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SECTION 8 Coronary artery bypass graft surgery inspecial situations
Fig.64.2 Intraoperative image showing coronary artery reimplantation in a patient with ALCAPA. Panel (a)shows the opened pulmonary artery;
the anomalous coronary artery has been detached and the defect in the pulmonary artery has been repaired (arrow). Panel (b)shows the anomalous
coronary artery after reimplantation into the aorta (arrows).
Reproduced from Rajbanshi BG, Burkhart HM, Schaff HV, Daly RC, Phillips SD, Dearani JA. Surgical strategies for anomalous origin of coronary artery from pulmonary artery in
adults. J Thorac Cardiovasc Surg. 2014;148(1):220– 24. doi:10.1016/ j.jtcvs.2013.08.026 with permission from Elsevier
Coronary arteryfistulas
Coronary artery stulas are abnormal communications between a
coronary artery and another cardiovascular structure, such as the PA,
coronary sinus, or cardiac chambers. Aconnection between a coronary artery and a cardiac chamber is known as a coronary– cameral
stula.
Coronary artery stulas occur in 0.1– 0.2% of all patients undergoing coronary angiography. e most common origin is the
right coronary artery, and the most common draining sites are the
coronary sinus, PA, and right ventricle. Complications that may
arise from coronary artery stulas include myocardial infarction,
arrhythmias, congestive heart failure, and coronary aneurysms.
Furthermore, infective endocarditis develops in approximately 5%
of cases of coronary artery stulas. Patients are usually asymptomatic
and commonly present due to an incidental nding of a continuous
murmur or cardiomegaly and plethora on chest radiography.
Closure of a coronary artery stula is indicated in all symptomatic
patients. In asymptomatic patients, surgery may be advised due to
the risk of the stula increasing in size and causing congestive heart
failure. Another reason for closure is their association with infective
endocarditis. e choice of surgical or transcatheter approaches remains controversial as similar eectiveness, morbidity, and mortality have been reported. Complications of both approaches include
early or late postprocedural myocardial infarction. Early myocardial infarction is most likely due to iatrogenic occlusion of distal
coronary ow, while late myocardial infarction is usually caused
by thrombosis of the enlarged native proximal coronary artery.
For this reason, systemic anticoagulation should be considered in all
patients undergoing coronary artery stula repair.,
Surgicaltechniques
Epicardialligation
Surgical closure can be achieved by ligating the stulous connection of the coronary artery close to its drainage site (Fig. 64.3a). is
does not necessarily involve putting the patient on cardiopulmonary
bypass, and depends on accessibility of the coronary artery stula,
the presence of a coronary aneurysm, and other coexisting cardiac pathologies. Prior to ligating a coronary artery stula, it is important to ensure that branches supplying the myocardium are not
occluded. Careful study of the preoperative coronary angiogram is
critically important in order to identify the stula and drainage site.
Intraoperatively, it is oen helpful to temporarily occlude or snare
the suspected site of the stula and observe for ST- segment changes
that would indicate occlusion of the coronary artery rather than the
stulous communication.,
Transcoronary, transcameral, and transpulmonaryclosure
If the coronary artery stula opens into a ventricle or if the stula
is very large, the coronary artery is opened and the stula is closed
using a running suture (Fig. 64.3b). If the coronary artery stula
opens into an atrium or the PA, the chamber is opened and the stula is closed from the inside.
Transcatheterembolization
Endovascular closure is performed if the stula arises at the proximal part of the coronary artery. It is contraindicated in large stulas,
if there are multiple stulas present, or if there are other concomitant
cardiac pathologies requiring surgical correction. Several methods,
such as occlusion coils, vascular plugs, and covered stents, have been
described.
64 Coronaryanomalies 439
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Fig.64.3 Illustrations of coronary fistulas and surgical techniques. Panel (a)shows direct epicardial ligation of a coronary fistula with preservation of
distal coronary artery flow. Panel (b)shows the transcoronary approach for closure of a coronary fistula used in large dilated coronary arteries.
Reproduced from Said SM, Burkhart HM, Schaff HV, Connolly HM, Phillips SD, Suri RM, etal. Late outcome of repair of congenital coronary artery fistulas- a word of caution. J
Thorac Cardiovasc Surg. 2013;145(2):455– 60.
REFERENCES
1. Angelini P. Coronary artery anomalies— current clinical
issues:denitions, classication, incidence, clinical relevance, and
treatment guidelines. Tex Heart Inst J. 2002;29(4):271– 8.
2. Alexander RW, Grith GC. Anomalies of the coronary arteries
and their clinical signicance. Circulation. 1956;14(5):800– 5.
3. Kayalar N, Burkhart HM, Dearani JA, Cetta F, Scha HV.
Congenital coronary anomalies and surgical treatment. Congenit
Heart Dis. 2009;4(4):239– 51.
4. Fedoruk LM, Kern JA, Peeler BB, Kron IL. Anomalous origin of
the right coronary artery:right internal thoracic artery to right
coronary artery bypass is not the answer. J orac Cardiovasc
Surg. 2007;133(2):456– 60.
5. Taylor AJ, Rogan KM, Virmani R. Sudden cardiac death associated
with isolated congenital coronary artery anomalies. J Am Coll
Cardiol. 1992;20(3):640– 7.
6. Peñalver JM, Mosca RS, Weitz D, Phoon CKL. Anomalous aortic
origin of coronary arteries from the opposite sinus:a critical
appraisal of risk. BMC Cardiovasc Disord. 2012;12:83.
7. Davies JE, Burkhart HM, Dearani JA, Suri RM, Phillips SD,
Warnes CA, etal. Surgical management of anomalous aortic origin
of a coronary artery. Ann orac Surg. 2009;88(3):844– 7.
8. Sharma V, Burkhart HM, Dearani JA, Suri RM, Daly RC,
Park SJ, etal. Surgical unroong of anomalous aortic origin of
a coronary artery:a single- center experience. Ann orac Surg.
2014;98(3):941– 5.
9. Gulati R, Reddy VM, Culbertson C, Helton G, Suleman S,
Reinhartz O, etal. Surgical management of coronary artery
arising from the wrong coronary sinus, using standard and novel
approaches. J orac Cardiovasc Surg. 2007;134(5):1171– 8.
10. Krasuski RA, Magyar D, Hart S, Kalahasti V, Lorber R, Hobbs R,
etal. Long- term outcome and impact of surgery on adults with
coronary arteries originating from the opposite coronary cusp.
Circulation. 2011;123(2):154– 62.
11. Sabik JF 3rd, Lytle BW, Blackstone EH, Khan M, Houghtaling PL,
Cosgrove DM. Does competitive ow reduce internal thoracic
artery gra patency? Ann orac Surg. 2003;76(5):1490– 6.
12. Angelini P, Uribe C, Monge J, Tobis JM, Elayda MA, Willerson
JT. Origin of the right coronary artery from the opposite
sinus of Valsalva in adults:characterization by intravascular
ultrasonography at baseline and aer stent angioplasty. Catheter
Cardiovasc Interv. 2015;86(2):199– 208.
13. Rajbanshi BG, Burkhart HM, Scha HV, Daly RC, Phillips SD,
Dearani JA. Surgical strategies for anomalous origin of coronary
artery from pulmonary artery in adults. J orac Cardiovasc
Surg. 2014;148(1):220– 4.
14. Peña E, Nguyen ET, Merchant N, Dennie C. ALCAPA
syndrome:not just a pediatric disease. RadioGraphics.
2009;29(2):553– 65.
15. Williams IA, Gersony WM, Hellenbrand WE. Anomalous
right coronary artery arising from the pulmonary artery:a
report of 7 cases and a review of the literature. Am Heart J.
2006;152(5):1004.e9– 17.
16. Said SM, Burkhart HM, Scha HV, Connolly HM, Phillips SD, Suri
RM, etal. Late outcome of repair of congenital coronary artery stulasa word of caution. J orac Cardiovasc Surg. 2013;145(2):455– 60.
17. Gowda ST, Forbes TJ, Singh H, Kovach JA, Prieto L, Latson LA,
etal. Remodeling and thrombosis following closure of coronary
artery stula with review of management:large distal coronary
artery stula— to close or not to close? Catheter Cardiovasc
Interv. 2013;82(1):132– 42.
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SECTION 9
Coronary artery bypass graing
and other surgery
Section editors:Marc Ruel and David Glineur
65. Coronary artery bypass grafting and mitral valve
surgery 443
Arman Kilic, Robert E.Michler, and Michael A.Acker
66. Combined coronary artery bypass grafting and
aortic valve replacement 451
Christopher Lau and Leonard N.Girardi
67. Coronary artery bypass grafting with the maze
procedure for atrial fibrillation 455
Hoda Javadikasgari and A.Marc Gillinov
68. Coronary artery bypass grafting with
postinfarction ventricular septal defect and
with ventricular pseudoaneurysm 461
Mitesh V.Badiwala
69. Coronary artery bypass grafting with concurrent
transmyocardial laser revascularization 469
Joshua L.Chan and Keith A.Horvath
70. Prior percutaneous coronary intervention and
surgical revascularization 475
Suvitesh Luthra, Sunil K.Ohri, and David P.Taggart
71. Guideline- directed medical therapy in coronary
artery bypass grafting 487
Ana- Catarina Pinho- Gomes and David P.Taggart
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65
Coronary artery bypass graing
and mitral valvesurgery
Arman Kilic, Robert E. Michler, and Michael A. Acker
Introduction
Mitral regurgitation (MR) is categorized as either primary or secondary. Primary MR refers to structural or degenerative disease of
the mitral valve or subvalvular apparatus. Secondary MR is related
to functional impairment of the le ventricle from non- ischaemic
or ischaemic causes in which the mitral valve is structurally normal.
Secondary MR in the setting of coronary artery disease is known
as ischaemic mitral regurgitation (IMR). IMR results from wall
motion abnormalities aecting papillary muscle function and location as well as adverse remodelling of the le ventricle with distortion of the ventricle and mitral annulus. ese conditions result
in apical and lateral migration of the papillary muscles and associated tethering forces that hinder leaet coaptation, thus leading to
regurgitation.
Approximately 50% of all myocardial infarctions are associated
with some degree of IMR. Moreover, 10– 20% of patients with ischaemic heart disease have moderate or severe MR. e development of any degree of MR is associated with a reduction in event- free
survival, an increase in the severity of heart failure, and a doubling
of mortality.
Critical to any discussion of IMR are the indications for surgery, the type of surgery, and the specic operative techniques for
addressing the mitral valve. In the setting of moderate IMR, an essential decision point is whether coronary artery bypass graing
(CABG) alone will be sucient to correct the MR or whether additional surgical intervention is required for the mitral valve. In severe IMR, the controversy is centred on whether mitral valve repair
or replacement is the better surgical therapy. ese points will be
discussed in further detail in this chapter.
Indications forsurgicalintervention
Although the data are clear that the presence of IMR is associated
with worse survival when compared to coronary artery disease patients without IMR, it is unclear if this association is a result of the
clinical sequelae of IMR itself or if the presence of IMR is a marker
of more advanced heart failure. In this context, it is also unknown
whether surgically addressing IMR at the time of CABG lessens
symptomatic burden, results in reverse remodelling, improves
quality of life, or improves survival.
e 2014 American Heart Association and American College of
Cardiology Guidelines provide a classIIa (‘should consider’) recommendation for mitral valve surgery in patients with chronic severe IMR who are undergoing CABG (Fig. 65.1). In the opinion
of these authors, this classIIa recommendation is insucient and
the mitral valve ‘must’ be addressed at the time of CABG, preferably
with mitral valve replacement. In addition, the European Society of
Cardiology and European Association for Cardio- oracic Surgery
Guidelines from 2017 provide a classIrecommendation for surgery
in severe IMR at the time of CABG in patients with a le ventricular
ejection fraction greater than 30%. ese guidelines also make a
classIIa recommendation for mitral valve surgery in patients with
symptomatic severe IMR with an ejection fraction less than 30%
but with an option for revascularization and evidence of myocardial viability. AclassIIb recommendation is made for considering
mitral valve surgery in patients in whom revascularization is not indicated, but who have severe IMR with an ejection fraction greater
than 30% and remain symptomatic despite optimal medical therapy
and have low surgical risk. e 2018 European guidelines on myocardial revascularization provide a recommendation for mitral valve
surgery in the setting of severe IMR. ese more recent guidelines,
however, suggest that no rm conclusions can be drawn for moderate IMR particularly in the setting of an eective regurgitant orice area of greater than 0.2cm and regurgitant volume greater
than 30 mL, where the decision to add mitral valve repair to CABG
should be made on a case- by- case basis and discussed in a Heart
Team format.
e 2014 American Heart Association and American College of
Cardiology guidelines provide a classIIb (‘could consider’) recommendation for mitral valve repair in moderate IMR at the time of
CABG. ese authors agree with a classIIa ‘should consider’ recommendation in this clinical circumstance. Further details regarding
operative indications in the setting of moderate and severe IMR are
provided later in this chapter.
SECTION 9 Coronary artery bypass grafting and other surgery444
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Severe MR
Vena contracta ≥0.7 cm
RVol ≥60 mL
RF ≥50%
ERO ≥0.4 cm
LV dilation
Symptomatic
(stage D)
LVEF >30%
YES
NO
Primary MR
2
LVEF 30% to ≤60%
or LVESD ≥40 mm
(stage C2)
Asymptomatic
(stage C)
LVEF >60% and
LVESD <40 mm
(stage C1)
Likelihood of successful
Expected mortality <1%
Mitral Regurgitation
New onset AF or
PASP >50 mm Hg
(stage C1)
repair >95% and
YES NO
Progressive MR
(stage B)
Vena contracta <0.7 cm
RVol <60 mL
RF <50%
ERO <0.4 cm
2
Symptomatic
severe MR
(stage D)
Persistent NYHA
class III-IV
symptoms
Secondary MR
CAD Rx
HF Rx
Consider CRT
Asymptomatic
severe MR
(stage C)
Class I
Class IIa
Class IIb
Progressive
MR
(stage B)
MV Surgery*
(IIb)
MV Surgery*
(I)
MV Repair
(IIa)
Periodic Monitoring
MV Surgery*
(IIb)
Periodic Monitoring
Fig.65.1 Surgical indications for mitral regurgitation. *Mitral valve repair is preferred over mitral valve replacement when possible. AF, atrial
fibrillation; CAD, coronary artery disease; CRT, cardiac resynchronization therapy; ERO, effective regurgitant orifice; HF, heart failure; LV, left
ventricular; LVEF, left ventricular ejection fraction:LVESD, left ventricular end- systolic dimension; MR, mitral regurgitation, MV, mitral valve; MVR,
mitral valve replacement:NYHA, NewYork Heart Association:PASP, pulmonary artery systolic pressure:RF, regurgitant fraction; RVol, regurgitant
volume; Rx, therapy.
Reproduced from Nishimura RA etal. 2014 AHA/ ACC guideline for the management of patients with valvular heart disease:a report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines. Circulation 2014; 129:e521– 643 with permission from Wolters Kluwer.
Operativetechniques
When indicated, the operative sequence for combined CABG and
mitral valve surgery is generally well scripted. As with all open cardiac
surgery and in particular with the mitral valve, the transoesophageal
echocardiogram is essential and may reveal ndings discordant with
the preoperative transthoracic echocardiogram. Important echocardiographic variables that are evaluated and can aid in the decision of
repair versus replacement include leaet length, tenting area, leaet
angles, apical displacement of the coaptation point, lateral and posterior displacement of the papillary muscles, and direction of the
regurgitant jet. Asimple assessment incorporates the severity of
posterior papillary muscle tethering, and in cases where there is signicant tethering and in particular when it is accompanied with a
posteriorly directed jet, replacement is typically preferred.
Aortic and bicaval cannulation is performed with an antegrade
cardioplegia and root vent catheter placed into the ascending aorta.
Many surgeons will also utilize retrograde cardioplegia. e distal
coronary anastomoses including those utilizing the le internal
thoracic artery are generally performed prior to the mitral valve
surgery. e choice of conduit for revascularization in this setting
is based on surgeon preference as well as patient characteristics
such as age and presence of diabetes or obesity, with some surgeons
utilizing a vein conduit to the circumex artery distribution and
others utilizing an arterial conduit such as the internal thoracic artery or the radial artery. One approach is to use vein conduit unless
the patient is under the age of 65years. In these younger patients, a
right internal thoracic artery either in situ that is brought through
the transverse sinus, or taken as a free conduit, is anastomosed to
the circumex distribution. Some surgeons prefer to use the radial
artery in this circumstance, and in particular for obese patients or
those with diabetes who are at higher risk of sternal wound issues
from a bilateral thoracic artery harvest. Exposure of the mitral valve
is then achieved via a le atriotomy through the interatrial groove or
a transseptal approach.
By denition, mitral valve analysis will reveal structurally
normal mitral valve leaets and chords in IMR, and oen, dipping
of a P3 scallop secondary to tethering of the leaet. Correction of
IMR is completed either by mitral valve repair using a restrictive
65 Coronary artery bypass grafting and mitral valvesurgery 445
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annuloplasty with or without papillary muscle sling or mitral
valve replacement. Apapillary muscle sling is typically performed
by inserting a Gore- Tex® gra around the bases of the papillary
muscles and then approximating the edges of the sling tightly.
is forms an intraventricular ring that once tightened, allows
for close approximation and juxtaposition of the papillary muscles. Following mitral valve surgery, the proximal anastomoses
are completed. In patients with atrial brillation, an ablation procedure and le atrial appendage ligation can also be performed
when technically feasible.
In performance of mitral valve repair, Bolling popularized the
concept of a restrictive annuloplasty with undersizing of the mitral
ring by at least one size below the standard measurement. Asize 26
or 28 ring usually suces for the majority of patients. Akey technical concept is in the type of ring that is used for IMR. It is now
generally accepted that the intertrigonal anterior brous portion of
the mitral valve dilates proportionally with the posterior annulus.
However, the greater circumference of dilation is in the posterior
annulus. erefore, partial or exible bands are not sucient to treat
IMR, oen resulting in residual functional MR and inhibiting reverse le ventricular remodelling. Small rigid and complete rings
are the preferred ring type to treat IMR. e absence of MR on
intraoperative transoesophageal echocardiogram aer separation
from cardiopulmonary bypass, and a zone of leaet coaptation
of 8– 10mm or greater mark a successful mitral valve restrictive
annuloplasty in IMR.
We recommend a complete chordal- sparing replacement of the
mitral valve for IMR when mitral valve replacement is the planned
operation. e rationale for this recommendation lies in the importance of maintaining the integrity of the mitral axis (valve leaets,
chords, papillary muscles, le ventricle) and its favourable impact
on le ventricular function in patients with IMR. Evidence from a
recent randomized controlled trial conrmed the benecial eects
of complete chordal- sparing mitral valve replacement compared to
partial chordal- sparing mitral valve replacement in IMR. Asimplied technique for complete chordal- sparing mitral valve replacement entails bisecting the anterior leaet, rotation of the leaet
tissue to the le and right, and placement of annular pledgeted sutures through the leading edge of the anterior leaet. e posterior
leaet tissue is usually generous and its leading edge can readily be
sutured in continuity with the pledgeted sutures placed through the
posterior annulus— tucking the chordal apparatus and leaets behind the prosthetic valve annulus.
Moderate ischaemic mitralregurgitation
e surgical treatment of moderate IMR is increasingly controversial, with approximately equal numbers of patients treated in
the United States with either combined CABG and mitral valve
repair/ replacement, or with CABG alone.– Operative mortality
for CABG as well as for CABG combined with mitral valve repair
has declined steadily over the past decade, but the additional aortic
cross- clamp time and cardiopulmonary bypass time associated with
the performance of mitral valve repair increases the risk of the combined procedure. erefore, selection of the appropriate patients is
imperative to ensure that the trade- o of the additional risk of mitral valve repair is necessary and provides additional short- and/ or
long- term benet.
Proponents for treating moderate ischaemic IMR with
revascularization alone argue that revascularization improves regional contractility and restores mitral valve– papillary muscle continuity, thus normalizing mitral valve function. On the other hand,
proponents for a more aggressive treatment strategy cite the negative consequences of ongoing IMR. Myocardial revascularization
alone may be insucient to restore normal ventricular physiology
once IMR develops. Correction of IMR may prevent progressive adverse remodelling and may improve cardiac function and attenuate
the risk of heart failure.
Until recently, evidence addressing treatment decisions for IMR
has been limited to small single- centre randomized trials, observational studies, and case series, where correction for signicant and
substantial imbalances in baseline patient characteristics is problematic, making it dicult to develop a clear understanding of appropriate treatment options.– ese studies were also limited by
variable denitions of the severity and aetiology of IMR, surgical
repair techniques, potential publication bias, limited patient followup, and lack of information on key secondary outcomes such as
quality of life.
e tide of understanding may now be growing clearer in the management of moderate IMR following the publication of three recent
randomized clinical trials. Atrial of moderate IMR by Fattouch and
colleagues, the Randomized Ischemic Mitral Evaluation (RIME)
trial, and the National Heart, Lung, and Blood Institute’s (NHLBI)sponsored Cardiothoracic Surgical Clinical Trials Network (CTSN)
moderate IMR trial. In all three of these trials, the mitral valve repair procedure performed was specically a restrictive annuloplasty.
Fattouch and colleagues randomized patients with moderate IMR
to CABG alone (n=54) or CABG plus mitral valve repair (n=48).
e mean follow- up was 32 ± 18months. Survival rates at 5years
were comparable at 88.8% versus 93.7% for CABG versus CABG
plus mitral valve repair, respectively. Importantly, the CABG plus
mitral valve repair group experienced a statistically signicant reduction in mean NewYork Heart Association class, le ventricular
end- diastolic dimension, le ventricular end- systolic dimension,
le atrial size, systolic pulmonary artery pressure, and grade of MR.
e RIME trial randomized 73 patients with moderate IMR (mean
eective regurgitant orice approximately 0.2cm) and a le ventricular ejection fraction greater than 30% to receive CABG alone
(39 patients) or CABG plus mitral valve repair (34 patients). e
study was discontinued aer review of the interim data revealed an
overwhelming benet for patients randomized to CABG plus mitral
valve repair. At 1year, the CABG plus mitral valve repair group compared to the CABG group demonstrated a marked improvement in
the primary end point of peak oxygen consumption (3.3 mL/ kg/ min
vs 0.8 mL/ kg/ min; P <0.001), le ventricular end- systolic volume
index (LVESVI; 22.2 mL/ m versus 4.4 mL/ m; P <0.002), mitral
regurgitant volume (28.2 mL/ beat vs 9.2 mL/ beat; P=0.001), and
plasma B- type natriuretic peptide (557.4 pg/ mL vs 394.7 pg/ mL;
P=0.003). ese benets for the CABG plus mitral valve repair
group were seen at the expense of longer operative times, and increased blood transfusion, intubation duration, and hospital length
of stay compared to CABG alone. ere was no statistically signicant dierence in mortality at 30days (3% vs 3%) and 1year (3%
vs 9%) between CABG plus mitral valve repair versus CABG alone
groups. erefore, the benet of adding mitral valve repair to CABG
SECTION 9 Coronary artery bypass grafting and other surgery446
(a) Death
CABG+MV repair
150
123
117
106
64
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appears to be an improvement in functional capacity as measured by
peak oxygen consumption, reverse remodelling, and MR severity.
e sustainability of these improvements and long- term outcomes
remain to be conrmed.
e CTSN trial compared 2- year outcomes between CABG alone
(n=151) and CABG plus mitral valve repair (n=151) in patients
with moderate IMR. e primary outcome was le ventricular remodelling as measured by LVESVI. Secondary outcomes included
a composite end point of major adverse cardiac or cerebrovascular
events, mortality, serious adverse events, residual MR, quality of life,
rehospitalization, and functional status. At 2- year follow- up, there
were no dierences between the cohorts with respect to a decrease
in LVESVI, or in other words, reverse remodelling. e rate of moderate or severe MR persistence or recurrence at 2years was higher
in the CABG alone group versus the CABG plus mitral valve repair
group:32.3% versus 11.2%, respectively (P <0.001). Other secondary
outcomes, including mortality, rehospitalization, and serious adverse events were comparable between the two groups (Fig. 65.2).
e authors concluded that there were no signicant improvements
100
Hazard ratio, 0.90 (95% Cl, 0.45–1.83)
90
P = 0.78
80
70
60
50
40
Patients (%)
30
20
CABG alone
10
0
0612
No. at risk
CABG alone
CABG+MV repair
151
150
138
142
in symptoms, major adverse events, survival, le ventricular reverse
remodelling, or ejection fraction with the addition of mitral valve
repair. ere was a signicant improvement in mitral valve regurgitation grade with the addition of mitral valve repair at 2years.
Interestingly, in both treatment groups an improvement in regional
wall motion in the inferior– posterior– lateral walls correlated with
a reduction in MR leading the authors to suspect the presence of
hibernating myocardium in the patients enrolled in the trial.
Important ndings from these randomized trials are discordant
and necessitate a careful examination of dierences in the enrolment
criteria, denitions of MR grade, and types of patients enrolled in
the three trials. For example, CABG alone may be sucient in patients similar to those enrolled in the CTSN trial. is includes patients with similar demographics (e.g. average age around 65years),
mildly reduced le ventricular ejection fraction (approximately
40%), non- severely dilated le ventricles, and, very importantly, reversible ischaemia where improvement in regional wall motion by
CABG appears to re- establish papillary muscle function and position resulting in an improvement in MR. In CTSN- like patients,
CABG + MV repair
18 24
Month
132
136
117
126
66
80
Fig.65.2 Rates of death and major cardiac and cerebrovascular adverse events in the CTSN moderate IMR randomized trial.
Source data from Michler RE etal. Two- year outcomes of surgical treatment of moderate ischemic mitral regurgitation. N Engl J Med 2016;374:1932– 41.
(b) Major adverse cardiac or cerebrovascular event
100
Hazard ratio, 0.89 (95% Cl, 0.60–1.34)
90
P = 0.58
80
70
60
50
40
Patients (%)
30
CABG
20
alone
No. at risk
CABG alone
10
0
0612
151
CABG + MV repair
121
Month
113
18 24
96
53
65 Coronary artery bypass grafting and mitral valvesurgery 447
70
Patients (%)
24-month visit
Replacemen
Replacemen
Replacemen
Replacemen
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relief of moderate IMR will occur in about 70% of patients, and in
the remaining patients, persistent MR is only moderate in severity
and well tolerated clinically. Progression to severe IMR did not occur
at 2years in patients treated with the addition of mitral valve repair.
In the trial by Fattouch etal. and RIME, the ventricles were larger
at baseline compared to CTSN- like patients and this alone may have
inuenced the benet seen in these two trials with respect to MR
grade, NewYork Heart Association class, reverse remodelling, and
symptoms.
Based on these trials, we recommend mitral valve repair in addition to CABG in patients with moderate IMR who have a large
ventricle (le ventricular end- diastolic dimension >55 mm or
LVESVI >50 mL/ m). Furthermore, concomitant mitral valve repair should be performed when the le ventricular ejection fraction is 35% or less, there are poor coronary bypass targets in the
posterior descending coronary or circumex coronary distributions
(inferior– posterior– lateral walls), there is posterior or inferolateral
le ventricular wall scarring, or a basal aneurysm or dyskinesia.
Further support for these recommendations comes from a study
of 135 patients with moderate IMR where the authors identied
predictors of improvement of MR in unrepaired moderate IMR in
patients undergoing CABG alone. ese predictors included the
identication of a large extent of viable myocardium and the absence
of dyssynchrony between the anterior/ lateral and posterior/ medial
papillary muscles. In patients meeting both of these criteria, 93%
showed an improvement in IMR with CABG alone.
In the setting of moderate IMR, treatment paradigms are easily biased and may in some instances lead to a premature or delayed recommendation for mitral valve repair surgery. Based on the current
literature and as active participants in clinical trials of IMR, these authors are condent in making these recommendations and remain
open to new evidence to adjust current treatment algorithms.
Severe ischaemic mitralregurgitation
Unlike moderate IMR, the crux of the controversy in severe IMR is
whether to repair or replace the mitral valve in addition to coronary
revascularization. Mitral valve repair is generally associated with
lower operative morbidity and mortality; however, MR recurrence
rates as high as 30– 40% in the setting of IMR have been demonstrated. Mitral valve replacement, while more eectively and durably
addressing mitral valve regurgitation, is associated with greater operative risk, and greater long- term risks of thromboembolism, valve
deterioration, and endocarditis.
e landmark CTSN trial for severe IMR sought to address this
controversy., Atotal of 251 patients with severe IMR were randomly assigned to mitral valve repair or chordal- sparing mitral valve
replacement. e primary end point was LVESVI at 12months.
e study demonstrated no signicant dierences in the primary
end point at 12- month follow- up. Furthermore, rates of death were
comparable at 14.3% in the repair group and 17.6% in the replacement group. ere were also no signicant dierences between the
study cohorts with respect to functional status, quality of life, or
major adverse cardiac or cerebrovascular events at 12months. Rates
of recurrent moderate or severe MR were substantially higher in the
repair group at 32.6% versus only 2.3% in the replacement group (P
<0.001). Collectively, these data supported the use of mitral valve
replacement in the setting of severe IMR.
A 2- year follow- up was performed for the same randomized
trial. Again, there were comparable decreases in LVESVI between the repair and replacement cohorts. Two- year mortality
was also similar at 19.0% and 23.2% in the repair and replacement
groups, respectively. Similar to the 1- year results, the recurrence
rate of moderate or severe mitral valve regurgitation was higher
in the repair group at 58.8% versus 3.8% in the replacement group
(P <0.001) (Fig. 65.3). Although the rate of serious adverse events
and overall hospital readmissions were comparable, patients
undergoing repair had more frequent serious adverse events related to heart failure and cardiovascular readmissions. e 2- year
data from the CTSN severe IMR trial underscored the ndings
of the 1- year analysis, with results that collectively advocate for
mitral valve replacement in the setting of concomitant CABG for
severe IMR.
Fig.65.3 Cumulative failure of mitral valve repair or replacement, as defined by death, moderate or severe mitral valve regurgitation, or mitral valve
reintervention in the 2- year severe IMR CTSN trial.
Source data from Goldstein D etal. Two- year outcomes of surgical treatment of severe ischemic mitral regurgitation. N Engl J Med 2016;374:344– 53.
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6-month visit
Death preceded by
recurrent MR or
reintervention
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by recurrent MR or
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Recurrent MR
or reintervention
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12-month visit
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