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Aortic Regurgitation Ali Mahajerin Echo Conference September 17, 2008.

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1 Aortic Regurgitation Ali Mahajerin Echo Conference September 17, 2008

2 Introduction Aortic regurgitation (AR) is characterized by diastolic reflux of blood from the aorta to the LV. Aortic regurgitation (AR) is characterized by diastolic reflux of blood from the aorta to the LV. AR may be caused by malfunction of the aortic valve leaflets themselves, by dilation of the aortic root and annulus, or a combination of these factors. AR may be caused by malfunction of the aortic valve leaflets themselves, by dilation of the aortic root and annulus, or a combination of these factors. Aortic root disease now accounts for >50% of all AVRs Aortic root disease now accounts for >50% of all AVRs Clinical presentation is highly variable and depends on multiple factors, including acuity of onset, aortic and LV compliance, hemodynamic conditions, and severity of the lesion. Clinical presentation is highly variable and depends on multiple factors, including acuity of onset, aortic and LV compliance, hemodynamic conditions, and severity of the lesion.

3 Epidemiology Incidence of clinically significant AR increases with age Incidence of clinically significant AR increases with age Typical peak in 4 th to 6 th decade of life Typical peak in 4 th to 6 th decade of life More common in men than women More common in men than women Overall prevalence of AR was 4.9% in Framingham Heart Study and 10% in Strong Heart Study Overall prevalence of AR was 4.9% in Framingham Heart Study and 10% in Strong Heart Study Prevalence of moderate or greater severity was 0.5% and 2.7%, respectively Prevalence of moderate or greater severity was 0.5% and 2.7%, respectively Most common cause of AR in developing countries is RHD Most common cause of AR in developing countries is RHD In developed countries the leading cause of AR is either congenital (particularly due to bicuspid leaflets) or degenerative disease (including annuloaortic ectasia). In developed countries the leading cause of AR is either congenital (particularly due to bicuspid leaflets) or degenerative disease (including annuloaortic ectasia).

4 Valve-Related Causes of AR Rheumatic disease Rheumatic disease Cusps become fibrotic and retract (usually also stenotic); MV involved as well Cusps become fibrotic and retract (usually also stenotic); MV involved as well Atherosclerotic degeneration Atherosclerotic degeneration Infective endocarditis Infective endocarditis Leaflet perforation Leaflet perforation Vegetation interferes with coaptation Vegetation interferes with coaptation Trauma (chest wall or deceleration injury) Trauma (chest wall or deceleration injury) Bicuspid aortic valve (can be associated with aortic root dilation as well) Bicuspid aortic valve (can be associated with aortic root dilation as well)

5 Other Valve-Related Causes of AR Myxomatous degeneration Myxomatous degeneration Structural deterioration of bioprosthesis Structural deterioration of bioprosthesis Other less common causes: Other less common causes: Ankylosing spondylitis (can cause disease of both the leaflets and the aortic root) Ankylosing spondylitis (can cause disease of both the leaflets and the aortic root) SLE, RA SLE, RA Takayasu disease Takayasu disease Anorectic drugs Anorectic drugs Membranous subaortic stenosis Membranous subaortic stenosis

6 Aortic Root Disease Dilation here is rare As little as 2mm of dilation here can cause AR Dilation here is common; especially in AS; does not lead to AR Between the annulus and the ascending aorta is a collagenous segment that forms the sinuses of valsalva. Between the annulus and the ascending aorta is a collagenous segment that forms the sinuses of valsalva.

7 Aortic Root Disease Dilation of the aortic ridge eliminates the normal overlap of the valves Dilation of the aortic ridge eliminates the normal overlap of the valves

8 Aortic Root-Related Causes of AR Idiopathic aortic root dilation Idiopathic aortic root dilation Aortoannular ectasia Aortoannular ectasia Marfan syndrome Marfan syndrome Ehlers-Danlos syndrome Ehlers-Danlos syndrome Osteogenesis imperfecta Osteogenesis imperfecta Aortic dissection Aortic dissection Syphilitic aortitis Syphilitic aortitis Trauma Trauma Ankylosing spondylitis Ankylosing spondylitis Bicuspid aortic valve with dilated aortic root Bicuspid aortic valve with dilated aortic root

9 Acute Aortic Regurgitation Most commonly caused by bacterial endocarditis, aortic dissection, or blunt chest trauma Most commonly caused by bacterial endocarditis, aortic dissection, or blunt chest trauma Sudden large regurgitant volume is imposed on an LV of normal size that has not had time to accommodate the volume overload. Sudden large regurgitant volume is imposed on an LV of normal size that has not had time to accommodate the volume overload. Abrupt increase in LVEDV leads to rapid and dramatic increase in LVEDP and LA pressures Abrupt increase in LVEDV leads to rapid and dramatic increase in LVEDP and LA pressures Inability of ventricle to develop compensatory chamber dilatation acutely results in a decrease in forward stroke volume. Inability of ventricle to develop compensatory chamber dilatation acutely results in a decrease in forward stroke volume. Tachycardia may develop as a compensatory mechanism to maintain cardiac output, but often insufficient. Tachycardia may develop as a compensatory mechanism to maintain cardiac output, but often insufficient.

10 Acute AR - Pathophysiology Patients often present with pulmonary edema or cardiogenic shock. Patients often present with pulmonary edema or cardiogenic shock. May present with myocardial ischemia: As LVEDP approaches diastolic aortic and coronary pressures, myocardial perfusion pressure in the subendocardium is diminished. May present with myocardial ischemia: As LVEDP approaches diastolic aortic and coronary pressures, myocardial perfusion pressure in the subendocardium is diminished. LV dilation and thinning of LV wall result in increased afterload, and combined with tachycardia leads to increased myocardial O2 demand LV dilation and thinning of LV wall result in increased afterload, and combined with tachycardia leads to increased myocardial O2 demand Ischemia and its consequences, including sudden death, occur commonly in acute AR. Ischemia and its consequences, including sudden death, occur commonly in acute AR.

11 Chronic Aortic Regurgitation Chronic AR imposes both volume and pressure overload on the LV. Chronic AR imposes both volume and pressure overload on the LV. Increased regurgitant volume  increased LVEDV and increased wall stress Increased regurgitant volume  increased LVEDV and increased wall stress Increased chamber compliance accommodates increased volume w/o increasing filling pressures Increased chamber compliance accommodates increased volume w/o increasing filling pressures Compensatory eccentric hypertrophy also occurs, helping to maintain normal stroke volume with the chamber enlargement Compensatory eccentric hypertrophy also occurs, helping to maintain normal stroke volume with the chamber enlargement LVEDV increases but LV wall compliance prevents increase in LVEDP LVEDV increases but LV wall compliance prevents increase in LVEDP

12 Chronic AR - Pathophysiology Early Compensated Enlarged chamber size  ↑ afterload  hypertrophy of LV which preserves compliance  normal filling pressures Enlarged chamber size  ↑ afterload  hypertrophy of LV which preserves compliance  normal filling pressures LVH  ↑ LV mass  normal LV vol/mass ratio & EF LVH  ↑ LV mass  normal LV vol/mass ratio & EF Progressive LV dilation and systolic HTN  ↑ wall stress and vol/mass ratio Progressive LV dilation and systolic HTN  ↑ wall stress and vol/mass ratio ↑ wall stress eventually leads to overt LV dysfunction. ↑ wall stress eventually leads to overt LV dysfunction. Decompensated LV systolic dysfunction accompanied by decreased LV diastolic compliance due to hypertrophy and fibrosis Leads to high filling pressures and CHF symptoms Exertional dyspnea common; angina can occur due to reduced coronary flow reserve with predominantly systolic coronary flow

13 Different Stages of AR Bekerdjian R, et al. Circulation 2005; 112:

14 Physical Exam - Auscultation A2 often soft/absent, P2 normal A2 often soft/absent, P2 normal S3 if LV function severely depressed S3 if LV function severely depressed High frequency decrescendo diastolic murmur over the 3 rd or 4 th intercostal space at left sternal border High frequency decrescendo diastolic murmur over the 3 rd or 4 th intercostal space at left sternal border Best heard sitting up, leaning forward at end expiration Best heard sitting up, leaning forward at end expiration Austin Flint murmur: mid-to-late diastolic apical rumble, possibly due to vibration of anterior mitral leaflet as it is struck by a posteriorly directed AR jet. Austin Flint murmur: mid-to-late diastolic apical rumble, possibly due to vibration of anterior mitral leaflet as it is struck by a posteriorly directed AR jet.

15 Physical Exam – Peripheral Findings Corrigan’s pulse – bounding “waterhammer” carotid pulse Corrigan’s pulse – bounding “waterhammer” carotid pulse deMusset’s sign – head bob with each heart beat deMusset’s sign – head bob with each heart beat Mueller’s sign – systolic pulsation of uvula Mueller’s sign – systolic pulsation of uvula Traube’s sign – pistol shot pulse over the femoral artery Traube’s sign – pistol shot pulse over the femoral artery Duroziez’s sign – systolic and diastolic bruits heard when femoral artery partially compressed Duroziez’s sign – systolic and diastolic bruits heard when femoral artery partially compressed Becker’s sign – visible pulsations of retinal arteries and pupils Becker’s sign – visible pulsations of retinal arteries and pupils Hill’s sign – popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg Hill’s sign – popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg Mayne’s sign – more than 15 mmHg decrease in diastolic blood pressure with arm elevation Mayne’s sign – more than 15 mmHg decrease in diastolic blood pressure with arm elevation Rosenbach’s sign – systolic pulsations of the liver Rosenbach’s sign – systolic pulsations of the liver Gerhard’s sign – systolic pulsations of the spleen Gerhard’s sign – systolic pulsations of the spleen

16 Natural History of AR Depends on AR severity, aortic root pathology, and adaptive response of LV. Depends on AR severity, aortic root pathology, and adaptive response of LV. Bonow et al: Bonow et al: 104 asymptomatic patients with severe AR and normal LVEF 104 asymptomatic patients with severe AR and normal LVEF Death, symptoms, or asymptomatic LV dysfunction was < 5%/year over 11-year follow-up Death, symptoms, or asymptomatic LV dysfunction was < 5%/year over 11-year follow-up Rate of sudden death was only 0.4%/year Rate of sudden death was only 0.4%/year At 11 years, 58% remained asymptomatic and had normal LV systolic function. At 11 years, 58% remained asymptomatic and had normal LV systolic function. Further strengthened serial changes in LV systolic function and/or LV dilatation as important to clinical outcome in AR and potential reasons for AVR. Further strengthened serial changes in LV systolic function and/or LV dilatation as important to clinical outcome in AR and potential reasons for AVR. Bonow RO, et al. Circulation 1991; 84:

17 Natural History of AR Dujardin et al: Dujardin et al: 246 patients with moderate-severe AR, mean follow- up 7 years 246 patients with moderate-severe AR, mean follow- up 7 years Not all asymptomatic with normal LV systolic function Not all asymptomatic with normal LV systolic function Ten-year mortality rate 34% Ten-year mortality rate 34% Independent predictors of survival were age, functional class, comorbidity index, atrial fibrillation, LVESD, and LVEF Independent predictors of survival were age, functional class, comorbidity index, atrial fibrillation, LVESD, and LVEF Dujardin KS, et al. Circulation 1999; 99:

18 Asymptomatic patients with normal LV function generally have a favorable prognosis Asymptomatic patients with normal LV function generally have a favorable prognosis Decline in LVEF with exercise or serial follow- up identifies patients who will likely require surgical intervention. Decline in LVEF with exercise or serial follow- up identifies patients who will likely require surgical intervention. Even moderate symptoms or evidence of LV dilatation are at higher risk and should be considered for early intervention. Even moderate symptoms or evidence of LV dilatation are at higher risk and should be considered for early intervention.

19 Natural History of Chronic AR

20 Diagnostic Tools: ECG LVH with or without strain pattern, LAD, LAE LVH with or without strain pattern, LAD, LAE One study suggests that in asymptomatic or mildly symptomatic patients with pure AR, the absence of ECG changes predicts LV systolic dimension 45% and >40% with exercise. One study suggests that in asymptomatic or mildly symptomatic patients with pure AR, the absence of ECG changes predicts LV systolic dimension 45% and >40% with exercise. Up to 83% of patients with rest or exercise ST segment abnormalities had an enlarged LV (>55mm) or reduced LVEF 55mm) or reduced LVEF < 45%. Conduction abnormalities rare except in late disease with severe LV dysfunction; sustained SVT or VT unusual in absence of significant LV dysfunction. Conduction abnormalities rare except in late disease with severe LV dysfunction; sustained SVT or VT unusual in absence of significant LV dysfunction.

21 Chest X-Ray Cardiomegaly Cardiomegaly Prominent Left Ventricle Prominent Left Ventricle Ascending Aortic dilatation Ascending Aortic dilatation LAE only if severe LV dysfunction LAE only if severe LV dysfunction

22 Chest X-Ray

23 Echocardiography Most important diagnostic test for evaluation of AR as well as for serial follow-up Most important diagnostic test for evaluation of AR as well as for serial follow-up Allows for: Allows for: Assessment of the anatomy of the aortic leaflets and the aortic root Assessment of the anatomy of the aortic leaflets and the aortic root Detection of the presence and severity of AR Detection of the presence and severity of AR Characterization of LV size and function Characterization of LV size and function

24 M-Mode Echocardiography The aortic regurgitation jet can cascade across the anterior mitral leaflet The aortic regurgitation jet can cascade across the anterior mitral leaflet Creates a high-frequency fluttering of the anterior mitral leaflet Creates a high-frequency fluttering of the anterior mitral leaflet Increased duration between E and A peaks Increased duration between E and A peaks Increased distance between the maximal anterior motion of the mitral valve in early diastole (E point) and the most posterior motion of the interventricular septum (e.g., increased E-point septal separation [EPSS]) Increased distance between the maximal anterior motion of the mitral valve in early diastole (E point) and the most posterior motion of the interventricular septum (e.g., increased E-point septal separation [EPSS]) In acute AR, premature closure of the MV can also be seen by M-mode In acute AR, premature closure of the MV can also be seen by M-mode Due to rapidly increasing LV pressure Due to rapidly increasing LV pressure

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26 AR by 2D Echo 2D Echo will give you a detailed evaluation of the aortic valve and root 2D Echo will give you a detailed evaluation of the aortic valve and root Detailed evaluation of LV size and function Detailed evaluation of LV size and function Many important causes of AR easily seen on 2D imaging Many important causes of AR easily seen on 2D imaging Even when AR is severe, sometimes 2D imaging is surprisingly normal Even when AR is severe, sometimes 2D imaging is surprisingly normal Indirect signs of AR: Indirect signs of AR: Diastolic curving of anterior mitral leaflet with concavity towards ventricular septum due to the direct effect of the regurgitant jet Diastolic curving of anterior mitral leaflet with concavity towards ventricular septum due to the direct effect of the regurgitant jet

27 Dilated aortic root due to aortoannular ectasia Large, mobile vegetation Bicuspid aortic valve with characteristic elliptical opening Acute AR due to aortic dissection Bekerdjian R, et al. Circulation 2005; 112:

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33 Color Flow Doppler Color flow jet composed of 3 distinct segments: Color flow jet composed of 3 distinct segments: Proximal flow convergence zone = area of flow acceleration into the orifice Proximal flow convergence zone = area of flow acceleration into the orifice Vena contracta = narrowest and highest velocity region of the jet at or just downstream from the orifice Vena contracta = narrowest and highest velocity region of the jet at or just downstream from the orifice The jet itself occurs distal to the orifice in the LV cavity The jet itself occurs distal to the orifice in the LV cavity Measurement of the jet area or penetration into the LV cavity is not accurate in assessing AR severity, though: Measurement of the jet area or penetration into the LV cavity is not accurate in assessing AR severity, though: If jet width/LVOT width < 25%  specific for mild AR If jet width/LVOT width < 25%  specific for mild AR If jet width/LVOT width > 65%  specific for severe AR If jet width/LVOT width > 65%  specific for severe AR This works best when regurgitant orifice is relatively round in shape. This works best when regurgitant orifice is relatively round in shape.

34 Color Flow Doppler Color flow Doppler is the most common technique to visualize AR Color flow Doppler is the most common technique to visualize AR Sensitivity > 95% Sensitivity > 95% False negatives can occur in tachycardia with mild AR False negatives can occur in tachycardia with mild AR Frame rate allows only a few diastolic frames to be displayed Frame rate allows only a few diastolic frames to be displayed Can be overcome by using CW -- has a higher sampling rate Can be overcome by using CW -- has a higher sampling rate Specificity ~100% Specificity ~100% Detects even trivial AR Detects even trivial AR 1% of subjects under age 40 1% of subjects under age % of patients greater than age % of patients greater than age 60

35 Eccentric AR jet Eccentric AR jet Width measured at origin of jet adjacent to leaflets Width measured at origin of jet adjacent to leaflets Jet width/LVOT width is <25% Jet width/LVOT width is <25% Case of mild AR Case of mild AR Jet width/LVOT width > 65% Case of severe AR Bekerdjian R, et al. Circulation 2005; 112:

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39 (Same patient – aortic valve endocarditis as cause of AR)

40 AR jet directed toward anterior mitral leaflet

41 Vena Contracta The narrowest diameter of flow stream The narrowest diameter of flow stream Independent of volume flow rate and driving pressure, relatively unaffected by instrument settings Independent of volume flow rate and driving pressure, relatively unaffected by instrument settings Narrow range of values though, so care needed to obtain optimal images. Ideal sample is: Narrow range of values though, so care needed to obtain optimal images. Ideal sample is: Perpendicular to jet width Perpendicular to jet width In zoom mode In zoom mode Narrow sector Narrow sector Minimum depth Minimum depth For AR, vena contracta can be measured in parasternal long-axis view preferably in zoom mode. For AR, vena contracta can be measured in parasternal long-axis view preferably in zoom mode.

42 Vena Contracta Vena contracta width of ≥ 6 mm correlates well with severe AR (sensitivity 95%, specificity 90%) Vena contracta width of ≥ 6 mm correlates well with severe AR (sensitivity 95%, specificity 90%) Vena contracta width of < 3 mm specific for mild AR. Vena contracta width of < 3 mm specific for mild AR. Enriquez-Sarano M, et al. NEJM 2004; 351:

43 Proximal Isovelocity Surface Area Acceleration of flow occurs proximal to the valve plane with a series of isovelocity “surfaces” leading to the high-velocity jet in the regurgitant orifice. Acceleration of flow occurs proximal to the valve plane with a series of isovelocity “surfaces” leading to the high-velocity jet in the regurgitant orifice. Velocity for a PISA can be determined as the aliasing velocity where a distinct red-blue interface seen (at this interface, velocity is equivalent to Nyquist limit). Velocity for a PISA can be determined as the aliasing velocity where a distinct red-blue interface seen (at this interface, velocity is equivalent to Nyquist limit). Assuming a hemispherical shape, the surface area of the PISA region is 2πr 2 Assuming a hemispherical shape, the surface area of the PISA region is 2πr 2 Peak regurgitant flow obtained by multiplying surface area by aliasing velocity, and effective regurgitant orifice area (EROA) is peak regurgitant flow divided by peak velocity obtained by CW Doppler. Peak regurgitant flow obtained by multiplying surface area by aliasing velocity, and effective regurgitant orifice area (EROA) is peak regurgitant flow divided by peak velocity obtained by CW Doppler.

44 PISA - Limitations Isovelocity contour flattens as it approaches the orifice, underestimating flow Isovelocity contour flattens as it approaches the orifice, underestimating flow Proximal structures can distort the isovelocity contour Proximal structures can distort the isovelocity contour Sensitive to errors in radius measurement Sensitive to errors in radius measurement 10% error in radius leads to 21% error in flow 10% error in radius leads to 21% error in flow

45 Continuous Wave Doppler Because AR jet is high velocity, CW Doppler necessary to record envelope of jet. Because AR jet is high velocity, CW Doppler necessary to record envelope of jet. Several types of info can be derived: Several types of info can be derived: Antegrade flow velocity Antegrade flow velocity Signal intensity relative to antegrade flow Signal intensity relative to antegrade flow Time course (shape) of velocity curve Time course (shape) of velocity curve AR results in increased antegrade volume flow rate across AV, which is reflected in an increase in the antegrade velocity across the valve. AR results in increased antegrade volume flow rate across AV, which is reflected in an increase in the antegrade velocity across the valve. The greater the severity of AR, the higher the antegrade velocity across the AV The greater the severity of AR, the higher the antegrade velocity across the AV Must also consider possibility of coexisting AS Must also consider possibility of coexisting AS

46 AR Antegrade Signal intensity is proportional to # RBCs contributing to regurgitant signal. Signal intensity is proportional to # RBCs contributing to regurgitant signal. Can compare intensity of regurgitant signal to antegrade flow as a qualitative estimate of regurgitant severity. Can compare intensity of regurgitant signal to antegrade flow as a qualitative estimate of regurgitant severity. Weak signal reflects mild severity; signal nearly equal to antegrade flow reflects severe regurgitation. Weak signal reflects mild severity; signal nearly equal to antegrade flow reflects severe regurgitation.

47 CW Doppler: Pressure Half-Time Shape of AR velocity curve depends on time course of diastolic pressure difference across AV Shape of AR velocity curve depends on time course of diastolic pressure difference across AV Chronic severe AR results in increased aortic pulse pressure with low aortic EDP. Rapid rate of decline in aortic pressure is reflected in steeper diastolic deceleration slope (even if LVEDP remains low). Chronic severe AR results in increased aortic pulse pressure with low aortic EDP. Rapid rate of decline in aortic pressure is reflected in steeper diastolic deceleration slope (even if LVEDP remains low). Thus, diastolic deceleration slope provides a semiquantitative measure of AR severity. Thus, diastolic deceleration slope provides a semiquantitative measure of AR severity. A flat slope (P 1/2 > 500 msec) is consistent with mild AR, and a steep slope (P 1/2 500 msec) is consistent with mild AR, and a steep slope (P 1/2 < 200 msec) indicates severe AR. For a given severity of AR, P 1/2 will be shortened by elevated LVEDP or vasodilator therapy that reduces AR. For a given severity of AR, P 1/2 will be shortened by elevated LVEDP or vasodilator therapy that reduces AR.

48 Pressure Half-Time With acute AR, LV compliance has not yet adapted leading to significant increase in LVEDP. In extreme cases, aortic and LV EDP may equalize at end-distole, resulting in a triangular-shaped CW-Doppler with linear deceleration slope from maximum velocity to baseline. With acute AR, LV compliance has not yet adapted leading to significant increase in LVEDP. In extreme cases, aortic and LV EDP may equalize at end-distole, resulting in a triangular-shaped CW-Doppler with linear deceleration slope from maximum velocity to baseline. Limitations of pressure half-time assessment: Limitations of pressure half-time assessment: Pressure half-time sensitive to chronicity of AR Pressure half-time sensitive to chronicity of AR Acute AR leads to much shorter values than chronic AR when LV is dilated with increased compliance Acute AR leads to much shorter values than chronic AR when LV is dilated with increased compliance Pressure half-time varies with SVR Pressure half-time varies with SVR Vasodilators may shorten the pressure half-time even as the aortic regurgitant fraction improves. Vasodilators may shorten the pressure half-time even as the aortic regurgitant fraction improves.

49 Pressure Half-Time

50 Regurgitant Volume or Fraction Can compare flow through AV versus MV or PV Can compare flow through AV versus MV or PV Stroke volume at any valve annulus is derived as the product of CSA and VTI of flow at the annulus Stroke volume at any valve annulus is derived as the product of CSA and VTI of flow at the annulus In the absence of regurgitation, SV determinations at different sites (LVOT, mitral annulus, pulmonic annulus) should be equal In the absence of regurgitation, SV determinations at different sites (LVOT, mitral annulus, pulmonic annulus) should be equal In the presence of regurgitation of one valve, without any intracardiac shunt the flow through the affected valve is larger than the other valves In the presence of regurgitation of one valve, without any intracardiac shunt the flow through the affected valve is larger than the other valves RV is the difference between the two flows RV is the difference between the two flows RF is the RV divided by forward stroke volume through the regurgitant valve. RF is the RV divided by forward stroke volume through the regurgitant valve.

51 Regurgitant Volume or Fraction

52 Regurgitant Volume (fraction): Regurgitant Volume (fraction): Mild: < 30 cc (< 30%) Mild: < 30 cc (< 30%) Mild-moderate: cc (30-39%) Mild-moderate: cc (30-39%) Moderately severe: cc (40-49%) Moderately severe: cc (40-49%) Severe: ≥60 cc (≥50%) Severe: ≥60 cc (≥50%) Limitations: Limitations: Assumes normal flow through comparison valve Assumes normal flow through comparison valve Cannot be used in presence of shunts Cannot be used in presence of shunts Sensitive to small measurement errors (measurement errors of the radius and tracing the VTI) Sensitive to small measurement errors (measurement errors of the radius and tracing the VTI)

53 RF by CW Doppler of Distal Arch Aortic regurgitant fraction can be estimated by ratio of reversed flow VTI / forward flow VTI in the distal aortic arch. Aortic regurgitant fraction can be estimated by ratio of reversed flow VTI / forward flow VTI in the distal aortic arch. Antegrade Retrograde

54 Aortic Flow Reversal An important supportive sign of severe AR is diastolic flow reversal in the descending aorta. An important supportive sign of severe AR is diastolic flow reversal in the descending aorta. Holodiastolic flow reversal usually indicates at least moderate AR Holodiastolic flow reversal usually indicates at least moderate AR Best measured with PW Doppler from a suprasternal probe position. Best measured with PW Doppler from a suprasternal probe position. If observed in the proximal abdominal aorta (from the subcostal position), is even more sensitive (100%) and specific (97%) for severe AR. If observed in the proximal abdominal aorta (from the subcostal position), is even more sensitive (100%) and specific (97%) for severe AR. False positives may occur if a PDA is present. False positives may occur if a PDA is present.

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58 Cardiac Catheterization May be needed to evaluate coronary anatomy in patients requiring surgical intervention. May be needed to evaluate coronary anatomy in patients requiring surgical intervention. Men age > 35 years, pre-menopausal women age > 35 years with risk factors for CAD, or postmenopausal women Men age > 35 years, pre-menopausal women age > 35 years with risk factors for CAD, or postmenopausal women Supravalvular aortography = semiquantitative way to grade AR, based on amount of contrast in LV after aortography Supravalvular aortography = semiquantitative way to grade AR, based on amount of contrast in LV after aortography Mild AR (1+): contrast appears in LV but clears after each beat. Mild AR (1+): contrast appears in LV but clears after each beat. Moderate AR (2+): faint opacification of entire LV over several cardiac cycles. Moderate AR (2+): faint opacification of entire LV over several cardiac cycles. Mod-severe AR (3+): opacification of entire LV with same intensity as aorta Mod-severe AR (3+): opacification of entire LV with same intensity as aorta Severe AR (4+): opacification of entire LV on first heart beat with intensity higher than aorta. Severe AR (4+): opacification of entire LV on first heart beat with intensity higher than aorta. Subjective, depends on amount of contrast injected and the size of the LV, and correlates poorly with regurgitant volume particularly in patients with dilated LVs. Subjective, depends on amount of contrast injected and the size of the LV, and correlates poorly with regurgitant volume particularly in patients with dilated LVs.

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64 Cardiac MR CMR is widely recognized as the non-invasive gold standard for quantification of LV volumes and ejection fraction. CMR is widely recognized as the non-invasive gold standard for quantification of LV volumes and ejection fraction. Can overcome the limitations of echo, such as studies limited by body habitus or cases with eccentric regurgitant jets. Can overcome the limitations of echo, such as studies limited by body habitus or cases with eccentric regurgitant jets. Phase velocity encoding is used to calculate forward stroke volume through the AV; total LV stroke volume is determined from LVEDV and LVESV, and the difference between aortic and LV stroke volumes is the regurgitant volume. Phase velocity encoding is used to calculate forward stroke volume through the AV; total LV stroke volume is determined from LVEDV and LVESV, and the difference between aortic and LV stroke volumes is the regurgitant volume. Volumetric CMR assessment of AR has been shown to be accurate and reproducible. Volumetric CMR assessment of AR has been shown to be accurate and reproducible. CMR has the potential to be a very useful tool for serial evaluations, though referring physicians are often more comfortable with qualitative interpretations of regurgitation severity such as those provided by echo assessment. CMR has the potential to be a very useful tool for serial evaluations, though referring physicians are often more comfortable with qualitative interpretations of regurgitation severity such as those provided by echo assessment.

65 Cardiac MR Gelfand et al. addressed the issue of concordance between quantitative CMR and qualitative echocardiographic determinations of regurgitant severity. Gelfand et al. addressed the issue of concordance between quantitative CMR and qualitative echocardiographic determinations of regurgitant severity. Compared echo and CMR findings in 141 consecutive patients with varying degrees of MR and/or AR, to identify CMR regurgitant fractions that correlated with qualitative mild, moderate, and severe regurgitaion by echo. Compared echo and CMR findings in 141 consecutive patients with varying degrees of MR and/or AR, to identify CMR regurgitant fractions that correlated with qualitative mild, moderate, and severe regurgitaion by echo. Average age 53 ± 15 yr, 43% female. 24 with AR, 83 with MR, 35 with no MR/AR. Median interval 31 days between CMR and Echo. Average age 53 ± 15 yr, 43% female. 24 with AR, 83 with MR, 35 with no MR/AR. Median interval 31 days between CMR and Echo. Gelfand EV, et al. Journal of CMR 2006; 8:

66 Cardiac MR The mean CMR aortic regurgitant fractions for each echocardiographic grade was significantly different (p < for trend, p<0.05 for each pairwise comparison) The mean CMR aortic regurgitant fractions for each echocardiographic grade was significantly different (p < for trend, p<0.05 for each pairwise comparison) The CMR-RF thresholds with maximal agreement for aortic regurgitation: The CMR-RF thresholds with maximal agreement for aortic regurgitation: Mild ≤ 15% Mild ≤ 15% Moderate 16-27% Moderate 16-27% Mod-sev or severe > 27% Mod-sev or severe > 27% These thresholds yielded 100% concordance within 1 regurgitation grade. For patients without AR on echo, the CMR aortic regurgitant fraction was 2 ± 2%. Gelfand EV, et al. Journal of CMR 2006; 8:

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74 Serial Testing with Echo If chronic nature of lesion uncertain and no initial surgical indication, should repeat exam and echo within 2-3 months after initial evaluation. If chronic nature of lesion uncertain and no initial surgical indication, should repeat exam and echo within 2-3 months after initial evaluation. Asx, mild AR, little/no LV dilation, normal LV systolic function: see yearly, echo q2-3 years Asx, mild AR, little/no LV dilation, normal LV systolic function: see yearly, echo q2-3 years Asx, severe AR, significant LV dilation (LVEDD > 60 mm), normal LV fx: echo q6-12 months Asx, severe AR, significant LV dilation (LVEDD > 60 mm), normal LV fx: echo q6-12 months Asx, severe AR, severe LV dilation (LVEDD > 70 mm), normal LV fx: echo q4-6 months. Asx, severe AR, severe LV dilation (LVEDD > 70 mm), normal LV fx: echo q4-6 months. Repeat echo for onset of symptoms, equivocal history of changing symptoms or exercise tolerance, or clinical findings to suggest worsening regurgitation or progressive LV dilatation. Repeat echo for onset of symptoms, equivocal history of changing symptoms or exercise tolerance, or clinical findings to suggest worsening regurgitation or progressive LV dilatation. Bonow RO, et al. Circulation 2006; 114: e84-e231.

75 Chronic AR Management - Surgery AR is a surgical disease. The timing of surgery is clinically dependent. AR is a surgical disease. The timing of surgery is clinically dependent. In patients with pure, chronic AR, AVR should be considered only if AR is severe. In patients with pure, chronic AR, AVR should be considered only if AR is severe. Operative mortality for AVR ~4%, higher with concomitant aortic root replacement or CABG or if comorbidities such as advanced age. Operative mortality for AVR ~4%, higher with concomitant aortic root replacement or CABG or if comorbidities such as advanced age. Death rate for Asx with normal LV <0.2%/year. Death rate for Asx with normal LV <0.2%/year. Symptomatic pts with chronic severe AR: >10%/yr Symptomatic pts with chronic severe AR: >10%/yr Bonow RO, et al. Circulation 2006; 114: e84-e231.

76 ACC/AHA 2006 Guidelines Class I indications for AVR in chronic, severe AR: Class I indications for AVR in chronic, severe AR: Symptomatic patients Symptomatic patients Asymptomatic with LVEF ≤ 50% at rest Asymptomatic with LVEF ≤ 50% at rest Undergoing CABG or other heart/aorta surgery Undergoing CABG or other heart/aorta surgery Class IIa for AVR in chronic, severe AR: Class IIa for AVR in chronic, severe AR: Asymptomatic, normal LV systolic function (LVEF ≥ 50%) but with severe LV dilatation (LVEDD > 75 mm or LVESD > 55 mm) Asymptomatic, normal LV systolic function (LVEF ≥ 50%) but with severe LV dilatation (LVEDD > 75 mm or LVESD > 55 mm) Bonow RO, et al. Circulation 2006; 114: e84-e231.

77 Surgical Outcomes 450 patients with severe AR: 450 patients with severe AR: Operative mortality 14%, 6.7%, and 3.7% for those with LVEF <35%, 36-49%, and ≥ 50%, respectively. Operative mortality 14%, 6.7%, and 3.7% for those with LVEF <35%, 36-49%, and ≥ 50%, respectively. Post-op outcome for pts with reduced LVEF pre-op depends on magnitude of reduction. Post-op outcome for pts with reduced LVEF pre-op depends on magnitude of reduction. Pre-op LVEF < 35%, 10- year post-op survival rate is 41% Pre-op LVEF < 35%, 10- year post-op survival rate is 41% Pre-op LVEF 35-49%, survival 56%. Pre-op LVEF 35-49%, survival 56%. Pre-op LVEF ≥ 50%, survival 70% at 10 years post-op. Pre-op LVEF ≥ 50%, survival 70% at 10 years post-op. Chaliki HP, et al. Circulation 2002; 106:

78 Post-Op Outcomes Surgery for symptomatic patients with severe AR reduces LV volumes, LV mass, wall stress and increases LVEF. Surgery for symptomatic patients with severe AR reduces LV volumes, LV mass, wall stress and increases LVEF. If asymptomatic, some say surgery is ideally performed when LVEF 50-55%. If asymptomatic, some say surgery is ideally performed when LVEF 50-55%. Dilated LV or low LVEF pre-op can still benefit from surgery. Dilated LV or low LVEF pre-op can still benefit from surgery. Patients with markedly decreased LVEF should not be denied surgery – these patients generally have an improvement in LVEF post-op as a result of relief of high afterload, especially if LV dysfunction has lasted less than one year. Patients with markedly decreased LVEF should not be denied surgery – these patients generally have an improvement in LVEF post-op as a result of relief of high afterload, especially if LV dysfunction has lasted less than one year. It is almost never “too late” to operate in chronic, severe AR. It is almost never “too late” to operate in chronic, severe AR.

79 Vasodilators? Short-term studies on the effects of vasodilators in acute severe AR have suggested improvement in hemodynamic and structural parameters. Short-term studies on the effects of vasodilators in acute severe AR have suggested improvement in hemodynamic and structural parameters. The long-term benefit of vasodilator therapy in chronic severe AR is unclear. The long-term benefit of vasodilator therapy in chronic severe AR is unclear. A total of 10 studies of vasodilator therapy in asymptomatic patients with chronic, severe AR have yielded conflicting and quite inconsistent results. A total of 10 studies of vasodilator therapy in asymptomatic patients with chronic, severe AR have yielded conflicting and quite inconsistent results. Only two studies have assessed clinical outcomes such as time to AVR (the remainder have only reported hemodynamic and/or structural parameters). Only two studies have assessed clinical outcomes such as time to AVR (the remainder have only reported hemodynamic and/or structural parameters).

80 Vasodilators – Clinical Outcomes Scognamiglio et al. randomized 143 asymptomatic patients with chronic, severe AR to nifedipine or digoxin. Scognamiglio et al. randomized 143 asymptomatic patients with chronic, severe AR to nifedipine or digoxin. Patients treated with nifedipine had a significantly lower rate of progression to AVR than digoxin patients. Patients treated with nifedipine had a significantly lower rate of progression to AVR than digoxin patients. By 6 years, a mean of 34% ± 6% of digoxin patients underwent AVR, while 15% ± 3% of nifedipine patients underwent AVR. By 6 years, a mean of 34% ± 6% of digoxin patients underwent AVR, while 15% ± 3% of nifedipine patients underwent AVR. Twenty digoxin pts. required AVR for reduced LV fx and/or onset of symptoms, while all 6 nifedipine pts who needed surgery were d/t reduced LVEF. Twenty digoxin pts. required AVR for reduced LV fx and/or onset of symptoms, while all 6 nifedipine pts who needed surgery were d/t reduced LVEF. Post-op LVEF after AVR significantly higher in nifedipine versus digoxin (65% ± 4% vs. 58% ± 8%). Post-op LVEF after AVR significantly higher in nifedipine versus digoxin (65% ± 4% vs. 58% ± 8%). Scognamiglio R, et al. NEJM 1994; 331:

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82 Vasodilators – Clinical Outcomes Evangelista et al. randomly assigned 95 patients with chronic, severe AR to nifedipine, enalapril, or placebo. Evangelista et al. randomly assigned 95 patients with chronic, severe AR to nifedipine, enalapril, or placebo. Followed patients for ~7 years. Followed patients for ~7 years. Rates of AVR were not significant across the 3 groups: Rates of AVR were not significant across the 3 groups: 12/31 (39%) of control group 12/31 (39%) of control group 16/32 (50%) of enalapril group 16/32 (50%) of enalapril group 13/32 (41%) of nifedipine group 13/32 (41%) of nifedipine group 11% of patients dropped out of study, though on-treatment analysis yielded similar rates of progression 11% of patients dropped out of study, though on-treatment analysis yielded similar rates of progression No significant changes in SBP, DBP, or HR noted; furthermore saw no significant changes in LVEF, LVESD, LVEDVI No significant changes in SBP, DBP, or HR noted; furthermore saw no significant changes in LVEF, LVESD, LVEDVI Evangelista A, et al. NEJM 2005; 353:

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84 Current Guidelines for Vasodilators Class I: Class I: Chronic therapy in severe AR with symptoms or LV dysfunction when not a surgical candidate. Chronic therapy in severe AR with symptoms or LV dysfunction when not a surgical candidate. Class IIa: Class IIa: Short-term therapy to improve hemodynamics in patients with severe CHF Sx and severe LV dysfunction before proceeding with AVR. Short-term therapy to improve hemodynamics in patients with severe CHF Sx and severe LV dysfunction before proceeding with AVR. Class IIb: Class IIb: Long-term therapy in asymptomatic patients with severe AR who have LV dilatation but normal systolic function (previously a class I indication before the Evangelista article). Long-term therapy in asymptomatic patients with severe AR who have LV dilatation but normal systolic function (previously a class I indication before the Evangelista article). Bonow RO, et al. Circulation 2006; 114: e84-e231.

85 Thank You!


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