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275 Mitral Regurgitation

are lower in young patients and may be twice as high in patients

65 years of age with significant comorbidities. Because there are also long-term complications of valve replacement, patients in whom preoperative evaluation suggests the possibility that MVR may be required should be operated on only if they have severe MS—i.e., an orifice area ≤1.5 cm2—and are in NYHA class III, i.e., symptomatic with ordinary activity despite optimal medical therapy. The overall 10-year survival of surgical survivors is ~70%. Long-term prognosis is worse in patients >65 years of age and those with marked disability and marked depression of the CO preopera­ tively. Pulmonary hypertension and RV dysfunction are additional risk factors for poor outcome.

PART 6 Disorders of the Cardiovascular System ■ ■FURTHER READING Connolly SJ et al: Rivaroxaban in rheumatic heart disease-associated atrial fibrillation. N Engl J Med 387:978, 2022. Nishimura RA et al: Mitral valve disease: Current management and future challenges. Lancet 387:1324, 2016. Otto CM et al: 2020 ACC/AHA guideline for the management of patients with valvular heart disease: A report of the American Col­ lege of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 143:e72, 2021. Patrick T. O’Gara, Joseph Loscalzo

Mitral Regurgitation The role of the physical examination in the evaluation of patients with valvular heart disease is also considered in Chaps. 44 and 246; of elec­ trocardiography (ECG) in Chap. 247; of echocardiography and other noninvasive imaging techniques in Chap. 248; and of cardiac catheter­ ization and angiography in Chap. 249. ■ ■ETIOLOGY Mitral regurgitation (MR) may result from an abnormality or disease process that affects any one or more of the five functional components of the mitral valve apparatus (leaflets, annulus, chordae tendineae, pap­ illary muscles, and subjacent myocardium) (Table 275-1). Acute MR can occur in the setting of acute myocardial infarction (MI) with pap­ illary muscle rupture (Chap. 286), following blunt chest wall trauma, or during the course of infective endocarditis (IE) owing to leaflet perforation or destruction. With acute MI, the posteromedial papil­ lary muscle is involved much more frequently than the anterolateral papillary muscle because of its singular blood supply. Transient, acute MR can occur during periods of active ischemia and bouts of angina pectoris. Rupture of chordae tendineae can result in “acute-on-chronic MR” in patients with myxomatous degeneration of the valve apparatus. Chronic MR can result from several disease processes (Table 275-1). Distinction should be drawn between primary (degenerative) MR, in which the leaflets and/or chordae tendineae are primarily respon­ sible for abnormal valve function, and secondary (functional) MR, in which the leaflets and chordae tendineae are usually normal but the regurgitation is caused by left ventricular (LV) and/or left atrial remodeling, annular dilation, papillary muscle displacement, dys­ synchrony, leaflet tethering, or their combination. Patient assessment, treatment approach, and long-term prognosis differ significantly between primary and secondary MR. Mitral valve prolapse (MVP) is discussed more extensively in Chap. 276. The rheumatic process produces rigidity, deformity, and retraction of the valve cusps and com­ missural fusion, as well as shortening, contraction, and fusion of the chordae tendineae. MR can persist after resolution of the acute phase

TABLE 275-1  Major Causes of Mitral Regurgitation (MR) Etiologies Acute   IE   Papillary muscle rupture (post-MI)   Chordal rupture/leaflet flail (MVP, IE)   Blunt trauma Chronic   Primary (affecting leaflets, chordae)     Myxomatous (MVP, Barlow’s, forme fruste)     Rheumatic fever     IE (healed)     Congenital (cleft, AV canal)     Radiation   Secondary (leaflets, chordae are “innocent bystanders”)     Ischemic cardiomyopathy     Dilated cardiomyopathy     HOCM (with SAM)     AF with LA enlargement and annular dilation (atrial functional MR)   Mitral annular calcificationa aMitral annular calcification may include elements of both primary and secondary MR (mixed) as the disease process may encroach on the leaflets, impair the normal sphincteric function of the annulus, or both. There are additional examples of “mixed” secondary MR such as the coexistence of MVP with an ischemic cardiomyopathy. Abbreviations: AF, atrial fibrillation; AV, atrioventricular; HOCM, hypertrophic obstructive cardiomyopathy; IE, infective endocarditis; LA, left atrial; LV, left ventricular; MI, myocardial infarction; MVP, mitral valve prolapse; SAM, systolic anterior motion. of infection and inflammation. MR may occur as a congenital anomaly (Chap. 280), most commonly as a defect of the endocardial cushions (atrioventricular cushion defects). A cleft anterior mitral valve leaflet accompanies ostium primum atrial septal defect. Radiation can result in leaflet thickening, retraction, and calcification, often in association with annular and chordal involvement and some degree of mitral ste­ nosis. Chronic MR occurs frequently after prior MI(s) associated with changes in LV size, shape, and function. Similar mechanisms of annular dilation and ventricular remodeling contribute to the MR that occurs among patients with nonischemic forms of dilated cardiomyopathy once the LV end-diastolic dimension reaches 6 cm. The MR associated with hypertrophic obstructive cardiomyopathy (HOCM) is usually dynamic in nature and dependent on systolic anterior motion of the anterior mitral valve leaflet into a narrowed LV outflow tract. Patients with chronic persistent atrial fibrillation (AF) may develop atrial remodeling and annular dilation with inadequate leaflet lengthening and MR (atrial functional MR). Secondary MR due to LV remodeling is more frequently encountered in the community than secondary MR that occurs in association with AF and annular dilation. Annular calci­ fication can result in MR when it encroaches on the leaflets or results in decreased sphincteric function, is especially prevalent among patients with advanced renal disease, and is commonly observed in women

65 years of age with hypertension and diabetes mellitus. Irrespective of cause, chronic severe MR is often progressive because enlargement of the left atrium (LA) places tension on the posterior mitral leaflet, pulling it further away from the mitral orifice and thereby aggravating the valvular dysfunction. Similarly, LV dilation increases the regurgi­ tation, which, in turn, enlarges the LA and LV further, resulting in a vicious cycle; hence the aphorism, “MR begets MR.” ■ ■PATHOPHYSIOLOGY The resistance to LV emptying (LV afterload) is reduced in patients with MR. As a consequence, the LV is decompressed into the LA during ejec­ tion, and with the reduction in LV size during systole, there is a rapid decline in LV tension. The initial compensation to MR is more com­ plete LV emptying. However, LV volume increases progressively with time as the severity of the regurgitation increases and as LV contractile function deteriorates. This increase in LV volume is often accompanied

by a reduced forward cardiac output (CO). LV compliance is often increased, and thus, LV diastolic pressure does not increase until late in the course. The regurgitant volume varies directly with the LV systolic pressure and the size of the regurgitant orifice; the latter, in turn, is influenced by the extent of LV and mitral annular dilation, as well as by leaflet morphology. Because ejection fraction (EF) rises in severe MR in the presence of normal LV function, even a modest reduction in this parameter (<60%) reflects significant contractile dysfunction. During early diastole, as the distended LA empties, there is a par­ ticularly rapid y descent in the absence of accompanying MS. A brief, early diastolic LA-LV pressure gradient (often generating a rapid filling sound [S3] and mid-diastolic murmur masquerading as MS) may occur in patients with pure, severe MR as a result of the very rapid flow of blood across a normal-sized mitral orifice. Measurements of LV ejection fraction (LVEF), CO, pulmonary arterial (PA) systolic pressure, regurgitant volume, regurgitant fraction (RF), and the effective regurgitant orifice area can be obtained during a careful Doppler echocardiographic examination. These measure­ ments can also be obtained accurately with cardiac magnetic resonance (CMR) imaging, although this technology is not widely available. Left and right heart catheterization with contrast ventriculography is used less frequently. Chronic, severe MR is defined by a regurgitant volume ≥60 mL/beat, RF ≥50%, and effective regurgitant orifice area ≥0.40 cm2. In patients with secondary MR, in whom the severity of MR can be underappreciated using echocardiographic/Doppler techniques, lesser degrees of regurgitation may carry relatively greater prognostic weight. The adverse prognosis in secondary MR related to adverse LV remod­ eling is intimately related to the degree of myocardial dysfunction. LA Compliance  In acute severe MR, the regurgitant volume is delivered into a normal-sized LA having normal or reduced compli­ ance. As a result, LA pressures rise markedly for any increase in LA volume. The v wave in the LA pressure pulse is usually prominent, LA and pulmonary venous pressures are markedly elevated, and pul­ monary edema is common. Because of the rapid rise in LA pressures during ventricular systole, the murmur of acute MR is early in timing and decrescendo in configuration ending well before S2, as a reflection of the progressive diminution in the LV-LA pressure gradient. LV sys­ tolic function in acute MR may be normal, hyperdynamic, or reduced, depending on the clinical context. Patients with chronic severe MR, on the other hand, develop marked LA enlargement and increased LA compliance with little if any increase in LA and pulmonary venous pressures for any increase in LA volume. The LA v wave is relatively less prominent. The murmur of chronic MR is classically holosystolic in timing and plateau in configuration, as a reflection of the near-constant LV-LA pressure gradient. These patients usually complain of severe fatigue and exhaustion secondary to a low forward CO, whereas symptoms resulting from pulmonary congestion are less prominent initially; AF is almost invariably present once the LA dilates significantly. ■ ■SYMPTOMS Patients with chronic mild-to-moderate, isolated MR are usually asymptomatic. This form of LV volume overload is well tolerated. Fatigue, exertional dyspnea, and orthopnea are the most prominent complaints in patients with chronic severe MR. Palpitations are com­ mon and may signify the onset of AF. Late-onset right-sided heart failure, with painful hepatic congestion, ankle edema, distended neck veins, ascites, and secondary tricuspid regurgitation (TR), occurs in patients with MR who have associated pulmonary vascular disease and pulmonary hypertension. Acute pulmonary edema is common in patients with acute severe MR. ■ ■PHYSICAL FINDINGS In patients with chronic severe MR, the arterial pressure is usually nor­ mal, although the carotid arterial pulse may show a sharp, low-volume upstroke owing to the reduced forward CO. A systolic thrill is often palpable at the cardiac apex, the LV is hyperdynamic with a brisk sys­ tolic impulse and a palpable rapid-filling wave (S3), and the apex beat is often displaced laterally.

In patients with acute severe MR, the arterial pressure may be reduced with a narrow pulse pressure, the jugular venous pressure and waveforms may be normal or increased and exaggerated, the api­ cal impulse is not displaced, and signs of pulmonary congestion are prominent.

CHAPTER 275 Auscultation  S1 is generally absent, soft, or buried in the holosys­ tolic murmur of chronic, severe MR. In patients with severe MR, the aortic valve may close prematurely (due to the reduced forward cardiac output), resulting in wide but physiologic splitting of S2. A low-pitched S3 occurring 0.12–0.17 s after the aortic valve closure sound, i.e., at the completion of the rapid-filling phase of the LV, is believed to be caused by the sudden tensing of the papillary muscles, chordae tendineae, and valve leaflets. It may be followed by a short, rumbling, mid-diastolic murmur, even in the absence of structural MS. In patients with isch­ emic or dilated cardiomyopathy, however, a third sound (S3) may also signify ventricular dysfunction. A fourth heart sound is often audible in patients with acute severe MR who are in sinus rhythm. A presystolic murmur is not ordinarily heard with isolated MR. Mitral Regurgitation A systolic murmur of at least grade III/VI intensity is the most char­ acteristic auscultatory finding in chronic severe MR. It is usually holo­ systolic (see Fig. 246-5A), but as previously noted, it is decrescendo and ceases in mid-to-late systole in patients with acute severe MR. The systolic murmur of chronic MR is usually most prominent at the apex and radiates to the axilla. However, in patients with ruptured chordae tendineae or primary involvement of the posterior mitral leaflet with prolapse or flail, the regurgitant jet is eccentric, directed anteriorly, and strikes the LA wall adjacent to the aortic root. In this situation, the systolic murmur is transmitted to the base of the heart and, therefore, may be confused with the murmur of AS. The murmur associated with anterior leaflet prolapse or flail is directed to the axilla. In patients with ruptured chordae tendineae, the systolic murmur may have a cooing or “seagull” quality, whereas a flail leaflet may produce a murmur with a musical quality. The systolic murmur of chronic MR not due to MVP is intensified by isometric exercise (handgrip) but is reduced during the strain phase of the Valsalva maneuver because of the associated decrease in LV preload. ■ ■LABORATORY EXAMINATION ECG  In patients with sinus rhythm, there is evidence of LA enlarge­ ment, but right atrial (RA) enlargement also may be present when pul­ monary hypertension is significant and affects right ventricular function and size. Chronic severe MR is frequently associated with AF. In many patients, there is no clear-cut ECG evidence of enlargement of either ven­ tricle. In others, the signs of eccentric LV hypertrophy are present. Echocardiogram (Fig. 275-1)  Transthoracic echocardiography (TTE) is indicated to assess the mechanism of the MR and its hemo­ dynamic severity. LV function can be assessed from LV end-diastolic and end-systolic volumes and EF. Observations can be made regarding leaflet structure and function, chordal integrity, LA and LV size, annu­ lar calcification, and regional and global LV systolic function. Doppler imaging should demonstrate the width or area of the color flow MR jet within the LA, the duration and intensity of the continuous wave Dop­ pler signal, the pulmonary venous flow contour, the early peak mitral inflow velocity, and quantitative measures of regurgitant volume, RF, and effective regurgitant orifice area. In addition, the PA pressures (PAPs) can be estimated from the TR jet velocity. TTE is also indicated to follow the course of patients with chronic MR and to provide rapid assessment for any clinical change. Transesophageal echocardiography (TEE) provides greater anatomic detail than TTE (see Fig. 248-5). Exercise testing with TTE can be useful to assess exercise capacity as well as any dynamic change in MR severity, PA systolic pressures, and biventricular function, for patients in whom there is a discrepancy between clinical findings and the results of other noninvasive testing. Chest X-Ray  The LA and LV are the dominant chambers in chronic MR. Late in the course of the disease, the LA may be mas­ sively enlarged and forms the right border of the cardiac silhouette. Pulmonary venous congestion, interstitial edema, and Kerley B lines

PART 6 Disorders of the Cardiovascular System FIGURE 275-1  Mitral regurgitation. Apical two-chamber transthoracic color flow Doppler echocardiographic display of a broad systolic jet of severe mitral regurgitation (yellow stream between the two white arrows) from the left ventricle directed posteriorly into the left atrium. LA, left atrium; LV, left ventricle; MV, anterior leaflet of the mitral valve. are sometimes noted. Marked calcification of the mitral leaflets occurs commonly in patients with long-standing, combined rheumatic MR and MS, as well as in patients with radiation-induced mitral valve dis­ ease. Calcification of the mitral annulus may be visualized, particularly Symptoms due to MR (Stage D) (regardless of LV function) LV systolic dysfunction (Stage C2) (LVEF ≤60% or ESD ≥40 mm) High or prohibitive surgical risk with anatomy favorable for transcatheter approach and life expectancy >1 y MV surgery (1) Degenerative MV disease Rheumatic MV disease Successful and durable repair possible Successful and durable repair possible MV surgery at primary or CVC (1) MV repair at primary or CVC (2a) Transcatheter edge-toedge MV repair (2a) MV repair or replacement (2b) MV repair at CVC (2b) FIGURE 275-2  Management of primary mitral regurgitation (MR). See legend for Fig. 272-4 for explanation of treatment recommendations (Class I, IIa, IIb) and disease stages (B, C1, C2, D). Preoperative coronary angiography should be performed routinely as determined by age, symptoms, and coronary risk factors. Cardiac catheterization and angiography may also be helpful when there is a discrepancy between clinical and noninvasive findings. Mitral valve repair is strongly preferred over valve replacement whenever feasible for surgical treatment of primary MR. Transcatheter edge-to-edge repair (TEER) is reserved for high or prohibitive surgical risk patients with appropriate anatomy on transesophageal imaging. CVC, comprehensive valve center; EF, ejection fraction; ERO, effective regurgitant orifice; ESD, end-systolic dimension; LV, left ventricular; MV, mitral valve; RF, regurgitant fraction; RVol, regurgitant volume; VC, vena contracta. (Reproduced with permission from CM Otto et al: ACC/AHA guideline for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021; 143(5):e72.)

on the lateral view of the chest. Patients with acute severe MR may have asymmetric pulmonary edema if the regurgitant jet is directed predominantly to the orifice of an upper lobe pulmonary vein. TREATMENT (FIGS. 275-2 AND 275-3) Mitral Regurgitation MEDICAL TREATMENT The management of chronic severe MR depends to some degree on its cause. Anticoagulation with either warfarin or a direct oral agent (e.g., apixaban, rivaroxaban) should be provided if AF inter­ venes, as guided by the CHA2DS2-VASc risk score. The direct oral anticoagulants should not be used if moderate or severe rheumatic mitral stenosis is also present (Ch. 274); they are also not approved for use in patients with mechanical prosthetic heart valves. Cardio­ version should be considered depending on the clinical context, AF chronicity, and LA size. In contrast to the acute setting, there are no large, long-term prospective studies to substantiate the use of vasodilators for the treatment of chronic, isolated severe primary MR with preserved LV systolic function in the absence of systemic hypertension. However, the severity of secondary MR in the setting of an ischemic or dilated cardiomyopathy may dimin­ ish with aggressive guideline-directed medical therapy (GDMT) of heart failure including the use of diuretics for decongestion, beta blockers, angiotensin-converting enzyme (ACE) inhibitors/angio­ tensin receptor blockers, angiotensin-neprilysin inhibitors, min­ eralocorticoid receptor antagonists, sodium-glucose cotransporter Primary mitral regurgitation Severe MR (VC ≥0.7 cm, RVol ≥60 mL, RF ≥50%, ERO ≥0.40 cm2) No symptoms due to MR (Stage C) Normal LV systolic function (Stage C1) (LVEF >60% or ESD <40 mm) Expected surgical mortality <1% with

95% likelihood of successful and durable repair without residual MR Progressive increase in LV size or decrease in LVEF on at least 3 studies No Yes

2 inhibitors, and biventricular pacing (cardiac resynchronization therapy [CRT]) when indicated. Antibiotic prophylaxis for pre­ vention of IE is indicated for MR patients with a prior history of IE. Asymptomatic patients with severe MR in sinus rhythm with normal LV size and systolic function should avoid isometric forms of exercise. Patients with acute severe MR require urgent stabilization and preparation for surgery. Diuretics, intravenous vasodilators (par­ ticularly sodium nitroprusside), and even mechanical circulatory support may be needed for patients with post-MI papillary muscle rupture or other forms of acute severe MR. SURGICAL TREATMENT In the selection of patients with chronic, severe, primary MR for surgical treatment, the often slowly progressive nature of the condition must be balanced against the immediate and longterm risks associated with operation. These risks are signifi­ cantly lower for primary valve repair than for valve replacement

(Table 275-2). In a 2023 analysis of outcomes reported to the Soci­ ety of Thoracic Surgeons Adult Cardiac Surgical Database, investi­ gators reported a mean perioperative mortality risk of 1.16% (<0.5% for patients <65 years of age) for repair of primary MR. Repair usu­ ally consists of valve reconstruction using a variety of valvuloplasty techniques and insertion of an annuloplasty ring. Repair spares the patient the long-term adverse consequences of valve replacement, including thromboembolic and hemorrhagic complications in the case of mechanical prostheses and late valve failure necessitating repeat valve replacement in the case of bioprostheses. In addition, Secondary mitral regurgitation GDMT supervised by a HF specialist (1) Severe MR Stage D RVol ≥60 mL, RF ≥50%, ERO ≥0.40 cm2) LV EF <50% LV EF ≥50% Persistent symptoms on optimal GDMT and AF Rx Persistent symptoms on optimal GDMT Mitral anatomy favorable LV EF 20–50% LV ESD ≤70 mm PASP ≤70 mm Hg MV surgery (2b) MV surgery* (2a) Transcatheter edge-toedge MV repair (2a) FIGURE 275-3  Management of secondary mitral regurgitation. See legend for Fig. 272-4 for explanation of treatment recommendations (Class I, IIa, IIb) and disease stages (B, C1, C2, D). Preoperative coronary angiography should be performed routinely as determined by age, symptoms, and coronary risk factors. Cardiac catheterization and angiography may also be helpful when there is a discrepancy between clinical and noninvasive findings. Surgery is recommended for patients with left ventricular ejection fraction (LVEF) >50%. Transcatheter edge-to-edge repair (TEER) is reasonable in selected patients after guideline-directed management and therapy (GDMT) has been optimized. *MV replacement may be preferred over MV repair for ischemic MR; AF, atrial fibrillation; CABG, coronary artery bypass grafting; EF, ejection fraction; ERO, effective regurgitant orifice; ESD, end-systolic dimension; HF, heart failure; LV, left ventricular; MR, mitral regurgitation, MV, mitral valve; PASP, pulmonary artery systolic pressure; RF, regurgitant fraction; RVol, regurgitant volume; Rx, treatment. (Reproduced with permission from CM Otto et al: ACC/AHA guideline for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021; 143(5):e72.)

TABLE 275-2  Mortality Rates After Mitral Valve Surgerya UNADJUSTED OPERATIVE MORTALITY (%) OPERATION NUMBER MVR (isolated) 10,699 4.5 CHAPTER 275 MVR + CAB

9.6 MVRp 12,424 1.2 MVRp + CAB

5.4 aData are for calendar year 2018 during which 1088 participant groups reported a total of 287,872 procedures. Surgical mitral valve commissurotomy cases are included in the mitral valve repair procedures. Abbreviations: CAB, coronary artery bypass; MVR, mitral valve replacement; MVRp, mitral valve repair. Source: Adapted from ME Bowdish et al: Ann Thorac Surg 109:1646, 2020. Mitral Regurgitation by preserving the integrity of the papillary muscles, subvalvular apparatus, and chordae tendineae, mitral repair and valvuloplasty maintain LV function to a relatively greater degree than does valve replacement. Surgery for chronic severe primary MR is indicated once symp­ toms occur, especially if valve repair is feasible (Fig. 275-2). Surgery should also be recommended for asymptomatic patients with LV dysfunction characterized by an EF ≤60% or an LV end-systolic dimension (LV ESD) ≥40 mm. Other indications for early con­ sideration of mitral valve repair in asymptomatic patients include a progressive decrease in LVEF or increase in LV ESD on serial imaging as well as mitral valve anatomy that would predict a >95% of a successful and durable repair in a low surgical risk patient. Undergoing CABG MV surgery (2b)

These aggressive recommendations for surgery are predicated on the adverse long-term consequences of waiting for LV function to decline further as well as the outstanding results achievable with mitral valve repair by reference surgeons at high-volume centers. Indeed, the majority of patients <75 years of age with degenerative MR, normal LV systolic function, and no coronary artery disease (CAD) can now undergo successful and durable repair of degenera­ tive MR (e.g., prolapse, flail) by an experienced surgeon at very low risk for perioperative death or major complication. Repair is feasible in up to 95% of patients with degenerative disease operated on by a high-volume surgeon in a referral center of excellence. Repair tech­ niques include chordal transfer, creation of neochords, limited leaflet resection, and insertion of an annuloplasty band. Long-term durabil­ ity is excellent; the incidence of reoperative surgery for failed primary repair is ~1% per year for the first 10 years after surgery. For patients with paroxysmal or persistent AF, left or biatrial maze surgery, or radiofrequency or cryoablative isolation of the pulmonary veins, along with left atrial appendage amputation, is performed to reduce the risk of recurrent postoperative AF and associated thrombus formation.

PART 6 Disorders of the Cardiovascular System The surgical management of patients with secondary MR is more complicated. Surgery for patients with ischemic MR most often involves simultaneous coronary artery revascularization. Current surgical practice includes either annuloplasty repair with an under­ sized, rigid ring or chord-sparing valve replacement for patients with moderate or greater degrees of MR. Valve repair for ischemic MR is associated with lower perioperative mortality rates than valve replacement but significantly higher rates of recurrent MR over time. Thus, replacement may be preferred over repair in this context. In patients with ischemic MR and significantly impaired LV systolic function (EF <30%), the risk of surgery is higher, recov­ ery of LV performance is incomplete, and long-term survival is reduced. Referral for surgery must be individualized and made only A B C D E F G4 NT G4 NTW G4 XT G4 XTW G4 NT AND NTW G4 XT AND XTW 4 mm 6 mm 4 mm 6 mm A PASCAL PASCAL Ace Retention elements Spacer Paddles Independent clasps B FIGURE 275-4  Clip devices used to grasp the free edges of the anterior and posterior leaflets in their midsections during transcatheter mitral valve repair of selected patients with mitral regurgitation. A. Fourth-generation of the first approved edge-to-edge repair device. B. System approved in 2022 includes a central spacer device and two paddles. The spacer is designed to reduce stress on the leaflets and preserve mitral valve area. (MitraClip is a trademark of Abbott or its related companies. PASCAL is an Edwards Lifesciences tradename.)

after aggressive attempts to improve symptoms with GDMT and CRT, when indicated. The routine performance of surgical valve repair in patients with significant secondary MR due to a dilated cardiomyopathy has not been shown to improve long-term survival compared with optimal GDMT, especially in the era of quadruple medical therapy for heart failure with reduced EF. Patients with acute severe MR can often be stabilized temporarily with appro­ priate medical therapy, but surgical correction will be necessary emergently in the case of papillary muscle rupture and within days in most other settings. When surgical treatment is contemplated, left and right heart catheterization and left ventriculography may be helpful in con­ firming the presence of severe MR in patients in whom there is a discrepancy between the clinical and TTE findings that cannot be resolved with TEE or CMR. Coronary angiography identifies patients who require concomitant coronary revascularization. TRANSCATHETER MITRAL VALVE REPAIR AND REPLACEMENT A transcatheter approach to the treatment of either primary or secondary MR may be feasible in selected patients with appropri­ ate mitral valve anatomy. One approach involves the deployment of a clip delivered via transseptal puncture that grasps the leading edges of the mitral leaflets in their mid-portion (anterior scallop to posterior scallop). The length and width of the gap between the leading edges of the leaflets, as well as other considerations such as leaflet thickening and calcification, dictate patient eligi­ bility. There are two commercially available transcatheter systems employing clip technology for the treatment of degenerative MR in symptomatic patients considered to be at high or prohibitive surgical risk (Fig. 275-4). Randomized trials of transcatheter 12 mm 9 mm 17 mm at 120° 22 mm at 120° Independent clasps