Valvular Heart Disease Flashcards
The most common etiology of mitral stenosis in adults is:
A. Congenital
B. Left atrial myxoma
C. Rheumatic fever
D. Severe mitral annular calcification
C. Rheumatic fever is the most common cause of mitral valve stenosis (99%). Congenital (e.g., parachute mitral valve), left atrial myxoma and severe mitral annular calcification are possible etiologies for mitral valve stenosis but are not as common as rheumatic fever. Rarely, mitral valve stenosis is a complication of malignant carcinoid heart disease, systemic lupus erythematosus, rheumatoid arthritis and the mucopolysaccharides of the Hunter-Hurley phenotype. In rheumatic fever, the mitral valve leaflet tips thicken and there is commissural fusion as well as thickening and shortening of the chordae tendineae.
The cardiac valves listed in decreasing order as they are affected by rheumatic heart disease are:
A. Aortic, pulmonic, tricuspid, mitral
B. Mitral, aortic, tricuspid, pulmonic
C. Pulmonic, aortic, tricuspid, mitral
D. Tricuspid, mitral, pulmonic, aortic
B. The mitral valve is the most common valve affected in rheumatic heart disease, followed by the aortic valve, tricuspid valve and rarely the pulmonic valve. Rheumatic fever results in four forms of fusion of the mitral valve apparatus leading to stenosis: (1) commissural, (2) cuspal,
(3) chordal and (4) combined.
Signs and symptoms of mitral stenosis secondary to rheumatic heart disease include:
A. Angina pectoris
B. Cyanosis
C. Pulmonary hypertension
D. Vertigo
C. Pulmonary hypertension is commonly associated with mitral stenosis because of (1) passive backward transmission of the elevated left atrial pressure, (2) arteriolar constriction and (3) organic obliterative changes in the pulmonary vascular bed. Eventually, right ventricular pressures increase which may lead to right ventricular failure.
Patients with mitral stenosis, left atrial enlargement and atrial fibrillation are at increased risk for the development of:
A. Left atrial myxoma
B. Left atrial thrombus
C. Left ventricular dilatation
D. Left ventricular thrombus
B. Thromboembolism is an important complication of mitral stenosis. The tendency for embolization correlates inversely with cardiac output and directly with age and the size of the left atrium with 80% of patients in whom systemic emboli develop are in atrial fibrillation.
Conditions that may lead to clinical symptoms that mimic those associated with rheumatic mitral stenosis include:
A. Aortic stenosis
B. Left atrial myxoma
C. Pericardial effusion
D. Ventricular septal defect
B. A mobile left atrial myxoma may prolapse into the mitral valve orifice during ventricular diastole and obstruct flow into the left ventricle mimicking mitral stenosis.
The equation used in the cardiac catheterization laboratory to determine mitral valve area is the:
A. Gorlin
B. Bernoulli
C. Doppler
D. Continuity
A. In most patients with mitral stenosis a detailed echocardiographic examination including two-dimensional echocardiography, a Doppler study with color flow Doppler provides the information required for optimal patient care. Cardiac catheterization may not be necessary to evaluate mitral stenosis hemodynamics including mitral valve area. Cardiac catheterization is required to evaluate coronary artery disease.
The M-mode being demonstrated below is an example of:
A. Mitral valve prolapse
B. Mitral stenosis
C. Left atrial myxoma
D. Aortic regurgitation
B. The three classic M-mode findings for mitral stenosis are:
• Thickened mitral valve leaflets
• Decreased mitral valve E-F’ slope
• Anterior motion of the posterior mitral valve leaflet
A strong indication for mitral stenosis on two-dimensional echocardiography is an anterior mitral valve leaflet that exhibits:
A. Coarse, chaotic diastolic motion
B. Diastolic doming
C. Reverse doming
D. Systolic bowing
B. Diastolic doming of the anterior mitral valve leaflet is an important two-dimensional finding in patients with rheumatic mitral valve stenosis. This classic finding is thought to be caused by commissural fusion.
Two-dimensional echocardiographic findings for rheumatic mitral stenosis include all of the following EXCEPT:
A. Hockey-stick appearance of the anterior mitral valve leaflet
B. Increased left atrial dimension
C. Reverse doming of the anterior mitral valve leaflet
D. Thickened mitral valve leaflets and subvalvular apparatus
C. Mitral stenosis is almost always caused by rheumatic involvement of the mitral valve. The mitral valve leaflets are thickened with diastolic doming (hockey-stick appearance) of the mitral valve. The left atrium is enlarged. In the parasternal short-axis of the mitral valve leaflets, the orifice of the mitral valve has a fish-mouth appearance.
Reverse doming of the anterior mitral valve may be seen in patients with severe aortic regurgitation.
The most accurate method for determining the severity of mitral valve stenosis is:
A. Determining the maximum velocity across the mitral valve by pulsed-wave Doppler
B. Measuring the E-F slope of the anterior mitral valve leaflet by M-mode
C. Measuring the thickness of the mitral valve leaflets
D. Performing planimetry of the mitral valve orifice by two-dimensional echocardiography
D. Obtaining the measurement of the mitral valve area by planimetry from the short-axis view of the mitral valve is an accurate method for quantifying the severity of mitral valve stenosis. The short-axis view of the mitral valve demonstrates the orifice of the stenotic valve and provides the opportunity for determining the degree of mitral valve stenosis.
Critical mitral valve stenosis is said to be present if the mitral valve area is reduced to:
A. < 1.0 cm^2
B. 1.0 to 1.5 cm^2
C. 1.5 to 2.5 cm^2
D. 2.5 to 3.5 cm^2
A. Severe critical mitral valve stenosis is present when the mitral valve area is <1.0 cm^2. Mitral valve operation is recommended in these patients. Mitral valve area of 1.1 to 1.5 cm^2 is considered moderate stenosis and 1.6 to 2.5 cm^2is mild.
The normal mitral valve area is 4 to 6 cm^2.
Typical echocardiographic findings in a patient with isolated rheumatic mitral stenosis include all of the following EXCEPT:
A. D-shaped left ventricle
B. Dilated left ventricle
C. Left atrial enlargement
D. Left atrial thrombus
B. In pure isolated mitral stenosis, the left ventricle does not become dilated. It may dilate if mitral valve regurgitation accompanies the stenosis. A D-shaped left ventricle which persists throughout ventricular systole and ventricular diastole suggests a right ventricular pressure overload. A D-shaped left ventricle during ventricular diastole which becomes circular in shape during ventricular systole suggests a right ventricular volume overload.
Secondary echocardiographic/Doppler findings in patients with rheumatic mitral stenosis include all the following EXCEPT:
A. Abnormal interventricular septal wall motion
B. Increase right heart dimensions
C. Increased tricuspid regurgitant jet velocity
D. Left ventricular dilatation
D. Because of the increase pulmonary artery pressure, the right ventricle and the right atrium will eventually dilate. As pulmonary artery pressure increases, the tricuspid valve systolic regurgitant peak velocity will follow. Abnormal septal wall motion due to right ventricular volume and/or pressure overload will lead to septal flattening and/or paradoxical septal motion.
The classic cardiac Doppler features of mitral valve stenosis include all the following EXCEPT:
A. Increased E velocity
B. Increased mitral valve area.
C. Increased pressure half-time
D. Turbulent flow
B. The expected cardiac Doppler findings in rheumatic mitral valve stenosis are increase velocities, turbulent flow and increased pressure half-time. The increased mitral inflow E velocity corresponds to the increased transmitral pressure gradient. The turbulent flow is due to the disturbance of flow caused by the valvular stenosis. The prolonged Doppler pressure half-time corresponds to the decrease in mitral valve area.
The abnormal mitral valve pressure half-time for patients with mitral valve stenosis is:
A. 0 to 30 msec
B. 30 to 60 msec
C. 60 to 90 msec
D. 90 to 400 msec
D. The abnormal range for the pressure half-time (PHT) in a patient with mitral valve stenosis is 90 to 400 msec. Mitral valve stenosis is considered severe when the pressure half-time is 220 msec or longer and the mitral valve area is 1.0 cm^2 or smaller.
MVA (cm^2) = 220 ÷ PHT (msec)
A deceleration time of 800 msec was obtained by continuous-wave Doppler in a patient with rheumatic mitral valve stenosis. The pressure half-time is:
A. 220 msec
B. 232 msec
C. 400 msec
D. 800 msec
B. The pressure half-time can be determined by the formula:
Pressure half-time (msec) = Deceleration time x 0.29
In this example, the pressure half-time is 800 msec x 0.29 = 232 msec
Mitral valve area (cm?) = 220 ÷ Pressure half-time
For this question: Mitral valve area (cm^2) = 220 ÷ 232 msec = .95 cm^2
Doppler mean pressure gradient across a stenotic mitral valve of 22 mm Hg is obtained. The severity of the mitral stenosis is:
A. Mild
B. Moderate
C. Moderately severe
D. Severe
D. Mild mitral stenosis is present when the mean pressure gradient of < 4 mm Hg, moderate 4 to 10 mm Hg and severe > 10 mm Hg.
Tracing the continuous-wave Doppler spectral waveform will allow computation of the peak velocity, peak pressure gradient, mean pressure gradient and velocity time integral.
Mitral stenosis is considered to be severe by all the following criteria EXCEPT:
A. Mean pressure gradient ≥ 10 mm Hg
B. Mitral valve area ≤ 1.0 cm^2
C. Mitral valve Doppler A wave peak velocity > 1.3 m/s
D. Pressure half-time > 220 msec
C. In the Doppler evaluation of mitral valve stenosis severity, the mitral valve A wave peak velocity is usually ignored.
Two-dimensional echocardiographic examination reveals thin mobile mitral valve leaflet tips and a Doppler E velocity of 1.8 m/s with a pressure half-time of 180 msec in an elderly patient. The most likely diagnosis is:
A. Abnormal relaxation of the left ventricle
B. Aortic regurgitation
C. Moderate to severe mitral annular calcification
D. Rheumatic mitral stenosis
C. In mitral stenosis due to severe mitral annular calcification, the Doppler and secondary echocardiography findings are similar to rheumatic mitral stenosis. This type of mitral obstruction is referred to as “functional” mitral stenosis.
All of the following are possible etiologies of anatomic mitral regurgitation EXCEPT:
A Mitral annular calcification
B. Mitral valve prolapse
C. Ruptured chordae tendineae
D. Dilated cardiomyopathy
D. Mitral regurgitation caused by segmental or global abnormalities without structural abnormalities of the mitral valve is termed functional mitral regurgitation and is commonly seen in patients with dilated cardiomyopathy or ischemic cardiomyopathy.
All of the following are causes for chronic mitral regurgitation EXCEPT:
A Rheumatic heart disease
B. Cleft mitral valve
C. Ruptured papillary muscle
D. Mitral annular calcification
C. Papillary muscle rupture is a rare complication of acute myocardial infarction and generally occurs during the second to third day following infarction. Rupture of the posteromedial papillary muscle is three times more common than rupture of the anterolateral papillary muscle. This is because the anterolateral papillary muscle is supplied by branches of the left anterior descending coronary artery and circumflex coronary artery. The posteromedial papillary muscle is supplied only by the posterior descending coronary artery.
The most common cause of acute mitral regurgitation is rupture of the chordae tendineae due to mitral valve prolapse.
The most common presenting symptom of significant chronic mitral regurgitation is:
A. Dyspnea
B. Hemoptysis
C. Systemic embolization
D. Ascites
A. The patient with significant chronic mitral regurgitation presents with the signs and symptoms of congestive heart failure: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, cough and weight gain due to the reduction of stroke volume and cardiac output as well an increase in pulmonary artery pressures.
Congestive heart failure in a patient with significant chronic mitral regurgitation occurs because of increased pressure in the:
A. Left atrium
B. Left ventricle
C. Right ventricle
D. Aorta
A. Congestive heart failure (inability of the heart to meet the metabolic demands of the body) can occur in patients with significant chronic mitral regurgitation due to the increase in left atrial pressure. The signs and symptoms of congestive heart failure include dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, cough and weight gain.
Possible signs and symptoms associated with acute severe mitral regurgitation include:
A. Hemoptysis
B. Anasarca
C. Pulmonary edema
D. Systemic embolization
C. Edema is the accumulation of fluid in cells, tissues or body cavities. Pulmonary edema is the accumulation of fluid in the lungs. In patients who develop severe acute mitral regurgitation, the left atrial pressure is reflected back into the pulmonary circuit. Because there is a rapid rise in pulmonary pressures at the venous level, fluid is forced out of the pulmonary capillaries and veins into the lungs.
Chronic significant mitral regurgitation may result in all of the following EXCEPT:
A Left atrial enlargement
B. Left ventricular enlargement
C. Left ventricular volume overload pattern
D. Mitral annular calcification
D. Chronic significant mitral regurgitation may lead to a volume overload in which the left atrium and the left ventricle bear the burden. If significant, the left ventricle will eventually fail because of the volume overload. The left ventricular volume overload pattern is left ventricular dilatation with hyperkinetic wall motion.
Mitral annular calcification is a common reason for the systolic murmur of mitral regurgitation in the elderly.
The most likely heart sound to be heard in patients with significant chronic pure mitral regurgitation is:
A. Loud S1
B. Fixed split S2
C. S3
D. Ejection click
C. The third heart sound (S3) (also referred to as the protodiastolic gallop or ventricular gallop) is the result of rapid filling and stretching of an abnormal left ventricle. It is frequently an early sign of left ventricular failure. The third heart sound may be present in patients with mitral regurgitation, aortic regurgitation, ventricular septal defect and patent ductus arteriosus. An S3 may also be a normal variant found especially in young adults.
The classic description of the murmur of chronic mitral regurgitation is:
A Holosystolic murmur heard best at the apex radiating to the axilla
B. Continuous machinery-like murmur
C. Systolic ejection murmur heard best at the right upper sternal border
D. Diastolic decrescendo murmur heard best at the left sternal border
A. The character of the murmur of mitral regurgitation depends upon whether the mitral regurgitation is mild, moderate or severe. It also depends on whether the anterior or posterior mitral valve leaflet is involved. In patients with posterior mitral valve leaflet defects, the direction of the regurgitant jet may be anterior and the mitral regurgitation murmur is best heard in the aortic area. In patients with mitral valve prolapse, the murmur may be crescendo and late systolic.
Cardiac magnetic resonance imaging provides all of the following information in the evaluation of mitral regurgitation EXCEPT:
A Regurgitant volume
B. Left ventricular volumes
C. Detailed visualization of the mitral valve apparatus
D. Left ventricular mass
C. Echocardiography provides reliable and detailed information concerning the mitral valve apparatus and function.
M-mode and two-dimensional findings associated with significant chronic mitral regurgitation include all of the following EXCEPT:
A. Fine diastolic flutter of the mitral valve
B. Left atrial enlargement
C. Left ventricular enlargement
D. Left ventricular volume overload pattern
A. Fine diastolic flutter of the mitral valve may indicate aortic regurgitation.
The two components of left ventricular volume overload are:
(1) left ventricular dilatation and (2) hyperkinetic left ventricular wall motion.
The M-mode shown is demonstrating:
A. Normal
B. Left ventricular volume overload pattern
C. Right ventricular volume overload pattern
D. Acute myocardial infarction
B. The two components of the left ventricular volume overload pattern are:
(1) left ventricular dilatation and (2) left ventricular wall hyperkinesis.
Systolic bowing of the inter-atrial septum toward the right atrium throughout the cardiac cycle may be an indication of:
A. Mitral regurgitation
B. Tricuspid atresia
C. Tricuspid regurgitation
D. Tricuspid stenosis
A. The inter-atrial septum may bow toward the right atrium in significant mitral regurgitation because left atrial pressure is markedly greater than right atrial pressure.
The inter-atrial septum may bow towards the left atrium throughout the cardiac cycle in patients with increased right atrial volume and/or pressure (e.g., significant tricuspid regurgitation, tricuspid stenosis, tricuspid atresia).
In patients with significant pure mitral regurgitation, the E velocity of the mitral valve pulsed-wave Doppler tracing is:
A. Decreased
B. Increased with inspiration
C. Increased
D. Unaffected
C. In the presence of mitral regurgitation, the velocity of antegrade mitral flow is increased because regurgitant flow is added to the normal mitral flow. Regurgitation produces an increased “v” wave in the left atrial pressure curve, resulting in an increased left atrial-left ventricular pressure difference in early diastole. This leads to an increased forward flow velocity (mitral E wave) in early diastole > 1.2 m/s.
The effect significant mitral regurgitation has on the pulsed-wave Doppler tracing of the pulmonary veins may be described as:
A. S wave increases, D wave decreases
B. S wave increases, D wave decreases
C. S wave reverses, D wave increases
D. Unaffected
C. In severe mitral regurgitation, the S wave is blunted or even reversed and the D wave is increased.
An accepted method for determining the severity of mitral regurgitation by continuous-wave Doppler is spectral:
A. Jet density
B. Length
C. Velocity
D. Width
A. By comparing the mitral inflow spectral density (strength) to the spectral jet density (strength) of the mitral regurgitation a semi-quantitative approach to the severity of mitral regurgitation can be achieved. A soft density with a parabolic flow signal suggests mild mitral regurgitation. A dense triangular continuous-wave tracing suggests the presence of severe mitral regurgitation.
In patients with significant mitral regurgitation, the continuous-wave Doppler tracing of the regurgitant lesion may demonstrate a(n):
A. Asymmetrical shape of the mitral regurgitation flow velocity
spectral display
B. Jet area of < 20%
C. Jet duration of < 85 msec
D. Symmetrical shape of the mitral regurgitation flow velocity spectral display
A. In patients with significant mitral regurgitation, the continuous-wave Doppler spectral display may demonstrate a dense, asymmetrical (triangular, tapered) shape which indicates a rapid rise in left atrial pressure due to the significant mitral regurgitation.
In patients with significant tricuspid regurgitation the continuous-wave Doppler spectral display may demonstrate a similar pattern (e.g., dense, asymmetrical) due to a rapid rise in right atrial pressure.
The peak mitral regurgitation velocity as determined with continuous-wave Doppler reflects the:
A Direction of the regurgitant jet
B. Etiology of the mitral regurgitation
C. Maximum pressure difference between the left atrium and left ventricle
D. Severity of the mitral regurgitation
C. The maximum velocity of the mitral regurgitant jet tells the examiner the maximum peak pressure difference between the left atrium and the left ventricle. The maximum velocity of the mitral regurgitation is generally 4 to 6 m/s since the pressure difference between the left atrium and the left ventricle is normally approximately 100 mm Hg during ventricular systole.
In patients with severe acute mitral regurgitation, the continuous-wave Doppler peak velocity of the regurgitant jet is:
A. Decreased
B. Dependent largely upon left ventricular global systolic function
C. Increased
D. Unaffected
A. In most cases the mitral regurgitation peak velocity is expected to fall between 4 to 6 m/s and is therefore not useful for determining the severity of mitral regurgitation. In patients with severe acute mitral regurgitation, the peak velocity may be < 4 m/s owing to an elevated left atrial pressure that reduces the pressure difference between the left ventricle and left atrium during ventricular systole. In addition, there may be tapering (triangular-shaped, asymmetrical) of the continuous-wave Doppler configuration.
In patients with significant mitral regurgitation, the isovolumic relaxation time may be:
A. Increased
B. Decreased
C. Affected by respiration
D. Unaffected
B. The isovolumic relaxation time (IVRT) is the period from aortic valve closure to mitral valve opening. The isovolumic relaxation time can be measured using pulsed-wave Doppler, continuous-wave Doppler or tissue Doppler imaging. With severe mitral regurgitation, the isovolumic relaxation time may be < 60 msec. This is due to the increase in left atrial pressure which causes the mitral valve to open sooner than normal. The normal isovolumic relaxation time is 76 + 13 msec for adults over 40 years of age.
A color flow Doppler method for semi-quantitating mitral regurgitation is regurgitant jet:
A. Area
B. Height
C. Length
D. Turbulence
A. The regurgitant jet area (RJA) compared to the left atrial area
(LAA) provides a semi-quantitative measure of the severity of mitral regurgitation. A RJA/LAA ratio of < 20% suggests mild mitral regurgitation while a RJA/LAA ratio > 40% indicates severe mitral regurgitation. The jet area may be used alone with a regurgitant jet area < 4 cm^2 indicating mild mitral regurgitation and > 8 cm^2 indicating severe mitral regurgitation. The above methods) is best to apply to central jets with the color velocity scale set to between 50 to 60 cm/s. The color gain can influence jet area. The blood pressure should be known since changes in blood pressure may change the jet area. It is important to note that the duration of the mitral regurgitation when using regurgitant jet area. Pulsed-wave Doppler, continuous-wave Doppler or color M-mode may be used to determine jet duration.
All of the following are useful color-flow Doppler techniques in the evaluation of mitral regurgitation EXCEPT:
A. Vena contracta width
B. PISA diameter
C. Peak velocity
D. Jet area
C. A vena contracta width of ≥ 0.7 cm indicates severe mitral regurgitation.
A PISA diameter of ≥ 0.9 cm indicates severe mitral regurgitation. A regurgitant jet area > 8 cm^2 indicates severe mitral regurgitation. Color flow Doppler demonstrates the mean velocity. In general, the peak velocity of mitral regurgitation is between 4 to 6 m/s and is determined with continuous-wave Doppler. In most cases, the peak velocity of the mitral regurgitation is not used to determine severity since the peak velocity represents the pressure gradient between the left ventricle and left atrium during ventricular systole. One exception is in the presence of severe mitral regurgitation (e.g., flail mitral valve due to papillary muscle rupture where a peak velocity of < 4 m/s may be obtained due a reduced systolic left ventricle - left atrial systolic pressure gradient.
Quantitative approaches to determine the severity of mitral regurgitation include all of the following EXCEPT:
A. Regurgitant volume
B. Regurgitant fraction
C. Regurgitant jet area
D. Effective regurgitant orifice
C. Regurgitant volume (RV), regurgitant fraction (RF) and effective regurgitant orifice (ERO) can be determined by using two-dimensional echocardiography with pulsed-wave Doppler. The proximal isovelocity surface area (PISA) method allows determination of regurgitant volume and effective regurgitant orifice. A regurgitant volume of ≥ 60 mL, a regurgitant fraction ≥ 50% and an effective regurgitant orifice ≥ 0.40 cm^2 indicate the presence of severe mitral regurgitation.
Cardiac Doppler evidence of severe mitral regurgitation includes all of the following EXCEPT:
A. Dense, triangular continuous-wave Doppler tracing
B. Mitral valve E wave velocity < 1.0 m/sec
C. Pulmonary vein systolic flow reversal
D. Regurgitant jet area/left atrial area ratio > 40%
B. With significant mitral regurgitation, the mitral valve E velocity will be increased (> 1.2 m/sec) due to the increased early diastolic pressure gradient between the left atrium and left ventricle. Mitral valve repair or replacement may be indicated in patients with significant mitral regurgitation when there is evidence of progressive ventricular dilatation, an end-systolic dimension > 45 mm, or a reduction in left ventricular global systolic function.
All of the following are true statements concerning mitral regurgitation EXCEPT:
A. Mitral regurgitation may be acute, chronic or intermittent
B. Mitral regurgitation may result in an increase in preload
C. Severity of mitral regurgitation is not affected by afterload
D. Regurgitant jet area, vena contracta width and proximal isovelocity surface area are recommended when determining severity
C. Afterload is the resistance to the ejection blood and can affect the severity of mitral regurgitation. An excellent example is when attempting to determine the severity of mitral regurgitation in the operating room when the patient is under anesthesia. The severity of mitral regurgitation is usually less than reported preoperatively. Noting the blood pressure and infusing isoproterenol may be required in the operating room to determine the severity of mitral regurgitation.
Diastolic mitral regurgitation is associated with:
A. Flail mitral valve
B. Mitral valve prolapse
C. Severe aortic regurgitation
D. Severe tricuspid regurgitation
C. Although mitral regurgitation is generally thought to occur during
systole, it may also occur during diastole. Diastolic mitral regurgitation is due to a positive left ventricular to left atrial pressure gradient. Other causes of diastolic mitral regurgitation include atrioventricular (AV)
block, atrial flutter, atrial fibrillation and disorders associated with
reduced ventricular compliance such as in restrictive cardiomyopathy or severe diastolic dysfunction.
The most common symptoms of mitral valve prolapse include all of the following EXCEPT:
A. Atypical chest pain
B. Palpitations
C. Syncope
D. Ascites
D. The vast majority of patients with mitral valve prolapse are asymptomatic. The symptoms of congestive heart failure (dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, cough, weight gain) may occur in patients with mitral valve prolapse who have significant mitral regurgitation. Panic attacks have been associated with mitral valve prolapse but this association has not been confirmed using the new, stricter criteria for the presence of mitral valve prolapse. Mitral valve prolapse appears to exhibit a strong hereditary component.
The complications of mitral valve prolapse include all of the following EXCEPT:
A. Increased risk of infective endocarditis
B. Significant mitral regurgitation
C. Mitral valve repair and replacement
D. Valvular stenosis
D. Other complications of mitral valve prolapse include cerebral embolic events and cardiac arrhythmias (e.g, paroxysmal supraventricular tachycardia, atrial fibrillation). Mitral valve prolapse appears to be the most common reason for mitral valve repair in the United States due to isolated significant mitral regurgitation. There may be an increased risk of sudden death in patients with mitral valve prolapse with severe mitral regurgitation, complex ventricular arrhythmias, QT interval
prolongation and a history of syncope and palpitations.
The associated auscultatory findings for mitral valve prolapse include:
A. Ejection click
B. Friction rub
C. Mid-systolic click
D. Pericardial knock
C . The classic auscultatory findings for mitral valve prolapse are mid-systolic click and late systolic murmur. The mid-systolic click is thought t o originate from the tensing of the chordae tendineae and the late systolic murmur originates from the mitral regurgitation.
A keyword that is often used to describe the characteristics of the valve leaflets in mitral valve prolapse is:
A. Dense
B. Doming
C. Redundant
D. Sclerotic
C. The terms redundant, thick and myxomatous are used to describe the valve leaflets in patients with classic mitral valve prolapse due to myxomatous degeneration. In non-classic mitral valve prolapse, the mitral valve leaflets are normal in thickness (< 5 mm).
The term myxomatous degeneration is associated with mitral valve:
A. Flail
B. Prolapse
C. Stenosis
D. Vegetation
B. Classic mitral valve prolapse is characterized by an increase in the amount of loose myxomatous tissue in the spongiosa component (the middle layer of the leaflet) which encroaches on the fibrosa
(the ventricular surface of the leaflet). The associated redundancy or myxomatous degeneration in the valve leaflet and chordae tendineae permit prolapse during ventricular systole. The terms thick, redundant or myxomatous may be used to describe a mitral valve prolapse if the valve leaflet thickness is > 5 mm. This is called classic mitral valve prolapse.
Echocardiographic characteristics of mitral valve prolapse include all of the following EXCEPT:
A. Increased mitral valve annulus diameter
B. Systolic bowing of the mitral valve leaflets towards the left atrium
C. Thickened, redundant, myxomatous leaflets
D. Diastolic doming of the mitral valve leaflets
D. Mitral valve prolapse is defined as systolic displacement (> 2 mm) of one or both mitral valve leaflets in to the left atrium above the plane of the mitral annulus. The parasternal long-axis view is the recommended view due to the fact the mitral annulus is saddle-shaped. The mitral annulus may be markedly dilated in patients with mitral valve prolapse. M-mode may be useful to determine whether the mitral valve prolapse
is mid to late systolic or holosystolic.
The gold standard two-dimensional echocardiographic view recommended to diagnose the presence of mitral valve prolapse is:
A. Parasternal long-axis
B. Parasternal short-axis of the mitral valve
C. Apical four-chamber
D. Subcostal five-chamber
A. Because the mitral annulus is saddle-shaped, the parasternal long-axis is the recommended view. A systolic displacement (> 2 mm ) of one or both leaflets into the left atrium suggests mitral valve prolapse. If the prolapsing leaflets) are > 5 mm in thickness, classic mitral valve prolapse is present. If the prolapsing leaflets) are < 5 mm in thickness,
non-classic prolapse is present. Use of the apical four-chamber view as the gold standard view for several years resulted in the over-diagnosis of mitral valve prolapse (5 to 15%). Using the stricter criteria described above, the prevalence of mitral valve prolapse is 1.7 to 2.4%. Mitral valve prolapse is twice as frequent in women than in men but significant mitral regurgitation occurs more frequently in older men (> 50 years of age) with mitral valve prolapse than in young women with mitral valve prolapse.
Secondary causes of mitral valve prolapse include all of the following EXCEPT:
A. Atrial septal defect
B. Bicuspid aortic valve
C. Cardiac tamponade
D. Primary pulmonary hypertension
B. A disease process that increases right ventricular dimension will decrease the left ventricular dimension thus causing the mitral valve to prolapse into the left atrium during ventricular systole (e.g., atrial septal
defect, primary pulmonary hypertension). Moderate to large pericardial effusion may exaggerate valve motion resulting in false positive mitral valve prolapse. Patients who are obese rarely present with mitral valve
prolapse because of increased left ventricular volumes.
All of the following are associated with mitral valve prolapse ЕХСЕРТ:
A. Mitral regurgitation
B. Tricuspid valve prolapse
C. Aortic valve prolapse
D. Pulmonary atresia
D. The mitral regurgitation may be mid to late systolic or holosystolic. Tricuspid valve prolapse may be present in up to 50% of patients with mitral valve prolapse. Aortic valve prolapse is uncommon but may
be found in patients with mitral valve prolapse (10% of patients with classic mitral valve prolapse) or with bicuspid aortic valve.
Which of the following is most commonly associated with mitral valve prolapse?
A. Left heart volume overload
B. Left heart pressure overload
C. Right heart pressure overload
D. Right heart volume overload
A. Mitral valve prolapse may result in significant chronic mitral regurgitation. Significant chronic mitral regurgitation initially results in left atrial dilatation, left ventricular dilatation and the left ventricular
volume overload pattern (left ventricular dilatation with hyperkinetic wall motion). With time, pulmonary hypertension may develop.
There is posterior mitral valve prolapse present. With color flow Doppler on, which direction will the mitral regurgitation jet be baffled?
A. Anterior
B. Posterior
C. Inferior
D. Cephalad
A. Anterior mitral valve prolapse will baffle the jet posterior. Prolapse of both mitral valve leaflets will result in a central jet.
Flail mitral valve can be differentiated from severe mitral valve prolapse on two-dimensional echocardiography because flail mitral valve leaflet demonstrates:
A. A thicker mitral valve
B. Chronic mitral regurgitation
C. Leaflet tip that points toward the left ventricle
D. Leaflet tip that points toward the left atrium
D. A flail mitral valve leaflet will present on two-dimensional echocardiography with exaggerated motion and the tip of the affected leaflet loses its point of coaptation and moves into the left atrium with its tip pointing superiorly into the left atrium. Severe mitral regurgitation is associated with flail mitral valve although the jet may
be baffled in such a way as to “hug” the valve leaflet and left atrial wall. This will make the regurgitant jet appear to be smaller with color flow Doppler on (coanda effect).
Mitral valve chordal rupture usually results in:
A. Aortic regurgitation
B. Mitral regurgitation
C. Pulmonary regurgitation
D. Tricuspid regurgitation
B. The most common cause of chordae tendinee rupture is mitral valve prolapse. Other causes include rheumatic heart disease, infective endocarditis, connective tissue disorders, myocardial infarction,
hypertrophic cardiomyopathy and trauma. Ruptured chordae tendineae may result in flail mitral valve leaflet and mitral regurgitation. The severity of the mitral regurgitation is dependent upon the number of chordae tendinee ruptured and if the ruptured chordae tendineae are primary, secondary or tertiary. If the mitral regurgitation is significant, the patient may present with acute pulmonary edema and congestive heart failure.
A common finding associated with a regurgitant murmur in the elderly is:
A. Aortic valve stenosis
B. Mitral annular calcification
C. Mitral valve stenosis
D. Mitral valve vegetation
B. The mitral annulus decreases in diameter by 25% during ventricular systole. Mitral annular calcification prevents that reduction during ventricular systole which allows blood flow back into the left atrium. Severe mitral annular calcification can result in obstructing blood flow during ventricular diastole resulting in functional mitral stenosis.
On M-mode and two-dimensional echocardiography dense echoes are noted posterior to normal mitral valve leaflets. The probable diagnosis is mitral valve:
A. Annular calcification
B. Aneurysm
C. Papilloma
D. Vegetation
A. The mitral valve annulus is part of the fibrous skeleton of the heart and begins to develop fibrosis and calcification by the age of 65 years. Echocardiography demonstrates a mass of dense and highly reflective echoes behind the posterior mitral valve leaflet. Mitral annular calcification may be accelerated by the presence of certain disease states such as systemic hypertension, aortic stenosis, diabetes, chronic renal failure and hypertrophic cardiomyopathy.
The etiology of aortic valve stenosis includes all the following ЕХСЕРТ:
A. Bacterial
B. Congenital
C. Degenerative
D. Rheumatic
A. Acquired aortic valve stenosis may be due to degenerative senile calcification or rheumatic fever. Congenital aortic valve stenosis may be unicuspid, bicuspid, tricuspid, or it may be due to a dome-shaped diaphragm. Quadricuspid aortic valve has been described, is usually not stenotic but may be regurgitant.
The most likely etiology of aortic valve stenosis in a 47-year-old patient is:
A. Annular
B. Congenital
C. Endocarditis
D. Degenerative
B. Differentiation of congenital (bicuspid) and acquired aortic valve stenosis may be difficult. An indication of a congenital etiology is the age of the patient. Patients with bicuspid aortic valve usually become
symptomatic between the ages of 20 and 50, while senile aortic stenosis occurs at a much later age.
The cardinal symptoms of valvular aortic stenosis include all the following EXCEPT:
A. Angina pectoris
B. Congestive heart failure
C. Anasarca
D. Syncope
C. The cardinal symptoms of valvular aortic stenosis, which commence most commonly in the sixth decade of life, are angina pectoris, syncope and congestive heart failure. Once these symptoms become manifest, the prognosis is poor. Survival curves show that the interval from the onset of symptoms to the time of death is about two years in patients with heart failure, three years in those with syncope and five years in those with angina.
The murmur of aortic stenosis is described as:
A. Holosystolic murmur heard best at the cardiac apex
B. Holodiastolic decrescendo murmur heard best at the right sternal border
C. Systolic ejection murmur heard best at the right upper sternal border
D. Diastolic rumble
C. The mid-systolic murmur of aortic valve stenosis is heard best at the right upper sternal border but is often well transmitted along the carotid vessels and to the apex. The murmur of aortic stenosis is harsh
and rasping, crescendo-decrescendo in shape at the right upper sternal border. High-frequency components may selectively radiate to the apex (the Gallavardin phenomena). A reversal of S2 or absent S1 is
associated with the auscultatory findings in these patients.
The pulse that is characteristic of significant valvular aortic stenosis is:
A. Pulsus alternans
B. Pulsus bisferiens
C. Pulsus paradoxus
D. Pulsus parvus et tardus
D. The arterial pulse associated with significant valvular aortic stenosis is one that rises slowly and is small and sustained (pulsus parvus et tardus). Pulsus parvus et tardus may be best detected by palpation of the right carotid artery.
Pulsus alternans is alternating weak and strong beats and is associated with severely reduced global ventricular systolic function.
Pulsus bisfierens is two beats within one and is associated with hypertrophic obstructive cardiomyopathy or severe aortic regurgitation.
Pulsus paradoxus is a drop in blood pressure with inspiration by more
than 10 mm Hg and is associated with cardiac tamponade.
The aortic valve area considered critical aortic valve stenosis:
A. < 3 cm^2
B. < 2 cm^2
C. < 1.5 cm^2
D. ≤ 0.75 cm^2
D. The aortic valve should be replaced in symptomatic patients with hemodynamic evidence of severe obstruction (aortic valve area ≤ 0.75 cm^2 or ≤ 4 cm^2/m^2). The normal aortic valve area is 3 to 5 cm^2. A recent recommendation states that an aortic valve area of < 1 cm^2 should be considered severe aortic stenosis.
The formula used to determine aortic valve area in the cardiac catheterization laboratory is the:
A. Bernoulli equation
B. Continuity equation
C. Doppler equation
D. Gorlin equation
D. In patients with valvular aortic stenosis, the peak-to-peak pressure gradient, mean pressure gradient and aortic valve area are calculated in the cardiac catheterization laboratory. The Gorlin equation for aortic
valve are (AVA) is:
AVA (cm^2) = (CO ÷ SEP) ÷ (43.3 x √MPG)
It should be noted that the peak-to-peak gradient calculated in the cardiac catheterization laboratory will usually be lower than the Doppler maximum peak instantaneous pressure gradient calculated
in the echocardiography laboratory. The mean pressure gradient and aortic valve area are comparable.
AVA, aortic valve area; CO, cardiac output; SEP, systolic ejection period; MPG, mean pressure gradient
All of the following may be measured in the cardiac catheterization laboratory when evaluating aortic stenosis ЕХСЕРТ:
A. Peak velocity
B. Maximum peak instantaneous pressure gradient
C. Peak-to-peak pressure gradient
D. Mean pressure gradient
A. Historically the peak-to-peak pressure gradient, mean pressure gradient and aortic valve area are measured in the cardiac catheterization laboratory when evaluating aortic stenosis.
It is important to note that cardiac Doppler measures the maximum peak instantaneous pressure gradient. The Doppler maximum peak instantaneous gradient is nearly always larger than the cardiac catheterization peak-to-peak pressure gradient. Comparing mean
pressure gradient and aortic valve area is important when evaluating cardiac Doppler and cardiac catheterization information since these values should be similar in aortic stenosis.
The Doppler maximum peak instantaneous pressure gradient in a patient with aortic stenosis is 100 mm Hg. The cardiac catheterization peak-to-peak pressure gradient will most likely be:
A. Equal to 100 mm Hg
B. Higher than 100 mm Hg
C. Lower than 100 mm Hg
D. Dependent upon respiration
C. Cardiac catheterization historically measures the peak-to-peak pressure
gradient, mean pressure gradient and aortic valve area in the evaluation of aortic stenosis. Doppler measures the maximum peak instantaneous pressure gradient, mean pressure gradient and aortic valve area by the continuity equation. The Doppler maximum peak instantaneous
pressure gradient will nearly always be greater than the cardiac catheterization peak-to-peak pressure gradient in aortic stenosis.
The Doppler mean pressure gradient and aortic valve area should be compared to the cardiac catheterization laboratories mean pressure gradient and aortic valve area because the values should be similar.
An effect of significant aortic valve stenosis on the left ventricle is:
A. Asymmetrical septal hypertrophy
B. Concentric left ventricular hypertrophy
C. Eccentric left ventricular hypertrophy
D. Protected in significant aortic valve stenosis
B. In significant aortic valve stenosis, left ventricular wall thickness is increased due to a pressure overload. When the capacity to develop left ventricular hypertrophy has been exhausted, the left ventricle dilates. Thus, left ventricular cavity dimension, wall thickness and global left ventricular systolic function should be measured in aortic
valve stenosis.
Pathologies that may result in a left ventricular pressure overload include all the following EXCEPT:
A. Discrete subaortic stenosis
B. Mitral valve stenosis
C. Systemic hypertension
D. Valvular aortic stenosis
B. Left ventricular hypertrophy results from left ventricular pressure overload. Physiologic hypertrophy may occur in competitive athletes. Eccentric left ventricular hypertrophy (hypertrophy with dilatation) may occur in volume overload cases (significant chronic aortic regurgitation, significant chronic mitral regurgitation).
Asymmetric hypertrophy is the non-uniform increase in wall thickness (e.g., hypertrophic cardiomyopathy).
The characteristic M-mode findings for aortic valve stenosis include all the following EXCEPT:
A. A lack of systolic flutter of the aortic valve leaflets
B. Diastolic flutter of the aortic valve leaflets
C. Reduced leaflet separation in systole
D. Thickening of the aortic valve leaflets
B. The characteristic M-mode echocardiographic findings in aortic valve
stenosis are marked thickening of the leaflets and reduced leaflet separation in systole. Thickening and/or calcification of the leaflets alone does not necessarily indicate hemodynamically important aortic
valve stenosis. Measurements of aortic valve leaflet separation by M-mode echocardiography correlate poorly with the clinical severity of aortic valve stenosis, with aortic valve gradients and with valve orifice
areas measured at cardiac catheterization.
Diastolic flutter of the aortic valve is associated with severe aortic regurgitation.
Possible two dimensional echocardiographic findings in significant aortic valve stenosis include all the following EXCEPT:
A. Aortic valve calcification
B. Left ventricular hypertrophy
C. Post-stenotic dilatation of the ascending aorta
D. Post-stenotic dilatation of the descending aorta
D. Two dimensional echocardiography is also useful in determining the severity of left ventricular hypertrophy, evaluating left ventricular global and segmental systolic function, detecting subvalvular obstruction
and evaluating the status of the other cardiac valves in patients with valvular aortic stenosis.
In the parasternal long-axis view, severe aortic valve stenosis is defined as an aortic valve leaflet separation that measures:
A. ≥ 14 mm
B. ≤ 12 mm
C. ≤ 10 mm
D. ≤ 8 mm
D. De Maria and colleagues reported that aortic leaflet separation of ≤ 8 mm, measured from the parasternal long-axis view, was reliable with a predictive value of 82% for severe aortic valve stenosis in patients with normal global left ventricular systolic function. They also observed that
aortic leaflet separation of > 20 mm reliably excluded the diagnosis of aortic valve stenosis.
Secondary echocardiographic findings associated with severe valvular aortic stenosis include all the following EXCEPT:
A. Decreased left ventricular systolic function (late in course)
B. Left ventricular hypertrophy
C. Post-stenotic dilatation of the ascending aorta
D. Right ventricular hypertrophy
D. In addition, left ventricular mass will also be increased. Left ventricular mass in grams may be calculated by M-mode with the formula:
0.8 x 1.04 [LVIDd + IVSd + PWLVd)^3 - LVIDd^3] + 0.6
The upper limit for men is 115 g/m^2 and for women is 95 g/m^2.
LVIDd, left ventricular internal dimension end-diastole;
IVSd, interventricular septum end-diastole;
PWLVd, posterior wall left ventricular end-diastole.
The two-dimensional view which best visualizes systolic doming of the aortic valve leaflets is the:
A. Apical five-chamber view
B. Parasternal long-axis view
C. Parasternal short-axis view of the aortic valve
D. Subcostal short-axis view of the aortic valve
B. Systolic doming, a feature commonly seen in a stenotic, non-calcified bicuspid aortic valve, is best visualized in the parasternal long-axis view. The parasternal and subcostal short-axis views of the aortic valve are the only two imaging planes in which a bicuspid valve can be reliably diagnosed because the shape of the systolic aortic valve opening can be evaluated. The normal trileaflet aortic valve will triangular in shape
when open during ventricular systole in the parasternal and subcostal short-axis views. A bicuspid aortic valve appears “football-shaped” (elliptical) when open during ventricular systole as viewed in the parasternal and subcostal short-axis views of the aortic valve.
Cardiac Doppler parameters used to assess the severity of valvular aortic stenosis include all the following EXCEPT:
A. Aortic pressure half-time
B. Aortic velocity ratio
C. Mean pressure gradient
D. Peak aortic valve velocity
A. In addition, the peak pressure gradient and cardiac output should be assessed in patients with valvular aortic stenosis. Severe aortic valve stenosis Doppler parameters are:
- Peak velocity > 4.0 m/sec*
- Peak pressure gradient > 64 mm Hg*
- Mean pressure gradient > 50 mm Hg*
- Aortic valve area ≤ 0.75 cm^2
- Aortic velocity ratio ≤ 0.25
- Assumes normal global left ventricular systolic function
Of the transvalvular pressure gradients that can be measured in the echocardiography laboratory, the most useful in examining
aortic valve stenosis is probably:
A. Mean diastolic gradient
B. Mean systolic gradient
C. Peak instantaneous pressure gradient
D. Peak-to-peak gradient
B. Clinically, the mean systolic gradient may be the most useful expression of aortic valve gradient, as it is directly comparable to the mean gradient measured in the cardiac catheterization laboratory.
The aortic valve area calculated in the cardiac catheterization laboratory should be similar to the aortic valve area determined in the echocardiography laboratory.
It should be noted that cardiac catheterization hemodynamic evaluation for aortic stenosis is not usually necessary since that can be accomplished in the echocardiography laboratory. The principal role of cardiac catheterization in patients with aortic stenosis is the evaluation of coexisting coronary artery disease.
A Doppler mean pressure gradient of 18 mm Hg is calculated in a patient with valvular aortic stenosis. The severity o f the aortic stenosis is:
A. Mild
B. Moderate
C. Moderately severe
D. Severe
A. Assuming normal global left ventricular systolic function, a mean pressure gradient of < 30 mm Hg usually indicates mild aortic valve stenosis while a mean pressure gradient > 50 mm Hg is severe. Tracing the continuous-wave Doppler tracing of the aortic valve will provide the aortic valve peak velocity, peak pressure gradient, mean pressure gradient and velocity time integral.
The onset of flow to peak aortic velocity continuous-wave Doppler tracing in severe valvular aortic stenosis is:
A. Increased
B. Decreased
C. Decreased with expiration
D. Increased with inspiration
A. As valvular aortic stenosis increases in severity, the acceleration time (onset of flow to peak velocity) becomes longer.
An asymmetric triangular contour with an early peaking of the continuous-wave Doppler aortic stenosis jet usually indicates mild aortic stenosis.
Symmetric and a rounded velocity contour with a late peaking velocity (peak > 50% of total ejection time) of the continuous wave Doppler spectral waveform is usually seen in severe aortic stenosis.
The severity of aortic valve stenosis may be underestimated if only the maximum velocity measurement is used in the following condition:
A . Anemia
B. Doppler intercept angle of 0°
C. Low cardiac output
D. Significant aortic regurgitation
C. A potential pitfall in the cardiac Doppler evaluation of aortic valve stenosis is low cardiac output. When there is pump failure, the maximum velocity across the valve may not be high, therefore leading to an underestimation of the severity of aortic valve stenosis. In cases where there is poor global left ventricular systolic function, the aortic valve area as derived by the continuity equation should be calculated. In addition, dobutamine may be used to improve global left ventricular systolic function during the Doppler examination. Planimetry of the aortic valve orifice may be attempted in the short-axis view of the aortic valve using transthoracic echocardiography or transesophageal echocardiography.
The Gorlin equation will underestimate the severity of aortic valve stenosis in patients with low cardiac output.
The echocardiographer may differentiate between the similar systolic flow patterns seen in coexisting severe aortic valve stenosis and mitral regurgitation by all the following EXCEPT:
A. Aortic ejection time is shorter that the mitral regurgitation time
B. Mitral regurgitation flow always lasts until mitral valve opening, whereas aortic valve stenosis flow does not.
C. Mitral diastolic filling profile should be present during recording of the mitral regurgitation, whereas no diastolic flow is observed in aortic valve stenosis.
D. Since both are systolic flow patterns, it is not possible to separate mitral regurgitation from aortic valve stenosis.
D. If two high-velocity signals of mitral regurgitation and severe aortic valve stenosis, coexist, the two jets must be clearly differentiated. The aortic ejection time is always shorter than the mitral regurgitation time because no aortic flow occurs during the isovolumic contraction and the relaxation periods. Even though mitral regurgitation may not occur until mid-systole, as with occasional cases of mitral valve prolapse, regurgitation lasts until the mitral valve opens. Simultaneously recorded diastolic signals are also helpful for differentiating these two high-velocity systolic flows; the mitral diastolic filling profile should be present during the recording of mitral regurgitation, whereas no diastolic flow or aortic regurgitation is observed during the recording of aortic valve stenosis.
The two-dimensional echocardiogram demonstrates a thickened aortic valve with reduced systolic excursion. On physical examination there was a crescendo-decrescendo systolic ejection murmur and a diastolic decrescendo murmur heard. The most likely diagnosis is aortic valve:
A. Flail
B. Regurgitation
C. Stenosis and regurgitation
D. Stenosis and mitral valve prolapse
C. Two-dimensional findings for aortic stenosis include thickened aortic valve with reduced systolic excursion, post-stenotic dilatation of the aorta, concentric left ventricular hypertrophy, left atrial dilatation and abnormal diastolic function.
When two dimensional evaluation of a systolic ejection murmur reveals a thickened aortic valve with normal systolic excursion and a peak velocity across the aortic valve of 1.5 m/s. The diagnosis is most likely aortic valve:
A. Regurgitation
B. Sclerosis
C. Stenosis
D. Prolapse
B. With aortic valve sclerosis the aortic valve leaflets are thickened with preserved systolic excursion (opening) and a normal aortic valve peak systolic velocity of < 2 m/s.
The most common etiology of chronic aortic regurgitation is:
A. Dilatation of the aortic root and aortic annulus
B. Infective endocarditis
C. Marfan’s syndrome
D. Trauma
A. The etiology of chronic aortic regurgitation may be primary aortic valve disease (e.g., bicuspid, calcific, rheumatic, myxomatous degeneration) or aortic root disease (e.g., degenerative aortic root dilatation, Marfan syndrome).
Aortic root disease represents the most common etiology of chronic aortic regurgitation and may account for more than 50% of patients undergoing aortic valve replacement for chronic aortic regurgitation.
All of the following represents possible etiologies for acute aortic regurgitation EXCEPT:
A. Infective endocarditis
B. Aortic valve sclerosis
C. Aortic dissection
D. Trauma
B. Infective endocarditis of the aortic valve may destroy the valve, cause a perforation or the vegetation may interfere with proper coaptation of the leaflets. The sudden increase in left ventricular filling will result in the left ventricular diastolic pressure to increase rapidly above the left atrial pressure during early ventricular diastole causing the mitral valve to close prematurely and a mitral valve pulsed-wave Doppler restrictive diastolic flow profile.
The LEAST common valve regurgitation found in normal patients is:
A. Aortic regurgitation
B. Mitral regurgitation
C. Pulmonary regurgitation
D. Tricuspid regurgitation
A. Aortic regurgitation is present in only 2% of young healthy subjects.
This compares to tricuspid regurgitation (70 to 90% of normals), pulmonary regurgitation (70 to 90% of normals) and mitral regurgitation (up to 50% of normals). It is important to identify the reason for the presence of aortic regurgitation (e.g., aortic root pathology, aortic valve disease, infective endocarditis, discrete subaortic stenosis, perimembranous ventricular septal defect, outlet ventricular septal defect, supravalvular aortic stenosis).
All of the following are associated with significant chronic aortic regurgitation EXCEPT:
A. Wide pulse pressure
B. Congestive heart failure
C. Holosystolic murmur heard best at the cardiac apex
D. Angina pectoris
C. With progressive severity of aortic regurgitation the systolic blood pressure increases and the diastolic pressure decreases resulting in a wide pulse pressure. In significant aortic regurgitation the systolic blood pressure may increase to 150 mm Hg and the diastolic blood pressure may fall below 70 mm Hg. The presence of a completely normal blood pressure in a patient with aortic regurgitation and normal global left ventricular systolic function virtually excludes the diagnosis of moderate to severe aortic regurgitation.
The characteristic feature of the murmur of chronic aortic regurgitation is a:
A. Diastolic decrescendo murmur heard best along the left sternal border
B. Diastolic crescendo-decrescendo murmur heard best along the left upper sternal border
C. Diastolic rumble following an opening snap
D. Harsh systolic ejection murmur heard best at the right upper sternal border
A. The murmur of aortic regurgitation is a high-pitched blowing decrescendo diastolic murmur heard best at the third and fourth interspace along the left sternal border. In certain cases, the murmur may only be heard in full expiration with the patient leaning forward.
The murmur associated with severe aortic regurgitation is:
A. Austin-Flint
B. Carvallo’s
C. Graham-Steell
D. Still’s
A. The Austin-Flint murmur is associated with severe aortic regurgitation and is described as a low-pitched mid and late diastolic rumble best heard at the cardiac apex.
Cardiac magnetic resonance imaging provides all of the following information in a patient with aortic regurgitation EXCEPT:
A. Detailed resolution of the aortic valve
B. Regurgitant volume
C. Effective regurgitant orifice
D. Left ventricular volumes
A. Cardiac magnetic resonance imaging provides accurate measurement of regurgitant volumes, effective regurgitant orifice, left ventricular end-diastolic and end-systolic volumes and left ventricular mass.
The hallmark M-mode finding for aortic regurgitation is:
A. Coarse diastolic flutter of the anterior mitral valve leaflet
B. Fine diastolic flutter of the anterior mitral valve leaflet
C. Chaotic diastolic flutter of the mitral valve
D. Systolic flutter of the aortic valve
B. High-frequency oscillation or flutter of the anterior mitral valve during ventricular diastole is the hallmark M-mode finding for aortic regurgitation. These oscillations of the anterior mitral valve leaflet indicate that the leaflet is caught between antegrade flow from the left atrium and retrograde flow from the aortic regurgitation. Fine diastolic flutter may also be seen on the interventricular septum.
Chaotic diastolic flutter of the mitral valve may indicate flail mitral valve.
Coarse diastolic flutter of the anterior mitral valve is associated with atrial flutter or atrial fibrillation.
Fine systolic flutter of the aortic valve is a normal finding.
Diastolic flutter of the aortic valve is associated with severe aortic regurgitation.
Reverse diastolic doming of the anterior mitral valve leaflet is associated with:
A. Flail mitral valve
B. Papillary muscle dysfunction
C. Rheumatic mitral valve stenosis
D. Severe aortic regurgitation
D. Reverse diastolic doming of the anterior mitral valve leaflet is associated with severe aortic regurgitation due to the mechanical deformation of the mitral valve caused by the large volume aortic regurgitation jet. This may be best visualized in the parasternal long-axis view, parasternal short-axis view of the mitral valve and apical four-chamber view.
All of the following are two dimensional echocardiography findings in a patient with significant chronic aortic regurgitation EXCEPT:
A. Left atrial enlargement
B. Abnormal aortic valve or aortic root
C. Left ventricular enlargement
D. Hyperkinetic left ventricular wall motion
A. Chronic aortic regurgitation is a volume overload characterized by left ventricular dilatation, increased wall motion and increased left ventricular mass. The left atrium is thought to be spared in chronic aortic regurgitation. In severe acute aortic regurgitation, early diastolic left ventricular pressure increases above left atrial pressure resulting in premature closure of the mitral valve and a mitral valve pulsed-wave Doppler restrictive diastolic flow profile.
In significant chronic aortic regurgitation, M-mode and two-dimensional evidence includes all of the following EXCEPT:
A. Hyperkinesis of the interventricular septum
B. Hyperkinesis of the posterior (inferolateral) wall of the left ventricle
C. Left ventricular dilatation
D. Paradoxical interventricular septal motion
D. Significant chronic aortic regurgitation is associated with the left ventricular volume overload pattern which is the combination of left ventricular dilatation with hyperkinetic wall motion. This pattern may be observed in patients with significant aortic regurgitation, significant mitral regurgitation, ventricular septal defect and patent ductus arteriosus.
Paradoxical interventricular septal motion combined with right ventricular dilatation are the two components of the right ventricular volume overload pattern. This pattern may be seen in patients with atrial septal defect, significant tricuspid regurgitation, significant pulmonary regurgitation and Ebstein’s anomaly.
The M-mode/two-dimensional echocardiography parameters that have been proposed as an indicator for aortic valve replacement in severe chronic aortic regurgitation are left ventricular:
A. End-diastolic dimension ≥ 55 mm and fractional shortening ≤ 25%
B. End-diastolic dimension ≤ 55 mm and fractional shortening of ≥ 25%
C. End-diastolic dimension ≥ 70 mm and left atrial dimension
≥ 55 mm
D. End-systolic dimension ≥ 55 mm and fractional shortening of ≤ 25%
D. End-systolic dimension of ≥ 55 mm and a fractional shortening of ≤ 25% have been suggested as indicators for valve replacement in asymptomatic as well as symptomatic patients with significant chronic aortic regurgitation. Once volume overload of the left ventricle produces clinically apparent cardiac decompensation irreparable damage occurs and replacing the aortic valve is usually ineffective.
Premature closure of the mitral valve is associated with all of the following EXCEPT:
A. Acute severe mitral regurgitation
B. Acute severe aortic regurgitation
C. First-degree atrioventricular block
D. Loss of sinus rhythm
A. Premature closure of the mitral valve is defined as when the C point of the mitral valve occurs on or before the onset of the QRS complex. This premature mitral valve closure occurs in acute severe aortic regurgitation because the left ventricular diastolic pressure quickly exceeds left atrial pressure resulting in premature closure of the mitral valve. Simply stated premature closure of the mitral valve indicates an elevated left ventricular end-diastolic pressure. A mitral valve pulsed-wave Doppler restrictive pattern will be present in patients with severe acute aortic regurgitation.
In a patient with severe acute aortic regurgitation the left ventricular end-diastolic pressure increases rapidly. This pathophysiology will affect which of the following?
A. Closure of the mitral valve
B. Systolic ejection period
C. Left ventricular dimension
D. Closure of the pulmonary valve
A. Acute severe aortic regurgitation will result in an increase in left ventricular end-diastolic pressure which may overcome the left atrial pressure and close the mitral valve prematurely (before or at the onset of the QRS complex). A pulsed-wave Doppler of the mitral valve may demonstrate a restrictive filling inflow pattern.
The M-mode finding that indicates severe acute aortic regurgitation is premature aortic valve:
A Closure
B. Systolic flutter
C. Mid-systolic closure
D. Opening
D. In severe acute aortic regurgitation the left ventricular diastolic pressure may be so great that the aortic valve opens prematurely (on or before the onset of the QRS complex).
Echocardiographic evidence of severe acute aortic regurgitation includes all of the following EXCEPT:
A. Premature closure of the mitral valve
B. Premature opening of the aortic valve
C. Premature opening of the mitral valve
D. Reverse doming of the anterior mitral valve leaflet
C. Severe acute aortic regurgitation rapidly increases left ventricular pressure which leads to premature closure of the mitral valve (increased left ventricular end-diastolic pressure overcomes left atrial pressure). Premature opening of the aortic valve is due to left ventricular pressure overcoming aortic diastolic pressure prematurely. With severe aortic regurgitation the regurgitant jet produces diastolic indentation (reverse doming) of the anterior mitral valve leaflet.
The mitral valve pulsed-wave Doppler flow pattern often associated with severe acute aortic regurgitation is grade:
A. Normal for age
B. I (impaired relaxation)
C. II (pseudonormal)
D. III or IV (restrictive)
D. The restrictive pulsed-wave Doppler mitral inflow pattern indicates an increase in left ventricular end diastolic pressure. It is characterized by an increase in the mitral E:A ratio (> 1.5) and a shortened deceleration time (< 140 msec). In acute severe aortic regurgitation there is a rapid rise in left ventricular diastolic pressure which will result in a restrictive mitral valve inflow pattern. Diastolic mitral regurgitation may also occur occasionally.
The pulmonary vein atrial reversal wave may be ________ peak velocity and duration in a patient with severe acute aortic regurgitation.
A. Increased
B. Decreased
C. Unchanged
D. Reversed
A. The pulmonary vein atrial reversal wave is useful in evaluating left ventricular end diastolic pressure. Since acute aortic regurgitation usually results in an increase in left ventricular end-diastolic pressure the pulmonary vein atrial reversal wave will be increased in velocity (> 35 cm/s) and/or increased in duration as compared to the mitral valve A wave duration (> 30 msec compared to the mitral valve A wave duration).
Severe aortic regurgitation is diagnosed with continuous-wave Doppler by all of the following criteria EXCEPT:
A. A maximum velocity of 4 m/s
B. A pressure half-time of < 200 msec
C. Increased jet density
D. Steep deceleration slope
A. The spectral density may be used as a semi-quantitative measure of the severity of aortic regurgitation. The denser the spectral display of aortic regurgitation the greater the severity. The aortic regurgitation pressure half-time may be measured to determine severity (mild > 500 msec; severe < 200 msec). A deceleration slope of > 3 m/sec may indicate significant aortic regurgitation. The peak velocity only indicates the pressure difference between the left ventricle and the aorta during ventricular diastole. The American Society of Echocardiography recommends that a peak velocity of 4 m/s be obtained when evaluating the spectral jet density and aortic regurgitation pressure half-time.
The continuous-wave Doppler signal of aortic regurgitation may be differentiated from the continuous-wave Doppler signal of mitral stenosis by the following guideline:
A. If the diastolic flow pattern commences before mitral valve opening then the signal is due to aortic regurgitation
B. If the diastolic flow pattern commences after mitral valve opening then the signal is due to aortic regurgitation
C. The Doppler flow velocity pattern of mitral valve stenosis is laminar while the Doppler flow pattern of aortic regurgitation is turbulent.
D. Cannot be differentiated by continuous-wave Doppler.
A. The continuous-wave Doppler flow velocity pattern of aortic regurgitation is a turbulent, holodiastolic high-velocity (3 to 5 m/s) pattern that begins with aortic valve closure. Aortic regurgitation is nearly always holodiastolic. Mitral regurgitation and tricuspid regurgitation are not always holosystolic.
The severity of aortic regurgitation may best be determined with color flow Doppler by all of the following methods EXCEPT:
A. Measuring the aortic regurgitation jet aliasing area in the parasternal long-axis view
B. Comparing the aortic regurgitation jet width with the left ventricular outflow tract width in the parasternal long-axis view
C. Measuring the vena contracta in the parasternal long-axis view
D. Determining the presence of holodiastolic flow reversal in the descending thoracic aorta and/or abdominal aorta
A. The following parameters may be useful when determining the severity of aortic regurgitation:
Regurgitant jet width/LVOT width ratio (mild < 25%; severe > 65%)
Regurgitant jet area/LVOT area (mild < 4%; moderate 4 to 24%; moderately severe 24 to 59%; severe > 60%
Vena contracta width (mild 0.3 cm; severe 0.6 cm)
Holodiastolic flow reversal in descending thoracic aorta and/or abdominal aorta suggests severe aortic regurgitation. The color flow velocity scale should be decreased and M-mode, pulsed-wave Doppler and/or continuous-wave Doppler should be used to determine if the duration of the flow reversal is holodiastolic.
Holodiastolic flow reversal in the descending thoracic aorta and/or the abdominal aorta may be present in each of the following EXCEPT:
A. Severe aortic regurgitation
B. Severe mitral regurgitation
C. Patent ductus arteriosus
D. Aortopulmonary window
B. A small degree of reversed flow can occur in the aorta in early diastole in normal patients immediately following aortic valve closure. Holodiastolic flow reversal in the descending thoracic aorta and/or abdominal aorta is an indication of significant aortic regurgitation. Other causes of holodiastolic flow reversal include ruptured sinus of Valsalva aneurysm, aorta-LV tunnel, cerebral arteriovenous fistula and upper extremity dialysis shunt.
All of the following are considered useful quantitative measurements to determine the severity of aortic regurgitation EXCEPT:
A. Peak velocity of aortic regurgitation
B. Regurgitant volume
C. Regurgitant fraction
D. Effective regurgitant orifice
A. Regurgitant volume: mild < 30 mL/beat; severe ≥ 60 mL/beat.
Regurgitant fraction: mild < 30%; severe ≥ to 50%, effective regurgitant orifice area: mild <0.10 cm^2; severe > 0.30 cm^2. The peak velocity of aortic regurgitation is determined by the diastolic pressure gradient between the aorta and left ventricle and ranges between 3 to 5 m/s regardless of severity. (P = 4 x V2^2).
P, pressure gradient between two-chambers in millimeters of mercury
V2^2, peak velocity across the obstruction in meters per second
Posterior displacement of the aortic valve leaflet(s) into the left ventricle outflow tract during ventricular diastole is called aortic valve:
A. Prolapse
B. Sclerosis
C. Stenosis
D. Perforation
A. Aortic valve prolapse is defined as the downward displacement of one or more of the aortic valve leaflets during ventricular diastole below a line joining the points of attachments of the aortic valve leaflets and is best evaluated in the parasternal long-axis view. Aortic valve prolapse has been referred to as diastolic doming of the aortic valve. Aortic valve prolapse has been associated with mitral valve prolapse, congenital aortic valve (e.g., bicuspid aortic valve), perimembranous ventricular septal defect, outlet ventricular septal defect, aortic root dilatation and infective endocarditis. Aortic valve prolapse may result in aortic regurgitation.
The most common etiology of tricuspid stenosis is:
A. Carcinoid heart disease
B. Infective endocarditis
C. Rheumatic fever
D. Right atrial myxoma
C. Tricuspid valve stenosis is almost always a result of rheumatic heart disease and it is invariably associated with mitral valve stenosis. Other etiologies of tricuspid stenosis include carcinoid heart disease (second most common cause), tumor, vegetation, congenital, valvular damage from catheter or pacemaker leads and sinus of Valsalva aneurysm.
The typical two-dimensional echocardiographic findings in rheumatic tricuspid stenosis include all of the following EXCEPT:
A. Leaflet thickening especially at the leaflet tips and chordae tendineae
B. Diastolic doming of the anterior tricuspid valve leaflet
C. Right atrial dilatation
D. Systolic bowing of the posterior tricuspid valve leaflet
D. The two dimensional findings for rheumatic tricuspid valve stenosis are similar to those of mitral valve stenosis. As with all valvular stenoses the hallmark diagnosis is diastolic doming of the affected valve. In addition to doming, thickening of the valve leaflets and restricted motion are signs that aid in the diagnosis of tricuspid valve stenosis. The right atrium, inferior vena cava, hepatic veins and superior vena cava are expected to be dilated in a patient with tricuspid valve stenosis.
All of the following are cardiac Doppler findings for tricuspid valve stenosis EXCEPT:
A. Increased tricuspid valve E wave velocity
B. Decreased pressure half-time
C. Decreased tricuspid valve area
D. Increased mean pressure gradient
B. A peak tricuspid valve E velocity of > 1 m/sec suggests the presence of tricuspid stenosis. Tricuspid stenosis is considered severe when the mean pressure gradient is > 6 mm Hg. A tricuspid valve area of < 2 cm^2 (normal tricuspid valve area is 5 to 8 cm^2) suggests severe tricuspid valve stenosis. A constant of 190 instead of 220 (Mitral valve area cm^2 = 220 ÷ pressure half-time) has been proposed to determine tricuspid valve area (Tricuspid valve area cm^2 = 190 ÷ pressure half-time). Because there is respiratory variation it is best to evaluate tricuspid valve stenosis with the patient holding their breath at end-expiration. Tricuspid regurgitation and rheumatic changes of the mitral valve and aortic valve should also be evaluated in patients with tricuspid valve stenosis.
Causes of anatomic tricuspid regurgitation include all of the following EXCEPT:
A. Carcinoid heart disease
B. Ebstein’s anomaly
C. Infective endocarditis
D. Pulmonary hypertension
D. There are several causes of anatomic (primary, organic) tricuspid regurgitation including carcinoid heart disease, Ebstein’s anomaly, infective endocarditis, tricuspid valve prolapse, ruptured chordae tendineae, flail leaflet and rheumatic heart disease.
The most common cause of tricuspid regurgitation is not anatomic but dilatation of the right ventricle and of the tricuspid valve annulus resulting in functional (secondary) tricuspid regurgitation (e.g., pulmonary hypertension).
The most common cause of chronic tricuspid regurgitation is:
A. Tricuspid valve prolapse
B. Rheumatic heart disease
C. Pulmonary hypertension
D. Ebstein’s anomaly
C. Functional tricuspid regurgitation is more common than anatomic tricuspid regurgitation. Pulmonary hypertension eventually results in right ventricular dilatation which leads to tricuspid regurgitation (functional tricuspid regurgitation). Other causes of functional tricuspid regurgitation include right ventricular infarction, pulmonary stenosis, pulmonary embolism and cor pulmonale. A systolic pulmonary artery pressure of > 55 mm Hg usually results in functional tricuspid regurgitation and may improve with a return to normal pulmonary pressures.
Signs of significant tricuspid regurgitation include all of the following EXCEPT:
A. Hepatomegaly
B. Jugular venous distention
C. Pulsus paradoxus
D. Right ventricular heart failure
C. The signs of right ventricular heart failure include jugular venous distention, hepatomegaly, peripheral edema, ascites and anasarca. The patient with significant tricuspid regurgitation may also have symptoms of left heart lesions because tricuspid regurgitation is a common response to left ventricular disease such as rheumatic mitral valve stenosis, coronary artery disease and significant mitral regurgitation.
Pulsus paradoxus is associated with cardiac tamponade.
The murmur of tricuspid regurgitation is best described as a:
A. Holodiastolic murmur heard best at the lower left sternal border
B. Pansystolic murmur heard best at the lower left sternal border
C. Pansystolic murmur heard best at the cardiac apex with radiation to the axilla
D. Systolic ejection murmur heard best at the upper right sternal border
B. The murmur of tricuspid regurgitation is maximal at the lower left sternal border or subxyphoid area, generally pansystolic and often, but not always, increased with inspiration. Augmentation of the murmur by inspiration is called Rivero-Carvallo. A right-sided S3 heart sound may also be detected.
All of the following are dilated in significant chronic tricuspid regurgitation EXCEPT:
A. Hepatic veins
B. Inferior vena cava
C. Pulmonary veins
D. Right atrium
C. Significant chronic tricuspid regurgitation causes dilatation of the vena cava, hepatic veins, right atrium, tricuspid annulus and right ventricle. A tricuspid valve annulus of ≥ 3.4 cm measured at ventricular end-systole suggests significant chronic tricuspid regurgitation.
M-mode and two-dimensional echocardiographic findings for chronic tricuspid regurgitation include:
A. Left ventricular volume overload
B. Paradoxical interventricular septal motion
C. Protected right ventricle
D. Right ventricular hypertrophy
B. Significant chronic tricuspid regurgitation leads to right ventricular volume overload which is manifested on echocardiography as paradoxical interventricular septal motion with right ventricular dilatation. With two-dimensional echocardiography, paradoxical interventricular motion is implied when in the parasternal short-axis of the left ventricle there is flattening of the interventricular septum during ventricular diastole with restoration of the circular shaped left ventricle during ventricular systole.
Left ventricular volume overload is left ventricular dilatation with hyperkinetic wall motion.
Methods for determining the severity of tricuspid regurgitation with pulsed-wave Doppler include all of the following EXCEPT:
A. Increased E wave velocity of the tricuspid valve
B. Holosystolic flow reversal of the hepatic vein
C. Laminar flow of the tricuspid regurgitant jet
D. Peak velocity of the tricuspid regurgitant jet
D. The maximum velocity of the tricuspid regurgitant jet reflects the pressure gradient between the right atrium and the right ventricle and does not necessarily indicate the severity of the tricuspid regurgitation. In patients with normal intracardiac pressures the peak velocity of tricuspid regurgitation is expected to be at least 1.7 m/s.
Cardiac Doppler findings associated with significant chronic tricuspid regurgitation include all of the following EXCEPT:
A. Concave late systolic configuration of the regurgitation signal
B. Increased E velocity of the tricuspid valve
C. Systolic flow reversal in the hepatic vein
D. Systolic flow reversal in the pulmonary vein
D. Severe tricuspid regurgitation parameters include:
• Tricuspid valve is abnormal
• Right atrium, right ventricle, inferior vena cava are dilated
• Regurgitant jet area (color flow Doppler) is > 10 cm^2
• Vena contracta (color flow Doppler) is > 0.7 cm
• PISA (color flow Doppler) > 0.9 cm
• Jet density (continuous-wave Doppler) is dense and triangular in shape
• Hepatic vein (pulsed-wave Doppler) holosystolic reversal
An intracardiac pressure that may be determined from the continuous-wave Doppler tricuspid regurgitation signal is:
A. Mean pulmonary artery pressure
B. Pulmonary artery end-diastolic pressure
C. Systolic pulmonary artery pressure
D. Systemic vascular resistance
C. The formula 4 x tricuspid regurgitation peak velocity^2 represents the peak systolic pressure gradient between the right atrium and right ventricle. By adding the right atrial pressure to the pressure gradient calculated from the tricuspid regurgitation peak velocity the right ventricular systolic pressure can be derived. In the absence of right ventricular outflow tract obstruction this represents the systolic pulmonary artery pressure.
RVSP (mm Hg) = 4 x TR peak velocity^2 + RAP (mm Hg)
The right atrial pressure may be estimated by evaluating the inferior vena cava. An inferior vena cava that is normal in dimension (< 1.7 cm) and collapses by > 50% with a sniff indicates a normal right atrial pressure (5 mm Hg).
RVSP, right ventricular systolic pressure;
SPAP, systolic pulmonary artery pressure;
TR, tricuspid regurgitation;
RAP, right atrial pressure
A tricuspid regurgitation peak velocity of 3.0 m/s is obtained.
This indicates:
A. Mild tricuspid regurgitation
B. Moderate tricuspid regurgitation
C. Severe tricuspid regurgitation
D. Pulmonary hypertension
D. The tricuspid regurgitation peak velocity represents the pressure gradient between the right ventricle and right atrium during ventricular systole and is generally not a parameter used to determine the severity of tricuspid regurgitation.
The formula: RVSP (mm Hg) = 4 x TR peak velocity^2 + RAP (mm Hg)
is used to determine the right ventricular systolic pressure and in the absence of right ventricular outflow tract obstruction, represents the systolic pulmonary artery pressure (SPAP).
A systolic pulmonary artery pressure of > 30 mm Hg is considered to be pulmonary hypertension.
RVSP, right ventricular systolic pressure;
TR, tricuspid regurgitation;
RAP, right atrial pressure;
SPAP, systolic pulmonary artery pressure
Possible echocardiographic and cardiac Doppler findings in a patient with carcinoid heart disease include all of the following ЕХСЕРТ:
A. Tricuspid regurgitation
B. Tricuspid stenosis
C. Tricuspid valve prolapse
D. Pulmonary regurgitation
C. The most common cardiac lesion found in carcinoid heart disease is tricuspid valve regurgitation. Tricuspid valve stenosis is less common and pulmonary valve stenosis and regurgitation rarely occur without coexisting tricuspid valve involvement.
Left heart involvement is rare in carcinoid heart disease (7% of cases).
The most common etiology of pulmonary regurgitation is:
A. Carcinoid heart disease
B. Infective endocarditis
C. Pulmonary hypertension
D. Rheumatic heart disease
C. By far the most common cause of pathologic pulmonary regurgitation is dilatation of the valve ring secondary to pulmonary hypertension. The second most common cause is infective endocarditis. Iatrogenic significant pulmonary regurgitation may be present in patients following treatment for pulmonary valve stenosis or tetralogy of Fallot.
Significant chronic pulmonary regurgitation is associated with:
A. Left ventricular volume overload
B. Right atrial hypertrophy
C. Right ventricular hypertrophy
D. Right ventricular volume overload
D. Isolated pulmonary regurgitation may lead to right ventricular volume overload. Right ventricular volume overload is diagnosed by the echocardiographic findings of right ventricular dilatation and paradoxical interventricular septal motion. Right ventricular volume overload may be diagnosed with two-dimensional echocardiography as right ventricular dilatation and flattening of the interventricular septum during ventricular diastole with restoration of the normal circular configuration during ventricular systole best seen in the parasternal short-axis of the left ventricle at the level of the papillary muscles.
All of the following color flow Doppler findings indicate significant pulmonary regurgitation EXCEPT:
A. Wide jet width at origin
B. Jet width/Right ventricular outflow tract width > 70%
C. Holodiastolic flow reversal in the main pulmonary artery
D. Peak velocity of < 1.0 m/s
D. In addition a jet length of > 10 mm suggests significant pulmonary regurgitation.
Which of the following pressures can be predicted when measuring the pulmonary regurgitation end-diastolic velocity?
A. Right ventricular systolic pressure
B. Systolic pulmonary artery pressure
C. Pulmonary artery end-diastolic pressure
D. Mean pulmonary artery pressure
C. PAEDP may be calculated by the formula:
PAEDP (mm Hg) = 4 x end-diastolic velocity PR^2 + RAP (mm Hg)
The normal pulmonary artery end-diastolic pressure is 4 to 12 mm Hg.
The estimation of the pulmonary artery end-diastolic pressure reflects the pulmonary artery wedge pressure.
PAEDP, pulmonary artery end-diastolic pressure;
PR, pulmonary regurgitation;
RAP, right atrial pressure
Which of the following pressures may be calculated when measuring the peak velocity of pulmonary regurgitation?
A. Right ventricular systolic pressure
B. Systolic pulmonary artery pressure
C. Mean pulmonary artery pressure
D. Pulmonary wedge pressure
C. MPAP may be calculated by the formula:
MPAP (mm Hg) = 4 x peak velocity PR^2
The normal range for the mean pulmonary artery pressure is 9 to 18 mm Hg.
MPAP, mean pulmonary artery pressure;
PR, pulmonary regurgitation
The most common symptom of infective endocarditis is:
A. Chest pain
B. Dyspnea
C. Orthopnea
D. Fever
D. Fever is the most common symptom (80 to 85% of infective endocarditis. Additional symptoms include chills, sweats, anorexia, weight loss, malaise, dyspnea, cough, stroke, headache, nausea/ vomiting, myalgia/arthralgia, abdominal pain, back pain and confusion. The onset of symptoms is estimated to be less than two weeks in patients with native valve endocarditis. The perioperative period post-cardiac valve replacement is two to five months or longer. Heart murmurs are noted in 80 to 85% of patients with infective endocarditis. The classic triad of infective endocarditis is fever, new murmur and positive blood cultures. The classic echocardiographic findings in infective endocarditis are valvular vegetation and valvular regurgitation.
The complications of infective endocarditis include all of the following EXCEPT:
A. Congestive heart failure
B. Embolization
C. Valve ring abscess
D. Annular calcification
D. Additional complications include valve leaflet vegetation, disruption (e.g., flail) with resultant regurgitation, perforation, aneurysm, fistula, dehiscence of a prosthetic valve, pericardial effusion and hemodynamic compromise (e.g., valvular regurgitation, premature mitral valve closure, restrictive mitral valve inflow pattern, valvular stenosis (rare) and shunt).
Infective endocarditis is a greater risk in patients with:
A. Atrial fibrillation
B. Coronary artery disease
C. Left ventricular aneurysm
D. Prosthetic heart valve
D. The classic clinical setting for infective endocarditis is pre-existent valvular heart disease (e.g., rheumatic, myxomatous, congenital, prosthetic heart valves, intravenous drug abuse).
A patient with a history of intravenous drug abuse presents to the echocardiography laboratory with complaints of fever, night sweats and weight loss. The most likely explanation is:
A. Congestive heart failure
B. Coronary artery disease
C. Infective endocarditis
D. Kawasaki disase
C. The clinical setting for infective endocarditis is pre-existing valvular disease. A mode of infection (e.g., dental, surgical, traumatic) is often identifiable. If a patient is an intravenous drug abuser normal right-sided cardiac valves can be affected. The classic presentation of infective endocarditis is fever, new murmur and positive blood cultures.
The classic echocardiographic findings for infective endocarditis are valvular vegetation and valvular regurgitation.
The classic manifestation of infective endocarditis is cardiac valve:
A. Vegetation
B. Doming
C. Sclerosis
D. Tumor
A. Vegetations are common to all types of infective endocarditis. They are situated most frequently on the valvular leaflets and less often on the endocardium of the ventricles or of the left atrium (McCallum’s patch of rheumatic carditis) and on the pulmonary or other arteries. The expected cardiac Doppler finding for infective endocarditis is valvular regurgitation. Approximately 15% of patients do not have a new murmur due to valvular regurgitation with one possible explanation being that the vegetation is located on the base of the leaflet which may not disrupt valve closure. Valvular stenosis is a rare complication of native valve infective endocarditis.
The usual site of attachment for vegetations on the mitral valve and tricuspid valve is the:
A. Annulus
B. Atrial side of the valve leaflets
C. Papillary muscles
D. Ventricular surface of the valve leaflets
B. The usual site of attachment for a vegetation is on the atrial side (low pressure side) of the mitral and tricuspid valve leaflets. Aortic and pulmonary valve vegetations are usually found on the ventricular side (low pressure side) of the valve.
The vegetation diameter as determined by two-dimensional echocardiography that is most often associated with systemic emboli is:
A. 3 mm
B. 5 mm
C. 7 mm
D. 10 mm
D. When the diameter of a vegetation exceeds 10 mm 50% of patients develop at least one complication of infective endocarditis. In tricuspid valve endocarditis, pulmonary embolism is the most common complication.
The essential two-dimensional echocardiographic finding of valve ring abscess secondary to infective endocarditis may be best described as:
A. Echolucent
B. Mural
C. Pedunculated
D. Sessile
A. Valve ring abscess usually presents as an area of echolucency (if cystic) or echoreflectant (if solid) around the valve ring or myocardium. Abscesses may be found in the aortic posterior annulus, peri-annular area, aortic-mitral intervalvular fibrosa, posterior aortic root and interventricular septum. For prosthetic heart valves, abscesses are usually seen around the sewing ring.
Valve ring abscess is usually caused by:
A. Infective endocarditis
B. Rheumatic fever
C. Valvular prolapse
D. Valvular regurgitation
A. Valve ring abscess is an uncommon but a serious typical complication of infective endocarditis and usually involves the aortic valve ring. A two-dimensional echocardiographic finding for valve ring abscess is an area of echolucency (if cystic) or echoreflectant (if solid). Rupture of aortic ring abscess can occur creating a fistula (e.g., communication between of the aorta to the right atrium, left atrium or right ventricle).
The test of choice for diagnosing the presence of vegetation and the complications of infective endocardits is:
A. Transthoracic echocardiography
B. Transesophageal echocardiography
C. Cardiac magnetic resonance imaging
D. Cardiac catheterization
B. The sensitivity of detecting a vegetation with transthoracic two-dimensional echocardiography is 65 to 80% and with transesophageal echocardiography it is 95%. It has been proposed that all patients with suspected infective endocarditis should undergo a transesophageal examination. The clinical utility of cardiac magnetic resonance imaging has not been determined but has been useful in determining the presence of perivalvular extension of infection, aortic root aneurysm and fistulas.
All of the following are types of prosthetic valve types EXCEPT:
A. Bioprosthetic (tissue)
B. Mechanical (metal)
C. Homograft (allograft)
D. Native
D. A bioprosthetic (tissue) valve is an actual valve or one made of biological tissue from an animal (heterograft) or human (homograft or allograft). A mechanical valve is made of nonbiological material (e.g., pyrolytic carbon). The Ross procedure is the placement of the patient’s pulmonary valve in the aortic valve position with placement of a homograft in the pulmonary valve position. This procedure is also called autograft.
All of the following are bioprosthetic (tissue) valves EXCEPT:
A. Starr-Edwards
B. Edwards Perimount
C. Medtronic Intact
D. Hancock
A. A bioprosthetic valve is an actual valve or one made of biologic tissue from an animal (heterograft, xenograft) or human (homograft, allograft) source. Stented porcine valves include the Hancock, Carpentier-Edwards and Medtronic Intact. Stented pericardial valves include the Carpentier-Edwards, Sorin Pericarbon and autologous pericardial valve. Stentless porcine valves include the Medtronic Freestyle, Edwards Prima and St. Jude Toronto SPV.
The Starr-Edwards is the most common ball and cage mechanical valve.
A pulmonic valve relocated to the aortic valve position is called a(n):
A. Allograft
B. Autograft
C. Heterograft
D. Xenograft
B. An autograft is a self-to-self bioprosthetic valve. The most common autograft procedure is the Ross procedure where the patient’s own pulmonary valve and adjacent main pulmonary artery are removed and used to replace the diseased aortic valve and aorta with re-implantation of the coronary arteries. A pulmonary or aortic homograft is placed in the pulmonary position. Allograft and homograft are from the same species (usually humans), heterograft and xenograft are from animals and autografts are from the patient themselves.
Which two cardiac valves need to be evaluated carefully in a patient with the Ross procedure?
A. Mitral valve; tricuspid valve
B. Aortic valve; pulmonary valve
C. Mitral valve; aortic valve
D. Aortic valve; tricuspid valve
B. The Ross procedure places the patient’s own pulmonary valve and adjacent main pulmonary artery in the aortic position with re-implantation of the coronary arteries. A human pulmonary or aortic homograft is placed in the patient’s pulmonary position. The presence of valve regurgitation, valve stenosis and global and segmental ventricular systolic function should be carefully evaluated.
The primary disadvantage of, the bioprosthetic (tissue) valve is:
A. Thrombus formation
B. Lack of durability
C. Pannus formation
D. Dehiscence
B. Tissue degeneration due to fibrocalcific changes which can lead to significant prosthetic valve regurgitation or stenosis usually occurs within ten years (30% by year 10; 30 to 60% by year 15) or more post-implantation. Other complications include surgical complication, valve thrombosis (more common in mechanical valves), pannus ingrowth, hemolysis, infective endocarditis and prosthesis-patient mismatch.
Degeneration is more common in the mitral valve than the aortic valve.
The primary advantages of the bioprosthetic valve includes lower risk of thromboembolism and no permanent anticoagulation therapy.
All of the following are mechanical valves EXCEPT:
A. Starr-Edwards
B. St. Jude
C. Hancock
D. CarboMedics
C. Mechanical valves are made of non-biologic material (e.g, pyrolytic carbon, titianium). Mechanical valves are classified into three major groups: caged-ball, tilting disc and bileaflet tilting disc valves The Starr Edwards is a ball and cage valve. The Omniscience and Medtronic-Hall are single tilting disc valves. The St. Jude (most common mechanical valve implanted) and CarboMedics are bileaflet tilting disc valves.
The Hancock is a porcine tissue valve.
The primary disadvantage of the mechanical valve is:
A. Dehiscence
B. Pannus ingrowth
C. Thrombogenicity
D. Durability
C. Patients with mechanical valves require long-term anticoagulation to reduce the risk of thrombosis and thromboembolism. Thrombosis of a mechanical valve in the tricuspid position is high followed by the mitral valve and then aortic valve and can result in significant prosthetic valve regurgitation and/or stenosis. Other disadvantages include mechanical failure (e.g., disk/poppet escape), pannus ingrowth, hemolysis, infective endocarditis and prosthesis-patient mismatch. The primary advantage of the mechanical valve is durability with the Starr-Edwards having an excellent history of over 40 years.
The most common ball and cage valve is the:
A. Starr-Edwards
B. Omniscience
C. St. Jude
D. Medtronic-Hall
A. The Starr-Edwards is a caged ball valve. The poppet is made of silicone rubber, the cage of Stellite alloy and the sewing ring of Teflon/polypropylene cloth. The Starr-Edwards valve is the oldest prosthetic valve of continuous use. Its primary disadvantage is size (bulky cage design) and is not indicated for use in patients who need a mitral valve replacement and have a small left ventricle. The Omniscience and Medtronic-Hall are tilting disc valves. The St. Jude is a bileaflet tilting disc valve.
The most common bileaflet tilting disc valve is the:
A. St. Jude
B. Starr-Edwards
C. Medtronic-Hall
D. Omniscience
A. The St. Jude bileaflet tilting disc valve is currently the most widely used prosthetic valve worldwide. It has two semi-circular discs coated with pyrolytic carbon which pivot open and closed without struts. The flow characteristics of the St. Jude are excellent with low transvalvular gradients and better cardiac output when compared to other mechanical valves. It may be the preferred valve for children because of its hemodynamic advantages.
Starr-Edwards is a ball and cage valve. The Medtronic-Hall and Omniscience are single disc tilting valves.
A prosthetic heart valve that is associated with a relatively high rate of outlet strut fracture and disc embolism is the:
A. Bjork-Shiley
B. Carpentier-Edwards
C. Starr-Edwards
D. Omniscience
A. Older models of the Bjork-Shiley tilting disc prosthesis are associated with an outlet strut fracture with embolization of the disc, a complication that is usually fatal.
Abnormal rocking motion of a prosthetic valve by two-dimensional echocardiography indicates prosthetic valve:
A. Dehiscence
B. Stenosis
C. Thrombus
D. Vegetation
A. Abnormal rocking motion of a prosthetic valve with respect to the surrounding cardiac-soft tissue structures reliably indicates dehiscence.
A qualitative way to determine dehiscence is to compare the motion of the prosthetic valve with the motion of the aortic root. If the prosthetic motion is greater than the aortic root motion, dehiscence may be present. Dehiscence may suggest the presence of infective endocarditis and usually results in significant valvular regurgitation.
The excessive ingrowth of tissue for a prosthetic valve is called:
A. Thrombus
B. Vegetation
C. Pannus
D. Dehiscence
C. Pannus is the excessive ingrowth of tissue and can occur with either a mechanical or a bioprosthetic valve. Pannus may result in prosthetic valve regurgitation or prosthetic valve stenosis.
Complications associated with prosthetic valve dysfunction include all of the following EXCEPT:
A. Dehiscence
B. Leaflet degeneration
C. Thrombosis
D. Tumor
D. Dysfunction of prosthetic valves may occur because of stenosis, regurgitation, perivalvular leak, leaflet degeneration, thrombosis, dehiscence, pannus, infective endocarditis, valve bed abnormalities (e.g., hematoma), hemolysis and prosthesis-patient mismatch). Leaflet degeneration (lack of durability) is a common problem for bioprosthetic valves and thrombus formation is a common problem for mechanical valves.
All of the following should be determined when evaluating a prosthetic valve with cardiac Doppler EXCEPT:
A. Peak velocity
B. Mean pressure gradient
C. Effective orifice area
D. Shunt ratio
D. Prosthetic valves are inherently stenotic and the flow velocity across a normal prosthetic valve will be higher as compared to a normal native valve. Each brand of valve has normal ranges according to size so a chart is usually referred to determine if the prosthetic valve is normal.
In general, a peak velocity of › 2 m/s may indicate an abnormal mitral valve prosthesis. A peak velocity of > 3 m/s may indicate an abnormal aortic valve prosthesis.
Cardiac Doppler evaluation of a prosthetic mitral valve should include all of the following EXCEPT:
A. Effective orifice area
B. Peak mitral valve A wave velocity
C. Peak and mean pressure gradients
D. Pressure half-time
B. The following hemodynamic data should be included in a mitral prosthetic valve Doppler examination:
• Peak velocity
• Peak (maximum) pressure gradient
• Mean pressure gradient
• Pressure half-time (mitral valve)
• Effective orifice area (continuity equation)
• Pulmonary artery pressure
These values should be collected at a baseline study during the first outpatient visit.
The best Doppler formula for calculating the effective orifice are
(EOA) in a patient with mitral valve replacement is:
A. 4 x (V2)^2
B. 4 x (V2^2 - V1^2)
C. (CSALVOT * VTILVOT) ÷ VTIMV
D. 220 ÷ pressure half-time
V2^2, velocity across the obstruction; V1^2, velocity proximal to the obstruction;
CSALVOT, cross-sectional area of left ventricular outflow tract;
VTILVOT, velocity time integral of left ventricular outflow tract;
VTIMV, velocity time integral of mitral valve
C. The effective orifice area of a mitral valve prosthesis is best determined by the continuity equation. The pressure half-time is useful in determining whether an increase in velocity is due to increased flow (i.e., prosthetic valvular regurgitation) or to obstruction. The pressure half-time method overestimates the area of mitral valve prosthesis because the constant 220 was derived for stenotic native mitral valves.
The continuity equation for mitral valve effective orifice area (EOA) is not valid when significant mitral regurgitation or significant aortic regurgitation is present.
The determination of prosthetic mitral valve regurgitation and prosthetic tricuspid valve regurgitation is made difficult by the artifact called:
A. Slice thickness
B. Shadowing
C. Mirroring
D. Enhancement
B. Due to the significant acoustic impedance mismatch between blood and prosthetic valve material shadowing (flow masking) occurs especially in the transthoracic apical windows. Examining for the flow convergence region (PISA) may be useful. An increased mitral peak E wave velocity (> 2 m/s) with a shortened pressure half-time (< 150 msec) may suggest significant prosthetic mitral valve regurgitation. A VTIPrMV / VTILVOT ratio of > 2.2 suggests significant prosthetic mitral regurgitation. Transesophageal echocardiography is the preferred test.
VTIPrMV, velocity time integral of prosthetic mitral valve;
VTILVOT, velocity time integral of left ventricular outflow tract
The best Doppler method for evaluating aortic valve replacement is probably:
A. Deceleration slope
B. Maximum peak instantaneous pressure gradient
C. Pressure half-time
D. Velocity ratio
D. The following parameters should be obtained during a Doppler evaluation of an aortic valve replacement:
• Peak velocity
• Maximum peak instantaneous pressure gradient
• Mean pressure gradient
• Effective orifice area (continuity equation)
• Velocity ratio
• Pressure half-time (aortic regurgitation)
• Pulmonary artery pressures
A velocity ratio (LVOTVTI / AVRVTI) of < .20 suggests aortic valve replacement obstruction.
LVOTVTI, left ventricular outflow tract velocity time integral;
AVRVTI, aortic valve replacement velocity time integral
All of the following are true statements concerning prosthetic valves EXCEPT:
A. A baseline study should be obtained post-surgery
B. Velocities depend upon the size and type of prosthetic valve
C. Prosthetic valve peak velocities are generally higher as compared to normal native valves
D. Prosthetic valve regurgitation is always abnormal
D. A small amount of so called built-in regurgitation is normal in all types of prosthetic valves. There are two types of normal (physiologic) prosthetic valve regurgitation: closure backflow and leakage. Closure backflow is the flow reversal due to valve closure. Leakage is due to flow in and around the occluding mechanism.
