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2	Chronic AR AT, 31 year old. Very active. 1-2 hours/day Asymptomatic Routine medical examination: BP 140/60, HR- 60/min, Diastolic murmur in the parasternal and apical region. Echo – Bicuspid arotic valve , severe AR
3	Chronic asymptomatic severe AR
4	AR - questions What is the etiology? What is the anatomy? What is the hemodynamic burden? What is the natural history? What are the methods of assessment? When to recommend medical therapy? When to recommend surgical therapy? - symptomatic - asymptomatic - Low EF?
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6	Etiologic Classification of Aortic Regurgitation Rheumatic Calcific – elderly IE Trauma – leaflet prolapse Bicuspid, Myxomatous Prosthetic – Bio, mechanical Congenital - unicuspid, quadri, VSD, DSS SLE, RA, Crohn, etc..
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8	Classification of AR – need for diagnostic tools
9	AR - questions What is the etiology? What is the anatomy? What is the hemodynamic burden? What is the natural history? What are the methods of assessment? When to recommend medical therapy? When to recommend surgical therapy? - symptomatic - asymptomatic - Low EF?
10	AR - hemodynamics AR- a state of volume and pressure overload - the entire LVSV is ejected into a high pressure chamber Compensatory mechanisms – high filling pressures, volume increase, eccentric and concentric hypertrophy In acute AR these mechanisms cannot be harnessed. In chronic AR wall stress during LV dilation is compensated by eccentric LVH (Laplace) – compensated asymptomatic state may last many years. FSV is maintained in the compensated state LVEF falls when compensatory mechanisms fail. Cor Bovinum – occurs in long term severe AR Vasodilator therapy has the potential to improve clinical state.
11	Hemodynamics of chronic AR
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13	Aortic Regurgitation
14	Acute AR- major causes Infective endocarditis Aortic dissection Trauma
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16	Acute AR- pathophysiology The regurgitant volume is sudden LVEDP and LAP increase rapidly LV dilatation cannot occur quickly Tachycardia occurs Cardiac output reduces Myocardial ischemia – LVED rise Pulmonary edema and cardiogenic shock may occur These events are more pronounced in pts with LVH (dissection in hypertensive pts, IE in AS, BAV in congenital AS)
17	Diagnosis – Acute severe AR Normal LV size may be found Pulse pressure not increased Equilibration of pressures : short diastolic murmur, S1 reduced, Echo- short AR diastolic half time (< 300 ms) , short MiF deceleration time (<150 ms), premature closure of MV TEE Sometimes additional data from CT, MR Cardiac cath, Aortography and coronary cath rarely needed and may delay treatment (only with known CAD).
18	Natural history – Acute severe AR Causes of death – pulmonary edema, ventricular arrythmias, EMD, circulatory collapse. Medical therapy is associated with early death. Compensatory tachycardia is desirable and BB should be avoided usually. (special consideration in dissection). Death may be sudden with ischemia Prompt surgical intervention is indicated. In IE with milder AR , and if hemodynamic allow , antibiotics. In IE with acute severe AR – surgery without delay
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21	Chronic AR- pathophysiology AR- a state of volume and pressure overload - the entire LVSV is ejected into a high pressure chamber Compensatory mechanisms – high filling pressures, volume increase, increased compliance to reduce the LV filling pressures, eccentric and concentric hypertrophy In chronic AR wall stress during LV dilation is compensated by eccentric LVH (Laplace) – compensated asymptomatic state may last many years. Compensated normal systolic function = normal LVEF FSV is maintained in the compensated state LVEF falls when compensatory mechanisms fail. Cor Bovinum – occurs in long term severe AR Vasodilator therapy has the potential to improve clinical state.
22	Chronic AR- pathophysiology FSV is maintained in the compensated state LVEF falls when compensatory mechanisms fail. Vasodilator therapy has the potential to improve clinical state. Preload reserve and gradual impairment of contraction lead to reduced LVEF. The transition may be insidious in spite marked LV dysfunction with a prolonged asymptomatic stage. Timely surgery – lead to reversal of impaired LV function. If surgery is late – recovery cannot be achieved.
23	Chronic AR - questions What is the etiology? What is the anatomy? What is the hemodynamic burden? What is the natural history? What are the methods of assessment? When to recommend medical therapy? When to recommend surgical therapy? - symptomatic - asymptomatic - Low EF?
24	Stages of chronic AR progression
25	Natural history of asymptomatic AR
26	Natural history of asymptomatic AR
27	Optimum time for AVR symptomatic AR (I) 50 pts, symptomatic AR, AVR, echo, cardiac cath, f/u
28	Optimum time AVR in asymptomatic AR (II) 37 pts, asymptomatic AR, serial echo + F/U, 14 AVR due to symptoms , 23 remained asymptomatic on f/u
29	Echo in AR- is AVR too late when ESD reaches 55 mm? 47 pts, AVR for pure AR. Echo, Cath, average clinical F/U 41m (6-76).
30	Criteria predictive of late survival after AVR for severe AR 39 pts, LV cath pressures and volumes, EF, 6 y clinical f/u.
31	AVR –preoperative LVF on survival 80 pts, AVR for symptomatic AR, 6y f/u, clinical, echo, RNA.
32	Mortality and morbidity of AR in clinical practice
33	Mortality and morbidity of AR in clinical practice (Mayo clinic)
34	Long term outcome of surigcally treated AR: early is better than late 170 pts, severe AR, 60 pts operated on early according to guideline, 100 pts – late, f/u 10+ 6 y 7 pts (12%) died in group A, 37 pts (37%) died in group B. Cardiac death occurred in 28 pts (28%) of group B and 7 (12 %) in group A
35	Chronic AR - Natural history Patient remains asymptomatic for years until considerable cardiomegaly and dysfunction occur. The transition to LV systolic dysfunction represent a continuum, and no single index represent an absolute boundary. LV systolic dysfunction: LVEF lower than normal at rest is initially reversible LVEF is determined by loading condition and contractile myocardial function Once impaired, LV function deteriorates over time. Gradual clinical deterioration: CHF, angina pectoris, rhythm disorders Once symptomatic - downhill course: Death within 4y of angina, 2y of CHF onset. Timely AVR may result in LV function recovery. If delayed LV function recovery and improved survival may not be achieved
36	Natural history in asymptomatic AR- Borer and Bonow siries
37	Natural history of aortic regurgitation Asymptomatic with normal LV systolic function: Progression to symptoms/ LVSD < 6%/y Progression to asymptomatic LVSD < 3.5%/y Sudden death < 0.2%/y Asymptomatic LV systolic dysfunction Progression to cardiac symptoms - > 25%/y Symptomatic pts mortality rate - angina > 10%/y Mortality rate – HF > 20%/y
38	Importance of symptomatology
39	Factors associated with worse functional and survival results (ACC/AHA 2006 guidelines) Pre operative systolic dysfunction Severity of symptoms Duration of LV systolic dysfunction
40	Factors associated with worse functional and survival results (ESC 2007 guidelines) Age End systolic diameter (volume) (>50 mm) or when corrected for BSA (>25 mm/sqm) EF at rest
41	Aortic root dilatation (ESC guidelines 2007) Predictors of outcome – aortic root dilatation at the sinus of valsalva When 6 cm: 3.6% rupture/year ; 3.7% dissection/year ; 10.8% death/year Death / year: 4% when 2.75 cm/sqm ; 3% when 2.75-4.24 sqm ; >20% when 4.25 cm/sqm. Bicuspid valve are rapid progressors!
42	Predictors of surgical outcome
43	Predictors of surgical outcome
44	AR - questions What is the etiology? What is the anatomy? What is the hemodynamic burden? What is the natural history? What are the methods of assessment? When to recommend medical therapy? When to recommend surgical therapy? - symptomatic - asymptomatic - Low EF?
45	Chronic Aortic Regurgitation
46	Clinical criteriae for chronic AR PND or orthopnea Effort intolerance Cardiomegaly Effort dyspnea Angina pectoris Rhythm disorders Increased systolic & PP, decreased diastolic pressure, Corrigan, Duroziez, Quincke, Hill and other signs.. Hyperdynamic diffuse apex. Diastolic murmur, 3^rd heart sound, Austin Flint Systolic murmur Signs of CHF
47	Working group of ESC- Recommendations on the management of asymptomatic pt with valvular heart disease -2002 Careful clinical examination should search for signs which suggest a severe valve disease. The presence of objective signs should be an incentive for complete and early evaluation. Echocardiography is the key examination. It is crucial to confirm the diagnosis, assess severity using quantitative assessment.
48	Recommendations for echo in AR – class 1 Confirm the presence and severity of acute AR Diagnosis of chronic AR when physical signs equivocal AR etiology assessment: valve, aortic root size LV dimensions and function Qualitative / quantitative assessment of AR severity Serial avaluation in asymptomatic severe AR pts. Serial testing of asymptomatic AR with dilated aorta Reevaluation in AR pts with changing symptoms RNA or MRA in sub-optimal echo studies
49	Recommendations for echo in AR – class 2a, class 2b ETT for functional capacity response in equivocal symptoms. ETT before participation in sport activity MRA for severity in unsatisfactory echo ETT with RNA for LV function in asymptomatic or symptomatic chronic AR
50	Assessment of Asymptomatic pts with chronic AR and normal LV function 104 pts, Asymptomatic severe AR, 2-16y (mean 8y f/u), serial echo +RNA rest & exercise.
51	Assessment of Asymptomatic pts with chronic AR and normal LV function Risk based on initial study measures
52	Assessment of Asymptomatic pts with chronic AR and normal LV function
53	Indications for AVR in a- or minimally symptomatic severe AR and normal LV function Criteriae for surgery in these pts controversial 104 pts, 1-18 y (7.3 y) clinicalf/u. Echo, RNV, + ETT. Endpoints & measures- cardiac death, operable symptoms & functional class, LV size & EF, ESS, EF,
54	Indications for AVR in a- or minimally symptomatic severe AR and normal LV function
55	EF response during ETT in AR “at the present time, clinical decisions should not be based on changes in EF on exercise , nor on data from stress echocardiography because these indices , though potentially interesting , have not been adequately validated”
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57	Aortic Regurgitation Anatomy of the Aortic Valve. Anatomy of the ascending aorta. LV size and function. EDD, ESD, EF. M- mode: closure of the mitral valve. Early closure in severe acute AR. M-mode: Flutter of the mitral leaflets. Mitral flow: Shortening of deceleration time. Restrictive pattern in severe AR. AR – CW pressure half time (Pt 1/2)
58	Aortic Regurgitation CFM: Size and extent of jet into LV. CFM: short axis width / area vs size of aortic root (from parasternal view, short axis view). Vena contracta Diastolic reversal of flow - descending aorta. Regurgitant volume Effective regurgitant orifice area Regurgitant fraction: Aortic regurgitant volume / LVOT stroke volume * 100.
59	Aortic Regurgitation Anatomy of the Aortic Valve. Anatomy of the ascending aorta. LV size and function. EDD, ESD, EF. M- mode: closure of the mitral valve. Early closure in severe acute AR. M-mode: Flutter of the mitral leaflets. Mitral flow: Shortening of deceleration time. Restrictive pattern in severe AR. AR – CW pressure half time (Pt 1/2)
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62	Bicuspid AoV
63	Aortic Regurgitation Anatomy of the Aortic Valve. Anatomy of the ascending aorta. LV size and function. EDD, ESD, EF. M- mode: closure of the mitral valve. Early closure in severe acute AR. M-mode: Flutter of the mitral leaflets. Mitral flow: Shortening of deceleration time. Restrictive pattern in severe AR. AR – CW pressure half time (Pt 1/2)
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67	Aortic Regurgitation Anatomy of the Aortic Valve. Anatomy of the ascending aorta. LV size and function. EDD, ESD, EF. M- mode: closure of the mitral valve. Early closure in severe acute AR. M-mode: Flutter of the mitral leaflets. Mitral flow: Shortening of deceleration time. Restrictive pattern in severe AR. AR – CW pressure half time (Pt 1/2)
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71	Aortic Regurgitation Anatomy of the Aortic Valve. Anatomy of the ascending aorta. LV size and function. EDD, ESD, EF. M- mode: closure of the mitral valve. Early closure in severe acute AR. M-mode: Flutter of the mitral leaflets. Mitral flow: Shortening of deceleration time. Restrictive pattern in severe AR. AR – CW pressure half time (Pt 1/2)
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78	Aortic Regurgitation Anatomy of the Aortic Valve. Anatomy of the ascending aorta. LV size and function. EDD, ESD, EF. M- mode: closure of the mitral valve. Early closure in severe acute AR. M-mode: Flutter of the mitral leaflets. Mitral flow: Shortening of deceleration time. Restrictive pattern in severe AR. AR – CW pressure half time (Pt 1/2)
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80	Aortic Regurgitation Anatomy of the Aortic Valve. Anatomy of the ascending aorta. LV size and function. EDD, ESD, EF. M- mode: closure of the mitral valve. Early closure in severe acute AR. M-mode: Flutter of the mitral leaflets. Mitral flow: Shortening of deceleration time. Restrictive pattern in severe AR. AR – CW pressure half time (Pt 1/2)
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82	CW in Establishing of Severity of AR
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86	Aortic Regurgitation CFM: Size and extent of jet into LV. CFM: short axis width / area vs size of aortic root (from parasternal view, short axis view). Vena contracta Diastolic reversal of flow - descending aorta. Regurgitant volume Effective regurgitant orifice area Regurgitant fraction: Aortic regurgitant volume / LVOT stroke volume * 100.
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92	Vena Contracta in AR
93	Vena Contracta in AR
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99	Aortic Regurgitation CFM: Size and extent of jet into LV. CFM: short axis width / area vs size of aortic root (from parasternal view, short axis view). Vena contracta Diastolic reversal of flow - descending aorta. Regurgitant volume Effective regurgitant orifice area Regurgitant fraction: Aortic regurgitant volume / LVOT stroke volume * 100.
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102	Holodiastolic Regurgitant Flow in Descending Aorta by PW in Severe AR
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104	Aortic Regurgitation CFM: Size and extent of jet into LV. CFM: short axis width / area vs size of aortic root (from parasternal view, short axis view). Vena contracta Diastolic reversal of flow - descending aorta. Regurgitant volume (LVOT – MiF or LVOT-PAFlow) Effective regurgitant orifice area Regurgitant fraction: Aortic regurgitant volume / LVOT stroke volume * 100.
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107	Echo in AR- ASE guideline
108	Echo in AR- ASE guideline
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111	Mild vs Severe AR
112	Serial testing: severity of AR, LV size and function, aorta Determine chronicity and severity BL (clinic, echo, Xray, ECG) and at 3 months. Asymptomatic mild AR, normal/ near normal LV Clinical 1per year, echo 1 per 2 years Asymptomatic severe AR, LVEDD>60mm: clinical 1 per 6-12m, echo 1 per 12m. Pts with LVEDD>70mm, ESD>50mm for whom risk of LVD and symptoms – 10-20% per year: echo / 4-6m RN or MRI can be used instead of Echo
113	Chronic Aortic Regurgitation-
114	Recommendations for cardiac catheterization in chronic AR Before AVR in pts with risk for CAD Assess severity of AR when noninvasive and clinical assessment inconclusive/discordant re – severity of AR or need for surgery. Assess severity of LVSD when noninvasive and clinical assessment inconclusive/discordant before decision re-need of AVR in severe AR. Class 3 indication too ridiculous to mention.
115	AR - questions What is the etiology? What is the anatomy? What is the hemodynamic burden? What is the natural history? What are the methods of assessment? When to recommend medical therapy? When to recommend surgical therapy? - symptomatic - asymptomatic - Low EF?
116	Chronic Aortic Regurgitation Medical therapy
117	Recommendations for vasodilator therapy in chronic AR In severe AR with symptoms or LVSD where surgery is not recommended for other cardiac or non cardiac reasons. Short term prior to AVR to improve hemodynamics and symptoms when in CHF with LVSD. Chronic in asymptomatic severe AR with LV dilation with normal systolic function.
118	Nifedipine vs Digoxin in severe asymptomatic AR & normal LV function 143 pts, nifedipine vs Digoxin, echo clinical 6y F/U.
119	Potential role of medical therapy Vasodilators: Hydralazine, nifedipine, ACEI. AVR and not medical treatment is recommended in symptomatic moderate to severe AR,
120	Medical Treatment - AR Vasodilators is intended to increase FSV and reduce RV. Acute nitroprusside, hydralazine, difedipine decreases EDV and increases EF ACEI have less consistent findings. May translate to reduced LV volume/mass BB should be used in Marfan with ascending aorta aneurysm. With severe AR , BB should be used with caution because of lengthening of diastole.
121	AR - questions What is the etiology? What is the anatomy? What is the hemodynamic burden? What is the natural history? What are the methods of assessment? When to recommend medical therapy? When to recommend surgical therapy? - symptomatic - Low EF? - asymptomatic
122	Goals of surgical therapy Acute AR – life saving Diminish symptoms Prevent development of heart failure Prevent mortality Prevent aortic complications in aortic aneurysm
123	Echo in AR- is AVR too late when ESD reaches 55 mm? 47 pts, AVR for pure AR. Echo, Cath, average clinical F/U 41m (6-76). Gr1 ESD<55mm, Gr2 ESD>55mm
124	Long term serial LV size and function after AVR 61 pts, severe AR, echo + RNA + clinic f/u before, 6-8m, 3-7y after AVR.
125	AR with LV dilatation – long term outcome 219 pts, severe AR, AVR; 31 pts, pre-op LVEDD>80 mm; 188 pts with LVEDD< 80 mm. 10 y f/u
126	AVR in severe AR and reduced LV- long term outcome 450 pts, isolated AR, 43 pts with lowEF<35%, 134 pts with medEF 35-50%, 273 normalEF>50%
127	Types of surgery in AR AVR when there is no aneurysm Aortic Aneurysm – ascending aorta replacement, reimplantation of coronary arteries, + AVR or valve sparing surgery. Supracoronary ascending aorta replacement when valsalva sinuses are spared.
128	Types of AoV replacement AVR with stented heterografts (pericaridial or bovine) AVR with stentless heterografts (porcine) AVR with valve homografts (cryopreservation improved durability), more complex surgery. Pulmonic valve autotransplantation (Ross) and a prosthesis in pulmonic position
129	AoV repair Decalcification and rheumatic repair – unsuccessful. Useful mainly in aortic root pathology Limited use in leaflet pathology
130	Indications for AVR or repair in chronic severe AR Symptomatic pts with severe AR irrespective of LV systolic function. Asymptomatic pts with chronic severe AR and LV systolic dysfunction (EF < 50%) at rest. Pts with chronic severe AR undergoing CABG or surgery on aorta or other valves Pts with severe AR preserved LV (EF>50%) and severe LV dilatation (EDD>75 mm, ESD>55mm) In moderate AR undergoing surgery for the Aorta In moderate AR undergoing CABG Asymtomatic pts with severe AR, EF>50%, LV dilatation (70 mm/ 50 mm), reduced effort tolerance, abnormal hemodynamic response to exercise.
131	Bicuspid AoV with dilated aorta (ACC/AHA guidelines 2006) Class 1 and Class 2a Echocardiogaphy to assess aorta dimensions CT/MRI or aorta when echo not conclusive Bicuspid AoV with dilated aorta (>4 cm) should undergo yearly serial testing (echo/Ct/MR) Aorta surgery (repair /replacement) in bicuspid AoV when diameter>5 cm or yearly increase 0.5cm In AVR for bicuspid AS/AR, aorta surgery (replacment / repair) indicated when diameter>4.5 cm BB can be given to bicuspid AoV pts with dilated (>4 cm) aortic root. CT/MR can be used to confirm aorta configuration
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133	Aortic root dilatation
134	Aortic root dilatation surgery Aortic root dilatation > 55 mm irrespective of AR grade Marfan syndrome > 45 mm Bicuspid AoV > 50 mm Mainly when rapid increase in aortic diameter ( > 5mm / year) or family history of aortic dissection
135	Indications for Surgery in AR Symptomatic (dyspnea, NYHA 2,3,4. angina) (1b) Asymptomatic with resting LVEF< 50% (1b) Pts undergo CABG or other valve surgery (1c) Asymptomatic with LVEF> 50% and ESD > 70 mm or ESD> 50mm (25 mm/msq) (2aC) Any grade of AR with diseased aortic root and - aortic root diameter > 45 mm in Marfan (1C) > 50 mm for bicuspid aortic valve (2aC) > 55 mm for other pts (2aC)
136	Operative mortality - surgery for valve disease
137	AR – questions – hope we answered all What is the etiology? What is the anatomy? What is the hemodynamic burden? What is the natural history? What are the methods of assessment? When to recommend medical therapy? When to recommend surgical therapy? - symptomatic - Low EF? - asymptomatic