mitral stenosis review

7/23/2019 Mitral Stenosis Review

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www.thelancet.com Vol 374 October 10, 2009 1271

Mitral stenosis

Y Chandrashekhar, Stephen Westaby, Jagat Narula

Mitral stenosis is a common disease that causes substantial morbidity worldwide. The disease is most prevalent indeveloping countries, but is increasingly being identified in an atypical form in developed countries. All treatmentsthat increase valve area improve morbidity. Mortality improves with surgery; the benefit of percutaneous balloonvalvuloplasty to mortality might be similar to that of surgery but needs further study. Percutaneous balloon valvuloplastyis the treatment of choice for patients in whom treatment is indicated, except for those with suboptimum valvemorphology, and even these patients are sometimes treated with this procedure if surgery is not feasible or if surgicalrisk is prohibitive. We review the pathology, diagnosis, and treatment options for patients with mitral stenosis.

IntroductionAlthough mitral stenosis is now rare in developedcountries, it has been recognised for more than300 yearsVieussens described the disease in 1705and

has provided major milestones in cardiology. It was thefirst disease to be diagnosed with echocardiography,1andthe first valve lesion to be successfully treated by surgery2or percutaneous balloon valvuloplasty (PBV).3 Mitralstenosis remains an important cause of morbidity despitethe ease with which it can be diagnosed and treated.

Mitrial stenosis is highly prevalent in developingcountries4because of its association with the prevalence ofrheumatic fever, but is also seen in developed countries.5Patients often have distinct social and demographicindicators dependent on their country of residence: indeveloping countries, patients tend to be young with apliable valve,6whereas in developed countries patients areof increased age with several comorbidities.7,8

EpidemiologyTwo-thirds of the worlds population live in developingcountries with a high prevalence of rheumatic fever orrheumatic heart disease (eg, 6 per 1000 schoolchildren inIndia vs05 per 1000 in developed countries4), resultingin a large population with mitral stenosis. In a survey ofrheumatic fever in India,4the mean age of presentationwas 151 years (SD 44), and two-thirds of the participantshad signs of mitral stenosis, of whom half had limitingsymptoms. Up to 30 million schoolchildren and youngadults have chronic rheumatic heart disease worldwide,and nearly a third of these also have mitral stenosis.9,10

Progression of mitral stenosis in developing countries

is malignant and intervention is often necessary duringteenage years.11 In developed countries,7 prevalencedetected by echocardiography is about 00202%. 12Thenatural history is distorted by a predominance of data

from PBV centres in developed countries becausepatients from these centres are older than are patientsin developing countries, have comorbidities,13and havesuboptimum outcome with interventions (table).21,22

AetiologyAlthough mitral stenosis most frequently followsrheumatic fever, fewer than half of affected patientsremember having rheumatic fever. Persistent inflam-matory valve damage23 and haemodynamic injury con-tribute to gradual progression; the rate of progressionand time to clinical detection is strongly associated withrepeated episodes of rheumatic fever.24This correlationcould partly explain the different natural history of mitralstenosis across the world.10,24,25

Degenerative causes are common in developedcountries (eg, 125% in Euro Heart Survey7). In 68% ofpatients with severe mitral annular calcification, who are

often elderly or dialysis-dependent, calcium encroachinginto the valve leaflets causes mitral stenosis. 26For thesepatients, physical findings are atypical and surgicaloptions are often unattractive.

Other rare causes are congenital deformities, whichoften present very early in infancy or childhood (eg,parachute mitral valve, double orifice mitral valve, supramitral ring27); infiltrating diseases (eg, mucopoly-saccharidosis); diseases affecting multiple systems (eg,Fabrys disease, systemic lupus erythematosus, andrheumatoid arthritis), but this cause is very rare; valvestenosis after mitral valve repair; and disorders associatedwith abnormal serotonin metabolism (eg, carcinoid andmethysergide treatment).

PathologyThe main features are leaflet thickening, nodularity, andcommissural fusion, all of which result in narrowing ofthe valve to the shape of a fish mouth (figure 1). 28Theleaflets might be calcified. Chordal fusion and shorteningadds a further resistance to blood flow. Continuedinflammation, injury, and repair affect the effectivenessof treatment, and treatments are tailored to target thesefeatures of disease.29,30

Whether left-ventricular systolic function is trulyreduced in patients with mitral stenosis and the clinicalsignificance of reduction is unknown. A third of patients

Lancet2009; 374: 127183

Published Online

September 10, 2009

DOI:10.1016/S0140-

6736(09)60994-6

Veterans Affairs Medical Center

and University of Minnesota,

Minneapolis, MN, USA

(Prof Y Chandrashekhar MD);

Oxford University, Oxford, UK

(Prof S Westaby MS); and

University of California, Irvine,

CA, USA (Prof J Narula MD)

Correspondence to:

Prof Y Chandrashekhar,

University of Minnesota, Division

of Cardiology (111c), VA Medical

Center, 1 Veterans Drive,

Minneapolis, MN 554 17, USA

[email protected]

Search strategy and selection criteria

We searched Medline for original articles published in English

between January, 1970, and March, 2008, using the root

search term mitral stenosis. We checked reference lists of

selected articles for further relevant articles. Only directly

relevant articles are included in the reference list of this report.


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1272 www.thelancet.com Vol 374 October 10, 2009

have some systolic dysfunction probably due to internal

constraint from a combination of a rigid mitral valve,31

reduced preload,32 and a reflex increase in afterload.33Although early studies have not found load-independentleft-ventricular contractile dysfunction,34 strain-rateimaging might show impaired long-axis function despitenormal global systolic function.35 Some patients mighthave systolic dysfunction that is not dependent on lowpreload.36 Successful PBV is not associated with clinicallysignificant changes in left-ventricular function, end-systolic wall stress, or preload-corrected ejection-fractionafterload relation,33except in rare reports.37 Low ejectionfraction does not seem to affect operative outcome.36

Diastolic function in patients with mitral stenosis is lesswell studied than systolic function is, but chamber

compliance is abnormal31

and superimposed diastolicdysfunction can negate the filling benefit of early diastolicsuction.38 Increased left-ventricular end-diastolic pressurecorrelates with poor outcome after PBV.39,40 Right-ventricular function is often reduced because of pulmonaryarterial hypertension, and affects prognosis for mitralvalve disease.41 Despite prompt reduction in pulmonaryhypertension after valvuloplasty, improvement of theright-ventricular ejection fraction can be slow.42 The leftatrium is stiffer (large V wave, which affects pulmonaryarterial pressure43 and exercise capacity44) with reducedsystolic flow and pump dysfunction proportional to theseverity of mitral stenosis.45 Atrial fibrillation worsens

stiffness and left-atrialfunction, which PBV can improve,46

but not entirely.47

Unlike aortic stenosis, the stenotic mitral valve behaveslike a fixed orifice despite changes in flow and pressure48

with exercise or dobutamine.49 Thus, patients with severemitral stenosis have little functional reserve and easilydecompensate with tachycardia or high flow. However,the valve does regain some valve reserve (increased sizewith increased flow) after PBV.

Procoagulation abnormalities that are common inmitral stenosis are changes in platelet activity; increasedconcentration of fibrinopeptide A, thrombin-antithrombinIII complex, and D-dimer; and changes in fibrinolyticactivity. These changes have most obvious effects in theleft atrium, probably originate in the left atrium or

hypertensive pulmonary circulation, and are correlatedpoorly with disease severity.50Atrial fibrillation might alsocreate or worsen many of these abnormalities. Anti-coagulation and PBV reduce hypercoagulability, whichmight partly explain the possible reduction of strokesafter valvuloplasty.51

PathophysiologyThe normal mitral valve area is 46 cm and a gradient israre unless the valve is less than 2 cm. Pathophysiology isclosely related to the amount of diastolic flow across thevalve and the diastolic filling period (figures 2 and 3).Generally, symptoms of dyspnoea correlate with increasing

Kothari et al

(1998)14Gamra et al

(2003)15Arora et al

(2002)16John et al

(1983)17*

Chen et al

(1995)18Iung et al

(2004)8Palacios et al

(2002)19Shaw et al

(2003)20

Country India Tunisia India India China France USA UK

Women 68% 46% 70% 80% 82% 95%

Age (years) 11 (12) 16 (28) 272 (112) 273 (93) 368 (123) 47 (15) 55 (15) 76 (44)

NYHA stage II 29% 555% 28% 241%

NYHA stage III 64% 575% 388% 67% 612%

NYHA stage IV 6% 69% 875% 415% 56% 35% 133%

Previous

commissurotomy

0% 136% 42% 156% 24% 18%

Previous embolism 11% 144% 95%

Atrial fibrillation 0% 6% 145% 125% 272% 31% 50% 85%

Calcified valve 21% 153% 31% 27% 10%

Mitral valve area (cm) 066 (004) 063 (01) 07 (02) 05 () 11 (03) 103 (023) 09 (03) 086 (027)

Mitral gradient (mm Hg) 243 (77) 23 (8) 295 (7) 183 (51) 103 (46) 14 (6) 114 (47)

Grade 2 mitral

regurgitation

09% 189% 128% 132% 26% 65%

Low ejection fraction 13%

Coronary artery disease 38%

Aortic valve involvement 133% 127% 155% 171% 23%||

Left-atrial thrombus 18%

Suitability for mitral

valve replacement

40%

Data are number of patients (%) or mean (SD). =data unavailable. NYHA=New York Heart Association stage of disease. *Surgical series from 1980s for comparison with more recent data. Data for NYHA stages

III and IV. Grades 34. Less than grade 3. Aortic regurgitation. ||Aortic stenosis.

Table:Range of patients with mitral stenosis treated by percutaneous balloon valvuloplasty


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mean left-atrial pressure, which is inversely related to RRinterval (figure 3). Atrial contraction helps to maintainflow across the stenotic mitral valve; atrial fibrillation,which is associated with tachycardia, irregular RR interval,and lack of atrial contraction, is often an importantprecipitating factor for symptoms of dyspnoea.

Symptoms start when mitral valve area (normally morethan 4 cm) reduces to 15 cm, and most patients haveobvious symptoms when the area is less than 1 cm(figure 3). Pulmonary oedema is rare but possible withmitral valve area of more than 1 cm, and affected patientsare treated as for severe mitral stenosis. Atrial fibrillation,anaemia, pregnancy, and infection can create discordancebetween symptoms and mitral valve area. Severity ofdyspnoea is associated with lung water,52and symptomaticrelief is achieved with decreased lung water53rather than

haemodynamic changes alone.54

Patients with persistentsevere mitral stenosis develop compensatory changes(eg, pulmonary arterial hypertension, dilated lymphaticvessels, and alveolar thickening) that moderate symptomsfor a short period. Left-atrial and left-ventricularcompliance changes due to age and pulmonary arterialhypertension can also affect symptoms and exercisecapacity.43,55,56

Clinical presentationPatients usually present with dyspnoea, often duringexercise or in combination with disorders that increaseheart rate or flow across the mitral valve.57,58The valve areanarrows gradually by 0103 cm per year,59 which

explains the variable onset of symptoms. The diseasecourse is accelerated in populations with recurrentrheumatic fever, in which the natural history is compressedto 510 years. Clinical presentation is affected by age-related comorbidities such as systemic hypertension,coronary artery disease, and diastolic dysfunction.60Frequency of adverse events increases with the onset oflimiting symptoms or substantial pulmonary arterialhypertension in the presence of severe mitral stenosis.

Other rare symptoms include haemoptysis, chest pain(often due to pulmonary hypertension), and pressureeffects on adjacent structures, for example from a dilatedleft atrium. Atypical presentations include fatigue(spontaneous or with diuresis) with a low transmitral

gradient61

and a syndrome of right heart failure withsevere pulmonary arterial hypertension. Patients withpulmonary oedema rarely have severe pulmonaryarterial hypertension, whereas those with severe hyper-tension (pulmonary vascular resistance >68 Woodunits) seem to present with right heart failure58 ratherthan pulmonary oedema. Occasionally, patients firstpresent with embolic episodes related mostly to atrialfibrillation, or very rarely while in sinus rhythm. Deathis mainly due to heart failure or systemic embolism.57,58Left-atrial myxoma, ball-valve thrombus, and cortriatriatum can be clinically mistaken as mitral stenosisand should be carefully excluded.

DiagnosisPhysical signs of mitral stenosis have been welldocumented.58 Moderate-to-severe disease is easilydiagnosed by auscultation in the left-lateral position or

after mild exercise, unless the patient has unfavourablebody habitus (severe obesity or chronic obstructivepulmonary disease), pulmonary oedema, very low cardiacoutput, or rapid atrial fibrillation. Diagnostic sensitivityand specificity is about 85% and accuracy is similar tothat of echocardiography (92% vs97%).62

Clinical issues that need to be addressed includeseverity of disease, pliability of the valve, extent of mitralregurgitation and pulmonary arterial hypertension, andpresence of atrial fibrillation. At present, severity ofdisease is assessed from symptoms (eg, shortness ofbreath, exercise intolerance), presence of long murmur(especially with presystolic accentuation in normal sinusrhythm or during long RR intervals in atrial fibrillation),

short interval of A2 to opening snap (OS), and signs ofpulmonary arterial hypertension or right ventricleoverload. Pliability of the valve is assessed from loud S1and prominent OS. Two useful assessment methods areelectrocardiography, which most commonly shows left-atrial enlargement and right-ventricle pressure overload,often with atrial fibrillation, and chest radiography, whichshows left-atrial enlargement, pulmonary arterialhypertension, and pulmonary congestion. However,imaging is the mainstay of diagnosis and treatmentselection (figure 4).

Echocardiography is used to diagnose and judge stage ofdisease, assess mitral regurgitation, exclude conditions

Figure :Pathological specimens of the mitral valve in mitral stenosis

Thickened, rigid, nodular appearance of the mitral valve leaflets viewed from the atria (A) and ventricle (B). Calcium

is present in commissural ends of the valve, and the commissures are fused resulting in a valve shaped like a fish

mouth. Subvalvular apparatus is thick, fused, and shortened (B, C). Healthy mitral valve leaflets (D).

A

C

B

D


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that mimic mitral stenosis, and provide information aboutsuitability for PBV (low echocardiography score,69absenceof commissural calcium70). Both valve area and gradientcan be accurately measured, but several measurementswith more than one method are often needed to accuratelyestimate haemodynamics of the mitral valve.48,71,72The mostreliable method to calculate valve area is planimetry with2D echocardiographycross-section images, and even morereliability might be achieved with 3D echocardiography.However, 2D echocardiography underestimates theseverity of mitral stenosis, especially moderate-to-severe

disease, in up to half of patients also examined with3D guided echocardiography,73,74 and underestimates theextent of commissural splitting by PBV.

Another common assessment method for mitral valvearea is pressure half-timethe time taken for thepressure to halve from the peak valuewhich is mosteffective for the native valve before surgical intervention.However, this method is affected by left-ventricularchamber compliance, left-ventricular chamber relaxationprofile, and heart rate; rarely, the mitral valve area can berecorded as normal even with clear valve obstruction.

Figure :Echocardiogram of mitral stenosis

Main resistance to flow is at the valve opening with contribution from the subvalvular apparatus. In the valve with mitral stenosis, anterior mitral leaflet (AML) and posterior mitral leaflet (PML) are thick

and move as a unit (A, C), whereas in the normal valve, AML and PML move separately (B, D) and have a mid-diastolic inward motion (arrow, B) that is decreased in mitral stenosis (arrow, A). Valve with

mitral stenosis is affected by variation in filling time corresponding to cycle lengths in atrial fibrillation (A) with a shorter filling time indicating higher gradients. The AML is thick and domes (arrow, E)

because of fusion at the commissural tips, that is absent in the normal valve (arrow, F). The flow channel is constricted and blood flow rushing into this narrow path results in a series of higher velocity

shells (G) unlike smooth, non-restrictive flow normally (H). The shell velocity and diameter are useful for calculation of valve area. Plotting velocities along a linear line through the mitral valve shows the

long length of turbulent flow with slow progression of the velocity fronts in mitral stenosis (G) unlike a smoother propagation in a normal valve (H); the difference in propagation is clear from doppler

waveforms (I, J, K, L). In a healthy valve (L), a sharp, narrow forward wave (E wave) with rapid up and down stroke precedes a period of diastases with low gradient between the left atrium and ventricle

because of mid-diastolic inward motion (B, D) and increased forward velocities due to atrial contraction (A wave). Increasing severity of mitral stenosis obliterates the normal mitral valve leaflet motion

(C vsD), and reduces E wave deceleration (K), and diastases (indicating persisting left-atrial to left-ventricle gradient). E wave deceleration is proportional to the severity of mitral stenosis, and therefore

the time for pressure to halve from the peak (pressure half-time) can be used to calculate valve area. The A wave contributes less to ventricular filling but still remains important since it allows filling with

less increase in mean gradient (pre-systolic accentuation of murmur). A wave is lost in atrial fibrillation, resulting in further increase in left-atrial pressure and mean gradient to allow left-ventricle filling.

LV=left ventricle. LA=left atrium.

Valve in mitral stenosis Healthy valve

AML

AML

PML

PML

LV

LV

LA

LALA

A

C

E

G

I

K

B

D

F

H

J

L


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Transoesophageal echocardiography provides animproved image of the anatomy, especially the com-missural anatomy and calcification, and additionalprognostic information. Cardiologists judge trans-oesophageal echocardiography to be nearly mandatory, iffeasible, before PBV, and is the only practically effi cientmethod to exclude the possibility of a clot in the leftatrium or in the left-atrial appendage.

Exercise echocardiography is occasionally needed for

patients with inconclusive symptoms or haemodynamics.Exercise can quantify haemodynamics or mitralregurgitation better than resting echocardiography can,assess disease severity in borderline symptomatic patients,and predict benefits from PBV.75 Dobutamine stressechocardiography can predict event rates in symptomaticpatients with moderate disease.76 Use of cardiaccatheterisation is rarely needed with imaging methodsthere are now available; occasionally this technique is usedto assess discrepancies between symptoms andechocardiography findings, or to image coronary arteriesin elderly patients. The role of techniques such as cardiacCT and MRI is being assessed.65,66

Conditions affecting mitral stenosisAtrial fibrillationOnset of atrial fibrillation, which is often caused by atrialinflammation and remodelling, is a pivotal moment inmitral stenosis. Atrial fibrillation occurs in 4075% ofpatients who are symptomatic for mitral stenosis,precipitates such symptoms, greatly increases the risk ofsystemic embolisation, and reduces cardiac output andexercise capacity.77,78 Exercise capacity is substantially

improved by restoration of sinus rhythm,77,78

especially inpatients with small atria and short duration of symptoms.79Maintenance of sinus rhythm is variable across patients,with most80 but not all studies79 showing substantialdiffi culty.

PBV does not seem to affect persistence of atrialfibrillation, but could allow conversion to normal sinusrhythm in suitable patients (left-atrial diameter


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of patients with embolic events 510 years after surgery)after PBV or surgical valvotomy, which necessitates

continuing anticoagulation. Addition of a maze proceduresubstantially reduces risk of embolism potential82 bymaintaining sinus rhythm more effectively.

Pulmonary hypertensionPulmonary arterial hypertension is often found insymptomatic patients with mitral stenosis; it could haveprognostic implications and trigger need for therapeuticinterventions.29Mechanical factors, vascular remodelling,and endothelial changes mediate such hypertension,83andneurohormones might affect the course.84,85 Moderatepulmonary arterial hypertension is often a passiveresponse to left-sided obstruction, and is readily reversed

with surgery or PBV. Most studies,86 but not all,87 showresidual pulmonary arterial pressure of 3040 mm Hg

after PBV. Occasionally, patients with pulmonary arterialhypertension who are hyper-responders present withstructural changes in the pulmonary bed,88 and theirhypertension is disproportionately severe89 and mightincompletely resolve after relief of mitral stenosis.Epoprostenol could have a role in combating pulmonaryarterial hypertension in such patients.90 Some cases ofpulmonary arterial hypertension might also be due toendothelial dysfunction.83,86

Generally, pulmonary arterial hypertension isreversible, and continually resolves after interventionwith increased pulmonary blood flow. The condition canrecur in cases of mitral re-stenosis or substantial mitral

A

E

I J K L

F G H

B C D

0

100

0

Peak E

Peak A

100

300

20 40 60 80 100

Time (% RR)

Pe

akvelocity(cm/s)

LA

LA

15 mm

LV

Figure :Imaging of the mitral valve in mitral stenosis

3D reconstruction from echocardiography images of a normal (A) and stenotic (B) mitral valve, with photomicrograph inset of a stenotic mitral valve from an unrelated patient to show similar valve

appearance. Successful percutaneous balloon valvuloplasty (PBV) splits the commissures (arrows, C), but non-commissural splits result in severe mitral regurgitation (arrow, D). 2D echocardiography

shows all pathological features of mitral stenosis: subvalvular apparatus is thickened and fused and calcium is present in the leaflets (E); left-atrial clot in a transoesophageal 2D echocardiography image

(F). Features in E and especially F make patients unsuitable for PBV. CT angiography can show valve and subvalvular anatomy (G) and can be used to planimeter the valve (H). MRI can show valve

structures in multiple axes (IK) to help make valve area planimetry more accurate (I, J). Flow through the jet is clearly seen (K), and velocity encoding can be used to calculate the pressure half-time (L).

Reproduced with permission from: BMJ Publishing Group (A63); Elsevier (B,64G and H,65I and J,66and K and L67); and Oxford University Press (C and D68). LA=left atrium. LV=left ventricle.


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regurgitation. Moderate-to-severe tricuspid regurgitationis recorded in up to a third of patients with mitral stenosisimmediately preceding PBV. It can be secondary torheumatic disease or severe pulmonary arterial hyper-tension. Tricuspid regurgitation and right-ventricularremodelling is not often improved after PBV.91Surgicalseries of mitral valve replacement also suggest thatrheumatic heart disease and a large left atrium with atrialfibrillation, both of which are present in mitral stenosis,are predictors of persistent tricuspid regurgitation.92Thus, PBV alone might not be suffi cient treatment forpatients with mitral stenosis and severe tricuspidregurgitation.

PregnancyMitral stenosis is one of the most common lesions found

during pregnancy93,94

and the diagnosis is usually madewhen symptoms are precipitated by blood volumechanges, often in the second trimester.95Mitral stenosis inpregnancy is associated with substantial morbidity(including pulmonary oedema), even in asymptomatic orminimally symptomatic patients with mild-to-moderatedisease (mitral valve area 115 cm in 36% of patients;>15 cm in 53%), and despite adequate medicaltreatment. Cardiac complication rates in women withmild, moderate, and severe disease are 26%, 38%, and67%, respectively.96 Many patients with New York HeartAssociation (NYHA) class I or II symptoms also showworsening during pregnancy,97which suggests that earlyaggressive management could be preferable to continuing

prolonged medical management. In India, researchersfound improved outcomes with complications in lessthan a quarter of patients, and only 20% of patientsneeded caesarean section.98

Complications strongly correlate with NYHA class andage.96,98 Maternal death is rare, even in developingcountries. Echocardiographic valve area is a moreconstant value than, and should be used in preference togradient for quantification of disease. Fetal complicationsinclude premature delivery and intrauterine growthretardation, and occur in 20% of pregnancies. Althoughhaemodynamics improve post partum, complicationssuch as pulmonary oedema are highly likely in the earlyperiod after delivery,99 and are probably related to

increased venous return after relief of inferior vena cavacompression.

PBV and surgical valvotomy (closed mitral valvotomy inpreference to methods needing cardiopulmonary bypass)seem to improve outcome,100,101 but surgical series havebeen associated with greater maternal and fetal morbidityand mortality.102 The usual indication that intervention isneeded is the occurrence of severe symptoms (NYHA classIII/IV or pulmonary oedema) that are refractory to medicaltreatment. Results of PBV are largely similar betweenpregnant and non-pregnant patients, although re-stenosishas been recorded in some subsequent pregnancies.98Theeffect of PBV on the fetus is controversialevidence

indicates both benefit103and absence of clear reduction infetal morbidity or prematurity.104

Natural history and prognosis after interventionThe natural history of untreated57,58,105,106 and treateddisease19,107127 has been well characterised. Such studies

have identified some key features about diseaseprogression and treatment (figures 5 and 6). First,progression in countries with recurrences of rheumaticfever tends to be rapid, whereas in those withoutrheumatic fever progression follows an indolent course.Second, all effective treatments that improve valve areareduce morbidity and very probably improve survival.PBV favourably changes the course of disease, and to anincreased extent if the patient is in NYHA class III or IVbefore intervention. Although symptoms improve, theeffect on natural history is less clear in NYHA class IIpatients; intervention very probably improves survival butthis association has not been studied rigorously. Third,although PBV might improve symptoms and mortality,

occurrence of adverse events is substantial and re-intervention is sometimes needed, especially in elderlypatients with less favourable anatomy. Fourth, freedomfrom occurrence of adverse events after PBV differsgreatly worldwide; age and echocardiography score areassociated but are not fully responsible for the difference(figure 6). Fifth, when intervention is needed, PBV ispreferred to surgery because of reduced morbidity andcost. However, unlike studies of PBV, which traditionallyinclude patients who will most likely prove optimum forsuccess, surgical series have often studied both good andsuboptimum patients, according to NHYA class, withgood overall results.

Figure :Natural history of mitral stenosis and effect of intervention

For some studies, percentage of patients with a specific stage of disease, or range of stages, is included.

NYHA=New York Heart Association class of disease. PBV=percutaneous balloon valvuloplasty.

100

80

Patientsurvival(%)

60

40

20

00 5

Follow-up (years)10

NYHA class II: India (1968)127

NYHA class III: Denmark (1962)105

NYHA class IV: Denmark (1962)105

NYHA class IIIIV treatedmedically: Germany (1991)106

NYHA class IIIIV treated bysurgery: Germany (1991)106

NYHA class II (24%)III (61%)treated by PBV: USA (19862000)19

NYHA class II (22%)III (73%)treated by PBV: France (198695)115

NYHA class II (42%)III (44%)treated by PBV: South Korea(198995)128

NYHA class IIIIV (76%) treatedby PBV: USA (198694)40

Open mitral valvotomy129


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Untreated mitral stenosis has a very poor prognosis

once symptoms are evident, and probability of survival isinversely proportional to the severity of NYHA class. Bothclosed and open valvotomy improve prognosis. PBVprobably improves overall survival: survival curves ofpredominantly NYHA class III patients after interventionare close to that of class II patients. Although symptomsimprove in nearly all patients after successful PBV, theeffect on survival is less evident in studies including alarge proportion (up to 4050%) of class II patients. Short-term and medium-term survival after PBV is similar tothat recorded after open valvotomy, albeit with reducedinitial morbidity, but comparison with surgery for verylong-term follow-up is not yet available.

Morbid events such as the need for mitral valve

replacement or re-intervention after re-stenosis are notuncommon after PBV. Echocardiography score, NYHAclass, and especially age affect event-free survival. Age atintervention is closely associated with geographicalregion, which affects prevalence and progression ofdisease, and comorbidities. In developing countrieseg,Tunisia (young patients with low scores) and Saudi Arabia(young patients with high scores)morbid events areless common after PBV than in developed countrieseg,Korea (middle-aged patients with high scores), and Franceand the USA (elderly patients with high scores). Webelieve that valves in countries with many rheumaticfever recurrences develop more commissural fusion than

in countries with few or no recurrences, in which patients

have valves with increased rigidity and participation ofsubvalvular components. Such geographical factors mightaffect results with PBV. Whether an association existsbetween geographical region and the components of theechocardiography score would be interesting to explore.

TreatmentTreatment by drugs or techniques other than surgery orPBV for mitral stenosis is not very effective and thereforeinterventional treatment is preferred except in cases of astrong contraindication. Drugs can be used to slow heartrate, deal with atrial fibrillation, do gentle diuresis, andcorrect secondary conditions such as anaemia, fever,infection, and volume overload. blockers or calcium

channel blockers (eg, diltiazem) are the mainstay forcontrol of heart rate; but blockers might worsen left-atrial appendage function (clinical significance unclear),and drugs that cross the placental barrier (eg, atenolol)during pregnancy have been associated with fetal growthretardation. ACE inhibitors have been tried in patientswith mitral stenosis and heart failure with some,131 butunproven, benefit. In view of the high occurrence ofembolic episodes, suggesting use of prophylactic warfarinin patients with mitral stenosis and normal sinus rhythmis tempting but not a proven treatment. Hypercoagulablepatients with mitral stenosis, patients with mitral stenosisand very large atria containing severe smoke or sludge in

Figure :Event-free patient survival after percutaneous balloon valvuloplasty

For some studies, percentage of patients with a specific stage of disease, or range of stages, is included. Stage of disease was scored by Wilkin score; University of

Southern California (USC) and Iung and colleagues115used separate scoring systems. Event-free patient survival was variably defined for different studies and mainly

included combinations of death, mitral regurgitation, surgery for mitral regurgitation, and re-stenosis and its treatment. NYHA=New York Heart Association class of

disease. PBV=percutaneous balloon valvuloplasty. MVA=mitral valve area.

100

90

80

70

60

50

40

30

20

10

0

0 5Follow-up (years)

Event-freepatientsurvival(%)

10 15

NYHA class III survival with no intervention:Denmark (1962);105 score not available

NYHA class IIIIV (69%) treated by PBV: Tunisia(198799);15 mean age 16 years (SD 28); score: 59

NYHA class IIIIV (89%) treated by PBV: Saudi Arabia(19892003);130 mean age 31 years (SD 11); score:>8 in 63% of patients

NYHA class II (42%)III (44%) treated by PBV:South Korea (198995);128mean age 42 years(SD 11); score: 78

NYHA class IIIIV (76%) treated by PBV: USA(198694);40mean age 44 years (SD 14); USC score:8 (broken line); score:


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images of the left atrium, or patients with a history ofprevious embolism could benefit from anticoagulants,but no data is yet available to support universal recom-

mendation of this approach. Prophylaxis for rheumaticand infective endocarditis prophylaxis should be used onthe basis of present guidelines.

Recommendations about the appropriate time forinterventional treatment29,127,132,133 have classically beensurgery or PBV for symptomatic patients with NYHA classIIIIV disease, and, if feasible, PBV could be considered ifsymptoms are less severe. Other considerations includeoperator skill, valve anatomy, onset of complications evenin absence of symptoms (eg, atrial fibrillation, pulmonaryarterial hypertension, and embolic events), and sometimesexercise haemodynamics (figure 7). Several excellenttreatment algorithms are based on expert opinion andoutline the strategies for treatment,29,126,131,133one of which is

shown in figure 7. In view of the suboptimum outcomewith drug treatment,127 we believe that even class II patientswho are not suitable for PBV should be considered forsurgery in an experienced surgical centre.

SurgerySurgical options include closed or open valvotomy, andmitral valve replacement. Closed valvotomy is mostlydone in developing countries when PBV is not an option;It is effective but less so than other methods. Openvalvotomy allows controlled reconstruction of the valves,and simultaneous tricuspid valve repair or mitral valvereplacement to be done if necessary. In fact data suggest

that patients with mitral stenosis and severe tricuspidregurgitation do better with surgical repair than withPBV; less than 50% of such patients improve with PBV,

especially if they also have atrial fibrillation or a largeright ventricle.134

Mitral valve surgery has similar results to PBV, albeitwith increased cost and morbidity.108 Mitral valvereplacement is a last resort in children, young adults, andwomen contemplating pregnancy, but is the treatment ofchoice in elderly patients with anatomy that isunfavourable for other options. Some risks are specific tomitral valve replacement, which carries higher mortalitythan does aortic valve replacement or mitral valve repair.135Patient prosthesis mismatch prevents regression of left-atrial enlargement and pulmonary arterial hypertension.In one study, 69% of patients were found to havemoderate mismatch and a probability of 6-year survival

of 84% (SD 1), and 9% had severe mismatch and a 74%(SD 5) 6-year probability of survival; by contrast, patientswith no mismatch had a 90% (SD 2) 6-year probability ofsurvival.136 Mitral prosthetic stenosis can worsen withtime because of the in-growth of pannus, especially withpersistent inflammation around the prosthetic valve ring,and this growth can cause prosthetic leaflet entrapment.

Percutaneous balloon valvuloplastySince the advent of PBV in 1984,3 the technique hasbecome the mainstay of treatment for mitral stenosis.The technique is as effective as open valvotomy and moreeffective than closed valvotomy, with reduced morbidity

Figure :Strategies for treating mitral stenosis

MVA=mitral valve area. NYHA=New York Heart Association class of disease. PBV=percutaneous balloon valvuloplasty. PAWP=pulmonary arterial wedge pressure. *Severe mitral stenosis is rarely

asymptomatic and, for such patients, we suggest use of the algorithm used for assessment of patients with moderate disease.

Moderate disease (MVA 1015 cm2, gradient 510 mm Hg)

Asymptomatic pat ient or, rarel y, a patient with few or atypic al symptoms Symptomatic patient (NYHA class IIIV)*

Suitable for PBV

PBV

Close follow-up with low threshold for surgery; makedecision based on surgical expertise and patientslifestyle needs

Palliative PBV

Surgery

NYHA c lass II NYHA class II IIV High risk for surgery

Unsuitable for PBVAssess exercise capacity

Low capacity; reproduciblesymptoms; abnormalhaemodynamics

Consider whether PBV is suitable;high threshold for surgery

High-risk indicators Severe pulmonary arterial

hypertension at rest orwith exercise

Clinically significant increasein PAWP with exercise

History of thromboemboli Very large left atrium or new

onset atrial fibrillation Evidence for right-heart dysfunction

Normal capacity; no symptomsof mitral stenosis

Severe disease (MVA 10 cm2, gradient 10 mm Hg)


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and cost in most patients, except for those withunfavourable anatomy.107110 In all permutations of thetechnique, a dilating device is passedeither antegrade(through the atrial septum) or retrograde (via the aorta)across the mitral valve. Dilation splits the commissuresand provides clinically significant improvement.Thickening, rigidity, calcification (especially com-missural), and subvalvular pathology have strongprognostic importance for valvuloplasty (figure 1).

The Inoue balloon technique has been the method ofchoice, but the balloon used is largely dependent on siteand operator expertise. Generally, the techniqueimmediately doubles the mitral valve area and halves thegradient. Almost 90% of patients show clinicallysignificant improvement in function with a final valvearea of more than 15 cm without severe mitral

regurgitation.8

Although shortness of breath improvesrapidly, exercise tolerance improves gradually.114 Mostpatients remain in NYHA class I or II. About 75% ofpatients are alive 710 years after intervention, and 60%are free of symptoms without secondary intervention forlong periods of follow-up.111

Centre volume and patient selection consistently affectresults.112 Success rates range from more than 95% inideal patients from highly selected centres, to about8085% in usual centres, and less than 5060% in patientswith suboptimum anatomy.110 Patients with favourablemorphology (echocardiographyscores of less than 8 andno commissural calcium) have more than 90% proceduralsuccess, very low occurrence of complications (


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10 WHO. Rheumatic fever and rheumatic heart disease. WHO Technical

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