late deaths was a patient diagnosed with DCM
who died 9 weeks after the Dor SVR procedure (Table VI). The cause of death was septic shock
after developing pneumonia in the context of pre-existing chronic obstructive pulmonary disease.
Table V. In-hospital and late deaths after Dor procedure for patients with LV Scar
Procedures
Patients
Hospital deaths
Late deaths (>4 weeks)
SVR + CABG
5
0
2
SVR + ASD + VSD
1
0
0
Total
6
0
2
SVR: surgical ventricular reconstruction; CABG: coronary artery bypass grafting; ASD:
atrial septal defect repair; VSD: ventricular septal defect repair. Both patients had triple
vessel coronary artery disease.
Table VI. In-hospital and late deaths after Dor procedure for patients with DCM
Procedures
Patients
Hospital deaths
Late deaths (>4 weeks)
SVR + MVR + AVR
1*
0
0
SVR without MVR
4
0
1
Total
5
0
1
SVR: surgical ventricular reconstruction; MVR: mitral valve repair; AVR: aortic valve
repair.
*The patient who underwent mitral and aortic valve reconstruction required a heart
transplantation 4 months after the Dor operation due to ventricular arrhythmias.
26
3.3
Batista PLV Procedure
The Batista PLV procedure was carried out in 3 patients: 1 diagnosed with idiopathic DCM, 1
who developed a secondary DCM as a consequence of myocardial infarction, and 1 post
infarction patient with a left ventricular scar (akinesia). Additional surgical procedures to the
Batista reduction included a mitral valve replacement for the patient with secondary DCM,
associated CABG for 3 diseased coronary arteries for the patient with akinesia, and an epicardial
defibrillator implantation for the one patient with idiopathic DCM as a precaution due to prior
episodes of ventricular tachycardia.
3.3.1
NYHA Status
In a range of NYHA class I - IV, for patients who underwent the Batista PLV procedure, the
patient with idiopathic DCM and the patient with ventricular akinesia improved from NYHA
class III to NYHA class II.
3.3.2
Echocardiographic Results to Determine Effect of Operation
Transthoracic echocardiographic parameters before and after the Batista PLV procedure are
presented in Table VII. Mean preoperative and postoperative EF for patients with DCM was
16.2% increasing to 20.0%, and for the 1 patient with akinesia, preoperative EF was 20.0%
increasing postoperative to 37%. Preoperative LVEDD for both DCM patients measured 78 mm
and decreased postoperatively to 68 mm (Table VII).
Table VII. Echocardiographic changes in patients before and after Batista PLV ejection
fraction, left ventricular end-diastolic diameter (LVEDD) and mitral valve insufficiency
Ejection Fraction (%)
LVEDD (mm)
Mitral Valve
Insufficiency
Pre-Op
Post-Op
Pre-Op
Post-Op
Pre-Op
Post-Op
Akinesia
20.0
37.5
-
-
3
2
2O DCM
17.5
15
84
69
4
(death)
15
25
71
66
3
2
IDCM
27
3.3.3
Hospital Mortality and Late Deaths under Batista PLV Procedure
Out of the 3 patients who underwent the Batista PLV procedure, one patient diagnosed with
secondary DCM who was in NYHA class IV, died 14 weeks after the operation (Table VIII).
The cause of death could not be determined due to missing records and an unlisted telephone
number.
Table VIII. In-hospital mortality and late deaths after Batista procedure for patients with
DCM and LV scar (Akinesia)
Procedures
Patients
In-hospital deaths
Late deaths (>4 weeks)
PLV + CABG
1
0
0
PLV + MVR
1
0
1
PLV without MVR
1
0
0
Total
3
0
1
PLV: Partial left ventriculectomy; MVR: Mitral valve repair; CABG: Coronary artery
bypass graft
28
4
DISCUSSION
In this retrospective study, 47 patients underwent the Dor surgical ventricular reconstruction for
ventricular dysfunction and remodeling after an infarction for either left ventricular akinesia or
dyskinesia and dilated cardiomyopathy. Results of the in-hospital deaths demonstrate that the
Dor SVR procedure is feasible due to the low perioperative mortality. The results of this study
also underscore the prognostic importance of associated coronary grafting to the procedure.
Although results of the clinical outcome for the 36 patients with ventricular aneurysm
(dyskinesia) indicate that the Dor SVR procedure has an immediate significant effect on LVEDD
and ejection fraction and in the long-term significantly improves NYHA functional class, these
parameters require critical reappraisal whether they permit valid assessment of the benefit of this
procedure. Transthoracic measurements of LVEDD and EF do not allow firm conclusion with
respect to the prognostic value of the Dor SVR procedure and its impact on long-term survival
and quality of life. Furthermore, a new approach to the classification of heart failure has been
developed since the NYHA classification has shown serious limitations.
Operative Feasibility
The overall operative mortality of only two out of fifty patients demonstrates the feasibility of
the Dor surgical ventricular reconstruction for patients with postinfarction left ventricular
aneurysm and scar and patients with idiopathic DCM. This result is similar to previous studies
that have also demonstrated the safety and efficacy of this surgical method on patients with
ventricular dysfunction after an infarction for either left ventricular akinesia or dyskinesia (4, 31,
33, 34, 38, 39, 41).
Immediate Improvement in Ventricular Function: LVEDD after the Dor SVR Procedure
for patients with postinfarction left ventricular aneurysm
The best assessment of left ventricular end-systolic volume reduction in our data was the
echographic measurement of the change in LVEDD before and after the operation, since endsystolic volume was not measured in this retrospective study. A significant decrease (p = 0.0002)
from a mean preoperative LVEDD of 61mm to postoperative 58mm was demonstrated for all
patients with a left ventricular aneurysm after Dor surgical ventricular reconstruction. Patients
with a left ventricular scar and patients with DCM also demonstrated a decrease in diameter
although the number of patients in each group were too small to be statistically significant. The
LVEDD measurement taken at the level of the posterior papillary muscles to the left ventricular
wall however, is not an accurate calculation of the reduction in volume. Due to the method of
29
measuring the LVEDD, particularly in the presence of an aneurysm a small reduction in the
diameter may severly underestimate a reduction in volume. Therefore, the reduction of LVEDD
is not an appropriate estimation of volume reduction when an aneurysm is present. More
efficient
is
the
direct
measurement
of
volume
reduction
with
three-dimentional
echocardiography or magnetic resonance imaging of the left ventricle.
Reducing left ventricular dilatation and end-systolic volume is of prognostic importance. Prior
studies have demonstrated that left ventricular dilatation after an infarction is a major risk factor
for severe ventricular dysfunction and cardiac death (52, 104) and end-systolic volume (ESV) as
one of the most significant predictive factors of prognosis (54, 73, 104, 109).
The advantage of the Dor SVR procedure over conventional medical therapy is the immediate
reduction of ventricular cavity and size and subsequent reduction of ventricular volume.
Although ACE-I therapy with enalapril have demonstrated the prevention of a progressive left
ventricle dilatation (53, 64), a mean reduction in ventricular dilatation was not achieved. In fact,
ACE-I with captopril beyond 1 year had no effect on progressive dilatation and declining late
ventricular dysfunction (94). Despite studies in canine ventricles (61, 70) that demonstrated a
reduction in ventricular volume after captopril treatment and a substudy of the Studies of Left
Ventricular Dysfunction (SOLVD) that also observed a volume reduction in response to
enalapril (53), the mean changes in ventricular volume have been small.
Whereas medical therapy has not demonstrated a significant reduction in ESV, Dor et al. and
other studies employing the Dor SVR procedure or the modified Dor have demonstrated a
significant reduction in end-systolic volume index (ESVI) (Figure 15).
ESVI (ml/m2)
180
160
Pre-operative
Post-operative
Figure 15. Change in
pre- and postoperative
mean
end-systolic
volume index (ESVI)
after
Dor
surgical
ventricular reconstruction
for
left
ventricular
akinesia and dyskinesia
as reported by 5 studies.
140
120
100
80
60
40
20
0
Ref.
41
32
4
34
90
30
Immediate Improvement in Ventricular Function: Ejection fraction after the Dor SVR
Procedure for patients with postinfarction left ventricular aneurysm
Ejection fraction as a measure of short-term success of the operation during hospital stay was
demonstrated in this study for patients after ventricular aneurysmectomy and surgical
reconstruction. When patients in the left ventricular aneurysm group with CABG were compared
to patients without CABG, only non-CABG patients demonstrated a significant increase in EF.
This is in contrast to previous studies that demonstrate a definite correlation between coronary
artery bypass grafting and improved EF (88, 3).
The explanation for a statistically insignificant difference in EF for patients with associated
CABG may have been the result of detecting with echocardiography. Poor image quality or the
foreshortening of the ventricular cavity by the tomographic plane leads to suboptimal
echocardiographic measurements (53). In this study, ejection fraction was calculated subjectively
with transthoracic echocardiography on the basis of an individual visual approximation. A less
observer-dependent and highly accurate measurement of ejection fraction for patients with heart
failure is achieved with diagnostic tools such as the radionuclide angiography and
ventriculography (101, 106, 107). Standardizing imaging planes and recording techniques, and
consistency with one or two examiners responsible for data analysis without knowledge of
patient's clinical course might result in a more accurate ejection fraction. Whether however,
ejection fraction is the most significant indicator of left ventricular function after a myocardial
infarction is unclear (72).
Although EF has been demonstrated in the past to be an indicator for left ventricular pump
function (28, 53, 54, 68, 86, 96), a low EF may be caused by persisting ischemia or contractile
dysfunction due to remaining myocyte damage or due to damaging secondary changes to the
noninfarcted myocardium (11, 52, 81). Furthermore, a low ejection fraction as a meaningful
index in predicting prognosis has been otherwise demonstrated. In one study, a low ejection
fraction (<=30%) was associated with an 80% one-year mortality for patients with an aneurysm,
however in the group without an aneurysm, a relatively low mortality (7%) was observed despite
the same low ejection fraction (72). The implication that the presence of an aneurysm is a greater
prognostic indicator than EF has been demonstrated in previous studies that showed a
significantly lower actuarial survival of patients with ventricular aneurysm than persons without
an aneurysm (46, 52, 72). Several explanations would account for this. When an aneurysm
exceeds 20-25% of the surface of the left ventricle, the rest of the functioning myocardium
would have to exceed its physiological contraction limit by an additional 30% of initial
myocardial fiber length, resulting in a decreased stroke volume (62). An increased wall stress as
a result of the expansion in the infarcted region leads to increased myocardial oxygen
31
requirement which may be a risk factor for ventricular fibrillation due to the reentry of electrical
impulses between normal myocardium and infarcted myocardium (104). Sudden death due to
ventricular tachycardia and rupture accounted for 55% mortality for patients with an aneurysm
(72).
Therefore, EF does not allow a firm conclusion with respect to its importance as a parameter for
determing the benefit of this procedure. Echocardiographic calculation of EF is dependent on the
practical skills of the examiner and the inherent shortcoming of detecting with echocardiography
as mentioned above. Furthermore, of the 41 out of 50 documented cases in this study, 37 patients
received positive intropes during the operation.
Other parameters such as the left ventricular end-systolic volume and the evaluation of right and
left ventricular filling pressures, and hemodynamic measurements in addition to ejection
fraction, such as cardiac output and stroke volume at rest and during exercise at steady-state
conditions (on a supine bicycle) are better prognostic indicators (52). However, these objective
parameters were not assessed in this retrospective study.
Long-term Function: NYHA Status after the Dor SVR Procedure for patients with
postinfarction left ventricular aneurysm and scar
The major objective of therapy besides improving survival, is to improve cardiac function. After
left ventricular aneurysmectomy and surgical reconstruction, 35 out of 36 recorded patients at a
median follow-up of 19 months (2-36 months) demonstrated a significant improvement (p =
0.0003) in NYHA functional class. Whereas 86% were in NYHA class III/IV before the
operation (66% in NYHA III and 20% in NYHA IV) only 31% were in NYHA III/IV after the
operation and the majority (51%) improved to NYHA II/I (43% in NYHA II and 8% in NYHA
I). These results are similar to other studies using the same surgical method that also
demonstrated an improvement from NYHA III/IV to NYHA I-II (4, 33, 36, 40, 74).
When patients in the left ventricular aneurysm group were subgrouped into CABG and nonCABG patients, a statistically significant (p = 0.0008) improvement in NYHA functional class
was demonstrated only for patients with associated coronary grafting. Before surgical ventricular
reconstruction, 67% of the patients were in NYHA class III. After the operation, 54% improved
to NYHA II and 13% improved to NYHA I.
Although statistical significance could not be assessed in the small number of patients with left
ventricular akinesia, the most impressive degree of change in functional class improvement and
recovery was observed in this group of patients who underwent the Dor SVR procedure with
associated coronary grafting. One patient out of 6 in the akinesia group, went from NYHA IV to
NYHA I and three advanced to NYHA class I and II. These observations support the findings of
32
previous investigators who have demonstrated the benefit of surgical reconstruction for patients
not only with ventricular dyskinesia but also for patients with left ventricular akinesia (4, 5, 10,
33, 40).
Whether the current NYHA classification will suffice as a reliable parameter in judging the
success of the Dor SVR procedure is questionable. Until recently, the American College of
Cardiology and the American Heart Association (ACC/AHA) developed a new approach to the
classification of heart failure. In the past, functional limitations on activity imposed by the
symptoms of heart failure was described in a classification according to the New York Heart
Association (NYHA). Unfortunately, this classification had major limitations since patients
symptoms varied from days to weeks and assessment was subjective according to each
physician. Furthermore, the structural prerequisites for the development of cardiac failure was
not included. As a consequence, a new approach to the classification of heart failure that focused
on the process of change and the progression of heart failure was developed (56). Although it is
not intended to replace NYHA classification, it was developed to objectively evaluate the
progression of the patients disease. Patients are evaluated and defined in four stages from A to D.
Stage A patients are at high risk for the development of heart failure, however have no structural
abnormality of the heart; stage B patients have structural ventricle abnormality, however has
never developed symptoms of heart failure; stage C patients have structural abnormality and
have past or current symptoms of heart failure; and stage D patients have end-stage symptoms of
cardiac failure that are unmanageable with standard treatment. For diagnostic and coding
purposes, stage C and D are recognized as clinical diagnosis of heart failure. The benefit of this
new classification is the focus on the development and advancement of cardiac failure and helps
to identify and screen patients who are at risk and patients who are chronically ill. This allows
for a more critical assessment of which patient would benefit from an operation such as the Dor
SVR procedure.
Prognosis and Survival after the Dor SVR Procedure for patients with postinfarction left
ventricular aneurysm
The 89% three-year survival and 96% with associated coronary grafting for patients with a
ventricular aneurysm who underwent the Dor surgical ventricular reconstruction is higher than
the three-year survival rate of previously published aneurysmectomies and medical therapy. In a
series of aneurysmectomies combined with CABG performed from 1979-1987, the mean threeyear cumulative survival rate with conventional aneurysmectomy was 73% (2, 8, 14, 20, 58, 60,
63, 85). The advantage of the Dor SVR procedure over conventional aneurysmectomy is the
exclusion of the scarred areas in the septum, which cannot be achieved with standard linear
33
suture, and use of an endoventricular patch in replacement of the excised dysfunctional
myocardium to establish normal fiber orientation and restoration of the physiological elliptical
form of the ventricle.
In comparison to the data reported in this study, medical therapy has demonstrated a 79% threeyear actuarial survival for patients with an aneurysm (50). From a series of conservative medical
therapy from 1954-1978 for patients with a ventricular aneurysm, the mean three-year
cumulative survival rate was 61% (12, 44, 78, 83, 87). Furthermore, in selected heart failure
trials, conservative medication with the use of enalapril and digoxin reported a 1-year mortality
that ranged from 12.5% - 52% (23, 24, 35, 90).
Whereas some studies have observed higher operative mortality with extensive coronary disease
and concomitant CABG to aneurysmectomy (20, 49, 80), and yet others (4, 8, 79, 80, 91, 108)
have observed a higher actuarial survival with associated CABG, the data in this study support
the prognostic benefit for patients when CABG is concomitantly performed. At a median followup of 19 months (2-36 months) there was a 96% over a 73% survival rate for patients with a left
ventricular aneurysm who underwent associated coronary grafting to the Dor SVR procedure in
comparison to non-CABG patients. When age, ejection fraction and NYHA functional class
were compared between the two groups, no differences were noted. The only difference was
seen in patient gender population. Gender bias, however, did not affect overall survival, (p =
0.345) although more women did not undergo associated CABG with the operation.
Patent arteries have been associated with a limited infarct expansion and improved prognosis
after a myocardial infarction (9, 49, 52, 88, 82, 84). Trachiotis et al. demonstrated in patients
with ischemia and poor left ventricular function (EF < 25%) relief of symptoms and possible
salvage of remaining viable myocardium after first-time coronary artery bypass grafting (100).
Improved left ventricular function and ejection fraction compared to patients with an occluded
artery have also been reported (88, CASS). By establishing patency in the infarct-related artery,
it has been postulated that the degree of remodeling is effected (82) since revascularization
would improve stress responses to the remaining contractile myocardium (21). The lower
survival rate in this study for patients with an aneurysm without associated CABG may be
caused by damaged myocardium not identified by symptoms or routine preoperative assessment.
More vigorous diagnostic efforts to identify asymptomatic ischemia are therefore warranted in
patients with symptoms of heart failure but without angina.
Although not statistically significant, differences between the ventricular dyskinesia with CABG
and the ventricular akinesia with CABG after the Dor surgical reconstruction should be
considered. There was a trend for superior outcome (p = 0.0587) for the dykinesia group. This
has partly to do with the technical difficulty of repairing a ventricle with akinesia (scar).
34
Distinguishing the border between noncontracting and normal tissue under cardioplegia is often
difficult (10, 40). The extent of scar resection and the positioning of the patch is dependent on
the surgeon's visual judgement. A miscalculated positioning of the patch could result in a smaller
residual cavity that would affect the diastolic function. Consequently, a modified Dor procedure
has been developed to address this problem. Rather than performing the ventricular
reconstruction under cardioplegic methods, surgery is conducted with an open-beating heart to
enable the surgeon to palpate between contractile and noncontractile myocardium (4, 10). This
allows a more precise excision of noncontracting muscle and a better assessment of the size and
placement of the patch. In this series of patients, 16 out of 36 patients with postinfarction left
ventricular aneurysm and 2 out of 4 patients with postinfarction ventricular scar underwent the
modified Dor. No significant difference was demonstrated between the Dor surgical ventricular
reconstructon and the modified Dor procedure.
Status and Survival of Patients with idiopathic dilated cardiomyopathy (DCM) after the
Dor SVR Procedure and the Batista partial left ventriculectomy (PLV)
This study included not only post myocardial infarction patients with evidence of ventricular
aneurysm or scar but also a few patients with idiopathic dilated cardiomyopathy. The reason was
the belief that reducing wall stress for a remodeled ventricle after ischemic cardiomyopathy
would also benefit DCM patients who also demonstrated chamber dilation and elevated wall
stress. There was a total of seven DCM patients, 5 who underwent the Dor procedure and 2 who
underwent the Batista partial left ventriculectomy. Although idiopathic DCM was initially
treated with the Batista PLV, 5 DCM patients in this study underwent the Dor surgical
ventricular reconstruction based on the assumption that restoration of the physiological geometry
is equally important as reducing wall tension.
DCM/Dor SVR Procedure
Follow-up for the DCM patients after the Dor SVR procedure in this study averaged 2-6 months.
Although improvement in NYHA functional class from III/IV to NYHA II was demonstrated in
3 out of 5 patients, long-term consequences have revealed limitations of this procedure on this
group of patients.
Two out of the 5 patients demonstrated shorty after the operation a slight increase in EF from
15% to 20-25%. However, 9 weeks after the Dor reconstruction surgery, one died due to
complications associated with preexisting chronic obstructive lung disease (37). Within the 3
patients who did not demonstrate a change in EF after the operation, 2 patients were
rehospitalized nine and twelve months after surgery, as a result of recurrent congestive heart
35
failure. Evaluation of LVEDD at the time of rehospitalization for both patients revealed an
increase from early postoperative values of an additional 17 and 18mm, respectively (37). They
were both subsequently listed for cardiac transplant.
One patient, who went from NYHA IV to NYHA II after the operation unfortunately
experienced severe ventricular arrythmias four months later. Although the patient received an
automated implantable cardioverter/defibrillator concomitant to the Dor SVR procedure due to
prior incidence of ventricular arrythmias, the electrode dislocated and the device did not function
properly. Symptoms of heart failure and eventual pulmonary complications lead to an emergency
cardiac transplantation (37). The requirement for cardiac transplantation for the patients
mentioned above reveal the restraints of the Dor SVR procedure for patients with idiopathic
dilated cardiomyopathy.
DCM/Batista PLV
There were 2 patients who underwent the Batista PLV and were included in this study as
comparison to the Dor procedure. One out of the 2 patients died 14 weeks after the operation.
The long-term benefits of PLV is under dispute.
A comprehensive analysis using pressure-volume relationships and time-varying elastance
theory examined the effects of heart reduction surgery for idiopathic DCM. The study
demonstrated that mass excision of myocardium depressed overall pump function by causing
changes in diastolic ventricular properties (6, 29). Atrip et al. supported this theory by
demonstrating that resection of viable, functioning myocardium has harmful effects on diastolic
compliance that offsets the beneficial effects of reducing wall stress (6). A recent study on the
long-term outcome of idiopathic DCM patients after treatment with PLV actually revealed 4
years after the operation an increase in diastolic volume, progressive dilatation and a decrease in
ejection fraction (75). In this study, 2 DCM patients underwent PLV, one for idiopathic DCM
and the other for secondary DCM as a consequence of myocardial infarction. Both patients
demonstrated a reduction in LVEDD shortly after the operation, however the one patient with
secondary DCM died 14 weeks after the operation. The cause of death could not be established.
The other patient with idiopathic DCM was still alive one year after the operation and showed
improvement from NYHA III to NYHA II, despite COPD as co-morbidity and prior episodes of
ventricular tachycardia. The long-term status of the patient is unknown.
The beneficial effects of the Dor SVR procedure or the Bastita PLV on this particular patient
population is uncertain because of the nature of the disease. The rationale of both operations is to
reduce wall tension in the already dilated ventricle and thereby improve ventricular function. The
Batista PLV achieves this reduction by resecting large sections of contracting left ventricular
36
wall. Although the ventricular diameter is decreased, the Batista PLV has been under criticism
since this procedure has been associated with a high rate of mortality (75, 76), requirement for
transplantation (37, 45, 92), sustained cardiac arrhythmias (13, 66, 69, 75, 76), and decreased
cardiac function (6, 7). Whereas the Dor SVR procedure with endoventricular patch attempts to
restore the elliptical shape of the dilated, spherical ventricle to improve cardiac function besides
reducing diameter, this procedure failed to demonstrate long-term benefits for idiopathic DCM
patients (37). A simple reduction in size will not eliminate the underlying pathophysiology of
DCM which lies in the cellular abnormality, degeneration, and/or inflammation of the myocytes.
When the pathophysiologic process that caused cardiomyopathy continues to progress, then it
may be postulated that reduction surgery does not help. Previous studies demonstrated that a
higher degree of myocardial fibrosis and hypertrophy in idiopathic DCM lead to a less favorable
prognosis after PLV (51, 69). In other studies, the recurrence of heart failure within one year and
required listing for transplantation was as high as 31% (45, 48) and 60% (37) and late mortality
as a result of progressive heart failure within one year was 13% (92) and 39% (75).
In conclusion, the results of this retrospective study imply the inferiority of the Dor SVR
procedure and the Batista PLV to cardiac transplantation for these patients with end-stage dilated
cardiomyopathy. This has led to the discontinuation of these procedures on this population of
patients in this department.
Whereas surgical reconstruction for idiopathic DCM is not associated with long-term benefits,
excluding areas damaged by infarction demonstrated a long-term beneficial outcome. However,
optimal care remains a matter of proper diagnosis, staging of the remodeling process, and early
intervention.
Prior studies have demonstrated that a shorter interval between infarction and aneurysm
resection lowers the risk of cardiac-related complications and death (67, 68). Eaton et al. have
observed that the risk period for infarct expansion is during the structurally vulnerable phase
when scar formation has not already developed in the infarct zone (46). This begins 3 days after
infarction and continues up to 14 days. Meizlisch et al. identified in over half the patients a
formation of a functional aneurysm already present within 24 hours after an acute myocardial
infarction and always detected by the time of hospital discharge. They also observed no new
visible topographic alterations within the infarct area after 3 months (72). Since formation of an
aneurysm occur frequently with anterior transmural infarctions, evaluation for the presence of an
aneurysm should be routinely conducted from the time of in-patient care and ambulatory up to
three months after the initial infarction. As soon as the diagnosis of an aneurysm is confirmed,
repair of aneurysm with surgical ventricular reconstruction should be considered since
37
significant risk of mortality is associated with an aneurysm (46, 72), and improvement in clinical
outcome with this procedure was demonstrated in this and previous studies.
Efforts to preserve the myocardium after an infarction should not only be directed on limiting
distortion in the infarcted area, but also on limiting ventricular remodeling. Since the extent of
myocardial reserve plays an important role in progressive dilatation and remodeling (51, 81), it is
important to accurately define the stage of the disease before beginning with treatment.
Consequently, when patients present with Stage B acccording to the new ACC/AHA
classification for heart failure, earnest consideration for surgical ventricular reconstruction
should be discussed with the patient.
Another important aspect for optimal treatment is evaluating risk factors that will predict either
the development of a limited ventricular dilatation or a progressive dilatation, since not all
myocardial infarctions lead to a detrimental progressive dilatation and cardiac failure. Avoidance
of unnecessary operation and medical therapy can be achieved when predictive variables that
lead to a worsening prognosis are evaluated. Patients that have a high risk of developing severe
left ventricular dysfunction as a result of progressive dilatation would then be candidates for
surgical ventricular reconstruction. Gaudron et al. studied 70 patients for 3 years after first
myocardial infarction and found in 20% the development of progressive dilatation and severe
ventricular dysfunction (52). Various factors have been defined and have also been separately
supported by numerous other studies that predict this subgroup of patients. Such factors include a
large transmural anterior infarct (46, 52, 71, 73, 81, 102), a low ejection fraction (52, 54, 65, 94)
and depressed stroke index at day 4 that persists after 6 months (52, 73), and severity of occluded
artery (9, 52, 73, 81, 82, 88, 102). Early surgical intervention for patients at high risk for late
cardiac failure might delay or perhaps interfere with the remodeling process, since excess
volume and a deleterious structural alteration would be restored to their normal, physiological
state.
As a consequence of the positive results after surgical intervention for patients with left
ventricular dyskinesia (aneurysm) and akinesia, an international, multicentered, pilot study
started in 1998 was organized to assess the clinical efficacy of surgical reconstruction as
treatment for a dilated, remodeled ventricle after a myocardial infarction. The cooperative effort
between cardiologists and surgeons under the name RESTORE (Reconstruction of Elliptical
Shape and Torsion of the ventricle) have published their preliminary results. The three-year
survival rate was 89.4% with an estimated mortality of 7.7%. Ejection fraction had an average
increase of 10% and end-systolic volume index decreased by approximately 37 ml/m2. The
positive results from the study prompted the coordination of a multicenter randomized,
38
prospective study funded by the National Institutes of Health. The study also known as STICH
(Surgical Treatment for IschemiC Heart Failure) began in July 2002 and is designated to last 7
years.
Conclusion
On the basis of this retrospective study, surgical ventricular reconstruction for a remodeled
ventricle for patients with postinfarction left ventricular aneurysm and scar may have long-term
beneficial effects. Importantly, this study revealed that associated coronary grafting has different
implications than when CABG is not performed. A low in-hospital mortality of 4% for all
patients who underwent the Dor SVR procedure demonstrates the feasibility and efficacy of this
operation. Patients with postinfarction left ventricular aneurysm demonstrated a significant
improvement in immediate function (EF and LVEDD) and long-term function (NYHA status).
However, these particular parameters must be critically reappraised with respect to the question
of their validity in concluding the benefit of the Dor SVR procedure. Survival for the group of
patients with left ventricular aneurysm when associated coronary grafting was performed was as
high as 96% at a median follow-up of 19 months (2-36 months). Patients with idiopathic DCM
however, demonstrate no long-term benefit from the Dor surgical ventricular reconstruction.
According to the measures mentioned above, patients with the highest risk of developing infarct
expansion/aneurysm and progressive dilatation should be identified and given the option for
surgical intervention.
39
5
SUMMARY
Background: Any disturbance of the functional cardiac anatomy will impair ventricular function
and cardiac output. It has been postulated that the Dor surgical ventricular reconstruction
procedure for patients with ventricular dysfunction after an infarction for either left ventricular
akinesia or dyskinesia results in better clinical outcome than classic aneurysmectomy or
conservative medical therapy. The reason is the focus of this procedure on restoring the
physiological dimensions of the remodeled ventricle by excluding noncontracting segments of
the heart, including the scarred septum, replacing the area with an endoventricular patch to
redirect normal muscle orientation, and reducing ventricular size, wall tension and volume. The
theory that this procedure might also be applied to other causes of cardiac remodeling has
introduced this application to patients with idiopathic dilated cardiomyopathy (DCM). The
purpose of this retrospective study was to analyze the clinical outcome and long-term survival of
patients who underwent the Dor surgical ventricular reconstruction (SVR) procedure.
Methods: Mortality, cardiac function, and long-term survival were analyzed retrospectively in a
cohort of patients with DCM, a ventricular aneurysm, or scar after a myocardial infarction who
underwent surgical ventricular reconstruction.
Results: The results of this study show an overall 85% three-year survival for patients after the
Dor surgical ventricular reconstruction. In-hospital mortality was 4%. Patients who underwent
the Dor SVR procedure after postinfarction left ventricular aneurysm demonstrated a survival of
89% at a median follow-up of 19 months (2-36 months). Importantly, patients with associated
coronary grafting to the Dor SVR procedure demonstrated a 96% survival rate over a 73% for
non-CABG patients. Significant improvement in EF and NYHA functional class was also
demonstrated in the ventricular aneurysm group. Patients operated on for left ventricular akinesia
had an overall survival of 67% at a median follow-up of 10.5 months (1-20 months) and
demonstrated the most impressive improvement in NYHA functional class. The five DCM
patients who underwent the Dor surgical reconstruction procedure revealed no long-term benefit
from the operation. The efficacy of surgical left ventricular reconstruction is currently being
investigated by a multicenter international randomized study funded by the National Institutes of
Health. The belief is that patients with a remodeled ventricle as a result of ischemic
cardiomyopathy will benefit significantly in clinical outcome and survival when the
physiological cardiac anatomy is surgically restored.
40
ZUSAMMENFASSUNG
Veränderungen der funktionellen Anatomie des Herzens führen zur Beeinträchtigung der
ventrikulären Funktion und Verschlechterung des Herzzeitvolumens. Daher wird postuliert, daß
Patienten mit ventrikulärer Dysfunktion aufgrund einer linksventrikulären Akinesie oder
Dyskinesie infolge eines Herzinfarktes durch die chirurgische Ventrikelrekonstruktion nach V.
Dor (Dor SVR) bessere klinische Ergebnisse als bei klassischer Aneurysmektomie oder
konservativer Therapie aufweisen. Das Prinzip der Dor-Operation besteht in der Resektion des
nicht kontrahierenden Myokardsegmentes mit dem vernarbten Septumanteil und Einnähen eines
endoventrikulären Dacron-Patches, um den normalen Muskelfaserverlauf des Ventrikels
wiederherzustellen. Hierdurch sollen Grösse, Wandspannung und Volumen des Ventrikels
verringert werden, um die physiologische Form des remodellierten Ventrikels zu rekonstruieren.
Da dieses Prinzip auch auf andere Ursachen einer kardialen Remodellierung anwendbar sein
könnte, ist die Dor SVR auch für die dilatative Kardiomyopathie (DCM) von Interesse. Das Ziel
dieser retrospektiven Studie ist die Beurteilung des Erfolges der Dor-Operation hinsichtlich des
klinischen Zustandes und Langzeitüberlebens der operierten Patienten.
Methoden: Mortalität, Ventrikelfunktion und Langzeitüberleben von Patienten mit dilatativer
Kardiomyopathie oder ventrikulärer Dyskinesie bzw. Akinesie nach Myokardinfarkt, die nach
Dor operiert worden waren, wurden aus den Krankenakten und mittels Telefoninterview
retrospektiv erfasst und ausgewertet.
Ergebnisse: Die 3-Jahres-Überlebensrate für Patienten nach der Dor-Operation betrug 85%. Die
Krankenhausmortalität lag bei 4%. Nach einer medianen Nachbeobachtungszeit von 19 Monaten
(2-36 Monate) hatten Patienten mit einem linksventrikulären Aneurysma nach Herzinfarkt
postoperativ eine Überlebensrate von 89%. Patienten, bei denen zusätzlich zur Dor-Operation
eine koronare Bypassoperation (CABG) durchgeführt worden war, hatten eine Überlebensrate
von 96% im Vergleich zu 73% für Patienten ohne CABG. Eine signifikante Verbesserung der
Ejektionsfraktion (EF) und des funktionellen NYHA-Grades durch die Operation wurde bei
Patienten mit Ventrikelaneurysma festgestellt. Operierte Patienten mit linksventrikulärer
Akinesie hatten eine Überlebensrate von 67% nach einer medianen Beobachtungsdauer von 10,5
Monaten (1-20 Monate) und ebenfalls eine beeindruckende Verbesserung der NYHA-Grades.
Für die 5 DCM-Patienten konnte kein Langzeiterfolg der Dor-Operation dokumentiert werden.
Obwohl EF, linksventrikulärer enddiastolischer Durchmesser (LVEDD) und die NYHAKlassifikation als Hauptparameter zur Beurteilung des Erfolges dieses Verfahrens benutzt
worden waren, sollte eine kritische Neubewertung der Zuverlässigkeit dieser Parameter
vorgenommen werden. Die Wirksamkeit der Dor-Operation wird zur Zeit in einer
randomisierten, internationalen Multizenterstudie der National Institutes of Health überprüft.
41
6
1.
REFERENCES
Abbate A, Bussani R, Biondi-Zoccai GG, Rossiello R, Silvestri F, Baldi F, Biasucci LM,
Baldi A. (2002) Persistent infarct-related artery occlusion is associated with an increased
myocardial apoptosis at postmortem examination in humans late after an acute myocardial
infarction. Circulation 106:1051-4.
2.
Akins CW. (1986) Resection of left ventricular aneurysm during hypothermic fibrillatory
arrest without aortic occlusion. J Thorac Cardiovasc Surg 91: 610-618.
3.
Alderman EL, Fisher LD, Litwin P, Kaiser GC, Myers WO, Maynard C, Levine F,
Schloss, M. (1983) Results of coronary artery surgery in patients with poor left ventricular
function (CASS). Circulation 68: 785-795.
4.
Athanasuleas CL, Stanley A. Jr., Buckberg GD, Dor V, DiDonato M, Blackstone EH, and
the RESTORE group. (2001) Surgical Anterior Ventricular Endocardial Restoration
(SAVER) in the dilated remodeled ventricle after anterior myocardial infarction. J Am Coll
Cardiol 37:1199-209.
5.
Athanasuleas CL, Stanley A. Jr., Buckberg GD. (1998) Restoration of contractile function
in the enlarged left ventricle by exclusion of remodeled akinetic anterior segment: Surgical
strategy, myocardial protection, and angioplastic results. J Card Surg 13: 418-428.
6.
Atrip JH, Oz MC, Burkhoff D. (2001) Left ventricular volume reduction surgery for heart
failure: A physiologic perspective. J Thorac Cardiovasc Surg 122: 775-782.
7.
Baretti R, Mizuno A, Buckberg GD, Child J. (2000) Batista procedure: elliptical modeling
against spherical distention. European Journal of Cardio-Thoracic Surgery 17: 52-57.
8.
Barratt-Boyes BG, White HD, Agnew TM, Pemberton JR, Wild CJ. (1984) The results of
surgical treatment of left ventricular aneurysms. An assessment of the risk factors affecting
early and late mortality. J Thorac Cardiovasc Surg 87: 87-98.
9.
Bates ER, Califf RM, Stack RD, Aronson L, George Bs, Candela Rj, Kereiakes DJ,
Abbottsmith CW, Anderson L, Pitt B, O'Neill WW, Topol EJ, The Thrombolysis and
42
Angioplasty in Myocardial Infarction Study Group. (1989) Thrombolysis and Angioplasty
in Myocardial Infarction (TAMI-1) Trial: Influence of infarct location on arterial patency,
left ventricular function and mortality. J Am Coll Cardiol 13: 12-18.
10.
Beyersdorf F, Doenst T, Athanasuleas C, Suma H, Buckberg GD. (2001) The beating open
heart for rebuilding ventricular geometry during surgical anterior restoration. Seminars
Thorac Cardiovasc Surg 13: 42-51.
11.
Beyersdorf F, Acar C, Buckberg GD, Partington MT, Sjostrand F, Young HH, Bugyi HI,
Okamoto F, Allen BS. (1989) Studies on prolonged acute regional ischemia. III. Early
natural history of simulated single and multivessel disease with emphasis on remote
myocardium. Thorac Cardiovasc Surg 98:368-80.
12.
Bluemchen
G,
Heid
Langzeitbeobachtungen
HP,
bei
Scharf-Bornhofen
27
Patienten
mit
E,
Reidemeister
nichtoperierten
JC.
(1978)
linksventrikulären
Aneurysmen. Z Kardiol 67: 736-748.
13.
Bocci EA, Bellotti G, Vilella de Moraes A, Bacal F, Moreira LF, Esteves-Filho A,
Fukushima JT, Guimaraes G, Stolf N, Jantene A, Pileggi F. (1997) Clinical outcome after
left ventricular surgical remodeling in patients with idiopathic dialted cardiomyopathy
referred for heart transplantation, Short term results. Circulation II: 165-172.
14.
Brawley RK, Magovern GJ, Gott VL, Dnahoo JS, Gardner TJ, Watkins L. (1983) Left
ventricular
aneurysmectomy-Factors
influencing
postoperative
results.
J
Thorac
Cardiovasc Surg 85: 712-717.
15.
Bristow MR, Gilbert EM, Abraham WT, Adams KF, Fowler MB, Hershberger RE, Kubo
SH, Narahara KA, Ingersoll H, Krueger S, Young S, Shusterman N. (1996) Congestive
Heart Failure/Myocardial Disease: Carvedilol produces dose-related improvements in left
ventricular function and survival in subjects with chronic heart failure. Circulation 94:
2807-2816.
16.
Buckberg GD. (2002) Basic science review: The helix and the heart. J Thorac Cardiovasc
Surg 124: 863-83.
43
17.
Buckberg GD. (2001) Congestive heart failure: Treat the disease, not the symptom-return
to normalcy. J Thorac Cardiovasc Surg 121: 628-37.
18.
Buckberg GD, Coghlan HC, Torrent-Guasp F. (2001) The structure and function of the
helical heart and its buttress wrapping. V. Anatomic and physiologic considerations in the
healthy and failing heart. Semin Thorac Cardiovasc Surg 13: 358-85.
19.
Buckberg GD, Coghlan HC, Hoffman JL, Torrent-Guasp F. (2001) The structure and
function of the helical heart and its buttress wrapping. VII. Critical importance of septum
for right ventricular function. Semin Thorac Cardiovasc Surg 13: 402-16.
20.
Burton NA, Stinson EB, Oyer PE, Shumway NE. (1979) Left ventricular aneurysm.
Preoperative risk factors and long-term postoperative results. J Thorac Cardiovasc Surg 77:
65-75.
21.
Christian TF, Milavetz JJ, Miller TD, Clements IP, Holmes DR, Gibbons RJ. (1998)
Prevalence of spontaneous reperfusion and associated myocardial salvage in patients with
acute myocardial infarction. Am Heart J 135: 421-7.
22.
Cohn JN. (1995) Structural Basis for Heart Failure, Ventricular Remodeling and Its
Pharmacological Inhibition. Circulation 91: 2504-2507.
23.
Cohn JN, Johnson GR, Shabetai R, Loeb H, Tristani F, Rector T, Smith R, Fletcher R.
(1993) Ejection fraction, peak exercise oxygen consumption, cardiothoracic ratio,
ventricular arrhythmias, and plasma norepinephrine as determinants of prognosis in heart
failure. The V-HeFT VA Cooperative Studies Group. Circulation 87: VI5-16.
24.
The CONSENSUS Trial Study Group. (1987) Effects of enalapril on mortality in severe
congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival
Study (CONSENSUS). N Engl J Med 316: 1429-35.
25.
Cooley DA, Collins HA, Morris GC Jr., et al., (1958) Ventricular aneurysm after
myocardial infarction: Surgical excision with use of temporary cardiopumonary bypass.
JAMA 167: 557-560.
44
26.
Cotran RS, Kumar V, Robbins SL. Robbins pathologic basis of disease. 4th Edition (1989)
W.B. Saunders Company. pp. 643-644.
27.
Couper GS, Bunton RW, Birjiniuk V, DiSesa VJ, Fallon MP, Collins JJ Jr, Cohn LH.
(1990) Relative risks of left ventricular aneurysmectomy in patients with akinetic scars
versus true dyskinetic aneurysms. Circulation 82: IV 248-56.
28.
De Feyter PJ, van Eneige MJ, Dighton DH, Visser FC, deJong J, Roos JP. (1982)
Prognostic value of exercise testing, coronary angiography and left ventriculography 6-8
weeks after myocardial infarction. Circulation 66: 527.
29.
Dickstein ML, Spotnitz HM, Rose EA, Burkhoff D. (1997) Heart reduction surgery: An
analysis of the impact on cardiac function. J Thorac Cardiovasc Surg 113: 1032-1040.
30.
Di Donato M, Toso A, Maioli M, Sabatier M, Stanley AW Jr, Dor V; RESTORE Group.
(2001) Intermediate survival and predictors of death after surgical ventricular restoration.
Semin Thorac Cardiovasc Surg 13: 468-75.
31.
Di Donato M, Sabatier M, Dor V, Toso A, Maioli M, Fantini F. (1997) Akinetic Versus
Dyskinetic Postinfarction Scar: Relation to Surgical Outcome in Patients Undergoing
Endoventricular Circular Patch Plasty Repair. J Am Coll Cardiol 29:1569–75.
32.
Di Donato M, Sabatier M, Toso A, Barletta G, Baroni M, Dor V, Fantini F. (1995)
Regional myocardial performance of non-ischaemic zones remote from anterior wall left
ventricular aneurysm. Effects of aneurysmectomy. Eur Heart J 16 (9):1285-92.
33.
Di Donato M, Sabatier M, Montiglio F, Maioli M, Toso A, Fantini F, Dor V. (1995)
Outcome of left ventricular aneurysmectomy with patch repair in patients with severely
depressed pump function. Am J Cardiol 76: 557-61.
34.
Di Donato M, Barletta G, Maioli M, Fantini F, Coste P, Sabatier M, Montiglio F, Dor V.
(1992) Early hemodynamic results of left ventricular reconstructive surgery for anterior
wall left ventricular aneurysm. Am J Cardiol 69: 886-90.
45
35.
The Digitalis Investigation Group. (1997) The effect of digoxin on mortality and mobidity
in patients with heart failure. N Engl J Med 336: 525-533.
36.
Doenst T, Schlensak C, Beyersdorf F. (2004) Modified ventricular reconstruction after
myocardial infarction. Deutsches Aerzteblatt 9: 474-478.
37.
Doenst T, Ahn-Veelken L, Schlensak C, Berchtold-Herz M, Sarai K, Schaefer M, van de
Loo A, Beyersdorf F. (2001) Left ventricular reduction for idiopathic dilated
cardiomyopathy as alternative to transplant- truth or dare? Thorac Cardiov Surg 49: 70-74.
38.
Dor V. (2002) Left ventricular reconstruction for ischemic cardiomyopathy. J Card Surg
17: 180-7.
39.
Dor V, Di Donato M, Sabatier M, Montiglio F, Civaia F; RESTORE Group. (2001) Left
ventricular reconstruction by endoventricular circular patch plasty repair: a 17-year
experience. Semin Thorac Cardiovasc Surg 13: 435-47.
40.
Dor V, Sabatier M, Di Donato M, Montiglio F, Toso A, Maioli M. (1998) Efficacy of
endoventricular patch plasty in large postinfarction akinetic scar and severe left ventricular
dysfunction: comparison with a series of large dyskinetic scars. J Thorac Cardiovasc Surg
116: 50-9.
41.
Dor V. (1998) Repair of Ventricular Aneurysm. Advances in Cardiac Surgery 10: 25-41.
42.
Dor V. (1997) The treatment of refractory ischemic ventricular tachycardia by
endoventricular patch plasty reconstruction of the left ventricle. Semin Thorac Cardiovasc
Surg 9:146-55.
43.
Dor V, Sabatier M, Di Donato M, Maioli M, Toso A, Montiglio F. (1995) Late
hemodynamic results after left ventricular patch repair associated with coronary grafting in
patients with postinfarction akinetic or dyskinetic aneurysm of the left ventricle. J Thorac
Cardiovasc Surg 110:1291-9.
44.
Douglas AH, Sferrazza J, Marici F. (1962) Natural history of aneurysm of ventricle. N.Y.
St. J. Med 62: 209-216.
46
45.
Dowling RD, Koenig S, Laureano MA, Cerrito P, Gray LA. (1998) Results of partial left
ventriculectomy in patients with end-stage idiopathic dilated cardiomyopathy. J Heart
Lung Transplant 17: 1208-1212.
46.
Eaton LW, Weiss JL, Bulkley BH, Garrison JB, Weisfeldt MD. (1979) Regionl cardiac
dilatation after acute myocardial infarction. N Engl J Med 300: 57-62.
47.
Eisen HJ, Tuzcu EM, Dorent R, Kobashigawa J, Mancini D, Valantine-von Kaeppler HA,
Starling RC, Sorensen K, Hummel M, Lind JM, Abeywickrama KH, Bernhardt P; RAD
B253 Study Group. (2003) Everolimus for the prevention of allograft rejection and
vasculopathy in cardiac-transplant recipients. N Engl J Med 349: 847-58.
48.
Etoch SW, Koenig SC, Laureano MA, Cerrito P, Gray LA, Dowling RD. (1999) Results
after
partial
left
ventriculectomy
versus
heart
transplantation
for
idiopathic
cardiomyopathy. J Thorac Cardiovasc Surg 117: 952-959.
49.
Faxon DP, Myers WO, McCabe CH, Davis KB, Schaff HV, Wilson JW, Ryan TJ. (1986)
The influence of surgery on the natural history of angiographically documented left
ventricular aneurysm: the Coronary Artery Surgery Study. Circulation 74:110-8.
50.
Faxon DP, Ryan TJ, Davis KB, McCabe CH, Myers W, Lesperance J, Shaw R, Tong TG.
(1982) Prognostic significance of angiographically documented left ventricular aneurysm
from the Coronary Artery Surgery Study (CASS). Am J Cardiol 50:157-64.
51.
Frazier OH, Gradinac S, Segura AM, Przybylowski P, Popovic Z, Vasiljevic J, Hernandez
A, McAllister HA, Bojic M, Radovancevic B. (2000) Partial Left Ventriculectomy: Which
patients can be expected to benefit? Ann Thorac Surg 69: 1836-41.
52.
Gaudron P, Eilles C, Kugler I, Ertl G. (1993) Myocardial Infarction: Progressive left
ventricular dysfunction and remodeling after myocardial infarction: Potential mechanisms
and early predictors. Circulation 87: 755-763.
53.
Greenberg B, Quinones MA, Koilpillai C, Limacher M, Shindler D, Benedict C, Shelton B.
(1995) Left Ventricular Function/Congestive Heart Failure: Effects of Long Term
47
Enalapril Therapy on Cardiac Structure and Function in Patients with Left Ventricular
Dysfunction: Results of the SOLVD Echocardiography Substudy. Circulation 91: 25732581.
54.
Hammermeister KE, DeRouen TA, Dodge HT. (1979) Variables predictive of survival in
patients with coronary disease: Selection by univariate and multivariate analyses from the
clincial electrocardiographic, exercise, arteriographic and quantitative angiographic
evaluations. Circulation 59: 421-430.
55.
Ho KKL, Anderson KM, Kanel WB, Grossman W, Levy D. (1993) Congestive Heart
Failure/Myocardial Responses/Valvular Heart Disease: Survival After the Onset of
Congestive Heart Failure in Framingham Heart Study Subjects. Circulation 88: 107-115.
56.
Hunt SA, Baker DW, Chin MH, Cinquegrani MP, Feldmanmd AM, Francis GS, Ganiats
TG, Goldstein S, Gregoratos G, Jessup ML, Noble RJ, Packer M, Silver MA, Stevenson
LW, Gibbons RJ, Antman EM, Alpert JS, Faxon DP, Fuster V, Gregoratos G, Jacobs AK,
Hiratzka LF, Russell RO, Smith SC Jr; American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines
for the Evaluation and Management of Heart Failure); International Society for Heart and
Lung Transplantation; Heart Failure Society of America. (2001) ACC/AHA Guidelines for
the Evaluation and Management of Chronic Heart Failure in the Adult: Executive
Summary A Report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the
Evaluation and Management of Heart Failure): Developed in Collaboration With the
International Society for Heart and Lung Transplantation; Endorsed by the Heart Failure
Society of America. Circulation 104: 2996-3007.
57.
Jantene A. (1985) Left Ventricular Aneurysmectomy, Resection or Reconstruction. J
Thorac Cardiovasc Surg 89: 321-331.
58.
Jehle J, Heerdt M, Spiller P, Loogen F, Krian A, Schulte HD. (1983) Results of surgical
therapy in patients with left ventricular aneurysm. Eur Heart J 4: 639-646.
59.
Jessup M, Brozena S. (2003) Heart Failure. N Engl J Med 348: 2007-18.
48
60.
Jones EL, Graver JM, Hurst JW, Bradfort DK, Bone P, Robinson J, Cobbs BW,
Thompkins TR, Hatcher CR. (1981) Influence of left ventricular aneurysm on survival
following the coronary bypass operation. Ann Surg 193: 733-742.
61.
Jugdutt BI, Schwarz-Michorowski BL, Khan MI. (1992) Effect of long-term captopril
therapy on left ventricular remodeling and function during healing of canine mayocardial
infarction. J Am Coll Cardiol 19: 713-721.
62.
Klein MD, Herman M, Gorlin R. (1967) A hemodynamic study of left ventricular
aneurysm. Circulation 35: 614-630.
63.
Knudsen MA, Lund O, Emmertsen K, Kristensen BO, Rasmussen K. (1987) Clinical
improvement and long-term survival after surgical treatment of postinfarction left
ventricular aneurysm. Scand J Cardiovasc Surg 21: 135-140.
64.
Konstam MA, Rousseau MF, Kronenberg MW, Udelson JE, Melin J, Stewart D, Dolan N,
Edens TR, Ahn S, Kinan D, et al. (1992) Effects of the angiotensin converting enzyme
inhibitor enalapril on the long-term progression of left ventricular dysfunction in patients
with heart failure. SOLVD Investigators. Circulation 86: 431-8.
65.
Lamas GA, Flaker GC, Mitchell G, Smith SC Jr, Gersh BJ, Wun CC, Moye L, Rouleau JL,
Rutherford JD, Pfeffer MA, et al. (1995) Effect of infarct artery patency on prognosis after
acute myocardial infarction. The Survival and Ventricular Enlargement Investigators.
Circulation 92: 1101-9.
66.
Lim KH, Griffiths EJ, Pryn SJ. Callaway M, Angelini GD. (1999) Left ventricular volume
reduction : new dawn or false horizon? Basic science and clinical doubts. J Card Surg 14:
38-45.
67.
Louagie Y, Alouini T, Lesperance J, Pelletier LC. (1987) Left ventricular aneurysm with
predominating congestive heart failure. A comparative study of medical and surgical
treatment. J Thorac Cardiovasc Surg 94: 571-81.
49
68.
Louagie Y, Alouini T, Lesperance J, Pelletier LC. (1989) Left ventricular aneurysm
complicated by congestive heart failure: An analysis of long-term results and risk factors
of surgical treatment. J Cardiovasc Surg 30: 648-655.
69.
McCarthy PM, Starling RC, Wong J, Scalia GM, Buda, T, Vargo RL, Goormastic M,
Thomas JD, Smedira NG, Young JB. (1997) Surgery for acquired heart disease. J Thorac
Cardiovasc Surg 114: 755-765.
70.
McDonald KM, Rector T, Carlyle PF, Francis GS, Cohn JN. (1994) Angiotensinconverting enzyme inhibition and beta-adrenoceptor blockade regress established
ventricular remodeling in a canine model of discrete myocardial damage. J Am Coll
Cardiol 24: 1762-1768.
71.
McKay RG, Pfeffer MA, Pasternak RC, Markis JE, Come PC, Nakao S, Alderman JD,
Ferguson JJ, Safian RD, Grossman W. (1986) Left ventricular remodeling after myocardial
infarction: a corollary to infarct expansion. Circulation 74: 693-702.
72.
Meizlisch JL, Berger HJ, Plankey M, Errico D, Levy W, Zaret B. (1984) Functional left
ventricular aneurysm formation after acute anterior transmural myocardial infarction.
Incidence, natural history, and prognostic implications. N Engl J Med 311: 1001-1006.
73.
Meneveau N, Bassand JP, Bauters C, Rozand JY, Petit JL, Beurrier D, Grollier G, Andre
F, Vahanian A, Viel JF. (1997) Influence of late reopening of the infarct-related artery on
left ventricular remodelling after myocardial infarction. IRIS Study Group. Eur Heart J 18:
1261-8.
74.
Menicanti L, Di Donato M. (2002) The Dor procedure: What has changed after fifteen
years of clinical practice? J Thorac Cardiovasc Surg 124: 886-90.
75.
Moreira LF, Stolf NA, de Lourdes Higuchi M, Bacal F, Bocchi EA, Oliveira SA. (2001)
Current perspectives of partial left ventriculectomy in the treatment of dilated
cardiomyopathy. Eur J Cardiothorac Surg 19: 54-60.
50
76.
Moreira LF, Stolf NA, Bocchi EA, Bacal F, Giorgi MC, Parga JR, Jatene AD. (1998)
Partial left ventriculectomy with mitral valve preservation in the treatment of patients with
dilated cardiomyopathy. J Thorac Cardiovasc Surg. Apr;115: 800-7.
77.
Morgan HE, Baker KM. (1991) Cardiac Hypertrophy: Mechanical, Neural, and Endocrine
Dependence. Circulation 83: 13-23.
78.
Mourdjinis A, Olsen E, Raphael MJ, Mounsey JPD. (1968) Clinical diagnosis and
prognosis of ventricular aneurysm. Brit Heart J 30: 497-513.
79.
Novick RJ, Stefaniszyn HJ, Morin JE, Symes JF, Sniderman AD, Dobell AR. (1984)
Surgery for postinfarction left ventricular aneurysm: prognosis and long-term follow-up.
Can J Surg 27: 161-7.
80.
Olearchyk AS, Lemole GM, Spagna PM. (1984) Left ventricular aneurysm. Ten years'
experience in surgical treatment of 244 cases. Improved clinical status, hemodynamics, and
long-term longevity. J Thorac Cardiovasc Surg 88: 544-53.
81.
Pfeffer MA, Braunwald E. (1990) Ventricular Remodeling After Myocardial Infarction,
Experimental Observations and Clinical Implications. Circulation 81: 1161-1172.
82.
Pfeffer MA, Lamas GA, Vaughn DE, Parisi AF, Braunwald E. (1988) Effect of captopril
on progressive ventricular dilatation after anterior myocardial infarction. N Engl J Med
319: 80-86.
83.
Proudfit WL, Bruschke AVG, Sones FM. (1978) Natural history of obstructive coronary
artery disease: Ten-year study of 601 nonsurgical cases. Progr Cardiovasc Dis 21: 53-78.
84.
Puma JA, Sketch MH Jr, Thompson TD, Simes RJ, Morris DC, White HD, Topol EJ,
Califf RM. (1999) Support for the open-artery hypothesis in survivors of acute myocardial
infarction: analysis of 11,228 patients treated with thrombolytic therapy. Am J Cardiol 83:
482-7.
51
85.
Rittenhouse EA, Sauvage LR, Mansfield PB, Smith JC, Davis CC, Hall DG, O'Brien MA.
(1982) Results of combined left ventricular aneurysmectomy and coronary artery bypass:
1974-1980. Am J Surg 143: 575-578.
86.
Sanz G, Castaner A, Betriu A, Magrina J, Roig E, Coll S, Pare JC, Navarro-Lopez F.
(1982) Determinants of prognosis in survivors of myocardial infarction: a prospective
clinical angiographic study. N Engl J Med 306: 1064.
87.
Schlichter J, Hellerstein HK, Katz LN. Aneurysm of the heart: a correlative study of 102
proved cases. (1954) Medicine 33: 43
88.
Schroder R, Neuhaus KL, Linderer T, Bruggemann T, Tebbe U, Wegscheider K. (1989)
Impact of late coronary artery reperfusion on left ventricular function one month after
acute myocardial infarction (results from the ISAM study). Am J Cardiol 64: 878-84.
89.
Silber S. (2003) [Early detection of myocardial infarct risk with cardio-CT. Can coronary
calcium calculation prevention sudden cardiac death?] MMW Fortschr Med 145: 37-40.
90.
The SOLVD Investigators. (1991) Effect of enalapril on survival in patients with reduced
left ventricular ejection fractions and congestive heart failure. N Engl J Med 325: 293-302.
91.
Stephenson, LW, Hargrove C, Ratcliffe MB, Edmunds LH Jr. (1989) Surgery for Left
Ventricular Aneurysm; Early survival with and without endocardial resection. Circulation
79: I-108-I-111.
92.
Suma H, Isomura T, Horii T, Sato T, Kikuchi N, Iwahashi K, Hosokawa J. (2000)
Nontransplant cardiac surgery for end-stage cardiomyopathy. J Thorac Cardiovasc Surg
119: 1233-1245.
93.
Sutton MGSJ, Sharpe N. (2000) Left Ventricular Remodeling After Myocardial Infarction:
Pathophysiology and Therapy. Circulation 101: 2981-2988.
94.
Sutton MGSJ, Pfeffer MA, Moye L, Plappert T, Rouleau JL, Lamas G, Rouleau J, Parker
JO, Arnold MO, Sussex B, Braunwald E. (1997) Cardiovascular death and left ventricular
remodeling two years after myocardial infarction: baseline predictors and impact of long52
term use of captopril: information from the Survival and Ventricular Enlargement (SAVE)
trial. Circulation 96: 3294-9.
95.
Swedberg K, Kjekshus J. (1988) Effects of enalapril on mortality in severe congestive
heart failure: results of the Cooperative North Scandinavian Enalapril Survival Study
(CONSENSUS). Am J Cardiol 62: 60A-66A.
96.
Taylor GJ, Humphries JO, Mellits ED, Pitt B, Schultze RA, Griffith LSC, Achuff SC.
(1980) Predictors of clincial course, coronary anatomy and left ventricular function after
recovery from acute myocardial infarction. Circulation 62: 960.
97.
Tebbe U, Kreuzer H. (1989) Pros and Cons of surgery of the left ventricular aneurysm - A
review. Thorac Cardiovasc Surgeon 37: 3-10.
98.
Tierney LM, McPhee SJ, Papadakis MA. Current Medical Diagnosis and Treatment, Adult
Ambulatory and Inpatient Management 2002; 41st edition.
99.
Torrent-Guasp R, Buckberg GD, Clemente C, Cox JL, Coghlan HC, Gharib M. (2001) The
structure and function of the helical heart and its buttress wrapping. I. The normal
macroscopic structure of the heart. Semin Thorac Cardiovasc Surg 13: 301-319.
100. Trachiotis GD, Weintraub WS, Johnston TS, Jones EL, Guyton RA, Craver JM. (1998)
Coronary artery bypass grafting in patients with advanced left ventricular dysfunction. Ann
Thorac Surg 66: 1632-9.
101. Vallejo E, Dione DP, Sinusas AJ, Wackers FJ. (2000) Assessment of left ventricular
ejection fraction with quantitative gated SPECT: accuracy and correlation with first-pass
radionuclide angiography. J Nucl Cardiol 7: 461-70.
102. Warren SE, Royal HD, Markis JE, Grossman W, McKay RG. (1988) Time course of left
ventricular dilation after myocardial infarction: influence of infarct-related artery and
success of coronary thrombolysis. J Am Coll Cardiol 11: 12-9.
103. Watson RDS, Gibbs CR, Lip GYH. (2000) ABC of heart failure: Clinical features and
complications. BMJ 320: 236-9.
53
104. White H, Norris RM, Brown MA, Brandt PWT, Whitlock RML, Wild CJ. (1987) Left
ventricular end-systolic volume as the major determinant of survival after recovery from
myocardial infarction. Circulation 76: 44-51.
105. Wilson JD, Braunwald E, Isselbacher KJ, Petersdorf RG, Martin JB, Fauci AS, Root RK.
Harrison's Principles of Internal Medicine. (1991) 12th Edition. McGraw Hill, Inc. pp.
975-977.
106. Wright GA, Thackray S, Howey S, Cleland JG. (2003) Left ventricular ejection fraction
and volumes from gated blood-pool SPECT: comparison with planar gated blood-pool
imaging and assessment of repeatability in patients with heart failure. J Nucl Med 44: 4948.
107. Wright GA, McDade M, Keeble W, Martin W, Hutton I. (2001) Are ejection fractions
from gated SPECT perfusion studies clinically useful? A comparison with radionuclide
ventriculography. Physiol Meas 22: 413-22.
108. Wright JS, Stacey RB, Albrecht H, Murton MM. (1987) Left ventricular aneurysm surgery,
Determinants of results. J Cardiovasc Surg 28: 85-88.
109. Yamaguchi A, Ino T, Adachi H, et al: (1998) Left ventricular volume predicts
postoperative course in patients with ischemic cardiomyopathy. Ann Thorac Surg 65: 434438.
54
LEBENSLAUF
Biographische Daten
Geburtsdatum:
15. September 1964
Geburtsort:
New York City, N.Y., USA
Staatsangehörigkeit:
USA
Familienstand:
Verheiratet seit 1993 mit Professor Dr. med. Hendrik Veelken
Kinder:
Charlotte Veelken, geb. 07.09.2000
Luise Veelken, geb. 03.10.2002
Ausbildung und beruflicher Werdegang
1982
High School Graduation, Paul D. Schreiber High School, Port Washington, N.Y.
1982 - 1986
Dickinson College, Carlisle, PA
Abschluß: Bachelor of Arts
1985 - 1986
Austauschstudentin an der Yonsei-Universität, Seoul, Republik Korea
1987 - 1991
Berufstätigkeit im Finanzmanagement in New York City:
Director of International Operations, Leslie Fay Companies
Finance Manager, Estee Lauder International Companies
1989 - 1991
Post-baccalaureate Pre-Medical Program, Columbia University, NY
1991 - 1993
Post-baccalaureate Pre-Medical Program, Harvard University, Cambridge, MA
Research Assistant, Department of Biological Chemistry and Molecular
Pharmacology, Harvard Medical School, Boston, MA
1994 - 1995
Studium der deutschen Sprache am Goethe-Institut Freiburg
Forschungstätigkeit, Abteilung Molekular- und Zellbiologie, Elias GmbH,
Freiburg
1995 - 2002
Studium der Humanmedizin, Albert-Ludwigs-Universität Freiburg
2001 - 2002
Praktisches Jahr des Medizinstudiums
Tertial Innere Medizin: Stanford University Medical Center, Stanford, CA
Tertial Chirurgie: Chirurgische Universitätsklinik Freiburg
Tertial Gynäkologie und Geburtshilfe: Universitäts-Frauenklinik Freiburg
11/2002
Ärztliche Prüfung
55
ACKNOWLEDGEMENTS
I thank Professor Dr. med. Beyersdorf, my doctoral thesis advisor and mentor, for his support
and for providing the opportunity for this doctoral thesis.
I extend my gratitude to Professor Dr. med. Werner for his time and effort in reviewing my
doctoral thesis.
I would especially like to thank Dr. med. Torsten Doenst for providing research guidance and
supervision, for his concrete advices and for many rewarding discussions which helped me
through this difficult and evolving subject.
My immeasurable gratitude to my husband, Hendrik, for his constructive criticism, his keen
scientific advice and his unending support.
56