Intro4u2u

HTML clipboardThe controller output (CO) is the input to the valve assembly and the process variable (PV) is the output as shown in figure 1-1. When the term Dead Band is used, it is essential that both the input and output variables are identified, and that any tests to measure dead band be under fully loaded conditions. Dead band is typically expressed as a percent of the input span. Dead Time: The time interval (Td) in which no response of the system is detected following a small (usually 0.25% - 5%) step input.

It is measured from the time the step input is initiated to the first detectable response of the system being tested. Dead Time can apply to a valve assembly or to the entire process. (See T63.) Disk: A valve trim element used to modulate the flow rate with either linear or rotary motion. Can also be referred to as a valve plug or closure member.

Equal Percentage Characteristic*: An inherent flow characteristic that, for equal increments of rated travel, will ideally give equal percentage changes of the flow coefficient (Cv) (figure 1-2). Final Control Element: The device that implements the control strategy determined by the output of the controller. While the final control element can be a damper, a variable speed drive pump, or an on-off switching device, the most common final control element in the process control industries is the control valve assembly. The control valve manipulates a flowing fluid, such as gasses, steam, water, or chemical compounds, to compensate for the load disturbance and keep the regulated process variable as close as possible to the desired set point. First-Order: A term that refers to the dynamic relationship between the input and output of a device. A first-order system or device is one that has only one energy storage device and whose dynamic transient relationship between the input and output is characterized by an exponential behavior. Friction: A force that tends to oppose the relative motion between two surfaces that are in contact with each other. The friction force is a function of the normal force holding these two surfaces together and the characteristic nature of the two surfaces. Friction has two components: static friction and dynamic friction. Static friction is the force that must be overcome before there is any relative motion between the two surfaces. Once relative movement has begun, dynamic friction is the force that must be overcome to maintain the relative motion. Running or sliding friction are colloquial terms that are sometimes used to describe dynamic friction. Stick/slip or “stiction” are colloquial terms that are sometimes used to describe static friction. Static friction is one of the major causes of dead band in a valve assembly. Gain: An all-purpose term that can be used in many situations. In its most general sense, gain is the ratio of the magnitude of the output change of a given system or device to the magnitude of the input change that caused the output change. Gain has two components: static gain and dynamic gain. Static gain is the gain relationship between the input and output and is an indicator of the ease with which the input can initiate a change in the Chapter 1. Introduction to Control Valves 4 Figure 1-2. Inherent Valve Characteristics A3449/IL output when the system or device is in a steady-state condition. Sensitivity is sometimes used to mean static gain. Dynamic gain is the gain relationship between the input and output when the system is in a state of movement or flux. Dynamic gain is a function of frequency or rate of change of the input. Hysteresis*:

The maximum difference in output value for any single input value during a calibration cycle, excluding errors due to dead band. Inherent Characteristic*: The relationship between the flow coefficient and the closure member (disk) travel as it is moved from the closed position to rated travel with constant pressure drop across the valve. Typically these characteristics are plotted on a curve where the horizontal axis is labeled in percent travel and the vertical axis is labeled as percent flow (or Cv) (figure 1-2). Because valve flow is a function of both the valve travel and the pressure drop across the valve, conducting flow characteristic tests at a constant pressure drop provides a systematic way of comparing one valve characteristic design to another. Typical valve characteristics conducted in this manner are named Linear, Equal-Percentage, and Quick Opening (figure 1-2). Inherent Valve Gain: The magnitude ratio of the change in flow through the valve to the change in valve travel under conditions of constant pressure drop. Inherent valve gain is an inherent function of the valve design. It is equal to the slope of the inherent characteristic curve at any travel point and is a function of valve travel. Installed Characteristic*: The relationship between the flow rate and the closure member (disk) travel as it is moved from the closed position to rated travel as the pressure drop across the valve is influenced by the varying process conditions. (See Valve Type and Characterization in Chapter 2 for more details on how the installed characteristic is determined.) Installed Valve Gain: The magnitude ratio of the change in flow through the valve to the change in valve travel under actual process conditions. Installed valve gain is the valve gain relationship that occurs when the valve is installed in a specific system and the pressure drop is allowed to change naturally according to the dictates of the overall system. The installed valve gain is equal to the slope of the installed characteristic curve, and is a function of valve travel.

(See Valve Type and Characterization in Chapter 2 for more details on how the installed gain is determined.) I/P: Shorthand for current-to-pressure (I-to-P). Typically applied to input transducer modules. Linearity*: The closeness to which a curve relating to two variables approximates a straight line. (Linearity also means that the same straight line will apply for both upscale and downscale directions. Thus, dead band as defined above, would typically be considered a non-linearity.)

Reconstruction of the aortic valve has been rarely performed during a half-century of cardiac surgery. The aortic valve repair was reported early after the beginning of open heart surgery by Albert Starr [1] and Frank Spencer [2] in congenital heart diseases. The satisfactory short and long-term results with valve replacements, together with the limited knowledge of the aortic root function were the main causes of the lack of interest for this surgical alternative. Paul Wojewski recently pointed out [3]: “We have lost our way in aortic valve surgery. We have made a lot of valves but we have never followed in general the principals dictated by nature”. Few surgeons in the world investigated the anatomy and complex physiology of the aortic valve, and later they have tried to apply their research findings to the surgical field. Magdi Jacoub and Tirone David have developed surgical techniques to spare the aortic valve when the aortic root replacement is mandatory, with very encouraging and predictable mid- and long-term results in a significant number of patients. Their original techniques and later modifications have widely accepted and they are now used by a growing number of surgeons.

Surgical reconstruction of the acquired aortic valve regurgitation has been explored with unpredictable results. During the eighties, Alain Carpentier [4,9] and Carlos G. Duran [5,7,8,11,12], at our Institution in Santander, have introduced different techniques to repair the aortic insufficiency with satisfactory mid-term results. During the last decade, several publications demonstrated an increasing interest with this challenging surgery. However, a variety of reconstructive techniques were used, without a clear categorization of the indications, or a separate analysis of the durability of each surgical technique.

Aortic regurgitation is produced by lack of coaptation of the leaflets due to prolapse of one or all cusps, the dilatation of the aortic annulus and/or the sinotubular junction, the damage or destruction of one leaflet, or the structural modification of the cusps. As John A. Carr and Edward B. Savage from Chicago have recently reported in an elegant review [6], the types of reconstructive technique used, mainly depends on the surgeon preferences. In general, these techniques could be classified as followed:

For isolated annular dilatation (non-aneurysmatic dilatation)

* Circular annuloplasty
* Commissural plication
* Pericardial valve extension
* Supraaortic crest enhancement

For leaflet damage or destruction

* Leaflet simple suture
* Pericardial patch repair
* Pericardial extension

For leaflet prolapse

* Free edge leaflet plication
* Leaflet resuspension
* Triangular resection

For leaflet retraction

* Lunulae unrolling
* Lunulae shaving
* Commissurotomy
* Pericardial extension

Duran et al [7] have reported the indications and limitations of aortic valve reconstruction, with the different repairs. Most of their patients did not required anticoagulation prophylaxis, only receiving antiplatelet drugs, with a low incidence of thromboembolic events (less than 1%).

Postoperative valve-related complications after aortic valve repair were low as shown in a meta-analysis of 761 patients [6]. The small incidence on thromboembolic events (1%) after aortic valve repair in patients without anticoagulation encourages for a persistent investigation on this surgical approach. Infective endocarditis is also low (average: 0.7%) over a mean follow-up of 4 years, significantly lower than the reported incidence after aortic valve replacement with bioprostheses. This incidence is appreciably higher (2.4%) after aortic cusp pericardial extension techniques [6].

Durability after aortic valve repair still remains uncertain. The reported 10-year freedom from reoperation rate was 64%, with a reoperation rate of 7.8%. This fact represents the determining factor in selecting this surgical alternative. Different authors agreed that the clinical outcome is significantly worse for the repaired rheumatic and bicuspid aortic valves than for the other etiologies, with higher recurrence and reoperation rates. Early causes of failure were suture dehiscence, incomplete repair, pericardial patch tear or detachment. Late failures were due to progression of the disease, pericardial patch or strip tissue degeneration (tear, fibrosis, retraction or calcification) [13]. Aortic leaflet extension with a strip of glutaraldehyde-treated autologous pericardium was used by Duran et al. [8] in patients with severe valve incompetence, but not long-term results have been described. Ahn et al. [10], from South Korea, have reported their experience in a group of 34 patients with pericardial leaflet extension technique, and only 8 patients were free from aortic valve regurgitation, but 93% of patients are free from reoperation one year after surgery. They concluded that a long-term follow-up study will be necessary to evaluate the durability of this reconstructive procedure.

Few years ago, we explored [14] whether or not the aortic valve repair was safe in patients with non-severe rheumatic aortic valve disease during other valvular procedures. In a group of 53 patients who underwent aortic valve repair with different repair techniques at the time of mitral or mitro-tricuspid valve surgery, only 12.7% were free from aortic valve structural deterioration 22 years after surgery; so, we concluded that the concomitant aortic valve repair did not seem appropriate. However, Al-Halees et al. [15] have later reported that, in their experience, repair of associated moderate aortic valve incompetence is worth considering even in predominantly young rheumatic population. They were more optimistic about the validity of this surgical approach, on a similar group of patients with a freedom from reoperation of 63.4% at 8-year follow-up. These authors pointed out that the lack of TEE in our series could explain the differences in our clinical outcomes.

Further analysis are necessary, separating the different etiologies, valve pathologies, and particularly the types of aortic valve repair technique used. Aortic valve repair will provide the patients with a better quality of life, no need for permanent anticoagulation, a lower incidence of thromboembolic events, endocarditis, and other valve-related complications. However, the durability of repair is still unclear, so it will require additional attention in order to establish the indications, to validate techniques, and above all to assess the durability of aortic valve repair in larger series of patients.

When treating aortic stenosis, the surgeon’s mission is to improve survival and alleviate symptoms by reducing or eliminating left ventricular outflow tract obstruction. Although logic suggests that it might be important to use the largest, most hemodynamically efficient prosthesis at aortic valve replacement, studies of the impact of prosthesis size and function on survival have generated controversy (1-5). In the patient with critical aortic stenosis, all available prostheses provide hemodynamic improvement over the diseased native aortic valve. But, as Dr. Kon points out, both geometric and functional assessments reveal clear differences between prostheses—and these differences may be particularly important in the patient with a “small” aortic root. In determining optimal surgical management in this situation, it is necessary to answer 3 questions: 1) What is a “small” aortic root?, 2) What is the impact of prosthesis-patient size on outcome after aortic valve replacement?, and 3) What surgical techniques should be employed to avoid the clinical syndrome of prosthesis-patient mismatch at aortic valve replacement?

Defining the “small” aortic root and prosthesis-patient size
When considering aortic valve replacement in a “small” aortic root, it is most appropriate to employ the concept of prosthesis-patient size, which incorporates measures of both valve size and patient size. Prosthesis-patient size may be expressed using geometric or functional measures of valve size. For geometric measures of prosthesis-patient size, prosthesis size is normalized to patient size by relating geometric dimensions of the prosthesis to body surface area (BSA) (1,2). This methodology is accurate (unbiased) and precise (reproducible), but does not describe specifically the function (transvalvular gradient) of the valve in a given patient at a particular time. Others have chosen to express prosthesis-patient size using the indexed in vivo effective orifice area (EOA), a functional assessment of prosthesis valve (4-6). However, both accurate and precise functional estimation of prosthesis size is elusive: it is related to patient factors, left ventricular outflow complex factors, time, measurement variability, inter-observer variability, method of computation, and myriad other factors. Nevertheless, the concept of indexed in vivo EOA does acknowledge the important interaction between prosthesis size and patient size. Using either geometric or functional assessments of prosthesis-patient size, values in a particular patient may be compared to those from a larger group or population, enabling identification of the patient with a small prosthesis-patient size.

Rather than focusing on prosthesis-patient size, much of the literature examines the issue of prosthesis-patient mismatch (4-8). These are closely related, but different concepts. No doubt a clinical syndrome of prosthesis-patient mismatch, as described by Rahimtoola, occasionally occurs, and such a patient “may be hemodynamically worse after valve replacement.” (9,10) Although Rahimtoola described a clinical diagnosis, over the years the definition of prosthesis-patient mismatch has ceased being a clinical diagnosis and has become arbitrarily inferred from postoperative echocardiographic velocity measurements. The challenge today is to relate the quantitative concept of prosthesis-patient size to the clinical syndrome of prosthesis-patient mismatch.

The impact of prosthesis-patient mismatch upon outcome
Dr. Kon has noticed that prosthesis-patient mismatch influences survival. Published reports confirm that at the small extremes of prosthesis-patient size, adverse clinical sequelae, or prosthesis-patient mismatch, occurs; this is most notable in its effect upon early mortality after aortic valve replacement (1, 4). In a study of 13,258 aortic valve replacements, Blackstone and coworkers found that 30-day mortality increased 1% to 2% when indexed orifice area decreased to less than 1.2 cm2/m2 after aortic valve replacement (1). They provided an algorithm to determine which patients were at risk of increased early mortality by virtue of small prosthesis-patient size. However, with nearly 70,000 years of patient follow-up, the latter study found no impact of prosthesis-patient size on intermediate or long-term survival, confirming other reported data (7,8).

Using in vivo EOA values from a variety of sources, Pibarot and coworkers determined that functional assessments of prosthesis-patient size also impact early survival after aortic valve replacement (4). Employing a somewhat arbitrary definition of prosthesis-patient mismatch, they found that both moderate and severe mismatch, defined as postoperative EOA less than or equal to 0.85 cm2/m2, reduced early survival after aortic valve replacement; although they did not examine EOA as a continuous variable, their data suggest that increasing severity of prosthesis-patient mismatch is associated with increased early mortality (4). In their study, the survival impact of severe prosthesis-patient mismatch was particularly pronounced in patients with reduced left ventricular function. Like Blackstone, they provide methodology to enable preoperative identification of patients at greatest risk of postoperative prosthesis-patient mismatch.

The preponderance of evidence suggests that very small prosthesis-patient size does influence early survival after aortic valve replacement (1,4,7). However, this is an important consideration in a relatively small proportion of patients having aortic valve replacement, and the magnitude of this effect is controversial (1, 8). Furthermore, variations in prosthesis-patient size have little impact on late survival (1,7,8).

These findings do not preclude an effect of prosthesis-patient size on functional status, particularly during exercise. In fact, recent data from Canada suggest that small prosthesis size is associated with late development of congestive heart failure (11). The impact of prosthesis-patient size on functional status after aortic valve replacement certainly warrants continued study.

Surgical techniques to avoid prosthesis-patient mismatch
Using geometric or functional reference values from the literature (1,4,6), it is possible to determine the prosthesis size required to avoid extremely small prosthesis-patient size in the individual patient. When the aortic root is small, the patient is usually small as well, and, in such instances, implantation of a relatively small prosthesis is unlikely to produce the clinical syndrome of prosthesis-patient mismatch. However, in the unusual circumstance of a large patient with a very small aortic root, it is reasonable to consider surgical options to avoid very small prosthesis-patient size and the potential for severe prosthesis-patient mismatch. In this rare situation, we favor aortic root enlargement followed by placement of a stented bioprosthesis or mechanical valve. Although Dr. Kon considers aortic root enlargement by the Manougian or Nicks techniques obsolete, these operations should not be discarded. They are relatively simple and quick, and generally enable implantation of a valve that is one size larger; in a patient at risk for prosthesis-patient mismatch, this may be enough to avoid sequelae attributable to this syndrome. Castro and coworkers achieved excellent results with a strategy of aortic root enlargement in patients identified to be at risk for prosthesis-patient mismatch (12). However, other experienced surgeons have noted increased operative mortality in patients having aortic root enlargement (13).

In contrast, when very small prosthesis-patient size is likely, Dr. Kon performs aortic root replacement with a stentless valve. This certainly provides a hemodynamically excellent result, although a randomized prospective trial failed to demonstrate superior hemodynamic indicies in comparision to stented valves up to 12 months after implantation. In the hands of very experienced surgeons like Dr. Kon, aortic root replacement is performed elegantly and safely, enabling extension of this operation to patients with poor left ventricular function. In contrast, it would be difficult to recommend such a complex strategy to a surgeon who performs only 1 or 2 aortic root replacements per year. Increased aortic cross clamp time and potential difficulties with bleeding and coronary button orientation might jeopardize results.

Summary
Prosthesis-patient mismatch is a real clinical syndrome; however, it is uncommon with modern prostheses and surgical techniques. Preoperative measurement of patient size and intraoperative sizing of the aortic root enable identification of patients at risk for prosthesis-patient mismatch before valve implantation. In the unusual circumstance that such a patient is identified, additional surgical techniques may be employed to optimize outcome.

Disclaimer
In responding to this presentation, we must acknowledge that we reside within the institution with the highest volume of valve operations on the North American continent. The practice at The Cleveland Clinic has not been to avoid using small sized valves in small aortic roots. Yet, hospital mortality for 881 isolated aortic valve replacements in the last 5 years was 1.2%, and for combined replacement and coronary artery bypass grafting 2% in 996 patients. In some instances, left ventricular outflow tract myectomy is performed for obstruction at that level; however, rarely is aortic root enlargement performed. We remain interested in performance of prostheses, but believe that available evidence suggests that other factors have a greater impact on long-term survival than prosthesis-patient size, however expressed

The small aortic annulus and the small aortic root represent one of the most vexing problems to the cardiac surgeon.  There are studies in the literature which support the belief that the size of the prosthesis inserted to replace the aortic valve has little influence on survival [1,2].  This is simply not true in our experience and many others.  When patient prosthesis mismatch (PPM) is looked at specifically one finds that it is an extremely important variable that predicts morbidity and mortality.  In a recent study by Blais, et al, PPM had a significant impact on mortality [3].  The risk of death was increased 2.1 fold in patients with moderate mismatch and 11.4 fold in patients with severe PPM (Slide 1).  All patients who died with severe PPM died of cardiac causes, low cardiac output syndrome, or myocardial infarction. Severe PPM was particularly deleterious in patients with poor LV function.  The mortality in this group of patients was 77% (Slide 2).
Slide 1

Slide 2

The significance of these findings are particularly important to analyze.  Cardiac surgeons today are faced with an ever increasing sub-population of patients with multiple co-morbidities.  Many of these, such as poor LV function, an exhausting list of complex medical problems, and advanced age, are beyond our control.  On the other hand, severe PPM is something we do have control over.  A strategy which preoperatively addresses the potential for PPM postoperatively will have a significant benefit on mortality.
Slide 3

The postoperative indexed EOA can be predicted preoperatively.  An EOA for each of the prostheses can be obtained from the literature.  Examples are in Table 1 from Blais article (Slide 3).  The indexed EOA is obtained simply by dividing the EOA by the recipient patient’s body surface area. PPM should not be clinically significant if the indexed EOA postoperatively is greater than 0.85 cm. sq./meter sq.  PPM will be moderate between 0.65 and 0.85 cm. sq./meter sq. Mismatch will be severe if the indexed EOA postoperatively turns out to be less than 0.65 cm. sq./meter sq.
Slide 4

The small aortic valve is most commonly seen in patients of small body size and is often associated with congenital heart disease.  It is in patients who have severe aortic stenosis that the adult cardiac surgeon confronts this problem.  In this situation we are asked to exchange one small valve for another.  Generally speaking, in the adult population we rarely confront an inadequate left ventricular outflow tract except in the instance of asymmetrical septal hypertrophy of the left ventricle.  This problem is easily recognized on the preoperative echocardiogram.  Turbulent flow is seen around a bulging septum on sagital view of the left ventricular outflow tract beneath the aortic valve. Measurements of the septum are significantly abnormal on echocardiography.  The cure is simply to perform a septal myomectomy after the aortic valve is removed.  The septum is incised just beneath the aortic annulus from the junction of the right and left coronary cusps to a point beneath the right coronary orifice (Slide 4).  The incision in the muscle is 2-4 mm deep and is carried towards the apex of the heart until one reaches the level of the papillary muscles.  There is no real danger of injuring the mitral valve as long as one stays on the ventricular septum.  Staying in line or to the left of the right coronary ostium keeps one away from the conduction system.  Obviously, the extent of the septal myomectomy is dependent on the degree of asymmetrical septal hypertrophy.

The smaller size traditional mechanical and bioprosthetic valves are inherently stenotic.  Under the best of circumstances they leave many patients with residual mild to moderate aortic stenosis.  Slide 5 shows the effective orifice areas for the most commonly available mechanical and bioprosthetic aortic valves.  Slide 6 shows that much of the space that these valves occupy in the LVOT is unavailable to blood flow and the flow through these valves is turbulent in nature (Slide 7).
Slide 5

Slide 6

Slide 7

The tradition has been to handle the small aortic annulus with an aortic annular enlargement procedure and the small aortic root with an aortic patch of some sort.  There are two commonly performed aortic annular enlargement techniques.  The Mannougian operation is considered the most simple and therefore the most common one utilized [4].  It is performed by cutting through the aortic annulus at the juncture of the left and right coronary cusps (Slide 8, 9).  This procedure only allows upsizing the prosthesis by 2 mm.  Any larger size would require incising too much of the anterior leaflet of the mitral valve, resulting in serious malfunction.  Upsizing by more than 2 mm requires the prosthesis to be placed on an oblique angle.  This would result in more turbulent flow patterns and thus be just as obstructive as a size smaller prosthesis.  One valve size increase is often insufficient to completely prevent PPM.
Slide 8

Slide 9

Slide 10

A much larger prosthesis can be inserted in the aortic root if one utilizes the aorto-ventriculoplasty technique described by Konno [5].  This technique requires transecting the first septal perforator artery when the ventricular septum is divided towards the apex of the heart.  The incision in the septum is initiated at the commissural junction where the right and left cusps of the aortic valve meet (Slide 10).  While this maneuver is well tolerated in children, many adults will develop a significant decline in left ventricular performance when this artery is divided.  Therefore, this may be a poor alternative for the adult patient with a small aortic annulus.
Slide 11

Pibarot and Dumesnil have evaluated many prostheses for the presence of mismatch [6,7].  They have clearly shown that natural aortic valve replacement options fare distinctly more favorably in patients with small aortic annuluses (Slide 11). Importantly, they have demonstrated that these differences are more pronounced when the patients are exercised.  The pulmonary autograft fares the best, followed by the aortic homograft and the stentless heterograft.  Some of the differences in the natural valve group may be related to the implant technique employed.  Most homografts and autografts were implanted using a free-standing root replacement technique, while most stentless heterografts were implanted as a sub-coronary implant.  We have found the root replacement technique reliable and can be performed with similar morbidity and mortality rates as a valve replacement [8].  Technique involves mobilizing the coronary arteries on buttons of aortic wall and removing excess sinus aorta.  The proximal suture line is accomplished with 28-32 simple interrupted 3-0 braided polyester sutures.  Coronary buttons are reattached with 5-0 polypropylene continuous suture and aortic continuity is re-established with a continuous 5-0 polypropylene suture (Slide 12-16).
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The armamentarium of natural valve substitutes available to the cardiac surgeon today make the Manougian operation and the Konno operation in the adult patient, with a small aortic annulus, an antiquated procedure.  Use of these valve substitutes will give larger EOAs, lower postoperative gradients, and more hemodynamically efficient laminar flow patterns than will upsizing with an aortic annular enlarging procedure. The most hemodynamically efficient way to implant a natural valve (stentless heterograft, cryopreserved aortic allograft, or a pulmonary autograft) is to use a free standing total aortic root replacement.  A stentless heterograft should be selected one size larger than the size of the left ventricular outflow tract.  When this is done, all the blood flow from the left ventricle sees is aortic valve leaflets and thus there is no impedance to flow (Slide 17).

In summary, PPM can largely be avoided today with a good preoperative strategy.  Eliminating PPM postoperatively will improve postoperative morbidity and mortality, particularly in patients with severe mismatch and/or depressed left ventricular performance.  If PPM is anticipated by preoperative predictions with a standard valve substitute, a natural valve substitute should be selected.  After one makes certain there are no obstructing lesions in the left ventricular outflow tract, an additional aortic annular enlarging procedure should not be necessary. Hemodynamic performance is best optimized by using a natural valve substitute (stentless heterograft, cryopreserved aortic allograft, pulmonary autograft) implanted with a total root replacement technique.

Despite half-century of experience in heart valve reconstruction, the tricuspid valve has been a “second class structure” for cardiac surgery. More than 20 years ago, the high incidence of tricuspid disease in our population, encouraged us to attempt to clarify the indications for repair, particularly in patients with functional tricuspid incompetence (1). Since functional tricuspid insufficiency always reflects some degree of right ventricular failure with elevated pulmonary resistance, or significant volume overload, we concluded that mild and moderate tricuspid incompetence can be surgically ignored only when the pulmonary resistance will predictably be reduced. However, the experience has demonstrated this beneficial postoperative event is not always well anticipated. On the other hand, some patients with postoperative low pulmonary vascular resistance continue with functional tricuspid insufficiency, because they do not recover the ability of the tricuspid valve annulus to shorten in systole.

Nowadays, with more than 900 functional tricuspid valve repaired at our Institution, it is time to analyse the state of the art of this commonly forgotten valve pathology. Current articles and meeting presentations on the functional tricuspid valve insufficiency are scarce and still asking the same type of questions: Should it be repaired? (2), What should be done? (3), Which should be the criteria for surgical repair? (4).

Functional tricuspid regurgitation is not a rare entity, since more than 25% of mitral valve insufficiency is associated with some degree of tricuspid dilatation with normal valve structures. This entity is often unrecognised, being only apparent during periods of increased preload or afterload. Dilatation of the annulus, involving the annular area supporting the anterior and posterior leaflets, is the only pathological finding at surgery. It is not always clear whether a functional tricuspid insufficiency, which may be expected to disappear or to improve, will remain and progressively increase the right ventricular cardiomyopathy, pulmonary hypertension, and chronic systemic venous hypertension, contributing to a poor outcome. One-third of symptomatic patients with an ignored functional tricuspid valve insufficiency, at the time of left side valves surgery, are referring to hospital for isolated tricuspid valve reoperation.

A better understanding of the natural history of the functional tricuspid incompetence and the progress made in transesophageal echocardiography has significantly contributed to clarify the indications and the limits for tricuspid valve repair. However, preoperative echo based on tricuspid valve grading at rest does not compare well with tricuspid dilatation found at surgery. Under general anesthesia, intraoperative echocardiography is not very useful to quantify the tricuspid regurgitation in order to indicate valve repair or to assure valve competence after correction.

Different methods and rules are used to indicate valve repair in the presence of functional tricuspid insufficiency. The indications were based on the clinical, echocardiography, and surgical findings. Moderate and severe tricuspid regurgitation should be repaired since it has been widely demonstrated that in those patients, tricuspid annuloplasty provides better symptomatic results and may improve survival. Further reoperation for isolated tricuspid valve repair after prior left heart valve surgery are also prevented. Dreyfus et al (2) recommend to examine the valve at the time of mitral valve surgery and to repair the tricuspid annulus if it is significantly dilated to more than twice normal (greater than 70 mm between the antero-septal and postero-septal commissures). Colombo et al. (5) surgically treated the tricuspid insufficiency when the indexed annulus dimension in more than 21 mm/m², been effective in term of clinical improvement and of late functional results.

Double venous cannulation is used in patients with mitral valve disease, and we always open the right atrium to inspect the tricuspid valve when pre- or per-operative echocardiography demonstrate a significant (moderate or severe) tricuspid regurgitation, in the presence of right atrial or ventricular dilatation, and in cases of high pulmonary artery systolic pressure.

Thirty years ago after the De Vega annuloplasty was described (6), this simple selective remodelling of the tricuspid annulus with a double suture at the anterior and posterior area continues as the most popular reconstructive surgical technique for significant functional tricuspid insufficiency. We have used a modified De Vega annuloplasty using interrupted pledgeted supported sutures. This segmental tricuspid annuloplasty (7) avoids tearing of the suture from the tricuspid annulus, “guitar string valve incompetence”, which leads to failure of De Vega annuloplasty early after surgery.

In our experience, multivariate analysis in a recent group 230 patients with functional tricuspid insufficiency demonstrates that the independent risk factors for tricuspid valve reoperation were the presence of residual tricuspid valve incompetence (OR: 3.25), pulmonary artery systolic pressure > 55 mmHg (OR:2.5) or ignored functional tricuspid insufficiency. Recently, Bhudia SK et al (8) from Cleveland Clinic has reported their experience with tricuspid valve repair in 790 patients, and they concluded that tricuspid valve annuloplasty did not consistently eliminate severe functional regurgitation and they identified as risk factors for repair failure the preoperative TR grade, poor left ventricular function, and repair type other than the Carpentier ring annuloplasty. These findings were not found in other important series, previously described.

In patients with severely dilated tricuspid annulus, we prefer a flexible ring annuloplasty to prevent the repair failure, allowing the physiological dynamic changes in the annular size and shape, and preventing the potential for future enlargement of the annulus. Controversy of whether a rigid or a flexible annuloplasty ring is better for tricuspid valve annuloplasty is still opened. The fact that a deformable (flexible) ring does not restore the physiological shape of the annulus and thus requires overcorrection resulting in a high incidence of residual tricuspid stenosis was not true in our experience.

Modern cardiac reconstructive surgery should pay more attention to a frequently forgotten valve pathology, which is killing many of our patients.

Ten years ago, Alfieri and colleagues from Milan introduced a simple and revolutionary method for mitral valve repair in patients with complex valve pathology requiring demanding surgical techniques for reconstruction or, when an unsuccessful result was expected, as in cases with prolapse of both leaflets, massive chordal elongation of the anterior leaflet, commissural lesions, endocarditis lesions, and leaflet prolapse associated with severe annular calcification (1). Initially, this still controversial operation was received with active criticism from those who believe that mitral valve anatomy should be respected and considered as a composite apparatus where every element (annulus, leaflets, chordae, papillary muscles and left ventricle) plays an important role in this complex valve mechanism. However, the “Alfieri stitch”, or more appropriately the “edge-to-edge” or “double orifice” technique, is gaining the attention of many surgeons who are now using this simple and innovative technique to extend the indications for mitral valve repair, after the satisfactory mid-term results and the stability of this method has been demonstrated (2). From the original paper in 1995, where Fucci et al.(1) reported using this technique in 12% of their mitral valve repairs, a few years later this group was performing the edge-to-edge plasty in 75% of cases (2).

Alfieri et al. (2) recommend a running 4-0 polypropylene suture to fix the free edges of the leaflets at the site of regurgitation, instead of a simple pledgeted supported stitch as the technique was initially reported. In patients with Barlow´s disease, this suture must plicate the leaflet redundancy to restore competence and prevent postoperative left ventricular outflow obstruction due to systolic anterior movement (SAM) of the anterior leaflet. This running suture also reduces the risk of rupture or tearing of the leaflets causing early failure, particularly in the presence of a friable leaflet, by adding two mattress sutures with pericardial pledgets to reinforce the repair. The major drawback is that suture length causes restrictive constraint of the leaflets movements. Long-term anticoagulation is not required with this operation, unless atrial fibrillation is present. Since most patients also receive a prosthetic annuloplasty ring, a 3-month anticoagulation is strongly recommended.

Since minimally invasive approach with the Heartport system is demanded by young patients, and robotic surgery is being performed in an increasing number of institutions, thus providing the opportunity for performing mitral valve repair percutaneously, the “edge-to-edge technique” is an attractive operation for surgeons, invasive cardiologists, and also for the industry which is trying to develop a device to staple the two mitral leaflets. Preliminary results and prospects for percutaneous approach were part of the program of the recent Cardiothoracic Techniques & Technologies meeting (9th Annual CTT Meeting 2003). However, this simple technique requires a concomitant annuloplasty to avoid repair failure and to reduce the risk of tissue degeneration; freedom from reoperation at 5 years in patients who underwent an annuloplasty procedure was 92 ± 3.4%, compared with 70 ± 15.0% in those without it (2). Localized fibrotic degeneration of the leaflets at the site of suture line was not reported but it should be expected, as with any fixed valve tissue. Votta et al. (5) has recently demonstrated that annular dilatation represents the most important influence on stress distribution in the region close to the suture, both in systole and diastole; the presence of an annuloplasty ring significantly reduces stresses acting on this critical area, as it was previously reported by Nielsen et al. (8) in an experimental model. Maximal stress was evidenced in marginal chordae inserted in the central region of the anterior leaflet, close to the suture line, as shown by a 3-D finite element model that simulated the stress pattern following the Alfieri´s operation. This elegant study also demonstrated that this technique produces a two fold increase in maximum stress with respect to the mechanics of a normal mitral valve. This computational analysis should be taken in consideration until long-term durability of this mitral reconstructive technique is established.

As Alfieri et al. (2) reported, the overall freedom from reoperation at 5 years was 90 ± 3.3%; significantly lower in patients with rheumatic disease (72 ± 14.5%) when compared with patients with degenerative disease (91 ± 3.7%). This finding is comparable to what is observed with every mitral reconstructive technique. Since rheumatic disease is frequently associated with relatively smaller effective orifices, this etiology is now considered a relative contraindication for the edge-to-edge operation. The cause of reoperation was recurrent severe mitral regurgitation (due, in most cases, or to leaflet prolapse, disruption of the suture), or severe hemolysis. Whether this technique should be used in cases of ischemic mitral disease, where geometric changes in the annulus, subvalvular apparatus and left ventricle are the causes of regurgitation, is still controversial (2), since the tethering effect may not be corrected with a central approximation of the leaflets.

A considerable reduction in the mitral valve effective orifice is the most important drawback with this procedure; however, no patient required reoperation for mitral valve stenosis in Alfieri´s experience (2). As Maisano et al. (4) have reported, the hemodynamic behavior of a double orifice mitral valve is not penalized by the new configuration of the valve after repair, with pressure drops and flow velocities across the leaflets similar to a single orifice valve. Timek et al. (7) have confirmed that the edge-to-edge mitral valve repair was not associated with substantial transvalvular obstruction during high flow conditions induced with dobutamine. However, a redundant subvalvular apparatus, as in Barlow´s disease, may decrease the pressure recovery within the left ventricle by generating vortexes, as these authors pointed out. Echo Doppler calculation of the maximum velocities is a consistent method for transvalvular pressure gradient estimation after “edge-to-edge” mitral valve repair.

Although long-term clinical results will be the ultimate test, a judicious use of this innovative and simple technique for complex mitral valve regurgitation, particularly in the degenerative disease, will prevent the mitral valve replacement in a significant number of patients. Furthermore, this operation will have a beneficial effect increasing the confidence of many surgeons and cardiologists and widening the indications of valve repair when a difficult mitral anatomy is present.

Mitral regurgitation is one of the most common valvular diseases in the adult population. Degenerative mitral valve diseases such as fibroelastic deficiency, Barlow’s disease and Marfan’s disease are among the most common etiologies of this condition in western countries. In patients with severe degenerative mitral regurgitation undergoing surgical correction, the superiority of mitral valve repair over replacement is now widely demonstrated (1).

Barlow’s disease, which is characterized by myxoid degeneration, appears early in life, often before the age of fifty. Patients typically present with a long history of systolic murmur. The valve leaflets are thick with considerable excess tissue, producing an undulating pattern at the free edges of the leaflets. The chordae are thickened, elongated and may be ruptured. Papillary muscles are also occasionally elongated. The annulus is dilated and sometimes calcified. In 1998, Tapia et al reported the surgical experience at Broussais hospital in a series of 320 consecutive patients with Barlow’s disease (2). Valve analysis showed that the mechanism of mitral regurgitation was type II Carpentier’s functional classification (leaflet prolapse) associated with annular dilatation in all patients. Segmental valve analysis revealed that isolated posterior and anterior leaflet prolapse was noted in 60% and 10% of patients respectively. Bileaflet prolapse was present in 30% of patients. Associated commissural prolapse was noted in 15% of patients. In this study, chordal rupture was the most common valvular lesion and annular calcification was present in 22% of patients.

In patients with degenerative mitral valve disease, valve repair using Carpentier’s techniques is the gold standard for surgical correction of mitral regurgitation and has provided excellent long-term results. Braunberger et al recently reported the very long-term results of valve repair with Carpentier’s techniques in non-rheumatic mitral valve insufficiency (3). In patients with isolated posterior leaflet prolapse, 10- and 20-year freedom from reoperation was 98.5% and 96.9% respectively. In those with isolated anterior prolapse, it was 86.2% and 86.2% respectively. Finally, in bilealfet prolapse it was 88.1% and 82.6% respectively. These data confirm the excellent results of Carpentier’s standard techniques of repair and their stability over a long period of time. Nonetheless, a recent analysis of the STS database showed that mitral valve repair is performed in only 37.7% of surgical procedures involving the mitral valve (4). We suspect that even fewer repairs are performed in patients with complex mitral regurgitation (e.g. Barlow’s disease, bileaflet prolapse and annular calcification).

In early 90’s, Alfieri introduced the concept of edge-to edge repair. This simple technique of repair consists of suturing the edges of the leaflets at the site of regurgitation. This technique can be applied at the paracommissural area (eg: A1-P1 segments: para commissural repair) or at the middle of the valve (e.g.: A2-P2 segments: double orifice repair). Initially Alfieri applied this technique in patients regardless of the etiology of mitral regurgitation (degenerative, ischemic, endocarditis, rheumatic). These studies showed a high rate of failure in patients with rheumatic mitral regurgitation (5). They also showed that isolated Alfieri repair is associated with a high rate of failure and that a concomitant annuloplasty should be performed in every patients (5).

In this presentation, Maisano and Alfieri review their use of the edge-to-edge technique with concomitant annuloplasty in Barlow’s disease. The underlying basis for this repair in bilealfet prolapse is, according to the authors, (1) to eliminate the primary regurgitant area by suturing the leaflet edge here (2) “to decrease leaflet mobility” and (3) “correct leaflet redundancy…to force coaptation…[and]…to restrict leaflet motion.”

The correction of mitral regurgitation by elimination of regurgitant site is not really a new concept. In 1959, Merendino et al reported their technique of posteromedial annuloplasty for the correction of mitral regurgitation (6). With this technique, multiples sutures were placed along the paracommissural area of anterior and posterior annulus and not at the free edges of the leaflets. The ultimate goal of this procedure was to correct mitral insufficiency by reducing the annular diameter and eliminating the regurgitant area. However, this procedure was not associated with good clinical outcome and was abandoned. Furthermore, most Barlow’s patients present with prolapse of multiple segments, not merely A2P2, resulting in more than one regurgitant jets. It is unclear to me why one would think that eliminating the central jet would lead to a satisfactory result. The authors suggest that the other segments benefit from overall decreased leaflet mobility forcing coaptation; however, they do not provide specific evidence to show that this actually occurs.

There are several additional specific fundamental concerns that need to be addressed with this technique. The edge-to edge technique, particularly the double orifice technique, results in a significant decrease in mitral valve area as demonstrated by the authors. Thus, the possibility of mitral stenosis should not be dismissed in Barlow’s patients even if the risk is less than in those with other etiologies (ischemic, rheumatic, etc.). Even without physiologic mitral stenosis, the decrease in orifice area increases flow velocities and turbulence, which can lead to fibrosis and calcification of the functioning (A1P1, A3P3) valve segments. This will likely impact the long-term durability of this repair.

Another factor, which may impact the long-term durability of the edge-to-edge technique, is the increased stress on the subvalvular apparatus of all segments. For example, in a patient with isolated A2 prolapse, suturing A2 to P2 will clearly increase the stress on the latter. In contrast, decreasing the stress on a still diseased subvalvular apparatus is one of the key principles behind Carpentier’s repair techniques and the likely explanation for the excellent long-term results.

Another interesting inconsistency in their technique relates to the sizing of the annuloplasty ring. The authors state that they use standard sizing parameters including the surface area of the anterior leaflet. It is unclear, however, whether they include the portion of the redundant anterior leaflet, which is incorporated in the edge-to-edge suture line. Sizing the ring prior to the edge-to-edge repair would result in an oversized annuloplasty, which could contribute to inferior late results.

Although the authors do not report their long-term results in this presentation, more complete clinical results in these 82 patients are available in their published manuscript (7). The 5-year freedom from reoperation was 86%, which is significantly lower than those of the standard Carpentier techniques reported above.

During the last decade, the introduction of the Alfieri technique has brought a new interest in broadening the application of mitral valve repair techniques, especially in patients with complex disease. At the present time, however, it appears to have raised more questions than answers. The standard repair techniques have a sound physiologic basis and have proven themselves over the very long-term. With proper training and a strong commitment, these techniques can be part of any surgeon’s armamentarium. Compromising long-term results in the name of simplification of surgical technique is not an acceptable tradeoff. In the same vein, the drive to perform valve repairs less invasively should proceed with the same attention to long-term results. The ultimate role of the Alfieri technique in Barlow’s disease, as well as other etiologies, remains to be clarified by longer-term follow-up

Thirty six years have elapsed since Grondin and associates published in The Journal of Thoracic and Cardiovascular Surgery the paper “The tricuspid valve: A surgical challenge.” Since then, and probably due to it, a lot of attention was placed in a valve whose patho-physiology was not very well understood at the time.

Surgeons now know that a severe degree of tricuspid regurgitation must be corrected at the time of mitral operation, and we now have in our armamentarium several techniques that have successfully passed the test of time to achieve a competent tricuspid valve. It is also true that we don’t know why so many patients, up to 20-25% according to different experiences, whose tricuspid valve was considered quite normal at the time of surgery, later develop right ventricular failure with concomitant severe tricuspid regurgitation. Once this situation is established neither medical nor surgical treatment are clearly effective.

After more than thirty years dealing with this problem and having visually explored many tricuspid valves of rheumatic and non-rheumatic patients at the time of surgery, we have the impression that most of the rheumatic valves have some degree of pathological changes in the leaflets or the subvalvular apparatus even in the absence of any tricuspid regurgitation detectable clinically or echocardiographically.

If these changes progress with time, the valve can became slightly incompetent and trigger a vicious circle that leads to the above mentioned situation with right ventricular failure. Could this vicious circle be interrupted by fixing the annulus with any of the available techniques?

If we admit this hypothesis, surely we are going to treat some patients unnecessarily. What is the price of that? To our knowledge, to wear a pair of sutures around the tricuspid annulus does not imply any risk in the long term. The low economical cost plus the short extra time of cardiopulmonary bypass necessary to perform a suture annuloplasty are added attractions. We lack the necessary experience to decide if such a policy will be applicable using prosthetic rings. Probably the relative high cost of rings can be an obstacle, especially in third world countries where rheumatic valvular disease is most prevalent.

Some technical tricks to properly perform a De Vega tricuspid annuloplasty:

• Place the sutures before doing anything in the mitral valve. Otherwise it may be difficult to place a good stitch in the antero-septal commissure.

• Try to keep your sutures as buried in the annulus as possible by going inside again close to the point you came out.

• If you just need to fix the annulus or to slightly reduce it, you don’t need a stitch at both ends; one suture doubly passed is enough. If you need to really reduce the annulus two sutures, one starting at either end, will produce a more uniform plication.

• In some cases, when the annulus is very much dilated, the plication can be done in two or even three parts. After the left heart valve surgery is completed, with the aortic clamp released, the sutures are tied over a progressive occluder.

Weight gain after quitting is a serious concern for some smokers. About 80 per cent of smokers put on weight when they quit. However most ex-smokers only gain a modest amount of weight. Women typically gain between 3 kilograms and 5.5 kilograms in the first year due to stopping smoking, while men tend to gain less. Research shows that in the long term, the average body weight of female ex-smokers is similar to women who have never smoked.

Smoking appears to change the distribution of fat in women to a less healthy male “apple” pattern. Women who smoke tend to put on more fat around their waist compared to women who do not smoke. Fat in this area is associated with risks such as stroke, heart disease, type 2 diabetes and a general increased death rate. When women quit smoking, any weight gain that occurs is in the normal and safer female pattern, with a preference to the hips rather than the waist.

It is possible to quit smoking and minimise weight gain if you pay attention to diet and exercise. However, it can be helpful to be prepared to accept at least a small increase in weight. It can be difficult to quit cigarettes and manage weight at the same time, because both activities require effort and commitment. If this is the case for you, concentrate first on quitting. See your doctor or dietitian for further information and advice if weight gain is a problem.

The causes of weight gain
The two main causes of weight gain when quitting smoking are thought to be:

* The effect of nicotine on the body – nicotine is the addictive substance in tobacco that causes smokers to continue their habit. Although nicotine isn’t thought to cause cancer, it does speed up the body’s food processing system, the metabolism. After many years of smoking, smokers tend to weigh slightly less than non-smokers. Researchers suggest that one of the reasons why some smokers tend to put on weight after quitting is because their metabolism slows down, and they burn fewer kilojoules than while they were smoking. This would explain why some ex-smokers put on weight even if they do not eat any more than usual.
* Eating more food – many smokers find their eating habits change when they quit cigarettes. Some smokers experience increased hunger as a withdrawal symptom, but research suggests that any increases in food intake after quitting eventually return to normal.

Eating instead of smoking
Some ex-smokers eat more, particularly in the first few days or weeks after quitting. Some of the reasons include:

* The restless, empty feeling of nicotine withdrawal can feel very similar to hunger pangs. The smoker may be ‘fooled’ into thinking they’re hungry when they are not.
* Missing the oral satisfaction of putting a cigarette into their mouths prompts some ex-smokers to substitute food for cigarettes. Instead of lighting up, they eat something.
* Food can be comforting. If an ex-smoker is having a hard time during the withdrawal period, they may reward themselves with treats and snacks in an attempt to feel better.
* Some smokers regularly skip meals – for example, breakfast may be a cup of coffee and a couple of cigarettes. Once you stop smoking, you may find that you don’t feel like skipping meals anymore.
* Many ex-smokers find that food tastes better, and this may lead to more helpings.

Tips on reducing weight gain
It is possible to maintain your current weight, or at least keep weight gain low, while you’re quitting cigarettes. Suggestions include:

* Exercise more often - being inactive is a risk factor for weight gain. Aim for around half an hour of moderate activity every day - for example, brisk walking, gardening, swimming or cycling. You can do 10 minutes of exercise at a time, adding up to a total of 30 minutes over the day, if you prefer.
* Muscle tissue burns more kilojoules than fat. You can boost your metabolic rate by including one or two weight training sessions into your weekly exercise program to build up muscle.
* Don’t crash diet. If you eat too few kilojoules, the body will respond by lowering the metabolism and burning muscle tissue for fuel.
* It can be tricky telling the difference between hunger pangs and withdrawal cravings. Get into the habit of ‘listening’ to your body before you decide to eat something.
* It takes about 15 minutes for your stomach to signal your brain that it’s full, so wait before having second helpings. You might find you don’t want it after all.
* Find ways other than eating to cope with withdrawal cravings. Some people drink water, while others count to 100 – experiment until you find your own method.
* Put safe, non-edible items in your mouth if oral cravings bother you. For example, you could use toothpicks or cinnamon sticks, or chew on sugarless gum.
* If you need to snack, keep raw vegetable sticks and other low fat, low kilojoule foods on hand.
* Increase your consumption of fruits, vegetables and wholegrain foods.
* Cut back on high fat, high salt and high sugar products. You can do this easily by not stocking these types of foods in your kitchen pantry.
* Alcoholic drinks can contain many kilojoules. Try alternating with water or other low kilojoule drinks.
* Be kind to yourself if you do put on a few kilos. You are boosting your health by quitting.

If you put on weight
If you’ve gained weight despite your best efforts, don’t despair. A few extra kilograms are a much lower risk compared to the risk of continuing to smoke. You would have to gain over 40 kilograms above your recommended weight to equal the risk of heart disease posed by smoking.

Don’t think that taking up smoking again will mean you will shed the weight – sometimes it doesn’t. Concentrate on improving your diet and increasing your physical activity. See your doctor or dietitian for help and advice.