Dipartimento di Medicina Clinica e Sperimentale
Dipartimento di Patologia Chirurgica, Medica, Molecolare e dell’Area Critica Dipartimento di ricerca transazionale e delle Nuove Tecnologie in Medicina e Chirurgia
Corso di Laurea Specialistica in Medicina e Chirurgia
Minimally invasive mitral valve surgery through
right minithoracotomy for degenerative disease in
asymptomatic patients:
a thirteen-year experience
at Ospedale del Cuore - Massa
Candidata Relatore
Abstract
The purpose of this thesis is to report and analyze early and long-term outcomes in asymptomatic patients who underwent minimally invasive mitral valve surgery through right minithoracotomy at Ospedale del Cuore - Fondazione Toscana Gabriele Monasterio in the setting of degenerative disease. A total of 374 patients satisfying these characteristics had benefited from minimally invasive mitral valve surgery, and thus avoided median sternotomy, from 2004 to 2016.
Mitral regurgitation (MR), currently the most frequent valvular heart disease, is mostly degenerative, linked to aging, and of increasing prevalence. Mitral valve surgery is the only current approved treatment of MR. Cumulative evidence obtained worldwide show that early surgery in asymptomatic patients is the preferred approach. “Watchful waiting”, meaning closely observing the manifestation of symptoms such as dyspnea, heart palpitation and fatigue, or echocardiographic evidence of left ventricular dysfunction, is a failed strategy, because symptoms are insensitive markers of risk and often unrecognized in a timely manner and, even after successful surgery, associated with poor outcome. Furthermore, in patients with severe organic MR, surgery is almost unavoidable and early mitral repair before the appearance of symptoms or overt LV dysfunction and irreversible anatomical modifications may restore life expectancy. At Ospedale del Cuore, OPA minimally invasive mitral valve surgery has become the standard approach since 2005, it is safe, reproducible, associated with low mortality and morbidity, high rate of mitral valve repair and excellent long-term results.
In this study, the mean age was 56 ± 13 years, 119 (31,8%) patients were female. Mean preoperative EF was 64 ± 4,9% and LVEDS 32,3 ± 4,6mm. MV repair
Overall in-hospital mortality was 0%. Incidence of stroke was 1,1%, and at discharge MR was trivial or none. At mean follow-up of 53 ± 13 months, overall survival was 98,7%, freedom from reoperation 98,4% and 362 (96,8%) patients denied symptoms or a reduction in quality of life.
Our results are in line with recent literature: early surgery in asymptomatic patients may restore life expectancy to that of persons of similar age and sex who never had MR and never had cardiac surgery, as long as minimally invasive valve repair is performed in high-volume centers.
CONTENTS
I. Literature review ... 11
1. Anatomy of the mitral valve ... 12
2. Mitral valve regurgitation ... 16
2.1 Epidemiology ... 16 2.2 Etiology ... 18 2.3 Functional Classification ... 23 2.4 Physiopathology ... 25 2.5 Clinical presentation ... 27 2.6 Imaging techniques ... 28
2.6 Disease progression and prognosis ... 31
3. Mitral valve surgery ... 32
3.1 Assessment ... 32
3.2 Indications ... 34
3.3 Repair techniques ... 35
3.4 Mitral valve replacement ... 44
4. Minimally Invasive Mitral Valve Surgery ... 46
4.1 The gold standard ... 46
4.2 History ... 47
4.3 The state of the art ... 57
II. Experimental work ... 67
5. Design and Methodology ... 68
5.1 Patient selection and data collection ... 68
5.2 Definitions ... 70 5.3 Follow-up ... 71 5.3 Surgical technique ... 72 5.4 Statistical analysis ... 74
6. Results ... 75
6.1 Baseline characteristic ... 75 6.2 Intraoperative data ... 78 6.3 In hospital outcomes ... 80 6.4 Late outcomes ... 827. Discussion and evaluation ... 87
8. Conclusions ... 93
8.1 Limitations ... 93
Bibliography ... 94
Ringraziamenti ... 109
List of Figures
1.1 The mitral valve apparatus 13
1.2 The mitral valve annulus 15
2.1 Prevalence of valvular heart disease 17
2.2.1 Barlow’s disease 21
2.2.2 Fibroelastic deficiency. 22
2.3 Carpentier’s functional classification of MR 24
2.6.1 Mitral valve with fibroelastic deficiency 29
2.6.2 Myxomatous mitral valve with bileaflet prolapse and severe valve regurgitation
30
3.1 Management of severe chronic primary mitral regurgitation 33 3.3.1 Posterior leaflet quadrangular resection, annular plication 38
3.3.2 Annular remodeling 39
3.3.3 Anterior leaflet triangular resection 40
3.3.4 Artificial chordoplasty 42
3.3.5 Alfieri edge-to-edge repair 43
4.2.1 Upper T ministernotomy 48
4.2.2 The right parasternal incision 49
4.2.3 Cohn’s ministernotomy approach 50
4.2.4 Chitwood’s micro mitral operation through right minithoracotomy 51
4.2.5 The Port-Access endovascular system 52
4.2.6 Technical solutions for minimally invasive surgery 55 4.3.1 Patient positioning for minimally invasive mitral valve procedure 58 4.3.2 Double stage venous cannula, the rib retractor, the custom
transthoracic atrial retractor, and the two ports
59
4.3.2 Anatomy of the left atrium following an atriotomy. Exposure is obtained using a left atrial lift system
60
6.4.1 Kaplan Meier cumulative survival curve 84
List of Acronyms
AF atrial fibrillation AKI acute kidney injury BMI body mass indexBNP brain natriuretic peptide CABG coronary artery bypass graft CAD coronary artery disease
COPD chronic obstructive pulmonary disease CPB cardio-pulmonary bypass
LVEF left ventricular ejection fraction GI gastroinstestinal
IABP intra-aortic balloon pump ICU intensive care unit
IMA myocardial infarction LAD left atrium diameter LMCA left main coronary artery LPM posterior mitral leaflet LV left ventricle
LVEDD left ventricular end diastolic diameter LVESD left ventricular end systolic diameter MIMVS minimally invasive mitral valve surgery MR mitral regurgitation
MVD mitral valve disease MVP mitral valve prolapse MVR mitral valve replacement
NYHA new york heart association functional classification P1 posterior lateral scallop
P3 posterior medial scallop
PAPs pulmonary artery systolic pressure RT right minithoracotomy
SAM systolic anterior motion
σ standard deviation
TEE transesophageal echocardiography TIA transient ischemic attack
TTE transthoracic echocardiography
List of Tables
2.2 Key differences between Barlow’s disease and fibroelastic deficiency at time of surgical presentation
19
4.2.1 Levels of ascent in minimally invasive cardiac surgery 47 6.1 Demographic characteristics (continuous variables) 75 6.2 Demographic characteristics and risk factors 76
6.3 Preoperative Echocardiography 77
6.4 Mitral valve procedure 79
6.5 Operative variables 79
6.6 Early outcomes 80
6.7 In-hospital outcomes 81
6.8 Late outcomes 82
6.9 Cox regression analysis of risk factors for late mortality 83 6.10 Cox regression analysis of risk factors for reoperation 83
Part I
1. Anatomy of the mitral valve
The mitral valve is located in the left atrioventricular groove and allows unidirectional flow from the left atrium into the LV during diastole.1 As shown in Figure 1, it consists of the annulus, the leaflets and commissures, the chordae, the papillary muscles, and the ventricle 2.
The mitral annulus is a “saddle” shaped fibromuscular ring (Figure 1.2) located in the left atrio-ventricular groove that serves as an attachment and hinge point for the mitral valve leaflets. It is divided into anterior and posterior segments based on the attachments of the anterior (or aortic) and posterior (or mural) mitral leaflets.3 The anterior portion of the mitral annulus is in continuity with the fibrous skeleton of the heart; thus fibrous in nature, the anterior portion of the annulus is much less prone to dilation in comparison to the posterior which is structurally weaker.1
The anterior leaflet is taller than the posterior leaflet but with a shorter base, attaching to one- third of the annular circumference between the right and left fibrous trigones. The posterior leaflet is usually subdivided by two indentations (or clefts) into three scallops, named, using Carpentier’s nomenclature: posterior-lateral scallop (P1), the most posterior-lateral and adjacent to the anteroposterior-lateral commissure, posterior-middle scallop (P2), in the middle and posterior-medial scallop (P3), next to the posteromedial commissure. The corresponding portions of the anterior leaflet are called anterior lateral scallop (A1), anterior middle scallop (A2) and anterior medial scallop (A3) respectively.4
Between the anterior and posterior leaflets, the mitral valve has posterior medial and anterior lateral commissures, which are small segments of leaflet tissue presenting at the insertional junction of the anterior and posterior leaflets. These two areas of leaflet tissue are supported by chordal fans and are critical to ensure a good surface of coaptation at the junctions of the two leaflets.1
From the attachment point of each leaflet at the annulus to the free edge, the leaflet is described as having basal, clear and rough zones. The basal zone is described as the area where the leaflet connects to the atrioventricular junction. The thin central portion of the leaflet is the clear zone. The thick rough zone at the free edge of the leaflet is the main area of chordal attachment and the region of coaptation (where the leaflets meet) and apposition (overlap of the leaflet free edge).5
Figure 1: The mitral valve apparatus. Superior view of the heart in diastole and systole without the atria and the great vessels. AC, anterior commissure; AL, anterior leaflet; AMC, aorto-mitral curtain; CA, circumflex artery, CS, coronary
Three orders of chords can be described: primary chords are attached to the free margins of the leaflets and ensure that the leaflets do not protrude into the atrium during systole. Secondary and tertiary chords distribute the pressure during systole and link the leaflets to the ventricle. Only the posterior leaflet has tertiary chords, these originate from the basal part of the leaflet and insert on the LV.6
The papillary muscles are a part of the LV, and they are attached by the chordae tendinae to the mitral leaflets. Each papillary muscle is identified according to the relationship to the valve commissures, and each provides a fan chord to its corresponding commissure as well as to both anterior and posterior leaflets. 1 The anterior papillary muscle can be vascularized by both the left anterior descending artery and the circumflex artery, whereas the posterior papillary muscle is dependent primarily on the posterior descending artery. 1.
The LV, due to the papillary muscles, supports the entire apparatus, and thus, ventricular dimensional changes in the setting of volume overload and remodeling, can lead to leaflet tethering and mitral valve regurgitation.7, 8
Two important structures surround the valve and its annulus: the circumflex coronary artery, which surrounds the left half of the mural leaflet, and the coronary sinus, adjacent to the right half of the same leaflet.9
Figure 1.2: The mitral valve annulus. The MV annulus has a saddle shape with the highest point (toward the left atrium) at the middle of the anterior leaflet adjacent to the aortic valve and at P2. LA indicates the left atrium; LV, left ventricle.3
2. Mitral valve regurgitation
2.1 Epidemiology
Mitral valve regurgitation is the most common valvular heart disease in the western world and the second most common requiring surgery.10, 11
In the past, valvular heart diseases were mainly caused by rheumatic heart disease, which remains a major burden in developing countries, however, in industrialized countries, rheumatic disease incidence has fallen substantially, and residual valvular diseases are now mostly degenerative.12
The prevalence of moderate (2+/3) or severe (3+/3) MR in the US 2000 general population is 1.7 % (95% CI 1.5-1.9), but affected 9.3% (95% CI 8.1-10.9) of individuals of 75 years or more. 11As shown in Figure 2.1, the incidence of valve disease increases with age. MR is often under diagnosed, especially in women. Moreover, many patients are not referred to surgery despite guideline-based indications, often because of age and comorbidities. 11
2.2 Etiology
MR can be defined as an abnormal leaking of the valve that fails to close properly during systole.
Although rheumatic heart disease is still the most common cause of mitral regurgitation worldwide, it is no longer a common cause of mitral regurgitation in developed countries.13 Additionally, although ischemic mitral regurgitation resulting from myocardial infarction still accounts for 10% to 20% of mitral regurgitation, earlier intervention in acute coronary syndromes may be limiting the number of such cases in the future.14
Degenerative mitral valve disease (DMVD) is now the leading cause of mitral valve disease and regurgitation.1 DMVD refers to a spectrum of conditions in which morphologic changes in the connective tissue of the mitral valve cause structural lesions that prevent normal function of the mitral apparatus. Degenerative lesions, such as chordal elongation, chordal rupture, leaflet tissue expansion, and annular dilation typically result in mitral regurgitation due to leaflet prolapse. Barlow’s disease and fibroelastic deficiency are the two dominant forms of DMVD.15
Table 2.2: Key Differences Between Barlow’s Disease and Fibroelastic Deficiency at Time of Surgical Presentation
Barlow’s disease Fibroelastic Deficiency
Pathology Myxoid infiltration Impaired production of
connective tissue
Typical age Young (<60 years) Older (60 years)
Duration of known mitral disease
Several years to decades Months
Long history of murmur Usually No
Familiar history Sometimes No
Auscultation Midsystolic click and late systolic murmur
Holosystolic murmur Echocardiography Bulky, billowing leaflets,
multi-segmental prolapse
Thin leaflets, prolapse of single segment, ruptured chord(s) Surgical lesion Excess tissue, thickened and
tall leaflets, chordal thickening or thinning, chordal elongation or rupture, atrialization of leaflets, fusion, fibrosis or calcification of chords, papillary muscle calcification, annular calcification
Thin leaflets, thickening and excess tissue (if present) limited to prolapsing segment, ruptured chordae
Barlow’s disease. It’s a degenerative mitral valve disease in which myxoid infiltration of the valve results in a myxomatous-appearing valve that is remarkable for excess thickened leaflet tissue.
Chordae are sometimes thin but more commonly are thickened, fused, or even calcified. Chordal elongation is more frequent than rupture. The etiology of the disease is unknown, and although some cases have a significant genetic or familial component, the majority of cases are sporadic.16
The pathological hallmarks are myxoid infiltration, which destroys the 3-layer leaflet architecture, and also collagen alterations seen on histological examination. This myxoid infiltration is responsible for the thick, redundant leaflets seen in Barlow’s disease. Because the infiltration affects the entire valve, billowing and/or prolapse of multiple segments of the valve are common findings.
Typically, patients with Barlow’s disease are young (age < 40 years), more often women, asymptomatic at first presentation having been found to have a murmur on physical examination.15 General physical examination is often unremarkable, but some patients have extra cardiac signs, such as skeletal abnormalities, which are suggestive of a forme fruste of Marfan’s syndrome.17 The auscultatory findings in Barlow’s disease were characterized in the 1960s18 and include a mid to late systolic click and a high-pitched, late, systolic murmur.
Echocardiographic assessment of the Barlow’s valve should:
1. Confirm the diagnosis of moderate to severe mitral regurgitation.
2. Confirm Carpentier type II and often associated type I valve dysfunction19 and identify which leaflet, and which segments of leaflets, prolapse or billow.
3. Delineate the primary lesions (excess leaflet tissue, chordal and leaflet thickening, chordal elongation and rupture) and secondary lesions (calcification, annular dilation).
Barlow’s disease will usually show billowing of the body of one or both leaflets with prolapse of the margin of either or both leaflets. Regurgitation results from the marginal prolapse and not from billowing of the leaflet body. If the prolapse is due to chordal elongation, the regurgitation typically occurs in the mid to late phase of systole as opposed to holosytole in the case of chordal rupture. The valve is typically large, with elongated and redundant billowing leaflets; leaflets are bulky and thickened.15 Leaflet thickness in diastole measured by M-mode echocardiography often exceeds 3 mm. Another common feature is displacement of the insertion of the posterior leaflet away from the ventricular crest and toward the atrium, creating an out-pouching at the leaflet base. Severe annular dilation is typical.
Figure 2.2.1: A. Large valve with redundant, thick, bulky leaflets; B. Tall, posterior leaflet with tip rising to anterior annulus; C. Calcified anterior papillary
Fibroelastic deficiency. The main pathological mechanism is connective tissue deficiency.20 While the 3-layer architecture of leaflet tissue is preserved, FD is the result of impaired production of connective tissue, with collagen deficiency.15 Secondary pathological change in prolapsing segments may result in myxoid deposition with resultant thickening and expansion, but this process is usually limited to the prolapsing segment.21 Histologically, elastic fiber alterations are more prevalent in fibroelastic deficiency compared with Barlow’s disease.20 The etiology is unknown but may be age related. Patients with FD are usually of middle or advanced age, and are typically asymptomatic until time of chordal rupture15.
In FD echocardiography usually shows a single, prolapsing segment, sometimes with a visible ruptured chord. Although the middle scallop of the posterior leaflet (P2) is the most often involved, any valve segment of the anterior or posterior leaflet may be affected. The valve leaflets are thin and do not show redundancy or billowing. Annular dilation is less pronounced than in Barlow’s. The regurgitation usually occurs throughout systole.
Figure 2.2.2: A. Prolapse of P2 due to multiple ruptured chordae; the leaflet tissue is thickened compared with other segments; B. Prolapse of P3 with ruptured chord; P3 is thickened, and the P2 (hook) and P1 segments are thin and of normal height.15
2.3 Functional Classification
As the techniques of valve reconstructions developed, it became clear that it was no longer sufficient to classify the valvular pathologies in the classical three groups: valve stenosis, valve regurgitation and combined stenosis and regurgitation. The aim to characterize valve pathology by an anatomical description of the lesions proved to be too complex to be practical. The anatomical approach was progressively abandoned and attention was placed on the valve dysfunction resulting from these lesions.22
This functional classification was introduced before echocardiography became available in the operating room, and resulted in a significant simplification and proved to be particularly important for the surgeon to restore normal function rather than normal anatomy of the valve.
The “functional approach” is based on the analysis, both by echocardiography and direct inspection by the surgeon, of the leaflet motion. Three functional types can be described depending upon whether the motion of the leaflet is normal (type I), increased (type II), or restricted (type III). Restricted leaflet motion may happen mainly during the opening of the valve (type IIIa) or during closure (type IIIb). While types I and II both result in valvular regurgitation, type III may result in regurgitation, stenosis or both.
• Type I: Valve dysfunction with normal leaflet motion. The course of the leaflets between systole and diastole has normal amplitude. The valve is regurgitant because of either leaflet perforation or lack of leaflet coaptation, a consequence of annular dilatation
• Type II: Valve dysfunction with excess leaflet motion (leaflet prolapse). The motion of one or more leaflets is increased and the free edge of one or several leaflets overrides the plane of the orifice during valve closure. The
• Type III: Valve dysfunction with restricted leaflet motion. The motion of one or more leaflets is limited, either during valve opening and closure (type IIIa), leading to various degrees of valve stenosis and regurgitation, or during valve closure (type IIIb), leading to valve regurgitation.
Figure 2.3: Carpentier’s functional classification of MR. The diagram represents the leaflets, papillary muscles and chords. Dotted lines trace the course of the leaflets in the cardiac cycle. Type I: normal leaflet motion. Type II: Leaflet prolapse. Type III: restricted motion (a) diminished opening and closure (b) diminished closure only.19
2.4 Physiopathology
MR imparts a volume overload on the LV because it must compensate for the volume lost to regurgitation. Severe mitral regurgitation can be divided into three stages: acute, chronic compensated, and chronic decompensate.1
In acute MR, as might occur from rupture of marginal chordae tendineae, a small unprepared LV is suddenly confronted with a large volume overload from blood returning from the pulmonary veins summed with the regurgitant volume from the LV. The volume overload causes existing sarcomeres to stretch maximally, increasing end-diastolic volume and also stroke work through the Frank-Starling mechanism.
The extra pathway for ejection into the left atrium reduces end-systolic volume. Increased preload, decreased afterload and a reflexive sympathetically mediated increase in contractility, act in concert to increase total stroke volume and ejection fraction. However, because 50% or more of the total stroke volume is regurgitated into the left atrium, forward stroke volume and cardiac output are reduced. Additionally, the left atrium, which is of normal size and compliance, receives its very high total volume at high filling pressure, in turn leading to pulmonary congestion. Thus, although LV function is normal, the patient suffers the low output and pulmonary congestion, typical of LV failure. Many patients will require immediate corrective surgery at the time acute severe mitral regurgitation develops.
In chronic compensated phase, eccentric hypertrophy develops, increasing LV volume. Because the radius term in the Laplace equation for wall stress has increased (stress = p × r/2th, where p = LV pressure, r = radius, and th = thickness), afterload returns from subnormal to normal. However, increased preload and normal contractility permit a higher than normal ejection fraction of a large end-diastolic volume so that total stroke volume is greatly increased.23 This
pressure and is likely to be asymptomatic even during exercise. Although the patient may enjoy a period of compensation which may lasts for years, eventually, contractile dysfunction, sustained from prolonged hemodynamic overload, ensues, and decompensation becomes manifest.24, 25
Impaired contractility causes increased end-systolic volume and reduced stroke volume and cardiac output. Filling pressure is now elevated, and the patient may develop heart failure symptoms. In decompensated mitral regurgitation, the increased radius term in the Laplace equation causes systolic wall stress to increase, and afterload is greater than normal, contributing to LV dysfunction. The relatively thin wall of the mitral regurgitant ventricle is beneficial to diastolic function and LV filling but is detrimental to LV systolic function because maladaptive LV remodeling causes increased afterload.1
It is important to note that ejection fraction may be held in the normal range by enhanced preload despite contractile dysfunction and afterload excess. The LV dysfunction caused by severe mitral regurgitation stems from multiple pathologic processes. At the cellular level, there is loss of contractile elements in the endocardium in experimental models of mitral regurgitation and in the papillary muscles of humans.26
Sympathetic overdrive, which is present in both human and experimental mitral regurgitation, contributes to the cellular pathology of the disease.27
The LV remodeling of mitral regurgitation is unique and probably dictated by the loading conditions present. Mitral regurgitation stands out as a pure volume overload. In most other volume overloads such as anemia, heart block, and aortic regurgitation, the extra volume generated by the LV is ejected into the aorta, where the high stroke volume generates a widened pulse pressure and an element of systolic hypertension. Thus, most volume overloads are in fact a combination of volume and pressure overload, and the LV remodels accordingly.
In mitral regurgitation, the extra volume is ejected into the left atrium, and systolic pressure is often low/normal. In turn, LV thickness is low-normal, producing a
2.5 Clinical presentation
The typical symptoms of mitral regurgitation are dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea. Other symptoms include reduced exercise tolerance, palpitation, fatigue, and chest pain.
On physical examination, the reduced forward stroke volume tends to reduce systolic blood pressure and pulse pressure, but this finding is quite variable, and some patients are actually hypertensive. The apical beat is displaced downward and to the left in chronic severe disease due to LV dilatation.
The typical murmur is holosystolic if the lesion is chordal rupture and is heard best at the apex and radiates to the axilla. Severe mitral regurgitation is often accompanied by an S3 produced by the emptying of the large left atrial volume under higher than normal pressure into the LV. The presence of an S3 is often evidence that the mitral regurgitation is severe, rather than indicating that the patient is in heart failure.
Mitral valve prolapse in Barlow disease is sometimes referred to as click-murmur syndrome, indicative of the typical findings on physical examination of a mid-systolic click followed by a late mid-systolic murmur. The click is generated as the elongated chordae are stretched taut. The valve leaflets then move past their coaptation point, and the murmur ensues.
Physical maneuvers that decrease LV volume, such as standing or the Valsalva maneuver, cause the click and murmur to come earlier in systole and consequently to increase in intensity. This occurs because a decrease in LV volume reduces tension on the mitral valve, in effect lengthening the valve apparatus. Maneuvers that increase LV volume, such as squatting or lying down, may cause the opposite effect or may cause the click and murmur to disappear altogether. 1
2.6 Imaging techniques
In patients with fibroelastic deficiency, echocardiographic findings typically include an isolated segmental prolapse with flail leaflet segment due to chordal rupture leading to holosystolic mitral regurgitation.
Conversely, echocardiographic findings in patients with Barlow disease include mid-systolic and frequently diffuse regurgitation with multiple jets consistent with chordal elongation affecting grossly thickened myxomatous leaflets. The posterior leaflet is often displaced toward the left atrium away from the ventricular hinge, resulting in a cul-de-sac along the posterior portion of the annulus, which potentially becomes a precipitating factor for the development of annular fissures and calcification.
Multiple echocardiography clues are used to determine the severity of a patient’s mitral regurgitation. All should be taken in the context of left atrial and ventricular size; severe mitral regurgitation is associated with chamber dilatation unless it is acute. In general, the severity of mitral regurgitation is graded using clues from the color flow mitral regurgitation jet.28 Jet size and depth are often used during visual
inspection to grade mitral regurgitation severity, but it can be misleading. Consequently, more quantitative measures, such as vena contracta width, effective regurgitant orifice area, and regurgitant fraction and flow, are often used to better establish the severity of mitral regurgitation. The PISA (proximal isovelocity surface area) method allows us to calculate the regurgitant orifice area (ERO).1 This method assumes that there is flow convergence in systole around one leaking orifice of the mitral valve. As such we can assume blood flow converges in a hemispherical shape as it goes from the left ventricle toward the left atrium in someone with a single central jet of MR. We can then use the continuity equation by using the area of the hemisphere of flow convergence and its velocity to calculate the area of the effective regurgitant orifice area (EROA), since we also know the peak mitral regurgitant velocity.
Figure 2.6.1: Mitral valve with fibroelastic deficiency. Prolapse and flail owing to ruptured chordae tendineae with related severe mitral regurgitation, as seen by a: 2D-TEE, b: color Doppler TEE, c: real-time 3D-TEE, and d: during surgery. 29
Figure 2.6.2: Myxomatous mitral valve with bileaflet prolapse and severe valve regurgitation. Imaged by a: 2D-TEE, b: color Doppler TEE, and c: real-time 3D-TEE, and d: during surgery. 29
2.6 Disease progression and prognosis
Heart contractility predicts surgical mortality, perioperative heart failure and postoperative LVEF. A rough estimate of heart contractility is the telesystolic diameter. AF adversely affects the prognosis.30 Without surgery, prognosis is poor, as MR can lead to heart failure, pulmonary hypertension, AF, stroke and death. However, timed and appropriate surgery restores life expectancy to levels comparable to that of the general population.29
3. Mitral valve surgery
3.1 Assessment
Echocardiography provides most of the relevant information for the decision-making process with regard to treatment of patients with MR, including the severity of MR, the type of lesion and mechanism according to the Carpentier classification for MR, and the anatomical features of the valve. 2D-transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) can provide useful information concerning the likelihood of MV repair.31
Severity should be estimated by measuring the width of the vena contracta, while the effective regurgitant orifice area (EROA) and regurgitant volume may be calculated through the proximal isovelocity surface area (PISA) method.10 Enlarged diameter and increased volume of the left atrium are other indicators of severity.
Real-time 3D transesophageal echocardiography (TEE) can help identify secondary prolapses and aid surgical planning.10
Neurohormonal activation in MR has been evaluated, with several studies suggesting the value of elevated BNP levels and a change in BNP as predictors of outcome. A cut-off BNP value ≥105 pg/ml determined in a derivation cohort was prospectively validated in a separate cohort and helped to identify asymptomatic patients at higher risk of developing HF, LV dysfunction or death on mid-term follow-up. Low-plasma BNP has a high negative predictive value and may be helpful for the follow-up of asymptomatic patients.10
3.2 Indications
Surgery is obviously indicated in symptomatic patients with severe primary mitral regurgitation. Parameters considered when deciding the patient’s course of treatment:
• LVEF ≤ 60% or LVESD ≥ 45mm33 • Atrial fibrillation34
• Systolic pulmonary pressure (PAPS) ≥50mmHg35
These predict a worse postoperative outcome independent of the symptomatic status and have therefore become triggers for surgery in asymptomatic patients. In patients with flail leaflet, an LVESD of 40–44 mm has been reported to predict a worse outcome compared with LVESD < 40 mm. Significant LA dilatation despite sinus rhythm has also been found to be a predictor of outcome.
Despite the absence of a randomized comparison between the results of valve replacement and repair, it is widely accepted that, when feasible, valve repair is the preferred treatment. Achieving a durable valve repair is essential. Degenerative mitral regurgitation due to segmental valve prolapse can be repaired with a low risk of mitral regurgitation recurrence and reoperation. Patients with a predictably complex repair should undergo surgery in experienced repair centers with high repair rates, low operative mortality and a record of durable results. When repair can’t be achieved, mitral valve replacement with preservation of the subvalvular apparatus is favored.32
3.3 Repair techniques
Mitral valve repair has become the gold standard for patients with MR36 since Alain Carpentier’s description of repair techniques in “The French Correction”.19 Mitral valve repair should be preferred over replacement whenever possible30: no randomized trial has compared yet replacement versus repair, but valve repair yields better results, including longer survival.32 In fact, durability and freedom from valve-related complications, including thromboembolism, hemorrhage and endocarditis, have been universally accepted as the main advantages of repair over replacement. 29, 37
Patients with repairable MR should be referred to centers with a high level of experience in the field in order to maximize the likelihood of a successful and durable reconstructive procedure. At the present time, more than 90% of degenerative lesions can be repaired successfully with contemporary techniques in expert centers.
Before attempting repair, the valve must be well exposed; the surgeon must understand the mechanism underlying the insufficiency by integrating preoperative TTE, intraoperative TEE and direct examination. Filling of the ventricle with saline is often a good approximation of the valve’s behavior during the cardiac cycle.9 The aim of surgery is maintaining leaflet mobility, remodeling the annulus, and allowing good coaptation of the valve.3 Simple, standardized repair procedures should be performed and a correctly sized annulus should be implanted. After testing for residual regurgitation, additional procedures may be performed.9
Important determinants of outcome are symptoms, age, AF, LVEF, pulmonary hypertension, and the reparability of the valve. While simple prolapse can easily be repaired, complex lesions and other etiologies cannot be predictably repaired.32 Surgery for MR carries a very low mortality risk. Long-term freedom from
Early surgical methods, such as chordal shortening or techniques that do not involve the use of annuloplasty rings, are associated with suboptimal results and have been abandoned.38 New technical solutions have been added to the list of fundamental methods of MV repair first described by Carpentier,15 including the use of artificial chordae39 and the edge-to-edge technique.40 From a technical point of view, valve repair for degenerative MR currently includes a large array of valvular, subvalvular, and annular procedures; the choice between these techniques depends on the type of lesions identified preoperatively and intraoperatively.
Surgical repair of posterior leaflet prolapse
Posterior leaflet quadrangular resection. In patients with isolated prolapse of the middle scallop of the posterior leaflet (P2), as encountered in the majority of patients with degenerative MR, MV repair usually involves the quadrangular resection of this scallop. The redundant portions of the prolapsing LPM must be removed to restore the correct coaptation with the anterior leaflet.The prolapsed segment is removed by excising a quadrangular portion of the leaflet. Freedom for reoperation at 20 years with this technique is 96,9%.9, 29
Annular plication and folding. Annular plication can be performed at the base of the resected segment, and the remaining portions of the posterior leaflet are then brought together and sutured directly.29 Annular plication carries the risk of infarct if the circumflex coronary artery is kinked,37 and has been abandoned in favor of sliding or folding plasty.29 Annular plication has been replaced in many institutions by other techniques, such as sliding plasty or folding plasty, which are particularly indicated in the presence of redundant leaflet tissue to reduce the risk of systolic anterior motion (SAM), a complication that occurs in 5–10% of patients submitted to simple quadrangular resection of the posterior leaflet.38 Folding plasty and sliding plasty decrease the height of the posterior leaflet and move the coaptation point of the MV posteriorly, thereby avoiding the possibility of dynamic obstruction of the LV outflow tract.
Figure 3.3.1: Posterior leaflet quadrangular resection, annular plication.
A: quadrangular resection of P3 is performed; B,C: compression sutures are
placed and then tied; D: the leaflet edges are re-approximated.22
Artificial chordae. In patients with posterior leaflet prolapse without redundant leaflet tissue, the most appropriate surgical solution may be the implantation of artificial chordae (also known as the “respect-rather-then-resect” approach). Alternatively a very limited triangular or quadrangular resection can be performed.29
Commissural prolapse. Possibly the simplest form of MR to repair, commissural prolapse can be treated with resection. Commissuroplasty, i.e. obliteration of the commissure, is even easier to implement and delivers the same results. 9
Annuloplasty. Almost all valve repairs include annuloplasty to correct annular dilation, restore the orifice area and shape of the annulus and to guarantee success in the long run.1, 19, 29 Annular size is estimated by measuring the surface area of the anterior leaflet.19 In the setting of degenerative MR, Cohn warrants oversizing of the annulus, as it is often functionally “too small” for a redundant prolapsing leaflet9. Undersized annuloplasty is also the cardinal treatment of IMR.36
Commercially available annuli have evolved over time: initially flat and rigid, they later became partially flexible and with a three-dimensional configuration. The latest are pathology-specific3.
Figure 3.3.2: Annular remodeling. A, annular dilatation persists after leaflet
Surgical repair of anterior leaflet prolapse
Lesions involving the anterior leaflet or both leaflets are not common, but they are more difficult to repair9, 29 and are associated with a higher risk of failure1. Still, some surgeons have published excellent results29.
Triangular resection. While large segments of the LPM can be removed and the remaining portions sutured together after annular plication; not the same can be done for the anterior leaflet, due to the rigid structure of the fibrous trigones and the anterior part of the annulus37. Carpentier discouraged triangular resection of the anterior leaflet19; still, if the prolapse is small, a triangular resection involving < 10% of the anterior leaflet followed by direct suture of the remaining leaflet portions usually yields good results29.
Figure 3.3.3: Anterior leaflet triangular resection. A,limits of resection are identified and small triangular resection is performed; B, the gap is closed by interrupted sutures22
Chordal shortening. Once more popular than today, chordal shortening has been abandoned because of concerns of insufficient durability1, 9, 29. It involves splitting the papillary muscles and suturing the elongated chords within it, thus effectively reducing their length9.
leaflet thus functionally transforming it into a primary chord29.
Chordal transposition involves the detachment of a segment of the posterior leaflet (with the corresponding chordae), which is then reattached at the free margin of the prolapsing portion of the anterior leaflet. The defect created on the posterior leaflet by chordal transposition is repaired by a standard quadrangular resection. The main advantage of these approaches is that transferred or transposed chordae usually already have the correct length and, unlike artificial chordae, do not need to be adjusted 29. With this technique, a 5-year freedom from reoperation after MV repair of 96% has been reported.39
Papillary muscle repositioning. Papillary muscle repositioning involves the
shortening of the anterior head of the papillary muscle, the chordae tendineae of which are anchored to the anterior leaflet of the MV to correct anterior leaflet prolapse. The fibrous segment of the anterior head is identified, separated from the other papillary muscle heads, and sutured down to the fibrous portion of the posterior head to decrease its height.29
Implantation of artificial chordae. In degenerative MR, one or more chordae
tendineae are often elongated or ruptured. A common way to address this issue is to replace them with artificial chordae made of 4.0 or 5.0 expanded polytetrafluoroethylene. The number of artificial chordae that need to be implanted depends on the extension of the prolapsing or flailing mitral leaflet segment. Each neochorda is sutured to the fibrous portion of the papillary muscle and to the free margin of the prolapsing portion of the mitral leaflet. The most challenging part of this technique is choosing the adequate length of the neo- chordae. If the prolapse involves only the anterior leaflet, the reference length to use is the length of the chordae tendineae that reach the non-prolapsing, facing part of the posterior leaflet. In the presence of bileaflet prolapse, the point of reference to consider is the anterior commissure, which is usually not affected by chordal elongation. Premeasured artificial chordae were introduced to clinical
biological adaptation and to be effective and safe. After 15 years, freedom from reoperation and recurrent MR were 92% and 85% respectively.43
Figure 3.3.4: Artificial chordoplasty. A, residual prolapse of A2 is evident on
saline testing. B, a Gore-Tex suture is passed through the fibrous tip of the papillary muscle and the margin of the prolapsing segment. C, optimal artificial chordae height is determined by intermittently testing valve competency by injecting saline into the ventricle. D, a final saline test confirms correction of prolapse.22
Alfieri’s edge to edge technique. The original idea behind the edge-to-edge technique was that the competence of a regurgitant MV can be restored effectively with a ‘functional’, rather than an ‘anatomical’ repair.44, 45
Figure 3.3.5: Alfieri edge-to-edge repair.46
The key is to identify the location of the regurgitant jet during the preoperative TEE. At precisely this location, the free edge of one leaflet is sutured to the corresponding edge of the opposing leaflet, thereby eliminating the incompetence of the MV. If the regurgitant jet is located in the center of the valve, edge-to-edge repair produces a MV with a double orifice configuration. If the jet is located in proximity of a commissure, the edge-to-edge procedure creates a single orifice MV with a smaller area than a normal valve. The technique is attractive because of its simplicity, reproducibility, and effectiveness, even in complex settings.29 In a series of patients with complex mitral lesions, who underwent edge-to-edge repair, freedom from reoperation at 5 years was 91 ± 4.2% (mean ± standard error); no patient required reoperation for MV stenosis.44 Long-term results in specific subsets of patients, such as those with segmental prolapse of the anterior leaflet, have been excellent. Freedom from reoperation at a follow-up of 4.50 ± 3.12
myxomatous degeneration of the MV have also been effectively treated with this approach.48
The edge-to-edge technique is contraindicated in patients with degenerative MR if they have multiple lesions involving segments of the anterior and posterior leaflets that do not face each other, or in patients with a small mitral annulus or rheumatic MR for the risk of inducing stenosis.29
3.4 Mitral valve replacement
The decision to replace the valve is taken based on the surgeon’s experience and the severity of the disease once the valve has been exposed. Generally speaking, MVR should be performed only if repair is unsuccessful or impossible.49 Barlow’s disease with bileaflet prolapse is commonly treated with valve replacement by inexperienced surgeons.1
When replacing the valve, it is important to preserve the ventricular-annular continuity whenever possible, as it helps maintain the shape of the LV and the LVEF. The leaflets and their chords should be incorporated in the stitches that anchor the prosthesis to the annulus.1 In fact, ventricle size increases with removal of the chords and chordal sparing improves survival.3 Sometimes however the leaflets must be removed to accommodate a prosthesis that otherwise would not fit.49
Guidelines recommend mechanical valve replacement in patients under the age of 70.1 Mechanical valves should also be offered to patients with AF who need anticoagulation therapy and those who do not want to undergo reoperation. Biological valves are preferred by patients that do not want to be committed to warfarin for the rest of their lives, and should be considered in patients at risk of serious bleeding, with a high risk lifestyle and in fertile women that do not exclude
reoperation at 15 years is 60% and most patients under the age of 60 years with a biological prosthesis will need another MVR. These valves are therefor particularly indicated in patients older than 65 years and in those that are not likely to outlive their prosthesis.49
4. Minimally Invasive Mitral Valve Surgery
4.1 The gold standard
The gold standard and most popular surgical incision for mitral valve surgery is median sternotomy.1, 29
The patient is anesthetized and intubated with a single lumen tube. A skin incision is made from the jugular notch to the xiphoid and the sternum is cut along the midline and spread with an appropriate retractor. After identification and isolation of the brachiocephalic vein, the heart is exposed through a pericardial incision.
The CPB pump drains blood from the right atrium or the venae cavae by gravity, and returns oxygenated blood through a cannula placed in the aorta, the axillary artery or the femoral artery. A vent is placed in the right inferior pulmonary vein to drain the left heart. Body temperature is maintained at around 34°C throughout the procedure. Cardioplegia is delivered as soon as the aorta has been clamped.
The mitral valve can be accessed either directly through an incision behind the venae cavae, parallel to the interatrial grove in Sondergaard’s plane or through the right atrium and the atrial septum. To improve the view of the surgical field, an atrial retractor is placed and the patient is tilted to the left. The valve is then repaired or replaced.
The surgical result is assessed at first with simple hydrodynamic tests.9 The final verdict is left to the TEE: residual MR, trans-valvular gradient and the presence of SAM should be carefully investigated.3 If the operation is successful, secondary hemostasis is completed, the patient is weaned off CPB and the wound is closed layer by layer.9
4.2 History
4.2.1 The trend
In the past 18 years cardiac surgery has been following the general trend of modern surgery towards less invasive operations, pursuing the goal of totally endoscopic mitral valve repair.9 According to a 2008 statement of the American Heart Association, “the term minimally invasive refers to a small chest wall incision that does not include a full sternotomy”.50 The main goals of MIMVS are avoiding median sternotomy and related complications, such as infection, mediastinitis and nerve injures, while achieving the same results of conventional sternotomy.51 Other advantages are higher patient satisfaction, better cosmetic result, less postoperative pain and lower number of transfusions.29 Minimally invasive surgery is also expected to shorten postoperative recovery, reduce costs, and improve patient satisfaction.52
In order to accept MIMVS as the standard of care, the same results must be obtained as in conventional sternotomy.9 In fact, less invasive options are more difficult, but safe: there is no evidence that mortality differs between MIMVS and the conventional approach.29, 51, 53, 54 However, CPB times are 3̃0 minutes longer.51
Minimally invasive surgery consists of a range of approaches, techniques and technologies that have the purpose of minimizing surgical trauma. According to the grade of invasiveness, these techniques have been classified as shown in Table 4.2.1.9
Surgical incisions
Level Description Type cm
1 Direct vision Limited incisions 10-12
2 Direct vision/video assisted Mini incisions 4-6
3 Video directed and robot assisted Micro incisions 1.2-4
4.2.2 First steps
While current less invasive approaches are the hemi-lower sternotomy and the right minithoracotomy1, a number of approaches have been proposed in the past.
In January 1996 Gundry proposed the upper sternal T-shaped ministernotomy for mitral valve operations. As shown in Figure 4.2.1, the sternum is cut horizontally in the third or fourth intercostal space, and vertically above this line. This way, the aorta, right atrium and superior vena cava can easily be cannulated for CPB. The left atrium is entered parallel to the right pulmonary artery.55
Figure 4.2.1: upper T ministernotomy56
In July 1996 Navia and Cosgrove published their parasternal approach, which involved resecting the third and fourth intercostal cartilages (Figure 4.2.2) and ligating the internal mammary artery. Exposure of the mitral valve was achieved through the atrial septum, and the dome of the left atrium when necessary. The parasternal approach was found to reduce pain, infection risk, blood loss and hospital stay while leaving a more aesthetic scar.57 As surgeons became more experienced, the femoral cannulation was progressively substituted by direct aortic cannulation. Early data showed a non-significant trend towards shorter hospital stay and a 7% decrease in direct costs. While pain was not measured, it appeared
potential concern of this approach was sacrificing the senatorial node artery, as the valve is accessed through the dome of the left atrium.58
Figure 4.2.2: The right parasternal incision59
Shortly thereafter, Cohn reported preliminary results using the same technique in a small cohort of patients. While pain, sternal infections, blood loss, recovery times and charges were reduced, there was an increased risk of aortic dissection related to the cannulation of the femoral artery.59 Other disadvantages of the parasternal approach included ligation of the internal mammary artery, and difficult conversion to full sternotomy.54
Both Cosgrove and Cohn later abandoned the parasternal approach as the resection of the costal cartilages could result in chest wall instability, and opted for a ministernotomy approach instead,58 modifying Doty’s original version.60 Preferred by Cohn and other surgeons49, 54 to RT, lower hemisternotomy for
interspace. The right atrium is drained through the femoral vein with the aid of suction, and the aorta can be cannulated and clamped directly.49, 61
Figure 4.2.3: Cohn’s ministernotomy approach61
4.2.3 Video assisted surgery and new clamping technique
In February 1996 Carpentier performed the video-assisted mitral valve repair through RT using ventricular fibrillation.62
Later that year, Chitwood modified this approach and called it the “micro-mitral” operation (see Figure 4.2.4). A double-lumen endotracheal tube was used to achieve selective lung ventilation. The incision was made at the midaxillary line and a segment of the fourth or fifth rib was removed to expose the field with a custom retractor. CPB was achieved through femoral cannulation assisted by suction drainage. Cardioplegia was delivered via a catheter placed in the coronary sinus. The most remarkable technical solution devised for this operation is the custom-built transthoracic aortic clamp. The actual valve replacement was performed visualizing the heart through a thoracoscopic camera.63 According to the author, thoracoscopy was particularly useful to expose the trigones, the commissures, and the subvalvular apparatus; this was especially true in obese
For the first 31 patients operated with his approach, Chitwood reported excellent surgical results, but a 30-day mortality of 3,2% despite good preoperative LVEF. CPB and cross-clamp times were 183 ± 7.2 and 136 ± 5.5 minutes respectively. Postoperative hospital stay was reduced by 3 days.65
Chitwood’s transthoracic cross clamp had several advantages over the parasternal approach and the Port-Access system that was being deployed in the same period: cartilages were not resected, the dome of the left atrium was left intact, and no endoaortic balloon related complications occurred. Moreover, Chitwood’s clamp was much cheaper than the Port-Access system.65 Still, some surgeons were concerned of potentially damaging the pulmonary artery and the left atrium when using this clamp.66
Figure 4.2.4: Chitwood’s micro mitral operation through right minithoracotomy63
4.2.4 The Port-Access endovascular system
The Port-Access endovascular cardio-pulmonary bypass system (EndoCPB, Heartport, Inc. Redwwod City, Calif.) was firstly deployed by Mohr and colleagues in June 1996. As shown in Figure 4.2.5, it consists of an aortic balloon with a distal lumen for cardioplegia and de-airing of the heart. After cannulation of the femoral artery, the device is placed with a guide wire alongside the arterial CPB cannula and pushed 1 cm above the sinotubular junction; while the correct positioning of the device was initially confirmed by fluoroscopy and TEE, soon TEE alone was deemed sufficient. The endoclamp is placed outside the surgical field, and does not obstruct the surgeon’s view, thus potentially simplifying surgery in a confined space. However, serious complications were associated with the use of this device, and overall morbidity and mortality increased.67
One major issue associated with this technique was migration of the balloon; it can migrate either proximally and cause acute aortic insufficiency and possibly damage the aortic valve, or distally, and obstruct the brachiocephalic trunk. Unfortunately, continuous monitoring of the right radial artery pressure has not proven to be a reliable indicator of balloon displacement. Moreover, high balloon pressure (235-360 mmHg), while necessary for continence, poses the risk of balloon rupture and potential damage to the aortic wall. Initial results also indicated increased incidence of retrograde aortic dissection.67 Initial results were overall encouraging, but not too promising: there was no reduction in postoperative pain, an increase in cross-clamp and CPB time and more neurological events were recorded.67 Moreover, the authors felt that the procedure was significantly more complicated.
Still, Mohr innovated RT beyond the Port-Access system: he abandoned the resection of the rib in favor of a rib retractor; he introduced a transthoracic atrial retractor, a 3D videoscope, and other custom made surgical instruments, including a transjugular pulmonary artery vent. Furthermore, he considered single-lumen intubation be sufficient.67
Later, as he grew more experienced, the same surgeon also improved and simplified the Heart Port technique. Double-lumen intubation was abandoned, as the chest could be opened after the onset of CPB through femoral cannulation, with collapsed lungs. Transcranial Doppler was introduced to monitor flow in the middle cerebral artery, and thus occlusion of the brachiocephalic trunk due to displacement of the balloon. Lastly, flooding of the operative field with CO2 was proposed to reduced air embolism.68 While morbidity and mortality were this time comparable to the conventional approach, the authors concluded that patient benefit was still questionable.68 Still today however, some surgeons strongly prefer the intra-aortic balloon for MIMVS and robotic surgery, despite the aforementioned risks.
4.2.5 Robotically assisted videoscopy
Mohr’s group was also the first to introduce the AESOP 3000, a voice controlled robotic arm that replaced the assistant surgeon in maneuvering the endoscopic camera: the “solo mitral surgery” was born.68
Chitwood’s team at East Carolina University later on also used the robotic camera arm.69 Even if some teams have written enthusiastic reports on the subject49, 68, compared to human control, the robotic arm increase both cardiac arrest and perfusion times by approximately 30-40 minutes, and for this reason its usefulness has been called into question.69 Notably, Chitwood’s approach included anterograde cardioplegia and maintained the safe and cheap transthoracic clamp.69
4.2.6 Technique refinements
Between 1996 and 1997 Carpentier and coworkers carried their work forward; they developed a two-stage venous cannula (Figure 4.2.6), to drain both venae cavae at the same time from the groin and cannulated the aorta directly. They also argued that ministernotomy provides better exposure of the heart structures as compared to minithoracotomy.70
Figure 4.2.6: The picture on the left shows the minithoracotomy, a 6 cm incision
through the fourth right intercostal space (horizontal line), and the ministernotomy, a 6 cm midline incision from the second to the fifth intercostal space (vertical line). The picture on the right shows (1) the double-staged venous cannula introduced through the iliac vein, allowing drainage of both superior and inferior venae cavae, (2) the video assistance using a thoracoscope introduced into the left atrium, and (3) the view of the heart seen through ministernotomy 70
4.2.7 Robotic surgery
On 7 May 1998 Carpentier was the first to adapt a robot, specifically a “Da Vinci” prototype, for cardiac surgery, performing the first robotic atrial septal repair.71 The system overcomes some of the most frustrating limitations of MIMVS, which requires long instruments that increase physiological tremor, reduce accuracy and have only four degrees of freedom.72 In 2000 the first totally endoscopic mitral valve repair was performed, using the Heartport system.73, 74 Robotic tracers are introduced in the third and fifth intercostal space at the anterior axillary line; an additional 2-3 cm incision in the fourth intercostal space anterior to the same line is used as working port and for camera access, while the atrial retractor is placed in the same intercostal space, lateral to the mid-clavicular line. 75
Early reports of robotic surgery indicated longer CPB and cross-clamp times but lower incidence of postoperative AF, transfusions, and shorter postoperative stay. Coupling extensive experience with the Cor-Knot device, the East Carolina Heart Institute has progressively reduced average cross-clamp and CPB time to 94.7 and 144.9 minutes respectively.75 The only obvious limitation of the system is the absence of tactile feedback.75
Remote control of the robot arms allows the surgeon’s assistant to actively participate in the operation: both surgeons cooperate in knot tying and pushing, and four instruments can work on the same site at the same time.76 As expected, robotic surgery can be used for both mitral valve repair and replacement.76, 77 In conclusion, the robotic approach is not common, as it is more expensive, and does not appear to have clinical benefits.1
4.3 The state of the art
4.3.1 Minithoracotomy
At Ospedale del Cuore - FTGM, OPA, almost all isolated mitral valve surgeries are performed through right anterolateral minithoracotomy.
Before the operation, a chest-x-ray is examined to assess the spatial relationships between the diaphragm, the right atrium and the intercostal spaces.
Anesthesia is provided according to the standard protocol used for a conventional mitral valve repair or replacement. The operation is performed under general intravenous anesthesia.
When all necessary arterial and venous lines are acquired the patient is intubated and anesthetized. Usually use a single lumen normal tube for intubation is used. A double lumen endotracheal tube can be used for single (left) lung ventilation if some difficulties during preparation are expected. Pleural adhesions, in case of reoperation, chest profile, and unfavorable intrathoracic working plane that can cause poor visualization of the ascending aortic cannulation site could be reasons for double lumen tube insertion. A transesophageal echocardiography (TEE) probe is positioned to obtain a clear anatomic image of the mitral valve and its functional morphology, monitor the venous cannula correct insertion/placement, and evaluate the valve function pre- and postoperatively.
Two defibrillator pads are placed across the chest wall to guarantee an effective electric conduction. The patient is in a supine position and an air sack is placed under the right scapula, to allow the patient’s right chest to be elevated slightly to provide the surgeon with a better working field exposure. This can be useful particularly in patients with a deep chest.
This sack can be inflated and deflated as necessary to lift and lower the right chest. The patient’s right arm should be moved slightly away from the body to provide space for the placement of the working ports.
Figure 4.3.1: Patient positioning for minimally invasive mitral valve procedure. 78
A 5-Fr catheter introducer sheath is placed percutaneously in the right femoral vein. This is done before the incision to avoid any possible femoral artery punctures before heparin administration. A prepared right femoral vein introducer sheath permits direct venous cannula insertion without any delay when the patient is anticoagulated.
The skin is then incised at the submammary crease or under the nipple, depending on the gender of the patient, for 5-7 cm; the RT is completed in the third or fourth intercostal space to access the pleura. Once the thorax has been opened with the aid of a reusable retractor, a soft-tissue retractor is then inserted to spread the ribs.
Two small stab wounds are then made for ports.One 5.5 mm working port is used for video assistance and for passing the pericardial stay sutures; the port is placed in the same intercostal space, in the mid-axillary line where the thoracotomy incision is made. Another 10.5 mm port is placed two intercostal spaces lower in the mid-axillary line. This port is used for the cardiotomy vent,
Figure 4.3.2: double stage venous cannula, the rib retractor, the custom transthoracic atrial retractor, and the two ports.
The pericardium is opened 3-4 cm anterior and parallel to the phrenic nerve and traction sutures are put into place. Purse strings are sewn in the ascending aorta; a guidewire is then introduced from the groin through the sheath and into the superior vena cava, according to Seldinger’s technique and under TEE guidance. A cannula is then positioned in the right atrium over the wire; double stage cannula is indicated if the surgeon must operate on the tricuspid valve as well. Again, TEE is used to confirm location of the venous cannula.
The aorta is then cannulated as in conventional sternotomy; similarly, a cardioplegia catheter is placed in the ascending aorta (see Figure 4.7c). Femoral cannulation may be an option for beginners and if exposure is difficult; however it requires radiological imaging and particular care when de-airing.
CPB is initiated; body temperature is kept at 34°C throughout the procedure. Meanwhile, the aorta is clamped with a flexible Cygnet flexible clamp, or Glauber’s detachable clamp (Figure 4.7b). Immediately after a 20ml/kg dose of anterograde crystalloid or hematic cardioplegia is delivered into the aortic root.
The mitral valve is exposed with a special transthoracic retractor after dissection of Sondergaard’s plane; the final operative setting is shown in Figure 4.3.3. The valve is repaired or replaced as described before. At the end of the procedure, the patient is temporarily weaned from CPB to assess the result.
Once a satisfactory result has been obtained, a ventricular vent is placed in the LV and through the valve itself. The heart is de-aired through the ventricular and the aortic vent. Lung ventilation aids the procedure. When TEE shows no more air bubbles, the aortic ventricular vent is removed and the patient is progressively weaned from CPB. Hemostasis is checked, the venous cannula is removed and protamine sulfate is administered; 15 minutes of groin compression are usually necessary to halt the venous hemorrhage. The field is checked again for bleeding and two drains are placed through the ports. The pericardium and the wound are closed in according to anatomical layers.79
Figure 4.3.3: Anatomy of the left atrium following an atriotomy. Exposure is obtained using a left atrial lift system80
