Stress-related mitral regurgitation.
Natural history of mitral regurgitation
Mitral regurgitation is a progressive disease, with average annual increases in the regurgitant volume (RVol) and in the effective regurgitant orifice (ERO). Anatomical changes are determinants of progression, which is faster in patients with mitral valve prolapse, especially in those with ruptured chordae, and in patients with mitral annular dilatation. The progression of MR can lead to adverse LV remodeling, and development of ventricular dysfunction. In these cases, ejection fraction (EF) may initially be "normal" (>50%) and symptoms may not be present, though prognosis is worse than in the unaffected population. Published estimates on long-term survival in patients with MR vary considerably. There was also substantial morbidity at 10 years, with incidences of atrial fibrillation (AF) and heart failure of 30% and 63%, respectively. At 10 years, 90% of patients had died or undergone surgery, making the operation almost inevitable in this population. Patients who were in New York Heart Association (NYHA) functional class III-IV showed high mortality (34% annually) if they were not operated on, but mortality was high (4.1% annually) even among those in functional class I-II. Patients with EF <60% also showed excess mortality compared to those with EF >60% on medical treatment. Sudden death is a major event in severe MR with rupture of chordae tendineae and causes about 25% of deaths of patients on medical treatment. Overall, the sudden death rate is 1.8% annually and even in patients without other risk factors (severe symptoms, LV dysfunction, and HF) is 0.8% per year. These data highlight the poor prognosis implied by severe organic MR, especially when ruptured chordae are involved.(Stout et al 2009; Enriquez-Sarano et al 1999; Braunbergher et al 2001)
Timing of surgery
Nowadays there are 2 directions in management of MR, concerning the optimal moment for correction. One of these recommends "watchful waiting" until the onset of symptoms or indicators of subclinical dysfunction in asymptomatic patients (eg. EF <60%, LVESD >40 mm), with echocardiographic evaluation of the patient every 6 or 12 months. The other approach recommends considering "early mitral repair," correction before symptoms or indicators of subclinical LV dysfunction are present. This approach stresses the need for sufficient evidence of MR severity, obtained by appropriate echocardiographic assessement (values of RVol and ERO), and a likelihood of successful repair of >95%, with operative mortality of 1% or less. These conditions require a cardiologist who is able to quantify the MR and critically evaluate the patient, a surgeon with experience in mitral repair, and an experienced postoperative team. Quantification of MR severity should include quantitative methods and indicators, the most widely used being the Doppler quantitative techniques based on the analysis of proximal isovelocity flow convergence and allowing for the calculation of RVol and ERO. (Otto 2012)
Risk factors for mitral regurgitation
There are different risk factors, which worsens the outcome of the MR patient. The first risk factor is age. Studies agree that patients >55 years are at greater risk of complications, probably because of decreased contractile reserve associated with age. However, it is difficult to establish a cut-off age above which risk increases significantly. Chordal rupture associated with severe MR (RVol >100 mL and ERO >0.5 [cm.sup.2]) is an important risk factor. The annual incidence of AF is 5% in patients with significant organic MR, and its appearance is associated with decreased survival. Even after valve repair, the presence of AF prior to the repair is associated with decreased survival at 5 years compared to normal sinus rhythm before repair (87% compared to 96%) Increased levels of brain natriuretic peptide (BNP) represent another risk factor, which was quantificated in studies. They are the consequences of regurgitation (e.g. LV and left atrium volume, AF, and symptoms) and represent an independent predictor of mortality and development of heart failure. The presence of pulmonary hypertension estimated by using echocardiography is another risk factor predicting a worse prognosis. Finally, whether or not the patient recognizes symptoms may be influenced by idiosyncratic differences in perception, fear of surgery, or because he performs little physical activity or has adapted levels of physical activity to accommodate the limitations imposed by mild symptoms. It is therefore essential to stress test patients when there is any degree of uncertainty about symptoms. These risk factors should be taken into account when deciding the appropriate surgery time for each patient. (Dal Bianco et al 2009)
Modern therapeutical approaches to mitral regurgitation
A successful surgical approach to mitral regurgitation was reported as early as 1951 by Bailey et al. Surgical and percutaneous interventions to treat MR have evolved tremendously ever since. At present, percutaneous means to repair the mitral valve or even replacing the MV appears to be on the horizon and promises to dramatically alter the treatment and selection of patients with MR. Bailey et al. first approached MR through a left thoracotomy, and the mitral annulus was narrowed by external constriction of the base of the heart in an approach not unlike recent attempts to perform mitral annuloplasty through the coronary sinus. Lillehei et al. performed the first direct suture annuloplasty of the MV in 1957 using cardiopulmonary bypass (CPB), and Starr and Edwards first replaced the mitral valve using a commercially successful device in 1960. Today, surgery for MR is performed in 40,000 patients each year in the United States. One should be aware that, in this age of rapidly advancing percutaneous technology that is used both by surgeons and interventional cardiologists, the term "surgical" could, in fact, be considered an anachronism.(Carpentier et al 2010)
Mitral regurgitation is the result of a mechanical dysfunction of the mitral valve and definitive correction is also mechanical (surgical). The mitral valve is not an isolated entity; it is closely related to the LV and ensures the latter's geometry and function via the connection through chordae tendineae. For that reason, mitral repair with preservation of the subvalvular apparatus forms the basis of current surgical treatment. In patients with organic MR, operative mortality has decreased considerably, especially with mitral repair. In the Mayo Clinic in Rochester, operative mortality is around 1% in patients under 75 years in cases of mitral valve repair or replacement, and <1% in isolated repair, by contrast, operative mortality in patients over 75 years is approximately 5%. Studies indicate lower perioperative mortality and greater long-term survival after valve repair. The experience of the surgical center is essential to achieving optimal results. Intraoperative transesophageal echocardiography is an essential component in successful valve repair and should be performed by experienced clinicians. They should supervise the procedure and assist in intraoperative decision-making. Currently, success rates in mitral repair are around 90%-95%. This high rate of success is possible once the surgeon's initial learning curve is completed and by using special techniques such as chordal transposition or insertion of artificial chordae, in particular to repair the ruptured chordae tendineae in the anterior leaflet. Unfortunately, mitral repair in rheumatic lesions is hardly successful. However, mitral repair in rheumatic MR should be performed when anatomically and functionally possible, because it is associated with longer survival than valve replacement. Mitral replacement decreases the need for re-intervention in rheumatic MR, but limits survival and increases the risk of embolic complications. (Gillinov et al 2008)
When referring for surgical correction a patient with MR, the etiology/mechanism of regurgitation should be determined. There are three basic mechanisms based on the mobility of the leaflets. The first is normal mobility with poor coaptation due to annular dilation or perforation of a leaflet. The second involves excessive mobility (prolapse or ruptured chordae tendineae) and the third, decreased mobility (inflammatory or ischemic disease).
Organic MR may be caused by a type 1 (e.g. cleft mitral valve), type 2 (e.g. MR arising from Barlow's disease) or type 3 (e.g. rheumatic mitral valve) dysfunction. Functional MR is usually a combination of dysfunction 1 and 3. Mitral regurgitation mediated by the second mechanism is the most susceptible of them all to repair, especially when the posterior leaflet is involved and the ring does not show severe calcification. However, repair in the case of Barlow's disease with severe bileaflet prolapse or prolapse isolated from the anterior leaflet is now as feasible as in isolated prolapse of the posterior leaflet. Repair is therefore possible in the vast majority of cases of mitral prolapse, when it is performed by experts. Once the organic mechanism has been assessed, it is necessary to quantificate the severity of MR. The echocardiografic exam, tranthoracic and sometimes transoesophageal, is an important tool. The presence of symptoms, EF <60% or LVESD e"40 mm means that ventricular dysfunction is manifest and the patient must be referred for surgery. The aim of such surgery is to repair the valve or replace it if repair is not possible. In the absence of manifest ventricular dysfunction, patient risk should be stratified. If the risk factors are present, the valve should be repaired early, but not before considering to evaluate surgical risk score: if the patient has a good life expectancy and the valve is repairable, the operation should be performed in a centre which can guarantee high surgical success rate and low operative mortality. If there are no such preconditions, "watchful waiting" (monitoring by a cardiologist with an echocardiogram every 6 months) can be implemented for signs echocardiographic and/or symptoms that indicate need for rescue, repair or replacement. There is thus a discrepancy between current guidelines and clinical practice recommendations, so that finding risk factors should be a class I indication for early repair. If there are no risk factors, 'watchful waiting' is safe and recommended. (McGee et al 2004)
Many factors can diminish the likelihood of mitral repair versus mitral replacement. Factors predicting replacement instead of repair include low surgeon/institution volume, anterior leaflet pathology or bileaflet pathology, rheumatic etiology, infectious etiology, functional/ischemic etiology, and secondary leaflet changes such as scarring and/or calcification. Although surgeons are under pressure to have high rates of MV repair, recurrent MR can often be worse than the consequences of initial mitral replacement. "Good" repairs are generally better than replacement, but replacement is generally better than "bad" repair with recurrent regurgitation. Freedom from reoperation at 20 to 25 years has been 90% in several large series. Factors such as anterior leaflet pathology or bileaflet pathology, rheumatic or infectious etiology, functional versus ischemic etiology, secondary leaflet changes such as scarring or calcification, lack of ring annuloplasty, and low volume for the surgeon or institution tend to predict a higher likelihood of reoperation. Several large studies with a high degree of echocardiography followup have recently reported residual or recurrent MR after mitral repair. The goal of surgical mitral repair has been to leave the operating room with free or only mild residual MR by transesophageal echocardiography under anesthesia, as more than that has been associated with a higher rate of reoperation. At 10 years, MR has been reported as at least moderate in 15% to 30% of patients having the myxomatous valve repaired and severe in 5% to 10%. For patients with functional or ischemic etiology, moderate or higher regurgitation has been reported in 20% to 30% of patients at 1 to 5 years (10), prompting some surgeons to consider mitral replacement or not addressing the MV insome patients. Others have criticized these studies because of their use of full-sized, partial, flexible rings, which many are often thought to allow for more unfavorable annular remodeling. Use of complete, rigid, and under-sized or reduced septal-free wall diameter rings is now favored for repair of ischemic or functional MR by many authors. (Hung et al 2007)
Mitral replacement had long been the standard surgical treatment for MR, but mitral repair is now favored over replacement in most patients. Advantages of mitral repair versus replacement include avoidance of mandatory anticoagulation, potentially better durability than bioprostheses, less impairment of LV function, less risk of LV posterior wall rupture, and lower early and late mortality. Some of the advantages of mitral repair over replacement come from the fact that previous mitral replacements tended to resect all of the native MV chords. However, many studies have now shown that mitral replacement with chordal preservation nearly eliminates the risk of ventricular-annular disruption and minimizes impairment of LV function. Indeed, to date, no definitive data exist to say that mitral repair has an advantage over chordal sparing mitral replacement, beyond the inherent issues of anticoagulation versus limited biological durability. Mitral replacement does have some inherent advantages over repair. The elimination of MR is more certain with replacement, especially when the quality of repair is in question. Elderly patients with limited life expectancy may have little issue with anticoagulation therapy or limited durability using modern bioprostheses. Mechanical mitral replacement with anterior leaflet resection was described by Krajcer et al. for hypertrophic obstructive cardiomyopathy with effective elimination of both MR and LV outflow tract obstruction. Some researchers believe that MV replacement may be a more effective therapy than mitral repair for patients with ischemic MR, especially if the mitral leaflet is restricted 1 cm below the plane of the mitral annulus. (Salvador et al 2008; Flameng et al 2008)
The selection of biological versus mechanical prostheses for mitral replacement remains controversial. The last decade has seen a significant shift toward biological mitral prostheses due to an aging population, hope that reoperation can be less invasive or percutaneous, patient dislike of anticoagulation therapy, and belief that modern bioprostheses are more durable. Unfortunately, replacement of a failed biological prosthesis remains a morbid procedure, and a significant percentage of patients having biological mitral replacement will require anticoagulation therapy for atrial fibrillation during their subsequent course. Actually data suggest that the durability of current bioprostheses in the mitral position remain limited, especially in patients under 60. Transapical replacement of failed biological mitral prostheses has been reported using percutaneous bioprostheses designed for the aortic position. Several new anticoagulants are on the horizon with the potential to eliminate frequent testing or minimize bleeding complications with mechanical prostheses. (Cerin et al 2010)
As the results of surgery for MR have improved, the threshold for operating on MR has been lowered. Today, mortality for isolated mitral repair is 1% to 2%, and mortality for isolated mitral replacement is 6%. Published guidelines for the management of valvular heart disease are data driven and useful, but guidelines need to be adjusted for each individual patient. For patients with a 90% likelihood of obtaining a mitral repair, surgery today is seldom performed as an isolated procedure for less than severe MR because of the low mortality and the low rate of symptoms for moderate MR. The indications for operation on functional MR remain more controversial than those for degenerative disease. Despite data that functional regurgitation is associated with impaired survival, nonrandomized studies have suggested that survival is not improved by mitral repair for functional regurgitation when the ejection fraction is 30%. Most people believe that heart failure symptoms can be improved after repair of functional regurgitation in patients with appropriate LV functional reserve. (Cerin et al 2012; Tesler et al 2009)
Two controversies in the early management of surgical patients are management of anticoagulation therapy and atrial fibrillation prophylaxis. Unless significant atrial fibrillation occurs in the postoperative period, most mitral repair or biological replacement patients can be managed with aspirin alone. Short-term anticoagulation therapy with warfarin for 3 months is not uncommon, as mitral patients have a 30% to 70% incidence of new atrial fibrillation after mitral surgery. Most of the large centers would use an antiarrhythmic like amiodarone in patients for 1 to 3 months to minimize postoperative atrial fibrillation and subsequent anticoagulation. Concurrent Maze procedure may have a role in minimizing but not eliminating atrial fibrillation in patients at high risk for atrial fibrillation. (Arsenescu 2013; Cerin et al 2006)
Ischaemic mitral regurgitation: a high risk group
Ischaemic mitral regurgitation remains one of the most complex and unresolved aspects in the management of ischaemic heart disease, because it is not only common, but it also significantly affects prognosis. Ischaemic MR occurs in approximately 20-25% of patients followed up after myocardial infarction and in 50% of those with post-infarct congestive heart failure. In patients with heart failure, even a mild degree of mitral regurgitation adversely affects survival. Increasing MR severity is associated with a progressively worse 5-year survival rate. Restrictive annuloplasty, combined with coronary artery bypass grafting (CABG), is currently the most commonly performed surgical procedure to treat ischaemic MR; however, subvalvular and ventricular approaches are under investigation. The poor results of current strategies create the need for a better understanding and preoperative assessment of mitral valve and left ventricular geometry and function. This will help to improve risk stratification and the identification of patient subgroups that are likely to benefit from various surgical strategies. Although knowledge about ischaemic mitral valve disease has increased dramatically over the past 15 years, a great amount of uncertainty concerning this subject remains. (Fattouch et al 2009; Fattouch et al 2010) Ischaemic mitral regurgitation has important prognosis implications in patients with coronary heart disease. It should not be underestimated and this underlines the need for a complete evaluation in which Doppler echocardiography plays a major role, but should be interpreted specifically, especially as regards quantification of the regurgitation. Therapeutic decisions are difficult and should involve a medico-surgical confrontation of all patient characteristics, if possible with surgeons who have expertise in the field of valve repair. Further evaluation of the different therapeutic options, including new repair techniques, is obviously mandatory to improve the answers to a number of questions pending, in particular the indications for surgery in patients with moderate ischaemic regurgitation and those with severe left ventricular dysfunction and no myocardial viability. A complete assessment of left ventricular geometry and function and of the mitral valve configuration prior to surgery may help improve patient risk stratification and better individualize the surgical strategy based on the patients specific characteristics.
The acute ischemic mitral regurgitation is a rare mechanical complication after myocardial infarction, due to elongation, partial or complete rupture of papillary muscle but has a poor prognosis and it needs urgent diagnosis and surgery. A careful echocardiographic exam, performed in ICU, is mandatory in acute patients with myocardial infarction, focusing on the presence of mitral regurgitation. In case of any suspicion of structural acute ischemic mitral regurgitation, the transesophageal exam must be done, in order to avoid the transformation of partial rupture of papillary muscle in a complete one. The complete rupture of the papillary muscle is often fatal and has to be considered as being too late a clinical and echocardiographic diagnosis; these patients need an emergent operation and very intensive perioperative pharmacologic and mechanical support. (Klein et al 2012)
From a conceptual point of view, chronic ischemic mitral regurgitation witnesses the loss of contractile myocardial tissue parallel with the presence of the post-infarction remodeling process. As known, ischemic mitral insufficiency develops on normally mitral leaflets. As the myocardial mass loss is larger, the remodeling processes and regurgitation become greater. Recognizing the mechanism of valve incompetence is an essential point for the surgical planning and for a good result of the mitral repair. In the patients candidates for surgery, the role of the echocardiographic exam is to identify the mechanisms of valve regurgitation and to quantify it. As noted, in most cases of chronic ischemic mitral regurgitation the mechanism is the restriction of one or both leaflets, caused by the tethering exercised by the displacedpapillary muscle. The transthoracic exam is common enough to clarify the mechanism of chronic ischemic mitral regurgitation. Only patients with papillary muscle elongation may raise difficulties in diagnosis. Loss of the normal shape of the 'triangle of coaptation' is one of the key characteristics of chronic ischemic mitral regurgitation. In case of post-ischemic elongation of the papillary muscle, the clue to diagnosis is obtained by looking not only to the mitral valve, but by focusing the exam on the papillary muscles, particularly when the patient presents a deformation of the coaptation triangle. In patients with type II[degrees] Carpentier's classifications (elongated papillary muscle and leaflets prolapse) alongside ring annuloplasty, use of PTFE Gore-Tex chordae is often required. In patients with chronic ischemic mitral insufficiency echocardiography may identify two different patterns of post infarction remodeling: a limited process of post infarction remodeling and an extensive one. The mitral repair is usually more challenging in patients with extensive pattern of post infarction remodeling where, due to left heart cavity enlargement, a phenomenon of "mitral valve--LV chamber mismatch" is present. (Levine et al 2002)
Although the mechanisms of ischemic mitral regurgitation are often complex, currently, undersized annuloplasty is considered to be the standard approach to reducing mitral insufficiency. Unfortunately this technique does not resolve the real mechanism of disease, the remodeled and sphericalized left ventricle. By this technique the persistence of ischemic mitral regurgitation is considered to range between 10 to 20% of the cases, and, at five years of follow up, half of the patient may develop recurrence. Thus, in advanced stages of left ventricular postinfarction remodeling with over-dilatation and important mitral valve tethering, ring annuloplasty has to be completed with leaflet extension. This approach seems to be coherent with the mechanism of mitral regurgitation, with the echocardiographic data and with the concept of "mitral valve--LV chamber mismatch." (Magne et al 2009)
The major challenge for cardiologists and surgeons is how to integrate data from different imaging techniques that assess mitral valve geometry and left ventricular size, geometry, function and potential functional recovery. In order to tailor and optimize the surgical approach to patients with chronic ischemic mitral regurgitation. Even as we speak, we have no reliable predictors for recurrent and persistent mitral regurgitation. However, the surgical treatment of ischemic mitral insufficiency continues to evolve and new methods addressing ventricular structures are being introduced: left ventricular restoration, papillary muscle relocation, sling, imbrication or reapproximation, chordal cutting or translocation. Despite remarkable progress in reparative surgery, further investigation is still necessary to find the best approach to treat ischemic mitral regurgitation. (Hvass et al 2010; Statescu et al 2011)
The serious implications of ischaemic mitral regurgitation are clearly established, but it has not been demonstrated that surgical correction of regurgitation improves the outcome. On the other hand, operative risk is not minor and late results are difficult to evaluate in this particularly heterogenous disease. In the absence of randomised controlled trails, the low level of evidence in literature does not invite recommendations. Nevertheless, the approach to different clinical situations may be summarised as follows in the light of our current knowledgeIn patients who have severe ischaemic mitral regurgitation (grade > 3/4 or, better, ERO > 20 [mm.sup.2]) and who should undergo CABG, correction of mitral regurgitation should be undertaken. Valve repair is frequently preferred, provided the surgeons have expertise with this technique and a careful intraoperative evaluation can be performed with the knowledge of potential pitfalls regarding quantification. When the type of coronary revascularisation is debated over, the association of severe ischaemic mitral regurgitation leads to combined surgery rather than percutaneous intervention. In patients who have severe ischaemic mitral regurgitation but no indication of coronary revascularisation, generally because there is no myocardial viability, the indication for isolated mitral surgery is debatable. Promising results have been reported by certain teams in non-controlled studies, but experience and follow-up remain limited. There is no consensus for surgery in such situations and it should be ascertained whether mitral regurgitation remains severe after optimisation of medical treatment. The first line of approach to these patients remains medical in most teams. Heart transplantation is the main alternative in end stage diseases. More recently, a debate has arisen concerning the opportunity to correct moderate ischaemic mitral regurgitation (grade 2/4, ERO < 20 [mm.sup.2]) in patients who should undergo CABG. The poor prognostic value of moderate ischaemic regurgitation, the uncertainties regarding the evolution of these regurgitations with ventricular remodelling, and the high risk of reoperation are criteria to associate valve repair with CABG. These widened indications should be balanced with the potential hazards which relate to the increased complexity of surgery and the lengthening of cardiopulmonary bypass in patients who have a poor left ventricular function. (Troubil et al 2010; Hashimet al 2012)
Percutaneous approaches to mitral regurgitation
Percutaneous therapy for mitral repair has emerged over the past several years as an investigational option for treating mitral regurgitation (MR). A variety of novel methods to treat MR using a percutaneous route have been developed. Most of these approaches are modifications of surgical techniques, some established and some obscure. The basic surgical approaches to mitral repair are annuloplasty and leaflet repair. Catheter-based devices mimic or approximate these surgical approaches. MR as a disease process is heterogeneous, and different therapeutic approaches are needed for different etiologies of MR and morphologies of the mitral apparatus. Primary leaflet diseases are mitral prolapse and fibroelastic deficiency. Secondary, or functional, MR exists when the leaflets are normal. Functional ischemic MR and functional MR related to heart failure occur in different populations and historically have had different responses to surgical therapy. Leaflet repair using a percutaneous clip has been accomplished for patients with mitral valve prolapse and also some patients with functional MR. Indirect annuloplasty via the coronary sinus has shown promising early human trial results in patients with functional MR. Direct annuloplasty and left ventricular chamber remodeling technologies are in the earliest stages of human application. This group of approaches is being studied as an alternative to surgery for selected patients. The MitraClip (Evalve, Menlo Park, CA) for leaflet repair has been approved for use in Europe and is being applied predominantly to high-risk surgical patients with either functional or degenerative, organic MR. One of the coronary sinus devices has received approval in Europe as well. This complex clinical landscape has made device development, trial design, and patient selection complicated. Steady progress in the field is being made. Many patients with functional MR who are currently treated medically will be the subject of upcoming trials. Catheter methods for mitral repair promise to serve some patients who are currently considered high risk for surgery, and some patients may have catheter therapy as an alternative to surgery. (Brinster et al 2006; Alfieri et al 2004)
Already today and increasingly in the future, the surgical and interventional approaches to MR will be made of a spectrum of approaches, spanning from maximally invasive to percutaneous. Patient selection for the appropriate approach will, thus, become increasingly important once we have data regarding the outcomes of each approach in different patient subsets. To further complicate decision making, procedure invasiveness/ morbidity may often be inversely related to procedure effectiveness. Thus, we may tend to favor less invasive but less effective approaches to treating MR in patients who are at higher risk and with limited life expectancy. Younger--and lower-risk patients may be more appropriate for more effective therapies while better tolerating any morbidity or risk. As less invasive approaches to MR become more available, some of the large pool of patients receiving little or no therapy for MR may become more likely to refer themselves, or to be referred, for some form of anatomic rather than medical treatment of their MR. Thus, technology continues to be a dominant driver of medical care for MR, just like most other diseases.
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Radu A. Sascau
Grigore T. Popa University of Medicine
Grigore T. Popa University of Medicine
Georgescu Grigore T. Popa University of Medicine
Correspondence concerning this article may be addressed to email@example.com, firstname.lastname@example.org or email@example.com
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|Author:||Sascau, Radu A.; Statescu, Cristian; Georgescu, Catalina Arsenescu|
|Publication:||Romanian Journal of Artistic Creativity|
|Date:||Mar 22, 2014|
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