Circulation. 2004;109:1064-1072
doi: 10.1161/01.CIR.0000115634.66549.4D
(Circulation. 2004;109:1064-1072.)
© 2004 American Heart Association, Inc.
Review: Clinical Cardiology: New Frontiers |
Novel Approaches to Cardiac Valve Repair
From Structure to Function: Part II
Magdi H. Yacoub, FRS;
Lawrence H. Cohn, MD
From Imperial College School of Medicine, Heart Science Centre, Harefield Research Foundation, Harefield, Middlesex, UK, and Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Magdi Yacoub, Heart Science Centre, Harefield Research Foundation, Harefield, Middlesex, UB9 6JH, UK. E-mail m.yacoub{at}imperial.ac.uk
 |
Introduction
|
|---|
In Part I of this article, several aspects of valve structure
and function and their possible clinical relevance were discussed.
We now review the clinical evolution and application for various
forms of valve repair and outline some of the factors relating
to the timing and choice of particular types of repair or replacement
and, whenever appropriate, repair versus replacement. In addition,
future prospects of valve repair based on understanding of the
sophisticated function and structure of valves and the possible
future contribution of tissue engineering are discussed.
|
Valve Repair: Evolution of a Concept
|
|---|
The very first attempts at surgical treatment of heart valve
disease were directed toward repair of mitral stenosis in the
early 1920s by Elliot Carr Cutler
1 in Boston and Sir Henry Souttar
2 in London. Although some of these operations were successful,
it was approximately 30 years before mitral valvotomy was established
by Bailey in the United States and Lord Brock and O.S. Tubbs
in the United Kingdom. The next heart valve operation to be
attempted was repair of mitral regurgitation by Lillehei et
al,
3 who in 1957 reported "surgical correction of pure mitral
regurgitation by annuloplasty under direct vision." Shortly
after that, Dwight McGoon,
4 at the Mayo Clinic, introduced "repair
of mitral regurgitation for ruptured chordae tendineae by triangular
resection of the prolapsing segment," a major contribution.
With the introduction of mechanical valve replacement by Harken,
Starr, and others and biological valves (homografts) by Donald
Ross and Brian Barratt-Boyes in the early 1960s, there was a
swing toward valve replacement. More recently, however, there
has been a gradual realization that the ideal operation may
be a restorative (repair) operation attempting to reproduce
some of the sophisticated functions of a normal valve. This
was accompanied by refining and evolving new techniques for
repair of different valves by Carpentier
5 and many others. During
the same period, valve substitutes have also been evolving,
with improvement in design and flow characteristics and reduction
of the rate of complications. However, some inherent problems,
such as thrombogenicity of mechanical valves and degeneration
of tissue valves, have not been eliminated. The availability
of many options offers opportunities but also problems of choice.
|
Decision-Making in Valve Surgery
|
|---|
Optimal management of specific lesions in individual patients
is critically dependent on appropriate decision-making with
regard to the timing and type of operation, 2 issues that are
closely related and interdependent. These decisions rely on
defining the goals of valve surgery, which include symptomatic
relief, restoration of both exercise capacity and quality of
life, and, importantly, longevity compared with age-matched
controls. The information needed to make these decisions is
sometimes incomplete, and therefore, clinicians have to depend
on predictions and possibly biases as well as the experience
and skills available to the group. Some of these uncertainties
are highlighted in the American Heart Association/American College
of Cardiology guidelines for management of valve disease.
6 Currently,
the information available in the literature is based primarily
on single-center observational studies involving a relatively
small number of patients and few prospective randomized trials
(the "gold standard").
7 Observational studies comparing the
results with matched controls using various statistical methods,
7–9 such as propensity scores or different modeling techniques,
10 are very useful but are not a substitute for randomized trials,
which are badly needed. The patient and valve specific information
required for decision-making regarding timing and type of operation
(
Table) include symptomatic status, because one of the goals
of the operation is to improve exercise capacity and quality
of life. In addition, the presence of symptoms in patients with
valve disease is often a strong prognostic
11 indicator. Although
symptomatic status can be self-evident, it may be clarified
in some patients by formal exercise testing with measurement
of gas exchange. For assessment of severity of valve dysfunction,
several echocardiographic and Doppler-derived indices
12,13 with
estimation of variables, such as regurgitant fraction and effective
orifice area, can be used. If necessary, these can be aided
by hemodynamic measurements. Information regarding the functional
anatomy of the hemodynamic lesion and the morphology and contribution
of each valve component can be studied by echocardiography and
MRI.
14,15 The presence and degree of calcification have been
shown to have prognostic value in patients with aortic sclerosis
and/or stenosis and can act as a predictor of progression.
16 The development of accurate methods of quantifying and characterizing
valve calcification by electron-beam tomography
17,18 can be
used for assessing suitability for repair and in follow-up of
patients with mild aortic stenosis or after bioprosthetic replacement
of heart valves and in patients at high risk of valve sclerosis,
such as patients with familial hyperlipidemia
19 or renal failure
requiring chronic dialysis. Assessment of left and right ventricular
function and secondary pulmonary hypertension evaluated by echo
or catheter techniques have traditionally played an important
role in timing of valve surgery. Other prognostic indicators,
such as genetic and biochemical markers, may be useful in the
future. The timing and type of procedure are specific to each
valve lesion and depend on comparing predicted long-term outcome
after each treatment strategy. This is exemplified by the timing
of mitral regurgitation in floppy-valve syndrome. Current knowledge
strongly suggests that repair of severe degenerative mitral
regurgitation is superior to replacement
20–23 and, when
applied relatively early in centers experienced in repair, can
result in survival comparable to that of age-matched controls.
|
Aortic Valve Repair
|
|---|
Application of reparative procedures to the aortic valve has
lagged behind because of the apparently irreversible changes
produced by cusp calcification, the common loss of substance
and retraction of cusp tissue in aortic regurgitation, and the
lack of durable biological material suitable for supplementing
valve tissue. Nevertheless, several reparative techniques are
being used successfully in specific types of aortic disease.
|
Aortic Stenosis
|
|---|
In neonates, infants, and children, severe congenital aortic
stenosis results in apparent disorganization of the valve with
complete or partial absence of one or more of the commissures.
Nevertheless, balloon valvuloplasty and/or open valvotomy or
repair can provide excellent palliation. Open valvotomy or repair
in these patients usually consists of transforming the valve
to bicuspid configuration with sharp division of the appropriate
commissure(s) and mobilization of the hinge mechanism. The mobility
of the cusps can be enhanced by "shaving" the aortic surface
of the commissural raphe and possibly by enlarging the noncoronary
sinus of Valsalva with an autologous pericardial patch. This
operation may allow children to grow normally to adolescence
or early adulthood, when a more definitive approach, such as
the Ross
24 operation, may be applied. More radical approaches,
such as the early application of the Ross procedure with or
without Konno-Rastan repair,
25 may be required in infancy but
are largely unwarranted before the age of 15 years.
|
Aortic Regurgitation
|
|---|
Recent advances in understanding the different mechanisms of
aortic regurgitation
26,27 have resulted in the evolution and
application of valve-conserving operations to an increasing
number of patients with aortic regurgitation.
In patients with aortic aneurysms or dissections involving the aortic root, 2 reparative approaches have been used. The first consists of a remodeling operation with radical excision of all diseased aortic tissue down to the annulus followed by reconstruction of the root using 3 tongue-shaped processes to recreate the aortic sinuses (Figure 1A).27 Several modifications to reshape the sinuses have been suggested.28–30 The main advantage of the remodeling technique is the preservation of "distensibility" of the aortic root and the near-normal pattern of instantaneous movements of the aortic cusps.30 This may translate into clinical benefit in the longer term. However, there is concern about the reproducibility and durability of this type of repair. In the original series, starting in 1978 and incorporating the "learning curve," the freedom from reoperation was 89% at 10 years. Progressive aortic regurgitation occurred only in patients with less than perfect results immediately after the operation. Appropriate timing of the operation before the onset of secondary changes in the cusps combined with technical refinements should minimize or abolish the need for reoperation. The technical refinements include slight undersizing of the Dacron tube (2 mm less than the echocardiographic measurements of the aortic root at the level of the attachment of the cusps) combined with the use of long Dacron "lips" to recreate the longitudinal curvature of the sinuses. This results in creating vortices that prevent progressive dilatation of the sinuses by creating inward forces at the level of the attachment of the cusps. The second approach (the tube operation), introduced by David and Findel31 from Toronto, consists of less radical excision of the diseased aortic wall followed by insertion of the mobilized valve inside a Dacron tube (Figure 1B). The perceived advantage of this technique is the strong splinting of the valve mechanism by the surrounding Dacron tube, which is thought to enhance competence and prevent future dilatation. There is, however, some concern about the fact that the cusps can touch the Dacron tube32 and the effect of the absence of distensibility30 and sinuses of Valsalva on long-term valve function. Longer periods of follow-up are needed to establish the exact role of these operations.
View larger version (25K):
[in this window]
[in a new window]
|
Figure 1. A, Diagram showing principle of remodeling operation for aortic regurgitation secondary to aortic wall disease (aneurysm or dissection). From Reference 27, Figure 2. B, Diagram of David operation for valve conserving repair of aortic regurgitation. From Reference 31, Figure 4.
|
|
View larger version (34K):
[in this window]
[in a new window]
|
Figure 2. Diagram illustrating a method for anatomic correction of syndrome of aortic regurgitation and ventricular septal defect. From Reference 35, Figure 10.
|
|
View larger version (33K):
[in this window]
[in a new window]
|
Figure 4. Diagram illustrating technique of quadrangular resection of a prolapsing (flail) posterior cusp combined with sliding plasty and insertion of a ring. Reprinted from Reference 49, with permission from the Society of Thoracic Surgeons.
|
|
The combination of ventricular septal defect and prolapsing aortic cusp has been the focus of attention for a relatively long time since the early description by Laubry and Pezzi.33 Several techniques for the associated aortic regurgitation have been described . One of the most commonly used is that introduced by Trusler et al34 from Toronto and consists of shortening the free border of the prolapsing cusp. More recently, the realization that the basic abnormality in this syndrome is the discontinuity between the aortic media and the crest of the interventricular septum has resulted in the evolution of a simple technique of reattaching the interventricular septum to the media of the aorta using a series of interrupted mattress sutures (Figure 2). 35 One of the advantages of this technique is that it does not involve touching the delicate aortic cusp tissue and therefore can be applied to infants before secondary changes in the valve occur.
Although the presence of bicuspid aortic valve predisposes to premature heavy calcification of the valve, a proportion of patients present with severe regurgitation with a pliable bicuspid valve.36,37 Some of these patients can be treated by repairing37,38 or redeveloping the fused commissure. The first technique consists of resecting a triangular part from the center of the fused redundant common leaflet to prevent its prolapse. An alternative technique consists of "recreating" the fused commissure by dividing the raphe and adding 2 triangular pieces of pericardium to reconstitute the commissure. This results in a competent trileaflet valve. A major disadvantage of this technique is that the material used for augmenting the cusps, whether autologous, homologous, or xenogenic, tends to shrink and calcify in the longer term. The same limitation applies to cusp augmentation used for repair of regurgitation of a tricuspid aortic valve38,39 in the presence of a pliable hinge mechanism
In patients with pure aortic regurgitation secondary to rheumatic disease, the essential lesion is retraction of the cusps with preservation of the hinge mechanism. The hemodynamic lesion results in progressive dilation of the aortic annulus with worsening of the regurgitation. In these patients, cusp augmentation using 3 separate strips of biological material38,39 (Figure 3) may be effective for various periods of time. The size of the patch is critically important, and the use of large redundant patches, particularly in the region of the left coronary cusp, can result in the redundant patch being sucked into the left coronary orifice, which could be fatal.
View larger version (136K):
[in this window]
[in a new window]
|
Figure 3. Technique of cusp augmentation using 3 strips of biological tissue. Reprinted from Reference 39, with permission from the Society of Thoracic Surgeons.
|
|
Materials used for this purpose include autologous pericardium, either "fresh" or treated with 0.6% glutaraldehyde for 8 minutes, processed calf pericardium, or human dura mater processed with glycerin. The use of the latter material has been discontinued because of the risk of transmitting spongiform disease. The durability of the tissues is unpredictable in different patients. Recently, the Carpentier group has reported 92% freedom from reoperation at 5 years after this type of procedure.39 Development of tissue engineered living patches could enhance the durability of this operation.
|
Mitral Valve Repair
|
|---|
Despite the complexity of the mitral valve apparatus, this valve
lends itself to repair in patients with both stenosis and regurgitation.
Application of these techniques, however, depends largely on
the pathogenesis of the valve disease, with >95% of patients
with the floppy-valve syndrome being suitable for repair.
Rheumatic Mitral Stenosis
Until recently, closed transventricular mitral valvotomy, introduced by Andrew Logan in Edinburgh and perfected by O.S. Tubbs through the introduction of an adjustable transventricular dilation, has produced good early and medium-term results and was cost-effective in developing countries. The availability of transcutaneous balloon valvuloplasty (PBV) or mechanical dilatation40 or open mitral valvotomy offers alternatives. The choice between these procedures depends on the morphology and function of the valve as well as economic and other factors. An echocardiographic scoring system was developed to assess the suitability for PBV.41 In a recent large series of PBVs from the Massachusetts General Hospital in Boston, the 12-year event-free survival after PBV was 38% for patients with an echocardiographic score of 
8, compared with 22% for those with an echocardiographic score of 
8.41 The use of transcutaneous mechanical mitral commissurotomy with a metallic dilator (commissurotome)40 can give very good immediate results (procedural success of 93% in selected patients with either stenosis or restenosis). Open mitral valvotomy42 is reserved for patients judged to be unsuitable for percutaneous procedures because of the presence of calcification, thrombus, or associated regurgitation. The operation consists of dealing with cusps, commissures, and subvalvar apparatus by use of fairly standardized techniques.42 The late results of this operation are good.42
Rheumatic Mitral Regurgitation
Severe pure mitral regurgitation continues to affect a large number of children and young adults in the developing world.43 The most common structural cause of regurgitation in these patients is dilatation of the mitral annulus, sometimes associated with elongation of the chordae tendineae, particularly those fixing the anterior cusp.44 This can be associated with restriction of the posterior cusp. These abnormalities result in prolapse of the anterior leaflet and can be corrected by the insertion of a posterior annuloplasty band or ring extending from one trigone to the other, thus displacing the posterior annulus forward. This has the effect of preventing prolapse of the anterior cusp and producing good coaptation of the cusps. Before the annuloplasty is performed, the valve should be evaluated and additional abnormalities or defects should be dealt with. Because rheumatic affection of the mitral valve produces progressive damage to the valve, the durability of this type of repair is not as good as repair of floppy valves. In a large series of 951 patients recently reported from Paris, with a follow-up of up to 29 years, freedom from reoperation was 89±19% at 10 years and 82±18% at 20 years.45
Myxomatous Mitral Valve Disease (Barlow’s Syndrome)
This entity is currently the most common cause of pure mitral regurgitation in western countries, with a continued increase in its prevalence because of a variety of causes, including increased life expectancy. In this syndrome, mitral regurgitation is caused by prolapse of one or more segments of cusp tissue into the left atrium, resulting in a spectrum of clinicopathological syndromes.46,47 This is produced by elongated and/or ruptured chordae associated with voluminous leaflet tissue and dilated annulus. The flail segments are readily definable by 2D echocardiography and at operation. Patients with flail segments present with severe mitral regurgitation in >85% of cases.47 The same authors have reported an increased mortality and morbidity in these patients even if they are asymptomatic or have relatively preserved left ventricular function. Sudden death accounted for approximately 25% of deaths occurring under medical treatment in this series.48 This association needs to be confirmed and its causes investigated in a larger series of patients. Fortunately, the vast majority of these patients are amenable to repair, as mentioned earlier, by fairly standardized techniques.49–54 The most commonly affected region is the posterior cusp, which can easily be dealt with by quadrangular resection of the flail segment in combination with compression sutures to reduce the size of the annulus in this region or sliding plasty49 to reduce the incidence of systolic anterior motion of the mitral valve49 (Figure 4). Prolapse of the anterior cusp requires a more complex type50–52 of repair, which could involve triangular resection, insertion of artificial chordae, chordal translocation from the posterior cusp, or occasionally edge-to-edge repair as described by Alfieri and Maisano.52 The repair operation is usually combined with annuloplasty using a variety of semirigid rings53,54 designed to reduce and possibly reshape the annulus. Although annuloplasty is thought to "stabilize" the repair and possibly enhance its durability, to date there have been no prospective randomized trials to validate this point. In addition, this type of annuloplasty may interfere with the mobility of the mitral annulus or rarely produce systolic anterior movement54 of the mitral valve, which can occur in 4.5% to 10% of patients.
Despite the diffuse nature of the disease, the durability of repaired mitral regurgitation in patients with degenerative valve disease is excellent. In 2 large series,55,56 the freedom from reoperation at 10 to 15 years was 90%.
The instantaneous hazard function for reoperation shows 2 phases, a peaking early hazard phase during the first year followed by a very low, slowly developing late phase.55 The cause of failure of the repair is technical reasons in approximately half of the patients,55 emphasizing the importance of experience and attention to detail in performing the repair, including the use of intraoperative transesophageal echo and ensuring lack of residual regurgitation at the time of operation. The incidence of postoperative endocarditis appears to be similar after repair compared with replacement. Several observational studies strongly suggest that long-term survival after repair is superior to that after replacement,20,23 which has stimulated operation on all or most patients with severe regurgitation, provided that repair can be performed.
Mitral Regurgitation Caused by Ischemic Heart Disease or Dilated Cardiomyopathy
This type of mitral regurgitation defines a group of patients at high risk.57 A small proportion of patients present acutely after myocardial infarction with complete or partial rupture of one of the papillary muscles, usually the posterior.58 Patients with partial rupture of one of the heads of a papillary muscle can be treated by excision of the flail segment in a manner similar to that for floppy valves. In complete rupture, reattachment58 of the papillary muscle may be achieved in a minority of patients who have localized infarction affecting the attachment of the papillary muscle (a rare event); however, usually the only effective treatment is urgent valve replacement.
The most common cause of ischemic mitral regurgitation is associated with chronic heart failure caused by repeated infarction. Because the valve components are anatomically normal, this type of mitral regurgitation is often referred to as "functional mitral regurgitation." The mechanisms responsible for "ischemic" functional mitral regurgitation are similar but not identical to those in mitral regurgitation associated with idiopathic dilated cardiomyopathy.59 Although this has been shown to be at least in part to be a result of dilatation of the mitral annulus,59,60 current evidence suggests that this is not the only factor and that one of the main causes of regurgitation in these patients is displacement of the papillary muscles downward and outward, thus leading to tethering of the mitral leaflets.61 Prognostically less severe degrees of functional mitral regurgitation, compared with mitral regurgitation caused by floppy-valve syndrome, have been shown to incur an excess mortality.62 Assessment of the severity of mitral regurgitation can be problematic, particularly perioperatively in patients under anesthesia or when the patients have been treated with intensive unloading therapy.63 When mild to moderate mitral regurgitation (effective regurgitant orifice of 20 mm2) is present preoperatively in patients requiring coronary artery bypass grafting, there is increasing evidence that this will not improve after revascularization and that it could have an adverse effect on long-term outcome.64 This supports the view that this degree of regurgitation should be repaired at the time of CABG. The use of an undersized annuloplasty is the most commonly performed method.65 Although this is effective, at least in the short term, it does not deal with the primary abnormality. Alfieri’s edge-to-edge repair has also been used in these patients.52 Other methods, such as septal-annular cinching66 and external plication67 and percutaneous repair68 have been used experimentally and may be useful clinically in the future.
In patients with functional mitral regurgitation who do not require revascularization, such as those with ischemic or idiopathic dilated cardiomyopathy, repair is considered only if regurgitation is judged to be severe.
Mitral Regurgitation Caused by Acute Endocarditis
Endocarditis of the mitral valve is the most common form of native heart valve endocarditis69 and carries a high morbidity and mortality in the acute phase. The most common organisms are Streptococcus veridans and Staphylococcus aureus and the enterococci. The disease results in various degrees of damage to the leaflets, chordae, and annular tissue and can cause abscesses involving the surrounding myocardium. Until recently, the condition was treated surgically only if intensive specific antibiotic therapy fails to control infection or if "uncontrolled" heart failure develops. The presence of large vegetations or abscesses did not necessarily constitute an indication for early surgical intervention. Recent evidence suggests that early repair could avoid excessive damage to the valve and give excellent long-term results.69–71 Repair usually consists of excision of infected tissue followed by direct reconstruction, as in the case of floppy-valve syndrome. More extensive damage to the valve could necessitate the use of autologous or xenogenic pericardium to repair defects in the leaflets, and artificial chordae may be used. The results of repair appear to be superior to those of replacement, in terms of both survival and incidence of complications or recurrence of infection.70
|
Tricuspid Valve Repair
|
|---|
Tricuspid Stenosis
Isolated tricuspid stenosis is very rare and is usually part
of rheumatic multivalvular disease. Although the hemodynamic
lesion can be tolerated for long periods of time,
72 the majority
of patients require repair. At operation, the cusps are fused
and produce a diaphragm-like structure; although the commissures
can be identified and divided, the cusps are usually retracted
and the subvalvar apparatus is affected. This necessitates the
use of annuloplasty. Other forms of tricuspid stenosis are extremely
rare.
Rheumatic Tricuspid Regurgitation
The most common cause of tricuspid regurgitation (TR) is functional TR secondary to rheumatic disease of left-sided valves, either before or after mitral valve operations.73–76 Although TR can regress after successful treatment of mitral valve disease, this is not always the case, with many patients having residual or progressive TR despite effective treatment of mitral valve disease with complete or partial normalization of the pulmonary artery pressure. TR in this setting can have adverse effects on clinical progress and outcome. Guidelines for repair73,75,76 of the valve include severity of TR assessed clinically and by imaging methods, indexed size of the tricuspid annulus (>2.1 cm/m2), ejection fraction of the tricuspid annulus (< 25%), and importantly, right ventricular function. Repair of the valve using ring, band, or suture annuloplasty is usually effective and does not increase the risk of the operation. In contrast, repair of isolated residual or recurrent TR after mitral valve surgery carries a higher risk (8.8% mortality).77
Tricuspid Valve Endocarditis
Another lesion that can require tricuspid repair is tricuspid endocarditis from intravenous drug abuse or after long-term catheterization of the right side, such as in patients in an intensive care unit. It can also be treated with reparative techniques, such as pericardial remodeling of the annulus, total excision of the tricuspid valve, or annuloplasty. Finally, in an even smaller subset of patients, reparative procedures can be performed for lupus endocarditis, diet drug-induced valvulitis, or carcinoid of the tricuspid valve. In patients who require tricuspid valve replacement, right-sided bioprosthetic valves are generally indicated, because they last longer than the similar valve placed in the left side of the circulation.
Ebstein’s Anomaly
This anomaly comprises a spectrum of abnormalities78 that need to be defined and corrected if possible. Early attempts at repair of the tricuspid valve in Ebstein’s anomaly concentrated on "correcting" the downward displacement of the hinge mechanism of the septal and inferior leaflets into the right ventricle and obliterating the "atrialized" ventricle. More recent methods of repair79,80 (Figure 5) depend on creating a monocuspid valve using the reconstructed anterosuperior leaflet, which is almost always present as a large sail-like structure with adequate tissue for repair. It is equally important, however, to realize that this leaflet is highly abnormal (a fact recognized by Wilhelm Ebstein in his original article in 1866)81 in shape, location, and size with limited mobility because of the presence of abnormal chordae and the frequent direct attachment of the free border of the cusp to the right ventricular myocardium.79,80 These latter abnormalities can produce stenosis and abnormal orientation of the orifice of the valve. Vertical plication of the atrialized right ventricle as advocated by Carpentier and Chauvaud has the advantage of reducing the size of the annulus and the atrialized ventricle but carries a small risk of injuring the right coronary artery. This can be prevented by identifying that artery before performing the repair. Ebstein’s anomaly should be operated on only when there are hemodynamically significant abnormalities, because the milder forms of the disease are very well tolerated. Most patients operated on are amenable to repair with the addition of biventricular Glenn shunt, if necessary, but valve replacement is rarely required.
View larger version (34K):
[in this window]
[in a new window]
|
Figure 5. Technique used for repair of TR due to Ebstein’s anomaly. A, Mobilization of anterosuperior leaflet. B, After division of abnormal chordae fixing ventricular aspect of leaflet to right ventricular wall, longitudinal plication of atrialized ventricle is started (A, B). C, Mobilized leaflet is reattached to its new position after completing plication of atrialized ventricle. Reprinted from Reference 80, with permission from the Society of Thoracic Surgeons.
|
|
|
Pulmonary Valve Repair
|
|---|
Diseases of the pulmonary valve are usually caused by congenital
abnormalities. Stenosis can be treated by balloon valvuloplasty,
which produces very good early results.
82 However, the longer-term
outcome in these patients has not been formally compared with
that obtained by surgical treatment. Although mild to moderate
degrees of pulmonary regurgitation can be tolerated for a relatively
long time, there is evidence that the condition is not entirely
benign and can cause right ventricular dysfunction
83 and/or
arrhythmias and therefore may have an adverse effect on symptomatic
status and possibly survival. In these patients, pulmonary valve
replacement with a pulmonary allograft is the treatment of choice.
Very few of these valves are amenable to repair.
|
Percutaneous Repair of Valve Regurgitation
|
|---|
As outlined earlier, percutaneous relief of valve stenosis by
balloon dilatation or mechanical devices is being applied routinely
in selected patients with mitral, pulmonary, and aortic stenosis.
More recently, percutaneous techniques for treating pulmonary
regurgitation by insertion of a bovine jugular vein inside a
stent have been developed and applied clinically
84 (
Figure 6).
Although similar techniques are being developed for treating
aortic regurgitation
85 (
Figure 7), this is more problematic
because of the proximity of the coronary ostia coupled with
exposure to high pressure.
View larger version (98K):
[in this window]
[in a new window]
|
Figure 6. Radiograph showing percutaneous insertion of a pulmonary valve substitute inside an expanded stent. Courtesy of Dr Phillip Bonhoeffer, Great Ormond Street Hospital, London.
|
|
View larger version (65K):
[in this window]
[in a new window]
|
Figure 7. Schematic views of device. Left, 3 parts of device are represented separately (from top: platinum stent, nitinol stent, and valve). Middle, Fully expanded device is shown longitudinally and axially. Right, diagrams demonstrate where nitinol and platinum stents are attached, which allowed stepwise approach. Reprinted with permision from Reference 85, Figure 2.
|
|
Percutaneous devices for treatment of functional mitral regurgitation introduced into the coronary sinus have been developed and tested in experimental models68 (Figure 8) with encouraging results.
View larger version (56K):
[in this window]
[in a new window]
|
Figure 8. Illustrations of principle of use of a percutaneous device (inserted through coronary sinus) to correct functional mitral regurgitation. Courtesy of Viacor.
|
|
|
The Future
|
|---|
Rapid progress in our understanding of the sophisticated functions
of heart valves should lead to continued efforts to reproduce
these functions at the cellular, molecular, and integrated tissue
levels. This may be achieved through the development of novel
reparative techniques or valve replacement using tissue-engineered
substitutes. The ultimate aim is to restore both longevity and
quality of life to normal after what is in effect a timely "corrective"
operation.
|
Footnotes
|
|---|
This is Part II of a 2-part article. Part I appeared in the
March 2, 2004, issue of
Circulation (
Circulation. 2004;109:942–950).
|
References
|
|---|
- Cutler EE, Levine SA, Beck CS. The surgical treatment of mitral stenosis: experimental and clinical studies. Arch Surg. 1924; 9: 689–821, 104–105.
- Souttar HS. The surgical diagnosis of mitral stenosis. Brit Med J. 1925; 2: 605.
- Lillehei CW, Gott VL, DeWall RA, et al. Surgical correction of pure mitral insufficiency by annuloplasty under direct vision. Lancet. 1957; 77: 446–449.[CrossRef]
- McGoon DC. Repair of mitral insufficiency due to ruptured chordae tendineae. J Thorac Cardiovasc Surg. 1960; 39: 357–362.
- Carpentier A. Cardiac valve surgery: the "French Correction." J Thorac Cardiovasc Surg. 1983; 86: 323–337.[Medline]
[Order article via Infotrieve]
- Guidelines for the management of patients with valvular heart disease. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 1998; 98: 1949–1984.[Medline]
[Order article via Infotrieve]
- Enriquez-Sarano M. Timing of mitral valve surgery. Heart. 2002; 87: 79–85.[Free Full Text]
- Grunkemeier G, Wu YX, Jin R. Statistical analysis of heart valve outcomes. J Heart Valve Dis. 2002; (suppl 1): S2–S7.
- Blackstone EH. Comparing apples and oranges. J Thorac Cardiovasc Surg. 2002; 123: 8–15.[Free Full Text]
- de Kruyk M, van der Meulen JHP, van Herwerden LA, et al. Monte Carlo technique: use of Markov series and Monte Carlo simulation in predicting replacement valve performances. J Heart Valve Dis. 1998; 7: 4–12.[Medline]
[Order article via Infotrieve]
- Tribouilloy C, Enriquez-Sarano M, Schaff H, et al. Impact of pre-operative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications. Circulation. 1999; 99: 400–405.[Medline]
[Order article via Infotrieve]
- Vandervoort P, Rivera J, Mele D, et al. Application of color Doppler flow mapping to calculate effective regurgitant orifice area: an in vitro study and initial clinical observations. Circulation. 1993; 88: 1150–1156.[Medline]
[Order article via Infotrieve]
- Enriquez-Sarano M, Miller FJ, Hayes S, et al. Effective mitral regurgitant orifice area: clinical use and pitfalls of the proximal isovelocity surface area method. J Am Coll Cardiol. 1995; 25: 703–709.[Abstract]
- Ringgaard S, Botnar RM, Djurhuus C, et al. High-resolution assessment of velocity fields and shear stresses distal to prosthetic heart valves using high-field magnetic resonance imaging. J Heart Valve Dis. 1999; 8: 96–103.[Medline]
[Order article via Infotrieve]
- Kozerke S, Hasenkam JM, Nygaard H, et al. Heart motion-adapted MR velocity mapping of blood velocity distribution downstream of aortic valve prostheses: initial experience. Radiology. 2001; 218: 548–555.[Abstract/Free Full Text]
- Rosenhek R, Burder T, Pozenta G, et al. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med. 2000; 343: 611–617.[Abstract/Free Full Text]
- Melina G, Rubens MB, Birks EJ, et al. A quantitative study of calcium deposition in the aortic wall following Medtronic Freestyle compared to homograft aortic root replacement: a prospective randomised trial. J Heart Valve Dis. 2000; 9: 97–103.[Medline]
[Order article via Infotrieve]
- Kizer JR, Gefter WB, deLemos AS, et al. Electron beam computed tomography for the quantification of aortic valvular calcification. J Heart Valve Dis. 2001; 10: 361–366.[Medline]
[Order article via Infotrieve]
- Deutscher S, Rockette HE, Krishnaswami V. Diabetes and hypercholesterolemia among patients with calcific stenosis. J Chronic Dis. 1994; 37: 407–415.
- Yacoub MH, Halim M, Radley-Smith R, et al. Surgical treatment of mitral regurgitation caused by floppy valves: repair versus replacement. Circulation. 1981; 64: 210–216.
- Sand ME, Naftel DC, Blackstone EH, et al. A comparison of repair and replacement for mitral valve incompetence. J Thorac Cardiovasc Surg. 1987; 94: 208–219.[Abstract]
- Lee EM, Shapiro LM, Wells FC. Superiority of mitral valve repair in surgery for degenerative mitral regurgitation. Eur Heart J. 1997; 18: 655–663.[Abstract/Free Full Text]
- Enriquez-Sarano M, Schaff HV, Orszulak TA, et al. Valve repair improves the outcome of surgery for mitral regurgitation: a multivariate analysis. Circulation. 1995; 91: 1022–1028.[Medline]
[Order article via Infotrieve]
- Ross DN. Replacement of the aortic valve with a pulmonary autograft: the switch operation. Ann Thorac Surg. 1991; 52: 1346–1350.[Abstract]
- Laudito A, Brook MM, Suelman S, et al. The Ross procedure in children and young adults: a word of caution. J Thorac Cardiovasc Surg. 2002; 122: 147–153.
- Becker AE. Surgical and pathological anatomy of the aortic valve and root. In: Cox JL, Sundt T, eds. Operative Techniques in Cardiac and Thoracic Surgery. W.B. Saunders Company. 1996; 1: 3–14.
- Yacoub MH, Gehle P, Chandrasekaran V, et al. Late results of a valve-preserving operation in patients with aneurysms of the ascending aorta and root. J Thorac Cardiovasc Surg. 1998; 115: 1080–1090.[Abstract/Free Full Text]
- Zehr KJ, Thubrikar MJ, Gong GG, et al. Clinical introduction of a novel prosthesis for valve-preserving aortic root reconstruction for annuloaortic ectasia. J Thorac Cardiovasc Surg. 2001; 121: 1220–1221.[Free Full Text]
- O’Cochran RP, Kunzelman KS, Eddy AC, et al. Modified conduit preparation creates a pseudo sinus in an aortic valve-sparing procedure for aneurysm of the ascending aorta. J Thorac Cardiovasc Surg. 1995; 109: 1049–1058.
- Leyh RG, Schmidtke C, Sievers HH, et al. Opening and closing characteristics of the aortic valve after different types of valve preserving surgery. Circulation. 1999; 100: 2153–2160.[Medline]
[Order article via Infotrieve]
- David TE, Findel CM. An aortic valve sparing operation for patients with aortic incompetence and aneurysm of the ascending aorta. J Thorac Cardiovasc Surg. 1992; 103: 617–622.[Abstract]
- Gallo R, Jumar N, al Halees Z, et al. Early failure of aortic valve conservation in aortic root aneurysm. J Thorac Cardiovasc Surg. 1995; 109: 1011–1012.[CrossRef][Medline]
[Order article via Infotrieve]
- Laubry C, Pezzi C. Traite des maladies congenitales du coeur. Paris, France: JB Balliere et Fils; 1921.
- Trusler GA, Moes CF, Kidd VSL. Repair of ventricular septal defect with aortic insufficiency. J Thorac Cardiovasc Surg. 1973; 66: 394.[Medline]
[Order article via Infotrieve]
- Yacoub MH, Khan H, Stavri G, et al. Anatomic correction of the syndrome of prolapsing right coronary aortic cusp, dilatation of the sinus of Valsalva and ventricular septal defect. J Thorac Cardiovasc Surg. 1997; 113: 253–261.[Abstract/Free Full Text]
- Sadee A, Becker AE, Verheul HA, et al. Aortic valve regurgitation and congenitally bicuspid aortic valve: a clinical pathological correlation. Br Heart J. 1992; 67: 439–441.[Abstract/Free Full Text]
- Cosgrove DM, Frazier CD. Aortic valve repair. In: Cox JL, Sundt TM, eds. Operative Techniques in Cardiac and Thoracic Surgery. W.B. Saunders Company. 1996; 1: 30–37.
- Duran C. Aortic valve repair and reconstruction. In: Cox JL, Sundt TM, eds. Operative Techniques in Cardiac and Thoracic Surgery: A Comparative Atlas. Philadelphia, Pa: WB Saunders; 1996: 15–29.
- Grinda J-M, Latremouille C, Berrebei AJ, et al. Aortic cusp extension valvuloplasty for rheumatic aortic valve disease: midterm results. Ann Thorac Surg. 2002; 74: 438–443.[Abstract/Free Full Text]
- Eltchaninoff H, Tron C, Cribier A. Effectiveness of percutaneous mechanical mitral commissurotomy using the metallic commissurotome in patients with restenosis after balloon or previous surgical commissurotomy. Am J Cardiol. 2003; 91: 425–428.[CrossRef][Medline]
[Order article via Infotrieve]
- Palacios IF, Sanchez PL, Harrell LC, et al. Which patients benefit from percutaneous mitral balloon valvuloplasty? Prevalvuloplasty and postvalvuloplasty variables that predict long-term outcome. Circulation. 2002; 105: 1465–1471.[Abstract/Free Full Text]
- Choudray SK, Dharcshwar J, Govil A, et al. Open mitral commissurotomy in the current era: indications, technique and results. Ann Thorac Surg. 2003; 75: 41–46.[Abstract/Free Full Text]
- John S. Surgery of the mitral valve. Indian J Chest Dis Allied Sci. 1996; 38: 223–225.[Medline]
[Order article via Infotrieve]
- Kalangos A, Beghetti M, Vala D, et al. Anterior mitral leaflet prolapse as a primary cause of pure rheumatic mitral insufficiency. Ann Thorac Surg. 2000; 69: 755–761.[Abstract/Free Full Text]
- Chavaud S, Fuzellier JF, Berribi A, et al. Long-term (29 years) results of reconstructive surgery in rheumatic mitral valve insufficiency. Circulation. 2001; 104 (suppl I): I-12–I-15.
- Yacoub M, McKay R. Spectrum of floppy mitral valve syndromes: clinicopathological study. Br Heart J. 1973; 35: 866–867.
- Ling H, Enriquez-Sarano M, Seward J, et al. Clinical outcome of mitral regurgitation due to flail leaflets. N Engl J Med. 1996; 335: 1417–1423.[Abstract/Free Full Text]
- Grigioni F, Enriquez-Sarano M, Ling L, et al. Sudden death in mitral regurgitation due to flail leaflet. J Am Coll Cardiol. 1999; 34: 2078–2085.[Abstract/Free Full Text]
- Perier P, Clausnizer B, Mistarz K. Carpentier "sliding leaflet" technique for repair of the mitral valve: early results. Ann Thorac Surg. 1994; 57: 383–386.[Abstract]
- El-Khoury G, Noirhomme P, Verhelst R, et al. Surgical repair of the prolapsing anterior leaflet in degenerative mitral valve disease. J Heart Valve Dis. 2000; 9: 75–81.[Medline]
[Order article via Infotrieve]
- Smedira NG, Selman R, Cosgrove DM, et al. Repair of anterior leaflet prolapse: chordal transfer is superior to chordal shortening. J Thorac Cardiovasc Surg. 1996; 112: 287–291;discussion 291–282.[Abstract/Free Full Text]
- Alfieri O, Maisano F. An effective technique to correct anterior mitral valve leaflet prolapse. J Card Surg. 1999; 14: 468–470.[Medline]
[Order article via Infotrieve]
- David T, Komeda M, Pollick C, et al. Mitral valve annuloplasty: the effect of the type on left ventricular function. Ann Thorac Surg. 1989; 47: 524–528.[Abstract]
- Kreindel MS, Schiavone WA, Lever HM, et al. Systolic anterior motion of the mitral valve after Carpentier ring valvuloplasty for mitral valve prolapse. Am J Cardiol. 1986; 57: 408–412.[CrossRef][Medline]
[Order article via Infotrieve]
- Gillinov AM, Cosgrove DM, Blackstone EH, et al. Durability of mitral valve repair for degenerative disease. J Thorac Cardiovasc Surg. 1998; 116: 734–743.[Abstract/Free Full Text]
- Braunberger E, Deloche A, Berrebi A, et al. Very long term results (more than 20 years) of valve repair with Carpentier’s techniques in non-rheumatic mitral valve insufficiency. Circulation. 2001; 104 (suppl I): I-8–I-11.
- Lamas GA, Mitchell GF, Flaker GC, et al. Clinical significance of mitral regurgitation after acute myocardial infarction. Circulation. 1997; 96: 827–833.[Medline]
[Order article via Infotrieve]
- Gula G, Yacoub MH. Surgical correction of complete rupture of the anterior papillary muscle. Ann Thorac Surg. 1981; 32: 88–91.[Abstract]
- Kwan J, Shiota T, Agler DA, et al. Geometric differences of the mitral apparatus between ischemic and dilated cardiomyopathy with significant mitral regurgitation: real-time three-dimensional echocardiography study. Circulation. 2003; 107: 1135–1140.[CrossRef][Medline]
[Order article via Infotrieve]
- Boltwood CM, Tei C, Wong M, et al. Quantitative echocardiography of the mitral complex in dilated cardiomyopathy: the mechanism of functional mitral regurgitation. Circulation. 1983; 68: 498–508.[Medline]
[Order article via Infotrieve]
- Otsuji Y, Handschumacher MD, Schwammenthal E, et al. Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation: direct in vivo demonstration of altered leaflet tethering geometry. Circulation. 1997; 96: 199–208.
- Grigioni F, Enriquez-Sarano M, Zehr K, et al. Ischemic mitral regurgitation: long-term outcome and prognostic implications with quantitative Doppler assessment. Circulation. 2001; 103: 1759–1764.[Medline]
[Order article via Infotrieve]
- Byrne JG, Aklog L, Adams DH. Assessment and management of functional or ischemic mitral regurgitation. Lancet. 2000; 355: 1743–1744.[CrossRef][Medline]
[Order article via Infotrieve]
- Adams DH, Filsoufi F, Aklog L. Surgical treatment of the ischemic mitral valve. J Heart Valve Dis. 2002; 11 (suppl 1): S21–S25.
- Bolling SF. Mitral reconstruction in cardiomyopathy. J Heart Valve Dis. 2002; 11 (suppl 1): S26–S31.
- Timek TA, Lai DT, Tibayan FA, et al. Septal-lateral annular cinching ("SLAC") reduces mitral annular size without perturbing normal annular dynamics. J Heart Valve Dis. 2002; 11: 2–10.[Medline]
[Order article via Infotrieve]
- Liel-Cohen N, Guerro JL, Otsuji Y, et al. Design of a new surgical approach for ventricular remodeling to relieve ischemic mitral regurgitation: insights from 3-dimensional echocardiography. Circulation. 2000; 101: 2756–2763.[Medline]
[Order article via Infotrieve]
- Osterle SN, Gillinov AM, Chin CH, et al. Percutaneous catheter-based mitral valve repair. J Am Coll Cardiol. 2002; 39: 432A.
- Sternik L, Zehr KJ, Orszulak TA, et al. The advantage of repair of mitral valve in acute endocarditis. J Heart Valve Dis. 2002; 11: 91–98.[Medline]
[Order article via Infotrieve]
Top
Introduction
Valve Repair: Evolution of...