Mitral Stenosis, Congenital

 

INTRODUCTION

Background: The mitral valve is the inlet valve to the left ventricle (LV). The normal mitral valve is a complex apparatus composed of an annulus and two leaflets that are attached by chordae tendineae to two papillary muscles. The papillary muscles arise from the walls of the LV and secure the chordae and mitral leaflets, preventing prolapse of the valve during ventricular systole.

Proper function of the mitral valve requires an intact mitral valve apparatus and satisfactory LV function. Mitral valve stenosis (MS) results from any pathologic process that narrows the effective mitral valve orifice at the supravalvular, valvular, or subvalvular levels. MS can be congenital or acquired.

Congenital MS, a rare entity, takes several forms. These include hypoplasia of the mitral valve annulus, mitral valve commissural fusion, double orifice mitral valve, shortened or thickened chordae tendinae, and parachute mitral valve, in which all chordae attach to a single papillary muscle. The most common associated malformations are coarctation of the aorta, aortic valve stenosis, and subvalvular aortic stenosis. The association of multiple levels of left-sided inflow and outflow tract obstruction is termed the Shone complex.

Severe hypoplasia, or atresia, of the mitral valve results in a hypoplastic left ventricular cavity size that is not capable of sustaining the systemic cardiac output. This situation is considered part of the spectrum of the hypoplastic left heart syndrome and is not considered further in this article. This article deals with MS that, while occasionally severe, allows enough blood flow into the LV to sustain the systemic cardiac output.

 

Pathophysiology: MS obstructs blood flow into the LV, elevating left atrial pressure in proportion to severity of the stenosis. This, in turn, restricts pulmonary venous return to the left atrium, elevating pulmonary vascular and, consequently, right heart pressures. Elevated hydrostatic pressure in the pulmonary capillaries forces fluid into the alveoli and interstitial space, producing pulmonary congestion. Congested bronchial veins may encroach on small bronchioles, with subsequent increase in airway resistance.

As a compensatory mechanism, pulmonary vasoconstriction occurs. The right ventricle (RV) pressure increases, resulting in RV hypertrophy. Elevated pulmonary pressure can progress to fixed pulmonary arterial hypertension from medial hypertrophy and intimal thickening of the pulmonary arterioles. The RV eventually fails and pulmonary blood flow decreases, decreasing systemic blood flow. If the reduction in cardiac output is critical, end organ failure with renal and/or hepatic insufficiency, shock, and metabolic acidosis can occur. RV failure results in systemic venous congestion with development of hepatomegaly, ascites, and pedal edema.

 

Frequency:

  • In the US: Congenital MS is rare, occurring in 0.5% of patients with congenital heart disease (CHD).

Mortality/Morbidity: In congenital MS in the fetus, mitral valve obstruction does not interfere with normal growth and development, even if the mitral valve is atretic, because the amount of pulmonary venous return to the left atrium is small and the fetal bronchocollateral circulation is adequate to relieve the obstructive effects. In this case, the RV supplies all of systemic blood flow via the ductus arteriosus and the patient presents with hypoplastic left heart syndrome. Less severe forms of MS permit normal fetal circulatory pathways to continue with normal development of the LV and ascending aorta. After birth, if congenital MS is left untreated, morbidity and mortality are high, with mean survival estimated at 3 years. Associated cardiac lesions, such as coarctation of the aorta (CoA) and aortic valve stenosis, increase morbidity and mortality.

Race: No racial predilection exists.

Sex: No sex predilection exists for congenital MS.

Age: Congenital MS is usually detected in infancy if MS and/or associated heart lesions are severe enough to produce physical findings or to provoke overt symptoms.

CLINICAL

History:

  • Congenital MS in infancy
    • Patients with severe MS may present with respiratory distress from pulmonary edema shortly after birth if a significant atrial septal communication does not exist. The presence of an atrial septal defect decompresses the left atrium, resulting in a clinical picture of pulmonary overcirculation and decreased systemic cardiac output.
    • Patients with mild-to-moderate MS present after the neonatal period with signs of low cardiac output and RV failure such as pulmonary infections, failure to gain weight, exhaustion and diaphoresis with feeding, tachypnea, and chronic cough.
  • Congenital MS in older children: Children with MS may present with the insidious onset of exercise limitation. These patients may present with the following signs:
    • Pulmonary congestion evidenced by increasing severity of dyspnea (depending on degree of MS) that may range from dyspnea during exercise to paroxysmal nocturnal dyspnea, orthopnea, or even frank pulmonary edema. Dyspnea may be precipitated or worsened by an increase in blood flow across the stenotic mitral valve (eg, pregnancy, exercise) or by a reduction in diastolic filling time achieved by increasing the heart rate (eg, emotional stress, fever, respiratory infection, atrial fibrillation with rapid ventricular rate).
    • Signs of right heart failure, including peripheral edema and fatigue may be present.
    • Patients with MS, including those previously without symptoms, may develop atrial fibrillation, although this is an uncommon event in childhood. It results from chronic distension of the left atrium. Atrial fibrillation may cause the following:

       

      • Loss of the atrial kick to LV filling reduces systemic output and this may precipitate or exacerbate congestive heart failure.

         

      • Thromboembolic events (seeding of systemic emboli) occur in 10-20% of patients with MS. Many of these emboli lodge in the brain, causing a stroke.

         

      • Infective endocarditis (a rare event) should be suspected when embolization occurs during sinus rhythm.
    • Hemoptysis may be caused by rupture of dilated bronchial veins. Pink frothy sputum may be a manifestation of frank pulmonary edema. Both are associated with end-stage severe MS but rarely occur in pediatric patients.
    • Chest pain occurs in approximately 15% of patients with MS.
    • Dysphagia can be produced by compression of the esophagus as a result of a dilated left atrium. It occurs rarely in children.
    • Hoarseness can occur if the dilated left atrium impinges on the recurrent laryngeal nerve. It is a rare manifestation of severe MS.

Physical: Physical examination findings vary according to the severity of MS.

  • Mild-to-moderate MS
    • Normal peripheral pulses and good perfusion
    • Loud S1 caused by abrupt closure of the stenotic mitral valve
    • Increased intensity of the pulmonic component of the second heart sound in proportion to elevation of pulmonary arterial pressure
    • A long low-frequency diastolic murmur beginning shortly after S2 best heard at the apex, with late diastolic accentuation (as long as sinus rhythm is present): Intensity and length of the murmur are in proportion to severity of the obstruction.

       

    • Possible demonstration of S4 at the apex in older children
  • Severe MS
    • Diminished peripheral perfusion and pulses
    • Palpation of an RV impulse (enlarged RV) when pulmonary hypertension is present
    • Soft S1 in the presence of heart failure and diminished left ventricular filling
    • Accentuation of the pulmonic component of S2 with minimal respiratory splitting of S2
    • Holodiastolic murmur with presystolic accentuation best heard at apex: The diastolic murmur may diminish secondary to low cardiac output from heart failure.
    • With severe pulmonary hypertension, possible occurrence of a high-frequency early diastolic murmur of pulmonic valve regurgitation in the pulmonic listening area
    • RV S3 or S4

Causes: The etiology of congenital MS remains unknown. However, incidence of MS in offspring of family members (especially the mother) with left ventricular outflow tract obstruction is increased.

DIFFERENTIALS

Cor Triatriatum
Mitral Stenosis, Acquired
Mitral Stenosis, Supravalvular Ring
Pulmonary Hypertension, Primary


Other Problems to be Considered:

Pulmonary vein stenosis
Shone complex
Atrial myxoma


WORKUP

Lab Studies:

  • Measure electrolyte balance and renal function if congestive heart failure is suspected.

Imaging Studies:

  • Chest radiography
    • Left atrial dilation
    • Posteroanterior (PA) dilation secondary to high pulmonary vascular pressure and resistance
    • Pulmonary venous congestion

       

    • Right ventricular enlargement
  • Echocardiography is the most important diagnostic tool to evaluate patients with MS. This noninvasive imaging modality provides excellent anatomic and hemodynamic assessment of MS. Echocardiography provides the following:
    • Direct anatomic data, such as visualization of valve leaflet morphology and motility as well as measurement of valve orifice dimensions

       

    • Evaluation of left atrial size and detection of left atrial thrombi
    • Indirect physiologic data (ie, estimation of pressure gradients across the mitral valve and right ventricular systolic pressure), which may be measured using Doppler echocardiography
    • Transesophageal echocardiography: Transesophageal echocardiography is used when transthoracic echocardiographic pictures are inadequate. It may also be used to guide intervention and assess results in the operating room and cardiac catheterization laboratory.
  • Cardiac catheterization may be used to obtain direct intracardiac pressure measurements, the mitral valve gradient, pulmonary vascular resistance, and systemic cardiac output. The mitral valve effective orifice can be calculated using the Gorlin formula. Currently, the diagnosis and hemodynamic assessment of most patients with MS is performed noninvasively with echocardiography. Cardiac catheterization is used only when echocardiography does not provide complete information or if the patient undergoes mitral balloon valvuloplasty.

Other Tests:

  • The electrocardiogram findings may be normal in patients with mild MS. Hemodynamically significant stenosis results in ECG findings of left atrial or biatrial enlargement and right ventricular enlargement in proportion to severity of the obstruction.
  • Magnetic resonance imaging is used infrequently; however, experience with this imaging modality in MS is more limited than with echocardiography.

TREATMENT

Medical Care:

  • Asymptomatic patients with mild MS require no significant therapy. They should undergo yearly follow-up care with physical examination, chest radiographs, and ECG with echocardiography as indicated by this assessment. These patients may remain stable for decades before MS progresses and the patient requires surgical intervention.
  • More significant stenosis producing mild symptoms can be managed with diuretics alone. Direct careful attention to proper diet and to early intervention for pulmonary disease.
  • For the patient with congestive heart failure, administer loop diuretics plus potassium-sparing diuretics. Digoxin may improve right ventricular function in the setting of pulmonary hypertension.
  • Address cardiac rhythm abnormalities with appropriate medications.
  • Patients with chronic uncontrolled atrial tachyarrhythmias should be on anticoagulant therapy.

Surgical Care: Surgical options depend upon specific mitral valve pathology.

  • Mitral valve repair
    • Commissurotomy consists of an incision of fused mitral valve commissures and shaving of thickened mitral valve leaflets. Open surgical commissurotomy is preferable.
    • Divide fused chordae tendineae and papillary muscles to relieve subvalvular stenosis.
    • Resect any supravalvular tissue contributing to the MS.
  • Mitral valve replacement with mechanical valve or bioprosthesis
    • This is reserved for patients with severe MS in whom mitral valve repair is not possible. In older children for whom coumadin therapy may be contraindicated, mitral valve replacement can be performed using a bioprosthesis, although the durability of tissue valves is less than mechanical protheses.
    • The risk of warfarin therapy should be weighed against the disadvantage of progressive bioprosthetic valve deterioration resulting in the certain need for reoperation.
    • Mitral valve replacement is best avoided in infants and small children because of frequent size mismatch between the smallest mechanical valves and the hypoplastic mitral valve annulus. In addition, somatic growth in children leads to the need for subsequent mitral prosthesis replacement(s).
    • Warfarin therapy also is more difficult to administer and to monitor in children. A less than perfect mitral valve repair frequently is preferable to mitral valve replacement in this group of patients.

       

    • Complications after mitral valve replacement include the risks of anticoagulation, valve thrombosis, valve dehiscence, infective endocarditis, valve malfunction, and embolic events.
  • Pediatric patients sometimes must undergo correction of associated LV obstructive lesions such as subaortic stenosis, aortic valve stenosis, coarctation of the aorta, and hypoplastic aortic arch.

Consultations: Consult a cardiologist and cardiothoracic surgeon.

Diet: Restrict salt and avoid excessive fluids. Maintain proper nutrition. Caloric supplementation may be necessary in the symptomatic infant.

Activity: Patients should avoid strenuous exercise because an increased heart rate decreases diastolic filling time. If atrial flutter/fibrillation coexists and atrial kick is lost, a further decrease in LV stroke volume occurs. This may result in syncope from decreased cerebral perfusion.

MEDICATION

Medical therapy is used to avoid or decrease pulmonary congestion as well as to treat atrial tachyarrhythmias. These require medical therapy to prevent thromboembolic complications.

Drug Category: Loop diuretics -- By promoting renal excretion of water and electrolytes, loop diuretics decrease pulmonary congestion. Pulmonary congestion results from back-flow to the lungs caused by obstruction across a narrowed mitral valve orifice.
Drug Name
 Furosemide (Lasix) -- Furosemide acts by inhibiting absorption of the electrolytes sodium and chloride in the proximal and distal tubules and in the loop of Henle, thereby promoting excretion of salt (sodium chloride) and water. It acts as a diuretic and as an antihypertensive.
Adult Dose 20-80 mg/d PO/IV divided q6-12h; not to exceed 600 mg/d
Pediatric Dose 0.5-2 mg/kg per dose PO/IV/IM q8-24h
Contraindications Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion
Interactions May increase aminoglycoside-induced ototoxicity; may be ototoxic if used with ethacrynic acid; may enhance salicylate toxicity in patients receiving high doses of these concomitantly; decreases lithium renal clearance, with subsequent increase in toxicity of lithium; may potentiate the effects of antihypertensive drugs such as ganglionic or peripheral adrenergic blockers; simultaneous sucralfate and indomethacin administration may reduce natriuretic and antihypertensive effects of furosemide
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions May be ototoxic when administered to severely oliguric patients; may precipitate gout (rare); excessive diuresis in MS may compromise cardiac output by reducing preload, may also precipitate circulatory collapse with the additional risk of thromboembolism; may cause electrolyte imbalance (eg, hypokalemic-hypochloremic metabolic alkalosis, hyponatremia, hypomagnesemia, hypocalcemia); use with caution in case of hepatic disease; prolonged use in premature infants may result in nephrocalcinosis; alterations in glucose tolerance test results have occurred, and precipitation of diabetes mellitus has been reported
Drug Category: Potassium-sparing diuretics -- Potassium-sparing diuretics are used to prevent potassium depletion induced by the more potent loop-diuretics (such as furosemide).
Drug Name
 Spironolactone (Aldactone) -- Spironolactone retains potassium by competing with aldosterone for the receptor sites in the distal convoluted renal tubules. This increases sodium and water excretion while retaining potassium and hydrogen ions.
Adult Dose 25-100 mg/d PO divided bid/qid; not to exceed 200 mg/d
Pediatric Dose 1-3.3 mg/kg/d PO divided bid/qid; not to exceed 200 mg/d
Contraindications Documented hypersensitivity; anuria; acute renal failure; hyperkalemia
Interactions May potentiate ganglionic-blocking agents; may potentiate antihypertensive drugs; may induce severe hyperkalemia when administered with ACE inhibitors or indomethacin; may increase the half-life of digoxin with the risk of developing digitalis toxicity
Pregnancy D - Unsafe in pregnancy
Precautions Potassium-sparing diuretics may cause hyperkalemia, especially when administered with ACE inhibitors; GI distress, rash, and gynecomastia have been reported; may cause transient elevation of BUN, especially in the presence of preexisting renal impairment; may cause mild metabolic acidosis; few cases of agranulocytosis have been reported; rat tumorigenesis has been shown with excess potassium-sparing diuretics; the dose should be decreased in case of hepatic impairment
Drug Category: Anticoagulants -- Anticoagulants are used in general for the prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. In the case of MS, they are used to prevent clot formation secondary to blood stasis in an enlarged, many times fibrillating, left atrium and in case of a prosthetic (mechanical) mitral valve.
Drug Name
 Warfarin (Coumadin) -- Warfarin inhibits vitamin K–dependent clotting factors II, VII, IX, and X and the anticoagulant proteins C and S. Its anticoagulation effect occurs 24 h after administration, but the peak effect may occur 72-96 h later. Antidotes are vitamin K and FFP.
Adult Dose Initial dose: 5-15 mg PO qd for 2-5 d, adjust to desired INR or PT
Maintenance dose: 2-10 mg/d PO qd
Pediatric Dose Initial dose: 0.1 mg/kg/d PO qd, adjust to desired INR or PT
Maintenance dose: 0.05-0.34 mg/kg/d PO qd
Therapeutic level: INR 2.5-3.5 or PT of 1.5-2 times baseline
Contraindications Documented hypersensitivity; severe hepatic and renal disease; uncontrolled bleeding; GI ulcers; malignant hypertension because of increased risk of intracranial hemorrhage; prior to invasive procedures (ie, spinal tap)
Interactions Anticoagulation effects are increased by chloramphenicol, cimetidine, fluconazole, metronidazole, indomethacin, salicylates, and sulfonamides; anticoagulation effects are decreased by carbamazepine, corticosteroids, chloral hydrate, griseofulvin, PO contraceptives, and vitamin K
Pregnancy X - Contraindicated in pregnancy
Precautions Patients on warfarin require periodic determinations of PT and INR

FOLLOW-UP

Further Inpatient Care:

  • Critically ill patients or patients unable to take oral medication may receive intravenous medications. Admission to the intensive care unit and endotracheal intubation may be required because of ineffective breathing caused by pulmonary edema.
  • Monitor the patient's anticoagulation therapy to prevent thrombus formation and to decrease the risk of embolization in case of a mechanical mitral valve. Remember that because these emboli come from the left atrium, embolization is to the systemic circulation, with many emboli reaching the brain.

Further Outpatient Care:

  • Regular visits to the pediatrician and/or generalist to monitor general health status, depending upon severity of MS
  • Regular visits to the pediatric cardiologist to monitor hemodynamic status, antiarrhythmic drug levels, and anticoagulation
  • Serial echocardiograms to monitor anatomic and hemodynamic progression of the MS: The frequency varies according to the patient's general health status and according to the cardiologist's criteria.
  • Stress Doppler hemodynamics using a supine bicycle or treadmill: Hemodynamics may be measured using transthoracic echocardiographic Doppler. This noninvasive test has replaced the traditional exercise stress test in the catheterization laboratory.

In/Out Patient Meds:

  • Inpatients may receive medications intravenously.

Transfer:

  • Transfer patient to an intensive care unit when general status is unstable because of low cardiac output or pulmonary edema.

Deterrence/Prevention:

    • In children, administer amoxicillin 50 mg/kg (not to exceed 2 g) PO 1 h before the procedure. In adults, administer amoxicillin 2 g PO 1 h before the procedure.
    • In high-risk patients (eg, those with prosthetic heart valves or previous history of endocarditis), administer ampicillin 50 mg/kg IV/IM in children and 2 g IV/IM in adults (not to exceed 2 g) plus gentamicin 1.5 mg/kg IV/IM for both children and adults (not to exceed 120 mg) within 30 minutes before starting the procedure. This is followed 6 h later by amoxicillin 25 mg/kg PO in children and 1 g PO in adults (not to exceed 1.5 g) or ampicillin 25 mg/kg IV/IM in children and 1 g IV/IM in adults. High-risk patients allergic to ampicillin/amoxicillin may receive vancomycin 20 mg/kg in children (not to exceed 1 g). High-risk patients allergic to ampicillin/amoxicillin should receive vancomycin 20 mg/kg IV in children (not to exceed 1 g) and 1 g IV in adults over 1-2 h plus gentamicin 1.5 mg/kg IV/IM for both children and adults (not to exceed 120 mg).
    • In penicillin-allergic patients, use erythromycin 20 mg/kg PO (not to exceed erythromycin ethylsuccinate 800 mg, stearate 1 g) 2 h before the procedure, then 10 mg/kg 6 h later. Other treatment options are clindamycin 20 mg/kg PO (not to exceed 300 mg) in children and 600 mg PO in adults 1 h before the procedure, cephalexin or cefadroxil 50 mg/kg PO in children and 2 g PO in adults 1 h before the procedure, and azithromycin or clarithromycin 15 mg/kg PO in children and 500 mg PO in adults 1 h before the procedure.
    • Avoid excessive salt intake, which increases fluid retention and may worsen symptoms.
    • Avoid excessive heat, excessive use of diuretics, and dehydration, which may decrease LV output by reducing preload.
    • Avoid contact sports in patients taking anticoagulants because of risks of cerebral, splenic, renal, or other internal organ bleeding. Pregnant women should avoid warfarin because of its teratogenic effects and risk of miscarriage.

Complications:

  • If MS is left untreated the following complications may arise:

     

    • Pulmonary edema

       

    • Right heart failure with progression to congestive heart failure

       

    • Renal insufficiency (due to congestive heart failure)

       

    • Progression to pulmonary hypertension

       

    • Atrial arrhythmias such as fibrillation or flutter

       

    • Thrombus formation in the dilated left atrium (due to stasis of blood)

       

    • Embolization of left atrial thrombus; stroke

       

    • Dysphagia from compression of esophagus by the enlarged left atrium
  • Complications of medical treatment
    • Diuretics may provoke dehydration (decreased preload) with subsequent compromise in cardiac output that may precipitate prerenal renal failure.
    • Warfarin may cause bleeding, such as intracranial hemorrhage and GI bleeding.
  • Complications of surgery
    • Mitral commissurotomy may cause significant postoperative mitral regurgitation, which may necessitate subsequent mitral valve replacement.
    • The risks of mitral valve replacement include those associated with anticoagulation, valve thrombosis, valve dehiscence, infective endocarditis, valve malfunction, and embolic events.
  • Complications of percutaneous balloon valvuloplasty
    • Safety depends on the mitral valve morphology and on the operator's experience. Very few forms of congenital MS are amenable to balloon valvotomy. Percutaneous balloon valvotomy should not be performed in patients with preexisting moderate-to-severe mitral valve regurgitation.
    • The most frequent complication after percutaneous balloon valvuloplasty is mitral regurgitation.

Prognosis:

  • Untreated newborns with severe MS have a grim prognosis. Surgical intervention is ideally avoided for as long as possible. Mechanical mitral valve replacement in a small infant or child is a high-risk procedure and carries a guarded prognosis.
  • Operative results and long-term outcome are extremely variable and highly dependent on coexisting abnormalities.
  • Mitral valve replacement entails a less than 5% mortality risk in young healthy patients without other significant cardiac abnormalities.

Patient Education:

  • Counsel patient and families regarding the appearance and/or worsening of symptoms.
  • Advise the patient regarding subacute bacterial endocarditis prophylaxis prior to any invasive or surgical application.
  • Monitor prothrombin time (PT) and international normalized ratio (INR) if the patient is on anticoagulation medication.
  • Advise pregnant mothers to avoid taking warfarin, avoid strenuous activity and excessive salt intake, and have their blood pressure frequently monitored.

.

MISCELLANEOUS

Medical/Legal Pitfalls:

  • Failure to diagnose primary problem
  • Failure to diagnose additional congenital cardiovascular abnormalities
  • Failure to refer a patient demonstrating increasing symptoms, especially those of congestive heart failure

Special Concerns:

  • Pregnancy
    • These patients have a higher risk of developing pulmonary edema because of the increased intravascular volume. For this reason, they should be monitored closely.
    • Asymptomatic or minimally symptomatic patients may only require close observation, but severely symptomatic patients may require urgent surgical intervention.
    • Pregnant women requiring anticoagulation because of a prosthetic mitral valve should receive heparin, which does not cross the placental barrier. They should not receive warfarin because of its teratogenic effects and fetal wastage.
    • Pregnant women with underlying heart disease require antibiotic prophylaxis with ampicillin and gentamicin or with amoxicillin if they undergo potentially bacteremic procedures.
    • Of note, cesarean delivery or uncomplicated abdominal delivery are not indications for antibiotic prophylaxis.

PICTURES

 

Caption: Picture 1. Hemodynamic changes in severe congenital mitral valve stenosis (MS). MS causes an obstruction (in diastole) to blood flow from the left atrium (LA) to the left ventricle (LV). Increased LA pressures are transmitted retrograde to pulmonary veins and pulmonary capillaries, resulting in capillary leak with subsequent development of pulmonary edema. To overcome pulmonary edema, the arterioles constrict, increasing pulmonary pressures. With time, capillaries develop intimal thickening, causing fixed (permanent) pulmonary hypertension. The right ventricle (RV) hypertrophies to generate enough pressure to overcome the increased afterload. Eventually, the RV fails, which manifests as hepatomegaly and/or ascites, edema of the extremities, and cardiomegaly on radiograph.
Click to see larger picture
Picture Type: Image
Caption: Picture 2. Two-dimensional echocardiogram, parasternal long axis view of a 5-month-old boy with congenital mitral valve stenosis. A small mitral valve annulus (star) is appreciated when compared to the normal-sized tricuspid valve annulus. Mitral valve stenosis has caused left atrial (LA) enlargement. Ao: Aorta; LA: left atrium; LV: left ventricle; RA: right atrium; RV: right ventricle.
Click to see larger picture
Picture Type: X-RAY
Caption: Picture 3. Two-dimensional echocardiogram, parasternal long axis view of a patient who required mitral valve replacement with a St. Jude's prosthetic mitral valve (star). He developed a stroke 1 month after mitral valve replacement despite anticoagulation with warfarin and required re-replacement of the prosthetic mitral valve. He will eventually outgrow this new prosthetic mitral valve and require subsequent mitral valve replacements with a larger mitral valve prosthesis. Ao: Aorta; LA: left atrium; LV: left ventricle; RA: right atrium; RV: right ventricle (see Image 2).
Click to see larger picture
Picture Type: X-RAY