# 37 - 275 Mitral Regurgitation

### 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