Discuss mitral valve apparatus

Clinical features, investigation and management of Mitral Stenosis

-Dr. Uphar Gupta

Moderator – Dr. Prabhakar K

The mitral valve

• AKA bicuspid valve or left

atrioventricular valve

• dual-flap valve

• lies between the left atrium

(LA) and the left ventricle

(LV)

The mitral apparatus

• composed of the left atrial wall, the annulus,

the leaflets, the chordae tendineae, the

papillary muscles, and the left ventricular wall.

Left atrial wall

• The left atrial myocardium extends over the

proximal portion of the posterior leaflet.

• Left atrial enlargement can result in mitral

regurgitation by affecting the posterior leaflet.

• The anterior leaflet is not affected, because of

its attachment to the root of the aorta

Mitral annulus

• fibrous ring that connects with the leaflets.

• not a continuous ring around the mitral orifice

• D-shaped

• The straight border of the annulus is posterior to the

aortic valve.

• The aortic valve is located between the ventricular

septum and the mitral valve.

• The annulus functions as a sphincter that

contracts and reduces the surface area of the

valve during systole to ensure complete closure of

the leaflets.

• Annular dilatation of the mitral valve causes poor

leaflet apposition - results in mitral regurgitation.

Mitral valve leaflets

• continuous veil inserted around the circumference of the mitral

orifice.

• The free edges of the leaflets have several indentations.

• Two of these indentations, the anterolateral and posteromedial

commissures, divide the leaflets into anterior and posterior.

• These commissures can be accurately identified by the insertions of

the commissural chordae tendineae into the leaflets.

• Normally, the leaflets are thin, pliable,

translucent, and soft.

• Each leaflet has an atrial and a ventricular

surface.

Anterior leaflet

• located posterior to the aortic root and is also anchored to the

aortic root, unlike the posterior leaflet.

• also known as the aortic, septal, greater, or anteromedial leaflet.

• The anterior leaflet is large and semicircular in shape.

• The 2 zones on the anterior leaflet are referred to as rough and

clear zones, according to the chordae tendineae insertion.

Posterior leaflet

• ventricular, mural, smaller, or posterolateral leaflet.

• The posterior leaflet is the section of the mitral valve

that is located posterior to the 2 commissural areas.

• It has a wider attachment to the annulus than the

anterior leaflet.

• It is divided into 3 scallops by 2 indentations or clefts.

Chordae tendineae

• Small fibrous strings that originate either from

the apical portion of the papillary muscles or

directly from the ventricular wall and insert

into the valve leaflets or the muscle.

Commissural chordae

• Commissural chordae are the chordae that insert

into the interleaflet or commissural areas located at

the junction of the anterior and posterior leaflets.

• Two types of commissural chordae exist.

• Posteromedial commissural chordae and

anterolateral commissural

Leaflet chordae

• insert into the anterior or posterior leaflets.

• Two types of chordae tendineae are connected to the

anterior leaflet.

• The first is rough zone chordae, which insert into the distal

portion of the anterior leaflet known as the rough zone.

• The second is strut chordae, which are the chordae that

branch before inserting into the anterior leaflet.

Papillary muscles and left ventricular wall

• represent the muscular components of the mitral apparatus.

• The papillary muscles normally arise from the apex and middle third

of the left ventricular wall.

• The anterolateral papillary muscle is normally larger than the

posteromedial papillary muscle and is supplied by the left anterior

descending artery or the left circumflex artery.

• The posteromedial papillary muscle is supplied by the right coronary

artery.

• Extreme fusion of papillary muscle can result

into mitral stenosis.

• On the other hand, rupture of a papillary

muscle, usually the complication of acute

myocardial infarction, will result in acute

mitral regurgitation.

Microscopic Anatomy

• The 3 layers of the ventricular wall are the

endocardium, the myocardium, and the epicardium.

• The endocardium consists of a simple squamous

endothelium and a thin subendothelial tissue.

• The myocardium consists of cardiac muscle fibers.

• The epicardium consists of a simple squamous

mesothelium and subepicardial tissue.

• There is a layer of dense fibrous connective tissue, called the

annulus fibrosus, located between the atrium and ventricle.

• The mitral valve connects the left atrium (LA) and the left

ventricle (LV).

• The mitral valve leaflets are composed of an outer layer of

endocardium and a dense connective tissue core, which is

continuous with the annulus fibrosus.

2- to 3-mm zone of overlap (the zona coapta).

Apical four-chamber view recorded in systole in a normal patient

MITRAL STENOSIS

• Obstruction to blood flow between the left atrium and the left

ventricle

• ETIOLOGY:-

– rheumatic carditis.

– Congenital MS is uncommon.

– MS, usually rheumatic, in association with atrial septal defect is called

Lutembacher syndrome.

– massive mitral valve annular calcification. This process occurs most

frequently in elderly patients and produces MS by limiting leaflet motion.

• Rheumatic changes present in 99% of stenotic mitral valves excised at

the time of mitral valve (MV) replacement.

• 25% - isolated MS

• 40% - combined MS and MR.

• Multivalve involvement - 38% of MS patients,

– Aortic valve 35%

– tricuspid valve 6%.

– pulmonic valve is rarely affected.

• Two thirds of all patients with rheumatic MS are female.

Acute rheumatic fever

inflammation and edema of

the leaflets

small fibrin-platelet thrombi along the leaflet contact zones.

Scarring

Earlier Stages • relatively flexible leaflets snap open in diastole into a curved shape

because of restriction of motion at the leaflet tips.

• This diastolic doming is most evident in the motion of the anterior leaflet

and becomes less prominent as the leaflets become more fibrotic and

calcified.

• The symmetrical fusion of the commissures results in a small central oval

orifice in diastole that on pathologic specimens is shaped like a fish

mouth or buttonhole because the anterior leaflet is not in the

physiological open position .

End-stage Disease

• thickened leaflets -adherent and rigid that they cannot open or

shut, reducing or, rarely, even abolishing the first heart sound and

leading to combined MS and MR.

• When rheumatic fever results exclusively or predominantly in

contraction and fusion of the chordae tendineae, with little fusion

of the valvular commissures, dominant MR results.

• Aschoff bodies, the pathologic hallmark of rheumatic disease, are

most frequently seen in the myocardium, not the valve tissue.

OTHER ETIOLOGIES

• rare complication of :-

– malignant carcinoid disease

– systemic lupus erythematosus

– rheumatoid arthritis

– mucopolysaccharidoses of the Hunter-Hurler phenotype,

Fabry disease, and Whipple disease

– Methysergide therapy is an unusual but documented cause of

MS.

Other causes of LA – LV Flow obstruction

– a left atrial tumor, particularly myxoma

– ball valve thrombus in the left atrium

– infective endocarditis with large vegetations

– congenital membrane in the left atrium (cor

triatriatum)

• Severity of mitral valve obstruction is the degree of valve

opening in diastole.

• In normal adults- 4 to 6 cm2

• 2 cm2 - mild MS - blood can flow from the left atrium to the

left ventricle only if propelled by a small pressure gradient.

• 1 cm2 - severe MS, a left atrioventricular pressure gradient of

approximately 20 mm Hg is required to maintain normal

cardiac output at rest

Pulmonary Hypertension

• mean left atrial pressure is elevated - prominent atrial contraction

(a wave), with a gradual pressure decline after mitral valve opening

(y descent).

• mild to moderate MS - pulmonary arterial pressure may be normal

or only minimally elevated at rest but rises during exercise.

• severe MS and those in whom the pulmonary vascular resistance is

significantly increased - pulmonary arterial pressure is elevated

when the patient is at rest.

(1) passive backward transmission of the elevated left atrial

pressure

(2) pulmonary arteriolar constriction, which presumably is

triggered by left atrial and pulmonary venous hypertension

(reactive pulmonary hypertension)

(3) organic obliterative changes in the pulmonary vascular bed,

which may be considered to be a complication of long-

standing and severe MS

• also exert a protective effect

• the elevated precapillary resistance makes the development of

symptoms of pulmonary congestion less likely to occur by

tending to prevent blood from surging into the pulmonary

capillary bed and damming up behind the stenotic mitral valve.

• However, this protection occurs at the expense of a reduced

cardiac output.

• In severe MS - pulmonary vein–bronchial vein shunts occur.

• Their rupture may cause hemoptysis.

• manifest a reduction in pulmonary compliance, increase in the work

of breathing, and redistribution of pulmonary blood flow from the

base to the apex.

• In time, severe pulmonary hypertension results in right-sided heart

failure, with dilation of the right ventricle and its annulus, secondary

tricuspid regurgitation (TR), and sometimes pulmonic regurgitation.

Left Ventricular Function

• The LV chamber typically is normal or small, with

normal systolic function and normal LV end-diastolic

pressure.

• However, coexisting MR, aortic valve lesions, systemic

hypertension, ischemic heart disease, and

cardiomyopathy may all be responsible for elevations

of LV diastolic pressure

Left Atrial Changes

• The combination of mitral valve disease and

atrial inflammation secondary to rheumatic

carditis causes the following:

– (1) left atrial dilation;

– (2) fibrosis of the atrial wall;

– (3) disorganization of the atrial muscle bundles.

• Premature atrial activation, caused by an automatic focus or reentry,

may stimulate the left atrium during the vulnerable period and

thereby precipitate AF.

• AF is often episodic at first but then becomes more persistent.

• AF per se causes diffuse atrophy of atrial muscle, further atrial

enlargement, and further inhomogeneity of refractoriness and

conduction.

• These changes, in turn, lead to irreversible AF.

Symptoms:- Dyspnea

• The most common presenting symptoms - dyspnea, fatigue, and

decreased exercise tolerance.

• Symptoms are caused by a reduced ability to increase cardiac

output normally with exercise or elevated pulmonary venous

pressures and reduced pulmonary compliance.

• Dyspnea may be accompanied by cough and wheezing.

• Vital capacity is reduced, presumably because of the presence of

engorged pulmonary vessels and interstitial edema.

• critical obstruction to left atrial emptying and dyspnea with ordinary

activity (NYHA functional Class III) - orthopnea as well and frank

pulmonary edema.

• The latter may be precipitated by effort, emotional stress, respiratory

infection, fever pregnancy, or AF with a rapid ventricular rate or other

tachyarrhythmia.

• In patients with a markedly elevated pulmonary vascular resistance, RV

function is often impaired and the presentation may also include

symptoms and signs of right heart failure.

Hemoptysis

• sudden and severe - caused by rupture of thin-walled, dilated bronchial

veins, usually as a consequence of a sudden rise in left atrial pressure.

• milder, with only blood-stained sputum associated with attacks of

paroxysmal nocturnal dyspnea.

• pink frothy sputum characteristic of acute pulmonary edema with

rupture of alveolar capillaries.

• also may be caused by pulmonary infarction, a late complication of MS

associated with heart failure.

Chest Pain

• not a typical symptom

• 15%

• indistinguishable from that of angina pectoris

• caused by :-

– severe RV hypertension secondary to the pulmonary vascular disease

– concomitant coronary atherosclerosis

– coronary obstruction caused by coronary embolization

Palpitations and Embolic Events

• Patients with AF often are initially diagnosed

when they present with AF or an embolic

event.

Other Symptoms

• Compression of the left recurrent laryngeal nerve by a greatly

dilated left atrium, enlarged tracheobronchial lymph nodes, and

dilated pulmonary artery may cause hoarseness (Ortner syndrome).

• repeated hemoptysis with pulmonary hemosiderosis.

• Systemic venous hypertension, hepatomegaly, edema, ascites, and

hydrothorax are all signs of severe MS with elevated pulmonary

vascular resistance and right-sided heart failure.

Physical Examination

• irregular pulse caused by AF and signs of left and right heart

failure

• systemic vasoconstriction may exhibit the so-called mitral

facies, characterized by pinkish-purple patches on the cheeks

• The arterial pulse is usually normal, but in patients with a

reduced stroke volume, the pulse may be low in volume.

• The jugular venous pulse usually exhibits a prominent a wave in patients with sinus rhythm and elevated pulmonary vascular resistance.

• In patients with AF, the x descent of the jugular venous pulse disappears, and there is only one crest, a prominent v or c-v wave, per cardiac cycle.

• Palpation of the cardiac apex usually reveals an inconspicuous left

ventricle; the presence of a palpable presystolic expansion wave or an

early diastolic rapid filling wave speaks strongly against serious MS.

• A readily palpable, tapping S1 suggests that the anterior mitral valve

leaflet is pliable.

• When the patient is in the left lateral recumbent position, a diastolic

thrill of MS may be palpable at the apex.

• RV lift is felt in the left parasternal region in patients with

pulmonary hypertension.

• A markedly enlarged right ventricle may displace the left

ventricle posteriorly and produce a prominent RV apex beat

that can be confused with a LV lift.

• A loud P2 may be palpable in the second left intercostal space

in patients with MS and pulmonary hypertension.

Auscultation

• accentuated S1

• As pulmonary arterial pressure rises, P2 at first becomes accentuated and

widely transmitted and can often be readily heard at both the mitral and

the aortic areas.

• With further elevation of pulmonary arterial pressure, splitting of S2

narrows because of reduced compliance of the pulmonary vascular bed,

with earlier pulmonic valve closure.

• Finally, S2 becomes single and accentuated.

• Other signs of severe pulmonary hypertension

– nonvalvular pulmonic ejection sound that diminishes during inspiration,

because of dilation of the pulmonary artery,

– systolic murmur of TR,

– Graham Steell murmur of pulmonic regurgitation,

– S4 originating from the right ventricle.

• An S3 gallop originating from the left ventricle is absent in patients

with MS unless significant MR or AR coexists

• The opening snap (OS) of the mitral valve is caused by a sudden tensing of the

valve leaflets after the valve cusps have completed their opening excursion.

• The OS occurs when the movement of the mitral dome into the left ventricle

suddenly stops.

• The OS can usually be differentiated from P2 because the OS occurs later,

unless right bundle branch block is present.

• In addition, the OS usually is loudest at the apex, whereas S2 is best heard at

the cardiac base.

• The mitral valve cannot be totally rigid if it produces an OS, so an OS

is usually accompanied by an accentuated S1.

• Calcification confined to the tip of the mitral valve leaflets does not

preclude an OS, although calcification of the body and tip does.

• The mitral OS follows A2 by 0.04 to 0.12 second; this interval varies

inversely with the left atrial pressure.

• A short A2-OS interval is a reliable indicator of severe MS

• The diastolic, low-pitched, rumbling murmur of MS is best heard at the

apex, with the bell of the stethoscope (low-frequency mode on electronic

stethoscopes) and with the patient in the left lateral recumbent position.

• When this murmur is soft, it is limited to the apex but, when louder, it

may radiate to the left axilla or the lower left sternal area.

• Although the intensity of the diastolic murmur is not closely related to the

severity of stenosis, the duration of the murmur is a guide to the severity

of mitral valve narrowing.

• The murmur persists for as long as the left atrioventricular

pressure gradient exceeds approximately 3 mm Hg.

• The murmur usually commences immediately after the OS.

• In mild MS, the early diastolic murmur is brief but, in the

presence of sinus rhythm, it resumes in presystole.

• In severe MS, the murmur persists until end-diastole, with

presystolic accentuation while sinus rhythm is maintained.

Differential Diagnosis

• rare diagnosis in developed countries

• In older patients - mitral annular calcification

• Left atrial myxoma

• HOCM

Radiography

• left atrial enlargement

• Extreme left atrial enlargement rarely occurs in

isolated MS - when present, MR is usually severe

• fluoroscopy is required to detect valvular calcification.

• Radiologic changes in the lung fields indirectly reflect

the severity of MS.

• Interstitial edema, an indication of severe obstruction, is manifested as Kerley

B lines (dense, short, horizontal lines most commonly seen in the costophrenic

angles).

• This finding is present in 30% of patients with resting pulmonary arterial

wedge pressures less than 20 mm Hg and in 70% of patients with pressures

greater than 20 mm Hg.

• Severe long-standing mitral obstruction often results in Kerley A lines (straight,

dense lines up to 4 cm in length, running toward the hilum), as well as the

findings of pulmonary hemosiderosis and rarely of parenchymal ossification.

• Kerley B lines • subpleural

perpendicular lines 1-3 cm in length

Calcification in the mitral ring(lateral view )

Electrocardiography

• Relatively insensitive for detecting mild MS

• shows characteristic changes in moderate or severe obstruction

• Left atrial enlargement (P wave duration in lead II >0.12 second

and/or a P wave axis between +45 and −30 degrees) is a

principal electrocardiographic feature of MS and is found in

90% of patients with significant MS and sinus rhythm.

• AF is common with long-standing MS.

• Electrocardiographic evidence of RV hypertrophy correlates with RV systolic

pressure.

• When RV systolic pressure is 70 to 100 mm Hg, approximately 50% of patients

manifest ECG criteria for RV hypertrophy, including a mean QRS axis greater

than 80 degrees in the frontal plane and an R:S ratio greater than 1 in lead V1.

• When RV systolic pressure is greater than 100 mm Hg in patients with isolated

or predominant MS, electrocardiographic evidence of RV hypertrophy is

consistently found.

Echocardiography • characteristic anatomy with leaflet thickening and restriction of

opening caused by symmetric fusion of the commissures, resulting

in “doming” of the leaflets in diastole

• As disease becomes more severe, thickening extends from the

leaflet tips toward the base with further restriction of motion and

less curvature of the leaflet in diastole.

• The mitral chords are variably thickening, fused, and shortened

and there may be superimposed calcification of the valve apparatus

• A score of 0 to 4+ is given for leaflet thickness, mobility,

calcification, and chordal involvement to provide an overall

score that is favorable (low) or unfavorable (high) for

valvuloplasty

• degree of anterior leaflet doming, symmetry of commissural

fusion, and distribution of leaflet calcification.

• left atrial size, pulmonary artery pressures, LV size and systolic

function, and RV size and systolic function.

• When pulmonary hypertension is present, the right

ventricle is frequently dilated, with reduced systolic

function.

• TR may be secondary to RV dysfunction and annular

dilation or may be caused by rheumatic involvement of

the tricuspid valve.

• Complete evaluation of aortic valve anatomy and

function is also important because the aortic valve is

affected in approximately one third of patients with MS.

• When transthoracic images are suboptimal, TEE is

appropriate.

• TEE is also necessary to exclude left atrial thrombus and

evaluate MR severity when percutaneous BMV is considered.

Characteristic Changes

• thickening at the leaflet edges, fusion of the commissures,

and chordal shortening and fusion.

commissural fusion that results in doming of the leaflets in the long-axis view and in a decrease in the width of the mitral orifice in the short-axis view.

M-mode echocardiogram - marked thickening of the mitral valve leaflets and the flat E-F slope during diastole.

the diffuse thickening of the mitral leaflets with the doming motion in diastole with diffuse thickening of the chordae

Exercise Testing with Doppler Echocardiography

• Exercise testing is useful for many patients with MS to ascertain the

level of physical conditioning and elicit covert cardiac symptoms.

• The exercise test can be combined with Doppler echocardiography to

assess exercise pulmonary pressure.

• Useful parameters on exercise testing include the following: (1) exercise

duration; (2) blood pressure and heart rate response; and (3) increase

in pulmonary pressures with exercise, compared with the expected

normal changes.

Cardiac Catheterization

• Catheter-based measurement of left atrial and LV pressures

• allows measurement of the mean transmitral pressure

gradient and, in conjunction with measurement of

transmitral volume flow rate, calculation of the valve area

using the Gorlin formula

• Routine diagnostic cardiac catheterization is not

recommended for the evaluation of MS.

Complications :- Atrial Fibrillation • The most common complication of MS is AF

• AF may precipitate or worsen symptoms caused by loss of the

atrial contribution to filling and to a short diastolic filling

period when the ventricular rate is not well controlled.

• predisposes to left atrial thrombus formation and systemic

embolic events.

• conveys a worse overall prognosis

Systemic Embolism

• caused by left atrial thrombus formation.

• most often occurs in patients with AF

• When embolization occurs in patients in sinus rhythm, the possibility

of transient AF or underlying infective endocarditis should be

considered.

• loss of atrial appendage contractile function, despite electrical

evidence of sinus rhythm, leads to blood flow stasis and thrombus

formation.

Infective Endocarditis

• MS is a predisposing factor for endocarditis in less than 1% of

cases in clinical series of bacterial endocarditis.

• The estimated risk of endocarditis in patients with MS is

0.17/1000 patient-years, which is much lower than the risk in

patients with MR or aortic valve disease.

Medical Treatment

• The medical management of MS is primarily directed

toward the following:

– (1) prevention of recurrent rheumatic fever;

– (2) prevention and treatment of complications of MS; and

– (3) monitoring disease progression to allow intervention at

the optimal time point.

• Patients with MS caused by rheumatic heart disease should

receive penicillin prophylaxis for beta-hemolytic

streptococcal infections to prevent recurrent rheumatic

fever

• Prophylaxis for infective endocarditis is no longer

recommended

• Anemia and infections should be treated promptly and

aggressively in patients with valvular heart disease.

• Anticoagulant therapy is indicated for prevention of systemic embolism

in MS patients with AF (persistent or paroxysmal), any prior embolic

events (even if in sinus rhythm), and documented left atrial thrombus.

• Anticoagulation also may be considered for patients with severe MS

and sinus rhythm when there is severe left atrial enlargement

(diameter >55 mm) or spontaneous contrast on echocardiography.

• Treatment with warfarin is used to maintain the international

normalized ratio (INR) between 2 and 3.

• Asymptomatic patients with mild to moderate rheumatic mitral

valve disease should have a history and physical examination

annually, with echocardiography every 3 to 5 years for mild

stenosis, every 1 to 2 years for moderate stenosis, and annually for

severe stenosis.

• More frequent evaluation is appropriate for any change in signs or

symptoms.

• All patients with significant MS should be advised to avoid

occupations requiring strenuous exertion.

• In patients with severe MS, with persistent symptoms after

intervention or when intervention is not possible, medical

therapy with oral diuretics and the restriction of sodium

intake may improve symptoms.

• Digitalis glycosides - slowing the ventricular rate in patients

with AF and in treating patients with right-sided heart failure.

• Hemoptysis is managed by measures designed to reduce

pulmonary venous pressure, including sedation, assumption

of the upright position, and aggressive diuresis.

Treatment of Arrhythmias • Immediate treatment of AF includes administration of intravenous heparin

followed by oral warfarin.

• The ventricular rate should be slowed, initially with an intravenous beta

blocker or calcium channel antagonist, followed by long-term rate control with

oral doses of these agents.

• When these medications are ineffective or when additional rate control is

necessary, digoxin or amiodarone may be considered.

• Digoxin alone for long-term management of AF may be considered in patients

with concurrent LV dysfunction or a sedentary lifestyle.

• Paroxysmal AF and repeated conversions, spontaneous or induced, carry the

risk of embolization.

• In patients who cannot be converted or maintained in sinus rhythm, digitalis

should be used to maintain the ventricular rate at rest at approximately 60

beats/min.

• If this is not possible, small doses of a beta-blocking agent, such as atenolol

(25 mg daily) or metoprolol (50 to 100 mg daily), may be added.

• Beta blockers are particularly helpful in preventing rapid ventricular responses

that develop during exertion.

• Multiple repeat cardioversions are not indicated if the patient fails to

sustain sinus rhythm while on adequate doses of an antiarrhythmic.

• Patients with chronic AF who undergo surgical MV repair or MV

replacement may undergo the maze procedure (atrial compartment

operation).

• Early intervention with percutaneous valvotomy may prevent the

development of AF.

Percutaneous Balloon Mitral Valvotomy

• Patients with mild to moderate MS who are asymptomatic frequently

remain so for years, and clinical outcomes are similar to age-matched

normal patients.

• However, severe or symptomatic MS is associated with poor long-term

outcomes if the stenosis is not relieved mechanically

• Percutaneous BMV is the procedure of choice for the treatment of MS

so that surgical intervention is now reserved for patients who require

intervention and are not candidates for a percutaneous procedure.

• BMV is recommended for symptomatic patients with – moderate to severe MS – with favorable valve morphology– no or mild MR– no evidence of left atrial thrombus.

• recommended for asymptomatic patients with– moderate to severe MS– when mitral valve obstruction has resulted in pulmonary hypertension

with a pulmonary systolic pressure greater than 50 mm Hg at rest or 60 mm Hg with exercise.

• BMV also is reasonable for symptomatic patients who are at

high risk for surgery, even when valve morphology is not ideal,

including patients with restenosis after a previous BMV or

previous commissurotomy who are unsuitable for surgery

because of very high risk.

• BMV may be considered for patients with moderate to severe

MS and new-onset AF and those with mild MS when

significant pulmonary hypertension is present .

• This percutaneous technique consists of advancing a small balloon

flotation catheter across the interatrial septum (after transseptal

puncture), enlarging the opening, advancing a large (23- to 25-mm)

hourglass-shaped balloon (the Inoue balloon), and inflating it within

the orifice

• Alternatively, two smaller (15- to 20-mm) side by side balloons across

the mitral orifice may be used.

• A third technique involves retrograde, nontransseptal dilation of the

mitral valve, in which the balloon is positioned across the mitral valve

using a steerable guidewire.