The MitraClip (Abbott Laboratories, Chicago, IL) device offers a novel, percutaneous, transvenous, transcatheter approach for patients suffering from severe mitral regurgitation, despite maximal medical therapy, in whom surgery is not an option. This chapter serves to describe mitral valve anatomy in the context of regurgitant pathology, provide a detailed description of the MitraClip procedure along with practical “pearls” to optimize deployment, and finally outline the current evidence base for MitraClip through a brief review of published literature.

The mitral valve apparatus is an elegantly complex structure that is comprised of the mitral valve leaflets, annulus, annular attachment at the atrioventricular junction, chordae tendineae, and the papillary muscles, all of which work synchronously throughout the cardiac cycle to deliver blood to the left ventricle.

The valve itself is composed of the aortic and mural leaflets, more often clinically referred to as the anterior and posterior leaflet, respectively.^1,2 The anterior leaflet of the mitral valve is broader than the posterior leaflet and comprises one-third of the annular circumference. This semicircular anterior leaflet shares a fibrous continuity with the left and noncoronary cusps of the aortic valve and between the aortic cusps adjacent to the membranous septum. This region of continuity is referred to as the intervalvular fibrosa or aortic-mitral curtain. The motion of the leaflet defines an important boundary between the inflow (during diastole) and outflow (during systole) tracts of the left ventricle. In contrast to the anterior leaflet, the posterior leaflet is narrower and extends two-thirds around the left atrioventricular junction within the inlet portion of the ventricle. The posterior leaflet is commonly described as having 2 clefts that separate the leaflet into 3 scallops along the free edge. The Carpentier nomenclature describes the most lateral scallop as P1, adjacent to the anterolateral commissure; the central scallop as P2; and the most medial as P3, adjacent to the posteromedial commissure.^1,2 The anterior leaflet is divided into 3 regions, named A1, A2, and A3, which correspond to the opposing scallops of the posterior leaflet (Fig. 46-1). Often, the free edge of the anterior leaflet is continuous and without indentation, making the distinction between different regions of the anterior leaflet somewhat challenging.

The mitral annulus gives a point of attachment for the mitral valve and separates the left atrium from the left ventricle (LV). The anterior, or aortic, aspect of the annulus is fibrous and less prone to dilatation. The posterior annulus is a dynamic, nonrigid, oval-shaped structure that alters shape throughout the cardiac cycle. The posterior, or mural, aspect of the annulus is muscular and therefore often subject to dilatation and calcification.

The chordae tendineae are fan-shaped chords that arise from the papillary muscles (PM) and insert into the mitral leaflets. The anterolateral and posteromedial PM arise from the mid to apical segments of the LV at the anterolateral and posterior walls, respectively. The posteromedial PM gives chords to the medial aspect of both leaflets (A3, P3, and half of A2 and P2), while the anterolateral PM chords attach to the lateral aspect of the leaflets (A1, P2, and half of A2 and P2).

Mitral regurgitation (MR) is the ejection of blood from the LV back into the left atrium during ventricular systole. This is due to failure of the leaflets to adequately coapt (close/seal) or appose (come together and overlap). There are numerous classification systems that describe the etiology of the regurgitation, which has relevant implications for therapeutic intervention. One such classification divides the etiologies into either primary or functional, also known as secondary, MR (Fig. 46-2). Primary MR is a consequence of valvular pathology, while secondary MR is due to anatomic distortions or functional impairment of the LV. In primary MR, the standard treatment is repair or replacement of the affected valve. In functional MR, therapy involves management of the underlying LV dysfunction or attempted restoration of normal annular size and shape. For select patients in whom optimized medical therapy is unsuccessful, surgical or percutaneous intervention may be pursued.

Primary Mitral Regurgitation

The most prevalent etiology of primary MR is valvular degeneration that causes morphologic changes to the valve, including leaflet thickening and stretching of leaflet tissue. This accounts for approximately 60% of MR cases. The severity of these changes can be limited to focal involvement of 1 leaflet or can range to severe involvement of both leaflets in their entirety. For example, fibroelastic deficiency may account for the single, localized prolapsing segment, which is often normal in appearance. This prolapse is due to focal chordal elongation with or without rupture. Barlow disease, on the other hand, occurs in the setting of extensive myxomatous changes to both leaflets and is associated with chordal thinning and elongation. Accordingly, segments of both leaflets prolapse into the left atrium. A more severe manifestation is a flail leaflet, characterized by complete eversion of the leaflet edge into the left atrium. A flail may be present in the event of primary chordal rupture and may result in severe mitral regurgitation.

Other less common causes of primary mitral valve disease include infective endocarditis, deep clefts, congenital mitral cleft, and rheumatic mitral disease. As a result of earlier and more effective treatments for rheumatic fever in the developed world, this disease process is decreasing in prevalence and accounts for approximately 12% of MR. This acquired valvulopathy often leads to commissural fusion of the leaflets and results primarily in mitral stenosis with associated regurgitation. Progressive inflammation leads to leaflet and chordal thickening. Over time, the leaflets may calcify and restrict leaflet motion, with subsequent malcoaptation during systole resulting in regurgitation.

Secondary (Functional) Mitral Regurgitation

Functional MR occurs in the context of morphologically normal leaflets and subvalvular apparatus, on a background of an underlying dilated cardiomyopathy or ischemic cardiomyopathy secondary to coronary artery disease. This accounts for approximately 25% of MR. The regurgitation is due to geometric perturbations of the LV, which may or may not be associated with dilatation. Regional or generalized wall motion abnormalities of the LV can distort the position of the papillary PMs during systole, resulting in chordal tension and leaflet restriction. Ventricular dilatation causes subsequent annular dilatation, resulting in failure of leaflet coaptation or inadequate apposition.

The clinical course of MR is usually indolent and progressive, except for the rare perimyocardial infarction complication of acute MR due to PM rupture. The posteromedial PM is more prone to rupture compared to the anterolateral PM due to single versus dual blood supply, respectively. The insidious nature of the disease in the majority of patients is a consequence of cardiac compensation for increasing regurgitant volume, initially through enlargement of the left atrium and by increasing LV systolic function as a measure to increase stroke volume and maintain cardiac output. As the valvular regurgitation progresses, the heart loses its ability to compensate for the increased regurgitant volumes and cannot maintain physiologic demands. The LV eventually dilates, with evidence of diastolic dysfunction, elevated pulmonary artery pressures, and ultimately systolic dysfunction, which may progress to decompensated heart failure. The presence of LV dilatation and attenuated systolic function, particularly in the context of symptoms or functional impairment, heralds a very poor prognosis if left untreated. Annual mortality rates with optimal medical therapy in patients age 50 years or older are approximately 3% for moderate MR and approximately 6% for severe MR.^4,5

Until recently, surgical valve repair and replacement were the only treatments proven to improve symptoms and prevent heart failure. Current American College of Cardiology (ACC)/American Heart Association (AHA) and European Society of Cardiology (ESC) guidelines recommend surgical intervention in symptomatic patients with chronic severe primary MR and in asymptomatic patients with chronic severe primary MR with evidence of systolic dysfunction or LV dilatation.^6,7 MV repair is the preferred method of surgical correction and has been shown to be superior to MV replacement in terms of morbidity and mortality.^8-10 Mortality has been shown to decrease by approximately 70% in such patients. As expected, the best outcomes are obtained in asymptomatic patients treated in high-volume advanced repair centers with low operative mortality (<1%) and high repair rates (>80%). These results highlight the importance of early detection, assessment, and management of MR by experienced physicians and surgeons.

Patients with secondary MR carry higher preoperative mortality compared to their primary MR counterparts, attributable to severe comorbidities of the latter patient population.^9,10 Accordingly, the ACC/AHA and ESC guidelines recommend surgery for patients with severe secondary MR and preserved systolic function only when undergoing coronary artery bypass grafting or aortic valve replacement.^6,7

Although surgery is the gold standard for treatment, there remains a cohort of patients who are either at prohibitively high risk for surgery or who may not benefit from a valve surgery, particularly those with functional MR. There is scant clinical evidence to demonstrate reduction in mortality following surgical repair in patients with systolic dysfunction and ventricular dilatation. Accordingly, treatment of such patients is debatable. The application of the MitraClip in such patients is the subject of an ongoing clinical trial.

The complete device apparatus is composed of (1) a steerable guide handle attached to the steerable sleeve and the clip delivery system, (2) the clip, (3) the delivery catheter handle, and (4) the delivery catheter (Fig. 46-3).

The MitraClip device is delivered using a 24-Fr catheter guide with a mobile steerable tip to precisely position the clip. The clip is a 4-mm wide and 8-mm long chrome-cobalt clip with 2 articulated arms that open from 0° (closed position) to 240° (open position), which facilitates grasping and drawing together the anterior and posterior leaflets. The inner parts of the clip’s arms are grippers, lined with small frictional elements that promote more effective grasping of the leaflets once the device has been deployed and is ultimately closed. The outer aspect of the clip is covered in a polyester mesh to promote epithelialization and tissue growth to facilitate a fibrous tissue bridge between the leaflets (Fig. 46-4). The clip delivery system has 2 knobs that control the anterior-posterior and medial-lateral steering of the catheter tip. The delivery catheter handle is composed of: (1) 2 levers to lock/unlock the clip and to lift/depress the gripper lines, respectively; (2) a knob to facilitate the opening and closing of the clips; and (3) a screw to enable release of the clip from the shaft of the delivery catheter.

Procedure

The MitraClip procedure is performed under general anesthesia, primarily to enable pauses in ventilation, which facilitates precise clip positioning and deployment. The additional advantage of general anesthesia is comfort to the patient, particularly in the context of a potentially lengthy procedure (which is contingent on operator experience and valvular anatomy) as well as extended periods of transesophageal echocardiography (TEE) evaluation.

One of the key advantages of the MitraClip procedure is that it is performed via venous access. It is recommended to use a micropuncture needle for veinotomy, in order to minimize vascular complications and ensure optimal sheath placement. Two sites of venous access are required. The first site is the jugular or femoral vein for right heart catheterization at the commencement of the procedure and immediately following release of the clip, which provides some indication of the efficacy of the intervention. A second venous sheath is placed in the femoral vein for eventual passage of the 24-Fr MitraClip apparatus. A Perclose Proglide suture can be placed in a “pre-close” fashion to achieve hemostasis at the conclusion of the case. Alternatively, a figure of 8 suture can be applied at the end of the case to provide local external hemostasis.