Valvular Stenosis Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE)

Valvular Stenosis Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE)
Need Edelman’s DVD Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE) Radiologic and Imaging Sciences - Echocardiography Grand Valley State University, Grand Rapids, Michigan

Basic Principles Approach to Evaluation Valvular Stenosis
Complete echocardiographic evaluation Diagnostic imaging of the valve to define the etiology of stenosis Quantification of stenosis severity Evaluation of coexisting valvular lesions Assessment of left ventricular systolic function Response to chronic pressure overload of other upstream cardiac chambers, and the pulmonary vascular bed Echocardiographic information integration with pertinent clinical data

Fluid Dynamics of Valvular Stenosis High Velocity Jet
Characterized by formation of a laminar, high velocity jet in the narrowed orifice Flow profile in cross section of origin is flat (blunt) – Remains blunt as the jet reaches the narrowest cross-sectional area in the vena contracta Physiologic cross-sectional area < anatomic cross-sectional area

Fluid Dynamics of Valvular Stenosis High Velocity Jet
Length of high velocity jet is dependent on: Orifice geometry Examples: Very short jet across a deformed, irregular calcified aortic valve Longer jet along smoother tapering symmetric rheumatic mitral valve

Rheumatic Heart Disease
Heart valves are damaged by a disease process that begins with a sore throat from streptococcal infection. Untreated, the streptococcal infection can develop into acute rheumatic fever. Rheumatic fever is an inflammatory disease that can affect many connective tissues of the body, especially those of the heart, joints, brain or skin. Who is at risk of rheumatic heart disease? Anyone can get acute rheumatic fever, but it usually occurs in children five to fifteen years old. The resulting rheumatic heart disease can last for life. What are the symptoms of rheumatic heart disease? The symptoms vary greatly from person to person. Often the damage to heart valves is not immediately noticeable. A damaged heart valve either does not completely close or does not completely open.

Mitral stenosis Progressive fibrosis Thickening and calcification of valve Enlargement of LA Formation of mural thrombi Funnel shaped “fish-mouthed” mitral valve MS and MR AS and AI

Non-dynamic images

4V2 Simply stated: Simplified Bernoulli equation
Fluid Dynamics of Valvular Stenosis Relationship between Pressure Gradient and Velocity Simply stated: Simplified Bernoulli equation 4V2

Fluid Dynamics of Valvular Stenosis Distal Flow Disturbance
Distal to stenotic jet Flowstream becomes disorganized w/multiple blood flow velocities and directions Distance that flow disturbance propagates downstream is related to stenosis severity Aortic proximal flow patterns Proximal to a stenotic valve Flow is smooth and laminar (organized) with normal flow velocity “Flat” flow profile

Mitral valve proximal velocities Left atrial to left ventricular pressure gradient drives flow passively from the left atrium abruptly across the stenotic orifice Proximal flow acceleration is prominent over a large region of the left atrium 3D velocity profile is curved: flow velocities are Faster adjacent to and in the center of a line continuous with the jet direction through the narrowed orifice Slower at increasing radial distances from the valve orifice Hemi-elliptical in comparison to a stenotic semilunar valve

Take home message Stroke volume Calculated proximal to a stenotic valve Based on knowledge of cross-sectional area of flow and spatial mean flow velocity over a period of flow

Aortic Stenosis

Classified as Three Types
Valvular Subaortic Supra-valvular

Diagnostic Imaging of the Aortic Valve
Aortic stenosis most often due to: Calcific aortic stenosis Congenital valve disease (most often bicuspid. In rare instances or unicuspid or quadracuspid) Rheumatic valve disease

Diagnostic Imaging of the Aortic Valve Calcific Aortic Stenosis
Most common etiology of aortic stenosis Degenerative age related calcification Occurs slowly over many years Initially presents as “sclerosis” area of increased echogenicity typically at base of valve leaflets sans significant obstruction to left ventricular outflow

Aortic Stenosis Calcific/Degenerative
Mean age 60 – 70 Clinically significant obstruction occurs typically from age years old Most common cause of aortic stenosis FIGURE A patient with mild aortic stenosis is shown Feigenbaum

Pathologic specimen of a severely stenotic trileaflet aortic valve, which demonstrates gross nodular athero-calcific changes on the aortic side of the leaflets.

Systolic leaflet excursion of less than 15 mm by 2D or M-mode Severe obstruction is reliably excluded FIGURE A patient with mild aortic stenosis is shown Again Feigenbaum

Planimetry of aortic valve is possible in some patients Interpretation with caution due to complex 3D anatomy of the orifice in calcific degenerative stenosis Ensure image plane is aligned at narrowest orifice of the valve 2D represents anatomic valve area – Doppler data reflects functional valve area FIGURE A patient with mild aortic stenosis is shown

Planimetry 10-006b Feigenbaum

Aortic Stenosis - Bicuspid Valve
Severe calcification: difficult to differentiate between bicuspid and tricuspid aortic valve

Average age of onset of calcific stenosis symptom is younger: usually 45 to 65 years old

Can be identified best in parasternal short-axis view Football shaped opening Long-axis: “dome-like” appearance Typically leaflets are unequal in size If anterior-posterior opening: anterior leaflet is larger If lateromedial opening: rightward leaflet is larger

Often have raphae (seam-like line or ridge) in the larger leaflet: closed valve appears trileaflet Identify as trileaflet only in systole 18-34a & b Feigenbaum

Aortic Stenosis – Unicuspid Valve

Aortic Stenosis - Rheumatic
Rheumatic valvular disease preferentially involves mitral valve Rheumatic aortic stenosis occurs concurrently with rheumatic mitral valve disease Results in commissural fusion of the aortic leaflets similar to rheumatic mitral disease Appears similar to calcific aortic stenosis (if mitral involved suspect aortic stenosis due to rheumatic disease)

Summary

Aortic Stenosis - Congenital
Usually diagnosed at childhood May not become symptomatic until young adulthood May be resultant from re-stenosis after surgical valvotomy

Aortic Stenosis Differential Diagnosis
Left ventricular outflow tract obstruction Fixed valvular obstruction Subaortic membrane or a muscular subaortic stenosis Dynamic subaortic obstruction Hypertrophic cardiomyopathy Supravalvular stenosis

Fixed valvular obstruction Subaortic membrane Suspect when valve anatomy is not clearly stenotic even though Doppler velocity and color flow indicates stenosis TTE vs TEE Feigenbaum

Subaortic Membrane – Fixed Subvalvular Stenosis
FIGURE A: An unusual cause of stenosis: A subaortic membrane is readily apparent in this apical four-chamber view. B: The presence of the membrane results in turbulence in the left ventricular outflow tract, proximal to the aortic valve. This high-velocity, turbulent flow can result in damage to the aortic cusps 18-30 Feigenbaum

Dynamic Subvalvular Stenosis
19-29a Feigenbaum

Supravalvular stenosis in a 30 year old with familial hypercholesterolemia
Non-dynamic

Aortic Stenosis Quantitation of Stenosis Severity
Measurement of maximum aortic jet velocity Calculation of mean and maximum gradient Determination of continuity equation valve area Ratio of outflow tract to aortic jet velocity

Dependence of pressure gradients on volume flow rate Coexisting aortic regurgitation = high transaortic pressure gradient Depressed ejection fraction/coexisting mitral regurgitation = low transaortic pressure Coexisting conditions common in adults with aortic stenosis

Continuity Equation Stroke volume proximal to valve = transvalvular stroke volume CSA LVOT X VTI LVOT = CSA Ao X VTI Ao

Aortic Stenosis Aortic Valve Index
Effect of body size into account AVA index = AVA/BSA

Aortic Stenosis Technical Considerations and Pitfalls
Continuity equation valve areas: well validated in comparison with Gorlin formula Continuous wave Doppler needed d/t high velocities Use of non-imaging transducer learning curve Parallel to flow: utilize several windows Outflow tract diameter: measure in mid-systole (inner edge to leading edge)

Aortic Stenosis Coexisting Valvular Disease
Approximately 80% of patients with predominate aortic stenosis have coexisting aortic regurgitation Regurgitation does not alter continuity calculation valve area calculations

Aortic Stenosis Response of the Left Ventricle to Valvular Aortic Stenosis
Chronic overload Concentric left ventricular hypertrophy LV systolic function typically preserved until late in disease course Dysfunction due to increased afterload and often reversible post repair

Aortic Stenosis Response of the Left Ventricle to Valvular Aortic Stenosis
Female vs. male Female: More hypertrophy Smaller ventricles Preserved systolic function Male: Less hypertrophy More left ventricular dilation Higher prevalence of systolic dysfunction

Aortic Stenosis Clinical Applications in Specific Patient Populations
Symptomatic Aortic Stenosis Doppler evaluation Aortic jet maximum velocity: simplest and most quantitative >4 m/sec considered surgical May have >4 m/sec and coexisting MR = not surgical <3 m/sec significant aortic stenosis unlikely; valve replacement unnecessary Caution: parallel to flow and systolic dysfunction

Asymptomatic Aortic Stenosis: Disease Progression and Prognosis Reproducibility Recording variability Intercept angle, wall filters, signal strength, acoustic window Measurement variability Identification of the maximum velocity, outflow tract diameter Physiologic variability Interim changes in heart rate, stroke volume, or pressure gradient

Asymptomatic Aortic Stenosis: Disease Progression and Prognosis Doppler echocardiography Prognosis depends o presence or absence of clinical symptoms and not on hemodynamics severity Rate of hemodynamic progression is variable from patient to patient On average: Increase of 0.3 m/sec per year Increase of mean pressure of 7 mmHg per year Valvular size decrease of 0.1 cm2 per year Concurrent decrease in volume flow rate may obscure disease progression resulting in no change in jet velocity

Aortic Stenosis 2D Criteria
Systolic “doming” and diastolic prolapse represent congenital features Usually thickened valve leaflets with restricted motion. Doming during early systole. Concentric left ventricular hypertrophy with normal LV cavity size. LA size will be increased (late in course of AS)

Aortic Stenosis Dobutamine Echocardiography
Dobutamine is a drug used to increase stroke volume across the stenotic valve. Mild to moderate stenosis valve leaflets will open wider with increase in stroke volume. True severe stenosis Valve will not open wider Dobutamine infusion will increase the maximum velocity of both the outflow tract and the jet proportionally. In milder forms of stenosis, increase in velocity of the left ventricular outflow tract will be much greater than that of the jet (due to the increase in valve area) Limitation of zero change in velocity results

Aortic Stenosis Dobutamine Stress Echocardiography
Feigenbaum

Additional Information

Mitral Stenosis

Mitral Stenosis Diagnostic Imaging of the Mitral Valve
Evaluate: Valve anatomy, mobility and calcification Mean transmitral pressure gradient 2D echo mitral valve area Doppler pressure half-time area Pulmonary artery pressures Coexisting mitral regurgitation

Technical Considerations
Accurate pressure gradient calculations depend on accurate velocity measurements PW Doppler signals may show better definition of the maximum velocity and early diastolic slope than CW Doppler Better signal-to-noise ratio

Mitral Valve Area-2D Simpler planimetry than with aortic valve
Well validated compared with valve area at surgery and catheterization-determined valve areas Shape of inflow region similar to a funnel Important to perform planimetry at leaflet tips Begin at apex and scan toward leaflet tips and low gain

Technical Considerations
Direct planimetry of mitral valve area on 2D shown to be a valid technique in most clinical situations Size may be underestimated if gain is too low (and vice versa) Image at leaflet tips

Mitral Valve Area Pressure Half-Time
Rate of pressure decline across the stenotic mitral orifice is determined by the cross-sectional area of the orifice Smaller the orifice, the slower the rate of decline Image right: maximum velocity and diastolic slope are identified. Pressure half-time of 226 ms corresponds to valve area of 1 cm2. No a-wave d/t atrial fibrillation

Mitral Valve Area Pressure Half-Time
Influence of atrial and ventricular compliance is assumed to be negligible Assumption not always warranted especially after percutaneous commissurotomy

Mitral Stenosis Differential Diagnosis
Includes other grounds of pulmonary congestion Standard echocardiography evaluation LV systolic function Aortic valve disease Presence of mitral regurgitation Diastolic LV function Rare case of atrial myxoma or other atrial tumor obstruction to LV inflow Rare case of cor triatriatum

Mitral Stenosis Rheumatic Disease
Predominately affects mitral valve Most common cause of mitral stenosis Characterized by commissural fusion Results in bowing or doming of the valve leaflets in diastole Base and midsections of leaflets move toward ventricular apex

Mitral Stenosis Rheumatic Disease - continued
Motion of the leaflet tips is restricted due to fusion of the anterior and posterior leaflets along the medial and lateral commissures Thickening of leaflet tips occurs frequently May have normal thickening of base and midportions Often calcification and fibrosis of chordae tendinae

Mitral Stenosis Rheumatic Disease
Leaflets become scarred and contracted. Adhesions cause fusion of the commissures of the valve,restricting movement of both leaflets. Leaflets become tethered in a downward position,creating a funnel-shaped structure. Over time there is progressive fibrosis at the initial site of fusion as well as throughout the more distal chordae and more proximal leaflets. Notice the classic “Hockey Stick” appearance of the anterior leaflet causing a doming effect. Note the belly of the leaflet is pliable (arrows) and there is little or no fibrosis, calcification, or thickening of the leaflets. Also not the secondary dilatation of the left atrium. Feigenbaum

Mitral Annular Calcification (MAC)
Common finding in elderly patients Mild MAC appearance Isolated area of calcification on the left ventricular side of the posterior annulus, near the base of the posterior mitral leaflet Area of fibrous continuity between aortic root and anterior mitral leaflet is rarely involved MAC may result in mid-to-moderate MR d/t increased rigidity of mitral annulus Occasionally MAC extends into based of mitral leaflets resulting in functional mitral stenosis (MS) due to narrowing of inflow area

Mitral Annular Calcification
Degenerative process seen frequently in older patients MAC can vary from very mild to very severe Precise cause of MAC is not fully known

Theory Natural step in the degeneration of the cardiovascular fibrous tissue that occurs in the older population Predisposing factors include: Advanced Age, Female Gender, Diseases that Increase Stress on Mitral Valve Apparatus

MAC May Contribute to the Following: Conduction Disturbances Stroke Infective Endocarditis Calcium deposits may extend into the membranous portion of the interventricular septum, involving the atrioventricular node and bundle of His and causing conduction disturbances. Stroke: Patients with MAC are twice as likely to have a thromboembolic event as patients without this condition in the absence of other potential sources. Thromboembolic events can be due either to the effects of mitral annular calcification on other structures such as left atrial enlargement, resulting in atrial fibrillation, or to calcific emboli or both. Feigenbaum

Mitral Stenosis: Left Atrial Enlargement and Thrombus
Chronic pressure overload Gradual enlargement of left atrium Stasis of blood due to low volume rate Results in thrombi Preferential to left atrial appendage May occur in body of atrium as protruding or as laminated thrombus along atrial wall or interatrial septum Most often occurs in conjunction with atrial fibrillation but may occur in NSR Br Heart J December; 37(12): 1281–1285

TTE High specificity for detection of left atrial thrombus Low sensitivity <50% Challenge is imaging left atrial appendage TEE High specificity >99% High sensitivity >99% Non-dynamic Non-dynamic

21-40a Feigenbaum

21-41 Feigenbaum

Pulmonary Hypertension
Left atrial pressure leads to Pulmonary venous hypertension leads to Pulmonary artery hypertension

Chronic Irreversible changes in the pulmonary vascular bed occur Elevated pulmonary vascular resistance and persistence of pulmonary hypertension even after relief of mitral stenosis

Suspect pulmonary hypertension in mitral stenosis when there is existing: Mid-systolic partial closure (“notching” of pulmonic valve m-mode Short interval between onset of flow and maximum velocity Severe pulmonary hypertension 2D echocardiographic finding RVH and RVE Paradoxic septal motion Tricuspid regurgitation secondary to annular dilation

Mitral Stenosis with Mitral Regurgitation
Coexisting regurgitation common in patients with mitral stenosis Mitral regurgitation will be covered in next lecture material

Mitral Stenosis with Co-Existing Other Valvular Disease
Rheumatic disease may also affect Aortic valve (second in frequency to mitral valve) Stenosis and/or regurgitation Aortic regurgitation may complicate assessment of mitral stenosis due to merging of two diastolic jets Tricuspid valve (less commonly) Tricuspid stenosis due to rheumatic disease difficult to appreciate on 2D imaging TR may also be caused by mitral stenosis resultant pulmonary hypertension

Mitral Stenosis –Left Ventricular Response
Left ventricle Small with normal wall thickness and normal systolic function Diastolic dysfunction is impaired due to mitral inflow restriction Presence of dilation suggests coexistent Mitral or aortic regurgitation Primary myocardial dysfunction (cardiomyopathy or ischemic disease)

Pre- and Postpercutaneous Commissurotomy
Balloon mitral balloon valvotomy/ commissurotomy Echo Doppler evaluation important for patient selection in terms of Predicted hemodynamic results Risk of procedural complications May use qualitative assessment, an additive scoring system or quantitative measurements of leaflet mobility (see Textbook written by Otto on Valvular Stenosis)

Best hemodynamic results Thin, mobile leaflets that have commissural fusion but little calcification or subchordal thickening Patients with most heavily calcified and deformed valves More likely to suffer procedure-related morbidity and mortality Contraindicated in conjunction with moderate or severe mitral regurgitation Left atrial thrombi dislodgement by catheters during procedure possibility TEE indicated prior to procedure

Post procedure Echo identification of complications and baseline for future assessments Complications Increase in severity of mitral regurgitaiton Presence of an atrial septal defect at the transseptal catheter puncture site

Mitral Stenosis and Pregnancy
Symptoms due to MS often initially occur during pregnancy due to Increased metabolic demands and volume flow rate

Tricuspid Valve Stenosis

Narrowing of the Tricuspid Valve Orifice Uncommon in adults
Tricuspid Stenosis Narrowing of the Tricuspid Valve Orifice Uncommon in adults

Tricuspid Valve Stenosis
<2.0 cm2 : severe tricuspid stenosis

Tricuspid Stenosis - Etiologies
Rheumatic Heart Disease – nearly all cases in association with rheumatic mitral involvement Systemic lupus erythematosus Loeffler’s endocarditis Metastatic melanoma Congenital heart disease Carcinoid Right atrial tumor/thrombus Whipple’s Disease Fabry’s Disease Infective Endocarditis Endocardial fibroelastosis Methysergide therapy Prosthetic valve

Symptoms Dyspnea Fatigue Right upper quadrant pain

Physical Examination Jugular venous distention Quiet precordium
Hepatomegaly Ascities Jaundice Peripheral edema without pulmonary congestion Signs and symptoms of mitral stenosis

Carvallo’s Sign Jose’ Manuel Rivero Carvallo (Mexican cardiologist 1905-1993)
The increase in the intensity of the pansystolic murmur of tricuspid regurgitation during inspiration. Distinguishes tricuspid from mitral involvement Best heard over left sternal border

Complications Increased risk of infective endocarditis
Decreased cardiac output

Cardiac Auscultation Opening snap (may occur later than mitral valve opening snap) Diastolic rumble best heard along the lower left sternal border Higher frequency than mitral stenosis rumble May be accentuated with inspiration Presystolic click with atrial contraction Both the opening snap and the diastolic rumble may be accentuated with inspiration Absence of normal respiratory splitting of S2 Tricuspid regurgitation murmur

Chest X-Ray (CXR) Right atrial enlargement Biatrial enlargement
Atrial fibrillation Right ventricular hypertrophy Suggests coexisting mitral stenosis with pulmonary hypertension

Cardiac Catheterization
Increased mean diastolic pressure gradient between the right atrium and right ventricle Increases with inspiration Increased right atrial pressure Persistence of end diastolic gradient between right atrium and right ventricle Aids in differentiating tricuspid stenosis from tricuspid regurgitation

M-Mode Criteria for Tricuspid Stenosis
Thickened tricuspid valve leaflets Decreased EF slope of the anterior tricuspid leaflet Anterior motion of the posterior valve leaflet Decreased/absent A wave of the anterior tricuspid valve leaflet Steep A-C slope of the tricuspid valve Pulmonary hypertension Due to coexisting mitral valve disease

2D Criteria for Tricuspid Stenosis
Thickened tricuspid valve leaflets, especially at leaflet tips and chordae tendinae with restricted motion Diastolic “doming” of the tricuspid valve with commissural fusion of the leaflets Right atrial dilatation Dilated inferior vena cava and hepatic veins Leftward protrusion of the interatrial septum Pulmonary hypertension (due to coexisting mitral valve disease)

TV Stenosis Doppler

Surgical Treatment Surgical/Balloon commisurotomy
Valve repair/valve replacement

Stenosis Tricuspid Valve
Rheumatic Heart Disease

Rheumatic Tricuspid Stenosis
Isolated rheumatic tricuspid almost never occurs Significant tricuspid stenosis occurs in roughly 3-5% of patients with rheumatic heart disease Rheumatic fever affecting the tricuspid valve is <6% and has a preponderance to females The tricuspid valve is in rheumatic heart disease is usually not as thickened or calcified as compared to mitral valve stenosis

M-Mode Criteria for Rheumatic Tricuspid Stenosis
Diminished EF slope Anterior displacement of the posterior leaflet Thickening of valve leaflets and apparatus

Caveats of M-Mode Criteria for Rheumatic Tricuspid Valve Stenosis
Accuracy is far lower than dx for mitral stenosis with M-mode Frequently concurrent pulmonary hypertension and right ventricular hypertrophy, which also lead to a diminished EF slope Anterior displacement of the posterior leaflet cannot always be well visualized and is therefore not a reliable finding Therefore, 2D is a more reliable technique in dx of rheumatic tricuspid stenosis

2D Criteria for Rheumatic Tricuspid Valve Stenosis
Doming of tricuspid valve leaflets in diastole, typically more toward the tips of the leaflets Thickening and reduced excursion of the posterior or septal leaflets, or both Reduced tricuspid orifice diameter relative to the diameter of the tricuspid annulus in the same scan plane

RVIT Rheumatic Stenosis
Note the thickening of the leaflets, which is maximal at the tips and chordae, and the preserved mobility of the mid portion of the leaflets in the real-time image Feigenbaum

Tricuspid Stenosis Important to Note
Tricuspid stenosis is pressure of the right atrium, which will eventually produce peripheral edema and reduced cardiac output Tricuspid stenosis almost never occurs as an isolated lesion; it generally accompanies mitral stenosis, so evaluate for mitral, aortic, and pulmonic valve disease due to rheumatic fever

Pulmonic Stenosis

Pulmonary Stenosis Pathophysiology
Systolic pressure overload leads to RVH Regional hypertrophy may lead to infundibular stenosis Commonly associated with other congenital malformations (VSDs, ASDs, tetrology of Fallot) RV chamber size usually normal, RA will enlarge Increased risk of endocarditis

Pulmonic Stenosis Etiology
Congenital (most common) Rheumatic (rare) Carcinoid Peripheral (PPS-junction of the R and L PAs) Infundibular (subvalvular) Prosthetic valve dysfunction

Physical Signs of PS Dyspnea on exertion
Systolic ejection murmur (LUSB) Pulmonary ejection sound, decreased/delayed P2 Sustained RV impulse at mid-lower LSB

Echo Findings M-mode may show an increase in the pulmonic “a” dip of more than 7 mm (useful for severe PS only) Valvular thickening and systolic doming (2D) Right ventricular hypertrophy Post-stenotic dilatation of the PA Narrowing of RVOT in infundibular PS Non-dynamic

Pulmonary Stenosis M-Mode and 2D
Mild pulmonary stenosis No abnormality is detectable either by M-mode or two- dimensional echocardiography. More severe obstruction, May be possible to detect right ventricular hypertrophy, Echocardiography is not a very sensitive method for diagnosing this. Non-dynamic

Pulmonary Stenosis M-Mode
Another sign that has been reported, confined to patients with severe obstruction, is an exaggerated "a-dip" on the pulmonary valve echocardiogram. “a-dip” or “diving W” Hypertrophied right atrium forcefully injects blood into an already full and stiff right ventricle during atrial systole. Pulmonary artery pressure is low, Sudden increase in right ventricular pressure is sufficient to partially open the pulmonary valve

Doppler Findings Increased velocity and turbulence at level of obstruction (valvular, subvalvular, or supravalvular) Use pulsed/color flow Doppler to locate level of obstruction Check for coexisting pulmonic regurgitation Measure peak and mean gradients (PSAX-Ao and RVOT are best)

Pulmonic Stenosis Doppler
CW Doppler spectral recording from PSAX-Ao view in a patient with mild pulmonic stenosis and mild pulmonic stenosis. Turbulent diastolic and systolic flows are noted with a slight increase in the peak systolic velocity to 1.4 m/s (normal < 1 m/s)

Subvalvular Stenosis Note the presence of muscle bundles in the area of the right ventricular outflow tract (arrow). 18-21 Feigenbaum

Pulmonic Valve Stenosis
18-24PV Feigenbaum A basal short-axis view demonstrates a thickened pulmonary valve (arrow). Doppler imaging demonstrates a peak gradient of 35 mm Hg.

Dysplastic Pulmonary Valve Stenosis
An example of dysplastic (Any abnormal development of tissues or organs. In pathology, alteration in size, shape, and organization of adult cells) pulmonary valve stenosis is provided. A: The pulmonary valve (arrow) is markedly thickened and immobile. Doming during systole is present. B: A maximal pressure gradient of approximately 65 mm Hg is demonstrated. PA, pulmonary artery; RVOT, right ventricular outflow tract. 18-24 Feigenbaum

Complication Right Heart Failure
An example of right ventricular pressure overload is shown due to pulmonary hypertension and consequentially infundibular hypertrophy. The right heart is severely dilated, and there is global right ventricular hypocontractility. 07-058a Feigenbaum

Complication Right Heart Failure
The short-axis view demonstrates marked flattening of the septum that was maintained in both systole and diastole. 07-058b Feigenbaum

Sources Feigenbaum H, Armstrong W. (2004). Echocardiography. (6th Edition). Indianapolis. Lippincott Williams & Wilkins. Goldstein S., Harry M., Carney D., Dempsey A., Ehler D., Geiser E., Gillam L., Kraft C., Rigling R., McCallister B., Sisk E., Waggoner A., Witt S., Gresser C.. (2005). Outline of Sonographer Core Curriculum in Echocardiography. Otto C. (2004). Textbook of Clinical Echocardiography. (3rd Edition). Elsevier & Saunders. Reynolds T. (2000). The Echocardiographer's Pocket Reference. (2nd Edition). Arizona. Arizona Heart Institute.

Valvular Stenosis Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE)

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