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Aortic regurgitation

The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.

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Aortic regurgitation

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Pratap Sagar Tiwari,Resident, Internal Medicine, NGMC
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• Anatomy ofAortic valve/variants • Aortic Regurgitation • Aortic Stenosis
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The AV islocated betwn the LVOT and the ascending aorta. It forms the centerpiece of t heart and closely approximates many other important cardiac structures; specifically, th PV anteriorly, MV posterolaterally, and TV posteromedially.[1] Ref: 1. Anderson RH. Clinical anatomy of the aortic root. Heart. Dec 2000;84(6):670-3.
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Picture ref: AndersonRH. Clinical anatomy of the aortic root. Heart. Dec 2000;84(6):670-3.
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Picture reference: AndersonRH. Clinical anatomy of the aortic root. Heart. Dec 2000;84(6):670-3.
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Bicuspid aortic valve •Bicuspid aortic valves are the most common cardiac valvular anomaly, occurring in 1- 2% of the general population. • It is twice as common in males as in females.[1] Ref: 1. Tzemos N, Therrien J, Yip J et al (September 2008). "Outcomes in adults with bicuspid aortic valves". JAMA 300 (11): 1317–1325
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• AR isa condition due to inadequate closure of the aortic valve leaflets leading to abnormal retrograde flow of blood through the aortic valve during cardiac diastole. • It can be induced either by damage to and dysfunction of the aortic valve leaflets or by distortion or dilatation of the aortic root and ascending aorta • In the developing world, the most common cause of AR is rheumatic heart disease. However, in developed countries, AR is most often due to aortic root dilation or a congenital bicuspid aortic valve .[1] Ref: 1. Maurer G. Aortic regurgitation. Heart. Jul 2006;92(7):994-1000.
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Leaflet abnormalities Aortic rootor ascending aorta Rheumatic fever Systemic hypertension Endocarditis Aortitis (eg, syphilis) Trauma Reactive arthritis Bicuspid aortic valve Ankylosing spondylitis Rheumatoid arthritis Trauma/ Dissecting aneurysm Myxomatous degeneration Osteogenesis imperfecta Ankylosing spondylitis Marfan syndrome/ EDS Acromegaly Inflammatory bowel disease AR is seen more commonly in men than in women. As in the Framingham study, AR was 13% of men versus 8.5% of women.[1] The greater prevalence of AR in men may reflect, in the male preponderance of underlying conditions such as Marfan syndrome[2] or bicusp valve[3] . Ref: 1. Singh JP, Evans JC, et al. Prevalence and clinical determinants of mitral, tricuspid, and AR (the Framingham Heart Study). Am J Cardiol. Mar 15 1999;83(6 2. Keane MG, Pyeritz RE. Medical management of Marfan syndrome. Circulation. May 27 2008;117(21):2802-13. 3. Ortiz JT, Shin DD, Rajamannan NM. Approach to the patient with bicuspid AVand ascending aorta aneurysm. Curr Treat Options Cardiovasc Med. Dec 200
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Law of laplace ↑LV Volume LV Hypertrophy
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Sudden large regurgitantvolume imposed on LV of normal size with normal compliance 1. Rapid ↑ LVEDP and ↑ LAP 2. LV attempts to maintain CO with ↑HR and ↑ Contractility Attempts to maintain forward SV/CO may be inadequate Cardiogenic Shock ↓ Forward SV/CO Pulmonary edema ↑ LVEDP and ↑ LAP Angina ↓ Coronary perfusion ↑demand myocardial O2
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Regurgitant Volume Load CompensatoryMechanisms: 1. ↑LV dilatation ↑ LVED vol and ↑chamber compliance 2. ↑ LV hypertrophy Decompensation Steadily increasing regurgitant volume load Further ventricular dilatation  ↑ wall stress Inability to continue further hypertrophy Contractile dysfunction  ↓ EF/SV/CO CHF symptoms Due to both congestion and ↓ CO Angina ↓ Coronary perfusion pressure & marked LVH
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deMusset's sign A headbob occurring with each cardiac cycle Mueller's sign Systolic pulsations of the uvula. Becker's sign Visible pulsations of the retinal arteries and pupils. Quincke's pulses visible Capillary pulsations in the nailbeds after holding the tip of the nail. Duroziez's sign A systolic and diastolic bruit heard when the femoral artery is partially compressed.to and fro murmur Traube's sign A pistol shot murmur (systolic and diastolic sounds) heard over the femoral arteries. Mayne's sign More than a 15 mmHg decrease in DBP with arm elevation from the value obtained with the arm in the standard position. Hill's sign Popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg. Rosenbach's sign Systolic pulsations of the liver. Gerhard's sign Systolic pulsations of the spleen.
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• The diastolicmurmur of AR begins immediately after A2 . • It is high pitched, often blowing in quality, and may be sustained in intensity or decrescendo. • It may be soft and barely audible, often appreciated only when the patient is sitting up, leaning forward, and holding his or her breath in expiration.
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• Patients witha longer diastolic murmur, a displaced left ventricular impulse, a wide pulse pressure, and the peripheral findings of a wide pulse pressure are considered to have severe AR. Note: When the Diastolic murmur of AR is louder in the 3rd /4th RICS than in the 3/4th LICS ,the AR is likely to result from Aortic root dilatation than deformitiy of leaflets alone. Ref: ACC/AHA Guidelines 2006
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• In areview of the literature, the presence of an early diastolic murmur, as heard by a cardiologist, was the most useful finding for establishing the presence of AR (positive likelihood ratio 8.8 [ie, the odds of AR are increased 8.8 fold]) and its absence the most useful finding for eliminating the presence of AR (negative likelihood ratio 0.2 to 0.3 [ie, the odds of disease are reduced by a factor of 0.2 to 0.3]) .[1] Ref: 1. Choudhry NK, Etchells EE. The rational clinical examination. Does this patient have aortic regurgitation? JAMA 1999; 281:2231
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• Laboratory testingin patients with aortic regurgitation should be guided by the clinical scenario. • For example, in patients with AR due to suspected infective endocarditis, peripheral blood counts and cultures may help clarify the diagnosis and identify the causative organism. • Specific serologic tests may assist in the diagnosis of rheumatological causes.
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• Aortic valvestructure and morphology (bileaflet versus trileaflet, flail, thickening) • Presence of vegetations • Severity of AR • Color Doppler jet width • Vena contracta width • Regurgitant volume, fraction, and orifice area • Premature closure of the mitral valve (seen in severe AR) • Associated lesions of the aorta, including dilation, aneurysm, dissection • LV structure and function • LV hypertrophy and dilation • EF and end-systolic dimension are key determinants of outcome
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MILD MOD SEVERE Structural parameters Left ventricularsize N N or dilated Dilated, except acute AR Aortic leaflets N or abnormal N or abnormal Abnormal/flail, or wide coaptation defect Color Doppler jet width Central jet, width <25 percent of LVOT Central jet, width 25 to 65 percent of LVOT Central jet width >65 percent of LVOT Doppler vena contracta width <3 mm 3 to 6 mm >6 mm Doppler parameters Quantitative parameters Regurgitant volume <30 mL/beat 30 to 59 mL/beat ≥60 mL/beat Regurgitant fraction <30 percent 30 to 49 percent ≥50 percent Regurgitant orifice area <0.10 cm2 0.10 to 0.29 cm2 ≥0.30 cm2 Severe chronic AR is typically a/w c/f including a longer diastolic murmur, a displaced LVI, a wide PP, and the peripheral findings of
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References: 1. ACC/AHA 2006guidelines 2. Gaasch WH, Andrias CW, Levine HJ. Chronic aortic regurgitation: the effect of aortic valve replacement on left ventricular volume, mass and function. Circulation 1978; 58:82 3. Schuler G, Peterson KL, Johnson AD, et al. Serial noninvasive assessment of left ventricular hypertrophy and function after surgical correction of AR. Am J Cardiol 1979; 44: 4. Borow KM, Green LH, Mann T, et al. End-systolic volume as a predictor of postoperative LVperformance in volume overload from valvular regurgitation. Am J Med 1980; 68: 5. Henry WL, Bonow RO, et al. Observations on the optimum time for operative intervention for AR. Evaluation of the results of AVR in symptomatic patients. Circulation 1980; 6. Kumpuris AG, Quinones MA, Waggoner AD, et al. Importance of preoperative hypertrophy, wall stress and end-systolic dimension as echocardiographic predictors of norma of left ventricular dilatation after valve replacement in chronic aortic insufficiency. Am J Cardiol 1982; 49:1091. 7. Gaasch WH, Carroll JD, Criscitiello MG. Chronic AR: prognostic value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio. J Am Coll Cardiol 19 8. Stone PH, Clark RD, Goldschlager N, et al. Determinants of prognosis of patients with aortic regurgitation who undergo aortic valve replacement. J Am Coll Cardiol 1984; 3:1 9. Bonow RO, Rosing DR, McIntosh CL, et al. The natural history of asymptomatic patients with aortic regurgitation and normal left ventricular function. Circulation 1983; 68:509 10. Bonow RO, Lakatos E. Serial long-term assessment of the natural history of asymptomatic patients with chronic AR and normal left ventricular systolic function. Circulation 11. Siemienczuk D, Greenberg B, Morris C, et al. Chronic aortic insufficiency: factors associated with progression to aortic valve replacement. Ann Intern Med 1989; 110:587.
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Class I indicationsfor CC under current ACC/AHA guidelines include the following:[1] • Assessment of coronary anatomy prior to aortic valve surgery in patients with risk factors for coronary artery disease. Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. .
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Class IIa -The weight of evidence or opinion is in favor of efficacy of the following test patients with AR in the above settings. Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with VHD.
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• In acutesevere AR, surgical intervention is usually indicated, but the patient may be supported medically with dobutamine to augment cardiac output and shorten diastole and sodium nitroprusside to reduce afterload in hypertensive patients. • In chronic severe AR, vasodilator therapy may be used in select conditions to reduce afterload in patients with systolic hypertension to minimize wall stress and optimize LV function; in normotensive patients, vasodilator therapy is not likely to reduce regurgitant volume (preload) significantly and thus may not be of Ref: 1. Bekeredjian R, Grayburn PA. Valvular heart disease: aortic regurgitation. Circulation. Jul 5 2005;112(1):125-34. clinical benefit.[1]
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• The acuteadministration of Na Nitoprusside , hydralazine, nifedipine or felodipine ↓PVR and results in an immediate augmentation in forward CO and a ↓ in regurgitant volume. • With nitroprusside and hydralazine ,these acute hemodynamic changes lead to a consistent ↓in EDV and an ↑in EF. References: 1. Miller RR, Vismara LA, .Afterload reduction therapy with nitroprusside in severe AR: improved cardiac performance and reduced regurgitant volume. AmJ Cardiol 976;38:564–7 2. Greenberg BH, DeMots H. Beneficial effects of hydralazine on rest and exercise hemodynamics in patients with chronic severe aortic insufficiency. Circulation 1980;62:49–55 3. FiorettiP, BenussiB.Afterload reduction with nifedipine in aortic insufficiency. AmJ Cardiol 1982;49:1728–32
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• Reduced EDVand ↑EF have also been observed in small number of pts receiving long term oral therapy with hydralazine and nifedipine for a period of 1-2 yrs. With nifedipine these effects are A/W ↓ in LV mass.[1,2] • Reduced BP with enalapril and quinapril has been A/W ↓ in EDV and mass but no change in EF.[3,4] References: 1. Scognamiglio R, Fasoli G. Long-term nifedipine unloading therapy in asymptomatic patients with chronic severe AR. J Am Coll Cardiol 1990; 16:424–9. 2. Greenberg B, Massie B, et al. Long-term vasodilator therapy of chronic AI: a randomized double-blinded, placebo-controlled clinical trial. Circulation 1988;7 3. Lin M, Chiang HT,etal.Vasodilator therapy in chronic asymptomatic AR: enalapril versus hydralazine therapy. J Am Coll Cardiol 1994;24:1046–53. 4. Schon HR, Dorn R. Effects of 12 months quinapril therapy in asymptomatic patients with chronic AR. J Heart Valve Dis 1994;3:500–9.
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• Indicated forlong-term therapy in patients with chronic, severe AR and symptoms of LV dysfunction but who are not candidates for surgery.( CLASS I: LOE-b) • Is reasonable for short-term therapy in patients with severe LV dysfunction and HF symptoms to improve their hemodynamic profile before proceeding with surgery.(CLASS IIa: LOE-c) • Is acceptable for long-term therapy in asymptomatic patients with severe AR and LV dilation with normal Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/A EF. (CLASS IIb: LOE-b) guidelines for the management of patients with valvular heart disease. Note: LOE = Level of Evidence
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• Antibiotic prophylaxisprior to dental procedures is no longer routinely recommended for all patients with AR under current ACC/AHA guidelines.[1] Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/A 2006 guidelines for the management of patients with valvular heart disease
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• Surgical treatmentof AR usually requires replacement of the diseased valve with a prosthetic valve, although valve-sparing repair is increasingly possible with advances in surgical technique and technology.
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• Patient issymptomatic. • Patient is asymptomatic, with a resting EF of ≤ 55%. • Patient is asymptomatic, with LV dilation (LV end-systolic dimension >55 mm). Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC 2006 guidelines for the management of patients with valvular heart disease.
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• For patientsundergoing AV replacement, careful consideration should be given to the relative risks and benefits of mechanical vs bioprosthetic valves. • Mechanical valves : more durable but require long-term anticoagulation with warfarin due to increased risk of thrombosis. • Bioprosthetic valves carry a greater risk of long-term deterioration and risk of reoperation but avoid the need for long-term warfarin.[1] Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/A 2006 guidelines for the management of patients with valvular heart disease. .
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• Inpatient careis required for most patients with acute severe aortic regurgitation (AR), particularly with symptoms or evidence of hemodynamic decompensation.
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ESD EDD Stable Dimension Incresing Dimension <45 mm <60 mm Evaluate 6-12 mn Repeat Echo in 12 mnth 3mnth 3 mnth 45-50 mm 60-70 mm Evaluate 6 mn Repeat Echo in 12 mnth 3 mnth 3 mnth 50-55 mm 70-75 mm Evaluate in 6 mn Repeat Echo 6 mnth 3 mnth 3 mnth >55 mm > 75 mm Surgery
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• Left untreated,acute severe AR is likely to lead to considerable morbidity and mortality from either the underlying cause (typically infective endocarditis or aortic dissection) or from hemodynamic decompensation of the LV. • Potential complications in patients with chronic severe AR include progressive LV dysfunction and dilation, CHF, MI, arrhythmia, and sudden death.
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The prognosis forpatients with severe AR depends on the presence or absence of LV dysfunction and symptoms, as follows:[1] • In asymptomatic patients with normal EF 1. Rate of progression to symptoms &/or LVD = < 6% per yr 2. Rate of progression to asymptomatic LVD = < 3.5% per yr 3. Rate of sudden death = less than 0.2% per yr • In asymptomatic patients with decreased EF, rate of progression to symptoms = >25% per year. • In symptomatic patients, mortality rate = >10% per yr. The strongest predictors of outcome are echocardiographic parameters (EF and LV end-systolic dimension). Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease.
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References: 1. 2008 updateon ACC/AHA 2006 Guideline on VHD. 2. Harrison’s Principle of Internal Medicine ,18th ed. 3. Washington manual; Cardiology Subspeciality Consult ,2nd ed. 4. Cardiology Secrets by Glenn L Levine, 3rd ed. 5. Uptodate 19.1 .Last literature review sep 30 2011. 6. Emedicine “ 7. Mayo Clinic

Editor's Notes

#4 The normal human heart contains 4 valves that regulate blood flow into and out of the heart. The aortic and pulmonic valves are known as the semilunar valves, whereas the tricuspid and mitral valves are referred to as the atrioventricular valves. All the valves are trileaflet, with the exception of the mitral valve, which has 2 leaflets. All 4 cardiac valves are surrounded by fibrous tissue forming partial or complete valvular rings, or annuli. These annuli join the fibrous skeleton of the heart and helps anchoring and supporting the valvular structures.The AV is located betwn the LVOT and the ascending aorta. It forms the centerpiece of the heart and closely approximates many other important cardiac structures; specifically, the pulmonic valve anteriorly, mitral valve posterolaterally, and tricuspid valve posteromedially.[1]
#5 The aortic valve functions to prevent the regurgitation of blood from the aorta into the left ventricle during ventricular diastole and to allow the appropriate flow of blood—the cardiac output—from the left ventricle into the aorta during ventricular systole. The aortic valve has 3 principle components: the annulus, cusps, and commissures.
#6 The aortic valve annulus is a collagenous structure lying at the level of the junction of the aortic valve and the ventricular septum.This area is also referred to as the aortic ring and serves to provide structural support to the aortic valve complex. There are 3 aortic valve cusps, each half-moon shaped or semilunar in appearance CONTAIN aortic sinuses and as it is named after the italian anatomist antoniovalsalva ,these aortic sinuses are also called sinus of valsalva. Their association with the respective coronary ostia identifies them: left, right, and posterior (or noncoronary). In the normal human heart, the left and right coronary arteries originate from the left and right aortic sinuses, 91% and 93% of the time, respectively.The rim of each valve cusp is slightly thicker than the cusp body and is known as the lunula. The lunulae of adjacent cusps slightly overlap each other at the time of valve closure, serving a role of increased valve support .The small spaces between each cusp's attachment point are called the aortic valve commissures .
#7 A bicuspid aortic valve (BAV) is most commonly a congenital condition of the aortic valve where two of the aortic valvular leaflets fuse during development resulting in a valve that is bicuspid instead of the normal tricuspid configuration.Bicuspid aortic valves are the most common cardiac valvular anomaly, occurring in 1- 2% of the general population. It is twice as common in males as in females.[1]In many cases, a bicuspid aortic valve will cause no problems.[4] However BAV may become calcified later in life, which may lead to varying degrees of severity of aortic stenosis or If the leaflets do not close correctly, aortic regurgitation can occur.The other uncommon variants can be unicuspid or quadricuspid.Pathophysiologic VariantsUnicuspid aortic valveUnicuspid aortic valve is a congenital valvular defect with an incidence of 0.02% in the general population. It is commonly associated with clinically significant aortic stenosis, usually manifesting during the third decade of life. All valves are unicommissural with the posterior commissural attachment. The free edge of the valve extends from the single commissure without further communication with the aorta. An estimated 50% of individuals with unicuspid aortic valve have associated ascending aortic dilatation. This is a rare cardiac anomaly but should be suspected in patients presenting at a young age with clinically significant aortic stenosis.[5, 9, 10]Bicuspid aortic valveBicuspid aortic valve is the most common congenital cardiac anomaly, occurring in 1-2% of the population, with a 2:1 male predominance. Evidence exists of familial clustering, with the incidence as high as 10% in some families. Bicuspid aortic valve may be clinically silent but can lead to early development of aortic stenosis or aortic insufficiency, most commonly in the fifth and sixth decades of life. Conditions associated with bicuspid aortic valve include patent ductusarteriosus,Williams syndrome, Turner syndrome, and coarctation of the aorta. Of clinical importance is the association of aortic root dilatation and ascending aortic aneurysm.[5, 11]Quadricuspid aortic valveQuadricuspid aortic valve (QAV), first described in 1862 by Balington, is a rare congenital valvular abnormality that affects both the pulmonic and aortic valves in a 10:1 ratio. The incidence of QAV is estimated at 0.0125–0.033% in the general population. Seven different subtypes of QAV have been identified, with the most common being 3 cusps of equal size with a fourth smaller cusp.QAV most commonly occurs as an isolated defect but has been associated with patent ductusarteriosus, Ehlers-Danlos syndrome, hypertrophic obstructive cardiomyopathy, and subaortic stenosis. Aortic valvular insufficiency is commonly observed in QAV. It occurs secondary to a central orifice formed from malcoaptation of the 4 valvular leaflets. In a small case series, 56% of subjects with QAV had significant valvular insufficiency, with a mean age at presentation of 46 years.[12, 13]
#8 AR is a condition due to inadequate closure of the aortic valve leaflets leading to abnormal retrograde flow of blood through the aortic valve during cardiac diastole.
#9 AR may be caused by either valvular or aortic root pathology. Valvular abnormalities that may result in AR include bicuspid aortic valve (the most common congenital cause), rheumatic fever, infective endocarditis, collagen vascular diseases, and degenerative aortic valve disease.Abnormalities of the ascending aorta, in the absence of valve pathology, may also cause AR, such as may occur with longstanding uncontrolled hypertension, Marfan syndrome, idiopathic aortic dilation, syphilitic aortitis, giant cell arteritis, Takayasu arteritis, ankylosing spondylitis, Whipple disease, and other spondyloarthropathies.The absence of a wide pulse pressure and of the characteristic arterial auscultatory signs of chronic AR in patients with acute AR is thought to be due to the much higher LV end-diastolic pressure (LVEDP) in the acute form. The acute development of a severe aortic valvular leak causes a much higher LVEDP in the normal-sized LV of patients with acute AR. Patients with chronic AR commonly have a dilated LV with increased compliance capable of accommodating large blood volumes without a significant rise of LVEDP.
#10 To understand the pathophysiology of condition like aortic regurgitation ,it is important to understand the law of laplace.As stated by Laplace law: left ventricular (LV) wall stress is directly proportional to the cavity pressure and inversely proportional to wall thickness. Due to the added regurgitantvol there is increase in lv volume that leads to An elevation in LV cavity pressure and it causes an increase in wall stress. If a hypertrophic response occurs, increasing thickness can return wall stress to normal. All forms of AR produce a similar hemodynamic abnormality. The inability of the aortic valve leaflets to remain closed or coapted during diastole results in a portion of the left ventricular stroke volume leaking back from the aorta into the left ventricle. The added volume of regurgitant blood produces an increase in left ventricular end-diastolic volume and that results in an elevation of wall stress. The heart responds with compensatory increase in wall thickness ,so that increasing thickness can return wall stress to normal.THIS compensatory myocardial hypertrophy occurs in chornic AR.The combination of hypertrophy and chamber enlargement raises the total stroke volume. AND also as we remember the starlings law ie the increase in lvedvie the preload results in increased stretching of the myocytes leading to increased contractility. The net effect is that forward stroke volume and hence cardiac output are initially maintained or the ef can even be supra normal despite the regurgitant lesion. Thus, the heart initially adapts well to chronic AR, functioning as a very efficient and compliant high output pump.
#11 But there is a slight different scenario in case of acute ar that can result from conditions like Endocarditis in which there occurs valve destruction and leaflet perforation or Aortic dissection or Traumatic rupture of the valve leaflets or even Iatrogenic ar that results during aortic balloon valvotomy..these all can result in acute ar . in chronic AR, the LV may undergo a series of adaptive changes over course of time but in cases of acute AR, the LV does not have time to dilate in response to the volume load.with acute AR the regurgitant volume fills a small ventricle that has not had time to dilate, resulting in an acute increase in left ventricular diastolic pressure and leading to increased LAP.Lv may attempt to maintain co with increase hr and contractility but usually becomes inadequate And results in a fall in forward cardiac output. The decline in forward stroke volume may be exacerbated by a shortening of diastolic filling time due to the combination of early closure of the mitral valve (due to high end diastolic pressures) and tachycardia (caused by a decrease in forward flow and cardiac output). The net effect is often profound hypotension and cardiogenic shock.As a result of rapidly increased LV end-diastolic pressure ,The elevated left ventricular end-diastolic pressure leads to elevated left atrial and pulmonary venous pressures .As pressure increases throughout the pulmonary circuit, the patient develops dyspnea and pulmonary edema. And correlating clinically ,unlike chronic ar , left ventricular stroke volume and diastolic filling volume are not increased with acute regurgitation.wide pulse pressure is may not be present and thereby the peripheral signs of wide pulse pressure are also not present. The pulse pressure is normal or may be reduced, but the pulse is usually weak, thready, and rapid. The cardiac apex is generally not displaced and is not hyperdynamic.Aortic dissection should always be suspected in patients with AR and chest or back pain. If aortic dissection is the cause, an inequality of pulses and blood pressure between the left and right arms may be observed. However, this finding may not be appreciated in the setting of profound hypotensionCardiac auscultation — Acute AR alters the quality of most of the heart sounds:due to the elevated lvdiastolicpresuure that close the mitral valve prematurely can result in reduced intensity of first heart sound.which can occasionally be heard in mid-diastole.The aortic component of S2 is often soft, while P2 is usually increased, reflecting pulmonary hypertension.An S3 is frequently heard but an S4 is absent.In contrast to the high pitched holodiastolic decrescendo murmur of chronic AR, the murmur with acute AR is a low pitched early diastolic murmur beginning after S2 .The murmur, however, may not be heard, especially when the diastolic gradient between the aorta and left ventricle lessens. A systolic murmur resulting from the increased volume of blood crossing the aortic valve may be heard, but is usually not loud. The combination of a soft systolic and a low-pitched diastolic murmur often produces a "to-and-fro" murmur at the cardiac base in acute AR.
#12 In chronic AR, the volume overload of the left ventricle is associated with a gradual increase in left ventricular size that maintains a normal forward cardiac output despite the regurgitant valve flow; left ventricular diastolic pressures remain normal.The resulting hypertrophy is necessary to accommodate the increased wall tension and stress that results from LV dilation .The combination of hypertrophy and chamber enlargement raises the total stroke volume .The net effect is that forward stroke volume and hence cardiac output are initially maintained despite the regurgitant lesion. although the LV vol is increased ,end diastolic pressure remains normal due to this ventricular complaince. Thus the heart initially adapts well to chronic ar functioning as a very efficient and compliant high output pump. As said During the early phases of chronic AR, the LV ejection fraction (EF) is normal or even increased (due to the increased preload and the Frank-Starling mechanism). Patients may remain asymptomatic during this period. As AR progresses, Eventually, the LV reaches its maximal diameter and diastolic pressure begins to rise, resulting in symptoms (dyspnea) that may be worse during exercise. Increasing LV end-diastolic pressure may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia, necrosis, and apoptosis. Patients with AR may remain asymptomatic for decades, even if there is progressive ventricular dilatation. If, however, there is a large regurgitant volume, the patient may complain of symptoms related to the increased mass of the enlarged left ventricle. These include:A sense of pounding and an uncomfortable awareness of the heartbeat. These symptoms are especially pronounced when lying down or lying on the left side which brings the left ventricular apex closer to the chest wall, augmenting the sensation during systolic contraction.Palpitations due to tachycardia or premature beats. The latter cause a compensatory pause and postextrasystolic potentiation with a further sense of variable cardiac motion by the patient.Symptoms of left-sided heart failure (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and eventual pulmonary edema) occur in the presence of left ventricular dysfunction.Physical examination — The physical examination in patients with chronic AR is often dramatic and frequently establishes the diagnosis without the need for laboratory testing. Both examination of the peripheral pulses and auscultation of the heart are important. The increased stroke volume results in abrupt distension of the peripheral arteries and an elevation in systolic pressure. Regurgitation back into the left ventricle then leads to a rapid fall in pressure with quick collapse of the arteries and a low diastolic pressure which may approach zero in severe disease.The net effect is a wide pulse pressure, which is manifested on examination as a "water hammer" or Corrigan pulse. This finding may be best appreciated by palpation of the radial or brachial arteries (exaggerated by raising the arm) or the carotid pulses. Other findings are associated with a hyperdynamic pulse:deMusset's sign — A head bob occurring with each cardiac cycle ..heart beat.Corrigan pulse :rapid carotid upstroke followed by arterial collapseTraube's sign — A pistol shot murmur (systolic and diastolic sounds) heard over the femoral arteries.Duroziez's sign — A systolic and diastolic bruit heard when the femoral artery is partially compressed.to and fro murmurQuincke's pulses —visible Capillary pulsations in the nailveds after holding the tip of the nail.Mueller's sign — Systolic pulsations of the uvula.Becker's sign — Visible pulsations of the retinal arteries and pupils.Hill's sign — Popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg.Mayne's sign — More than a 15 mmHg decrease in diastolic blood pressure with arm elevation from the value obtained with the arm in the standard position.Rosenbach's sign — Systolic pulsations of the liver.Gerhard's sign — Systolic pulsations of the spleen.Although all of these clinical signs have been described as ancillary findings useful in the diagnosis of AR, there are few published studies that have assessed the predictive value of any of these findings [5]. Exaggerated or bounding pulses and these physical signs are not specific for AR, since they can be seen in any condition associated with a marked increase in stroke volume and a hyperdynamic circulation. Included in this group are sympathetic hyperactivity, anemia, fever, pregnancy, thyrotoxicosis, large arteriovenous fistula, patent ductusarteriosus, and severe bradycardia. Severe mitral regurgitation also can cause rapid rising arterial pulses, but the pulse pressure is not increased.The combination of left ventricular enlargement and forceful systolic function results in the apical impulse being displaced laterally and inferiorly and being diffuse and hyperdynamic. A prominent pulsation (and occasionally a thrill) may be felt at the sternal notch due to concurrent dilatation of the ascending aorta.
#13 Sherman sign ; prominently located and palpated dorsalispedis pulseLandolfi sign: alternating constriction and dilatation of pupilDuroziez sign: systolic portion of murmur was caused by forward flow into the lower extremity and the diastolic segment was caused by aortic regurgitation towards the heart.Seagull murmur: it is murmur with musical qualities such as that heard occasionally in aortic insufficiency. A sea gull cry murmur is defined as a murmur imitating the cooing sound of a seagull.this type of murmur is typically characterised by a music timbre and a high frequency and may occur as a result of various valve disease.it is usually described as a sign of tight calcific aortic stenosis when the murmur high frequency components are transmitted to the lower left sternal border and the cardiac apex during most of the systole (gallavardin phenomenon).in this condition,the typical harsh timbre of the ejective murmur tends to assume a musical high pitched quality ,resembling that of mitral regurgitation which may be reminiscent of the cry of a seagull. A protodiastolic murmur with similar characteristics ,typically in decrescendo ,may occur in severe AR particularly when the flow presents high velocities. However, a seagulls cry murmur may also be the sign of MR or prolapse. Similarly the muscial and holosystolic sound reflects the presence of high frequency components due to high velocities of reflow.
#14 On palpation, the point of maximal impulse may be diffuse or hyperdynamic but is often displaced inferiorly and toward the axilla. Chronic AR is associated with changes in the heart sounds and a distinctive murmur. The heart sounds typically have the following characteristics. S1 may be soft, often reflecting a long PR intervalS2 is variable; it may be soft, absent, or singleA2 is often soft or absent while P2 may be normal, but obscured by the diastolic murmurA systolic ejection sound may be due to abrupt aortic distension caused by the large stroke volumeA third heart sound (S3 gallop) is heard when left ventricular function is severely depressedThe diastolic murmur of AR begins immediately after A2 . It is high pitched, often blowing in quality, and may be sustained in intensity or decrescendo. It may be soft and barely audible, often appreciated only when the patient is sitting up, leaning forward, and holding his or her breath in expiration.The intensity of the murmur does not correlate well with the severity of AR. However, the timing and duration of the murmur may be helpful.In mild AR, the murmur occurs only in early diastole and is blowing.As the regurgitation becomes more severe, the murmur extends through more of diastole, may become holodiastolic and is often rougher in quality. Patients with a longer diastolic murmur, a displaced left ventricular impulse, a wide pulse pressure, and the peripheral findings of a wide pulse pressure are considered to have severe AR.The intensity of the murmur can also be affected by certain maneuvers. As examples, the murmur increases with squatting and decreases with the Valsalva maneuver. The site at which the murmur is best heard varies with the cause. The murmur is heard best along the left sternal border, at the third and fourth intercostal space, when AR is due to valvular disease. In contrast, when the diastolic murmur of ar is louder in the 3rd /4thRics than in the 3/4thLics ,the ar is likely to result from aortic root dilatation than deformitiy of leaflets alone.A systolic murmur can be heard in many patients. It typically resembles the ejection type of murmur heard in aortic stenosis, ie, a crescendo-decrescendo harsh murmur beginning after S1. This murmur does not necessarily reflect concurrent aortic stenosis, since the increased ejection rate and large stroke volume across the aortic valve can lead to a "functional" stenosis. A second type of diastolic murmur (the Austin Flint murmur) may also be appreciated. volume.An Austin Flint murmur may be present at the cardiac apex in severe AR and is a low-pitched, mid-diastolic rumbling murmur due to blood jets from the AR striking the anterior leaflet of the mitral valve, which results in premature closure of the mitral leaflets.Distinguishing features from mitral stenosis include the absence of both a loud S1 and an opening snap of the mitral valve.However, the physical findings are not sufficiently reliable and echocardiography is typically used to assess severity.In very severe regurgitation with ventricular decompensation, the murmur may become soft or even absent. This change in character reflects the near equivalence of aortic diastolic and left ventricular end-diastolic pressures which markedly diminishes regurgitant flow. A similar situation can occur when AR is acute and the left ventricular end-diastolic pressure is very high.
#16 Discovery of a diastolic murmur is essential for the diagnosis of AR. In a review of the literature, the presence of an early diastolic murmur, as heard by a cardiologist, was the most useful finding for establishing the presence of AR (positive likelihood ratio 8.8 [ie, the odds of AR are increased 8.8 fold]) and its absence the most useful finding for eliminating the presence of AR (negative likelihood ratio 0.2 to 0.3 [ie, the odds of disease are reduced by a factor of 0.2 to 0.3]) [6].
#17 Laboratory testing in patients with aortic regurgitation (AR) should be guided by the clinical scenario. For example, in patients with AR due to suspected infective endocarditis, peripheral blood counts and cultures may help clarify the diagnosis and identify the causative organism. Specific serologic tests may assist in the diagnosis of rheumatological causes. Laboratory assessment of renal and hepatic function may play an important role in determining a patient's eligibility for certain vasodilator or other drug therapy.
#18 Echocardiography is part of the standard evaluation of patients with ARTransthoracic echocardiography should be performed in all patients with suspected AR, and periodically in patients with confirmed AR of significant severity.and it is of class I b recommendation acc to acc/aha 2006 guideline. Echocardiography is a highly accurate test in AR, with sensitivity and specificity well in excess of 90%. In addition, echocardiographic parameters are used to determine the optimal timing of surgery in many cases.[5]Important echocardiographic findings in AR include the following:Aortic valve structure and morphology (bileaflet versus trileaflet, flail, thickening)Presence of vegetations or nodules (may require transesophageal echocardiography in selected cases)Quantitative measurements of regurgitantvolume,fraction and orifice area assessed .Transeesophageal echo is done To clarify whether there is bicuspid valve if unclear on tteBetter sensitivity and specificity for aortic dissection than tteClarify whether there is endocarditis or root abscess if unclear on tteBetter visualisation of av in pt with prosthetic avSeverity of ARColor Doppler jet width (the vena contracta width is usually >65% of the width of the left ventricular outflow tract in severe AR)Vena contracta widthRegurgitant volume, fraction, and orifice areaPremature closure of the mitral valve (seen in severe AR) and opening of the aortic valve (with severely elevated LV end-diastolic pressure)Pressure half-time (usually < 300-350 ms with significant AR)Associated lesions of the aorta, including dilation, aneurysm, dissection, or ectasiaLV structure and functionLV hypertrophy and dilationEF and end-systolic dimension are key determinants of outcomeSurgery recommended if EF is ≤ 55% or if end-systolic dimension is >55 mm[5]
#19 Standard chest radiography shows cardiomegaly due to the dilatation of the left ventricle, which enlarges in an inferior and leftward direction. The ascending aorta (and often the aortic arch or knob) are typically markedly dilated.Left atrial enlargement does not occur unless there is significant left ventricular dysfunction. Apart from evidence of structural abnormalities (aortic dilation, ) The chest radiograph shows may also show stage of functional compromise (pulmonary edema).Electrocardiography findings are nonspecific The electrocardiogram (ECG) reflects the adaptive changes that occur in the left ventricle as a result of the volume overload.may include evidence of the following:LV hypertrophyLeft axis deviationLeft atrial enlargementLV volume overload pattern (prominent Q waves in leads I, aVL, and V3 to V6 and relatively small r waves in V1)LV conduction defects (typically late in the disease process)Exercise treadmill testing may be used to guide recommendations for surgical therapy in patients with chronic severe AR and equivocal symptoms.[5] However, the role of stress echocardiography in patients with AR remains uncertain, and further studies may be needed before it can be recommended for routine clinical use.[21]
#20 Stages and course — Data from patients undergoing aortic valve replacement, in addition to clinical information, has been used to develop criteria for the definition of compensated and decompensated stages of chronic AR (table 3) [8,10-16].An LV end-diastolic dimension less than 65 mm and an LVEF >55 percent indicate a compensated stage.An LV end-systolic volume greater than 60 mL/m2, an LV end-systolic dimension greater than 50 mm, or an LVEF <50 percent usually indicates serious depression of LV systolic function (decompensated stage).The nature of the transition from a compensated to a decompensated stage is poorly understood and the definitions of these stages have not been validated in a prospective fashion. Thus, they should only be used as general guidelines in a decision analysis that includes all other clinical data and patient preferences. Nevertheless, this information has been useful in defining limits that are predictive of the future need for aortic valve replacement [17,18].For example, one report included serial studies in 77 asymptomatic patients with moderate to severe AR [9]. Most patients had LV enlargement but all had normal LV systolic function. During a mean follow-up duration of 49 months, there were no deaths but 12 underwent surgery because of the development of symptoms and/or LV dysfunction. By life table analysis, the percent of patients not requiring surgery was 90 percent at three years, 81 percent at five years, and 75 percent at seven years.Thus, asymptomatic patients with moderate to severe AR and a normal LVEF at baseline require aortic valve replacement at the rate of approximately 4 percent per year. Similar findings were noted in a later study [10].The prognosis is not as good in asymptomatic patients with LV dysfunction. As many as two-thirds of such patients develop symptoms and require surgery within three years [11].One factor that may play a role in the progression of left ventricular dysfunction is vascular adaptation. In some patients, total arterial elastance, determined by measuring left ventricular pressure and left ventricular volumes during different loading conditions, decreases to maximize left ventricular work and to maintain performance [20]. However, in other patients, elastance increases, enhancing afterload excess and leading to a reduction in left ventricular work and pump performance; this is most apparent in those with depressed left ventricular contractility.
#22 Cardiac catheterization is not always required in all patients with chronic AR but may provide extremely valuable clinical information, especially in patients who are contemplating surgery. Class I indications for cardiac catheterization under current American College of Cardiology/American Heart Association guidelines include the following:[5]Assessment of coronary anatomy prior to aortic valve surgery in patients with risk factors for coronary artery diseaseAssessment of severity of AR, LV function, or aortic root size when noninvasive tests are inconclusive or discordant with clinical findingsAortic angiography, which may be performed during a cardiac catheterization procedure, may provide useful information regarding the severity of the patient's AR. Traditional angiographic grading is as follows:Mild (1+): A small amount of contrast enters the left ventricle during diastole and clears with each systole.Moderate AR (2+): Contrast enters the LV with each diastole, but the LV chamber is less dense than the aorta.Moderately severe AR (3+): The LV chamber is equal in density with the ascending aorta.Severe AR (4+): Complete, dense opacification of the LV chamber occurs on the first beat and the LV is more densely opacified than the ascending aorta.An intraaortic balloon pump is contraindicated because inflation of the balloon in diastole will worsen the severity of AR.
#24 The role of medical therapy in pt with ar is limited.In acute severe aortic regurgitation (AR), surgical intervention is usually indicated, but the patient may be supported medically with dobutamine to augment cardiac output and shorten diastole and sodium nitroprusside to reduce afterload in hypertensive patients.In chronic severe AR, vasodilator therapy may be used in select conditions to reduce afterload in patients with systolic hypertension to minimize wall stress and optimize LV function; in normotensive patients, vasodilator therapy is not likely to reduce regurgitant volume (preload) significantly and thus may not be of clinical benefit.[22]Therapy with vasodilating agents is designed to improve forward sv and reduce the regurgitantcolume.these effects should translate into reductio n in lvedv,wall stress, and afterload ,resulting in preservation of lv systolic function and reduction in lv mass.The acute administration of sodium nitoprusside ,hydralazine,nifedipine or felodipine reduces peripheral vascular resistance and results in and immediate augmentation in forward cardiac output and a decrease in regurgitant volume.With nitroprusside and hydralazine ,these acute hemodynamic changes lead to a consistent reduction in edv and an increase in ef.Reduced edv and increased ef have also been observed in small number of patients receiving long term oral therapy with hydralazine and nifedipine for a period of 1 to 2 years.withnifedipine these effects are associated with a reduction in left ventricular mass.Reduced bp with enalapril and quinapril has been associated with decrease in edv and mass but no change in ejection fraction.
#25 Therapy with vasodilating agents is designed to improve forward sv and reduce the regurgitantcolume.these effects should translate into reductio n in lvedv,wall stress, and afterload ,resulting in preservation of lv systolic function and reduction in lv mass.The acute administration of sodium nitoprusside ,hydralazine,nifedipine or felodipine reduces peripheral vascular resistance and results in and immediate augmentation in forward cardiac output and a decrease in regurgitant volume.With nitroprusside and hydralazine ,these acute hemodynamic changes lead to a consistent reduction in edv and an increase in ef.Reduced edv and increased ef have also been observed in small number of patients receiving long term oral therapy with hydralazine and nifedipine for a period of 1 to 2 years.withnifedipine these effects are associated with a reduction in left ventricular mass.Reduced bp with enalapril and quinapril has been associated with decrease in edv and mass but no change in ejection fraction.
#26 Reduced edv and increased ef have also been observed in small number of patients receiving long term oral therapy with hydralazine and nifedipine for a period of 1 to 2 years.withnifedipine these effects are associated with a reduction in left ventricular mass.Reduced bp with enalapril and quinapril has been associated with decrease in edv and mass but no change in ejection fraction.
#27 The current American College of Cardiology/American Heart Association (ACC/AHA) guidelines say the following about vasodilator therapy:Vasodilator therapy is indicated for long-term therapy in patients with chronic, severe AR and symptoms of LV dysfunction but who are not candidates for surgery.Vasodilator therapy is reasonable for short-term therapy in patients with severe LV dysfunction and heart failure symptoms to improve their hemodynamic profile before proceeding with surgery.Vasodilator therapy is acceptable for long-term therapy in asymptomatic patients with severe AR and LV dilation with normal EF.COntraindicatedLong-term therapy in asymptomatic patients with less than severe AR (mild to mod)and normal EFLong-term therapy in asymptomatic patients with LV dysfunction who are otherwise candidates for surgeryLong-term therapy in symptomatic patients with less than severe LV dysfunction who are candidates for surgery
#28 Although diuretics, nitrates, and digoxin are sometimes used to help control symptoms in patients with AR, not enough data in the clinical literature justify routinely recommending or discouraging these therapies. Also, no data support drug therapy of any class in patients with less than severe AR.[5]Antibiotic prophylaxis prior to dental procedures is no longer routinely recommended for all patients with AR under current ACC/AHA guidelines.[5]However, select patient groups for whom prophylactic antibiotic therapy prior to dental procedures may be reasonable include the following:Patients with prosthetic material in their hearts (such as artificial valves or valves repaired with prosthetic material)Patients with prior infective endocarditis.Patients with the following forms of congenital heart disease (CHD):Cyanotic CHD that is incompletely or not repaired (including patients with palliative shunts and conduits)Repaired CHD using prosthetic material, for the first 6 months post-procedurally (ie, prior to endothelialization of the material)Repaired CHD but at risk of inhibited endothelialization (ie, with residual defects at or adjacent to the site of the prosthetic material)Patients following cardiac transplantation who have valve regurgitation due to a structurally abnormal valve
#29 Surgical treatment of AR usually requires replacement of the diseased valve with a prosthetic valve, although valve-sparing repair is increasingly possible with advances in surgical technique and technology.
#30 Under current ACC/AHA guidelines[5] , aortic valve surgery is recommended for patients with chronic severe AR under the following circumstances:Patient is symptomaticPatient is asymptomatic, with a resting EF of ≤ 55%Patient is asymptomatic, with LV dilation (LV end-systolic dimension >55 mm)Additional circumstances in which aortic valve surgery may be reasonable include the following:Patient has moderate AR and is undergoing coronary artery bypass surgery or other surgery involving the ascending aortaPatient has severe AR with no symptoms, normal EF, and less severe LV dilation (LV end-systolic dimension >50 mm or LV end-diastolic dimension >70 mm) if the patient experiences (1) progressive LV dilation on serial imaging studies; (2) deteriorating exercise tolerance, or (3) abnormal hemodynamic responses to exercise, such as inability to augment blood pressure during a treadmill studyOngoing improvements in surgical technique and technology have enabled many patients with even severe LV dysfunction to undergo surgery (rather than cardiac transplantation).[23]In patients undergoing aortic valve surgery for bicuspid aortic valve disease who also have a dilated or aneurysmal ascending aorta with a diameter of >4.5 cm, concurrent aortic root repair or replacement is indicated.Aortic valve surgery is generally not indicated in asymptomatic patients with normal EF and less LV dilation (LV end-systolic dimension < 50 mm or LV end-diastolic dimension < 70 mm)
#31 For patients undergoing aortic valve replacement, careful consideration should be given to the relative risks and benefits of mechanical versus bioprosthetic valves. Traditionally, mechanical valves have been thought to be more durable but require long-term anticoagulation with warfarin due to increased risk of thrombosis, whereas bioprosthetic valves carry a greater risk of long-term deterioration and risk of reoperation but avoid the need for long-term warfarin.[24] In some cases, a clear choice is apparent (eg, a homografts is often preferred to a mechanical valve in the setting of active infective endocarditis).While further discussion is beyond the scope of this article, the reader is referred to the current ACC/AHA guidelines, which include major criteria for aortic valve selection as well as recommendations for antithrombotic therapy (including aspirin for all prosthetic valve recipients along with long-term anticoagulation with warfarin for selected patients).[5]
#32 Inpatient care is required for most patients with acute severe aortic regurgitation (AR), particularly with symptoms or evidence of hemodynamic decompensation. Patients with chronic severe AR may be followed as inpatients or outpatients, depending on the stage of their disease and severity of their symptoms and LV dysfunction.
#33 Asymptomatic patients with chronic severe AR require ongoing clinical surveillance with periodic echocardiography because in many cases, significant LV dysfunction may arise even before the patient becomes symptomatic.The recommended frequency of clinical evaluation is based on the stability of the left ventricular end-systolic dimensions (ESD) and end-diastolic dimensions (EDD) as listed below. After the initial study, clinical evaluation and repeat echocardiogram are recommended in 3 months. Subsequent follow-up is based on the results of the 2 evaluations.For patients with ESD < 45 mm or EDD < 60 mm and stable dimensions, clinical evaluation is recommended every 6-12 months and repeat echocardiography is recommended every 12 months.For patients with ESD < 45 mm or EDD < 60 mm and increasing dimensions, clinical evaluation and repeat echocardiography are recommended in 3 months.For patients with ESD 45-50 mm or EDD 60-70 mm and stable dimensions, clinical evaluation is recommended every 6 months and repeat echocardiography is recommended every 12 months.For patients with ESD 45-50 mm or EDD 60-70 mm and increasing dimensions, clinical evaluation and repeat echocardiography are recommended in 3 months.For patients with ESD 50-55 mm or EDD 70-75 mm and stable dimensions, clinical evaluation and repeat echocardiography are recommended every 6 months.For patients with ESD 50-55 mm or EDD 70-75 mm and increasing dimensions, clinical evaluation and repeat echocardiography are recommended in 3 months.For patients with ESD >55 mm or EDD >75 mm, surgery is recommended.
#34 Left untreated, acute severe AR is likely to lead to considerable morbidity and mortality from either the underlying cause (typically infective endocarditis or aortic dissection) or from hemodynamic decompensation of the LV.Potential complications in patients with chronic severe AR include progressive LV dysfunction and dilation, congestive heart failure, myocardial ischemia, arrhythmia, and sudden death. Additional complications may arise as a result of the patient's underlying condition (such as aortic root dissection in a patient with a bicuspid aortic valve and a severely dilated aortic root
#35 The prognosis for patients with severe AR depends on the presence or absence of LV dysfunction and symptoms, as follows:[5]In asymptomatic patients with normal EFRate of progression to symptoms or LV dysfunction = < 6% per yearRate of progression to asymptomatic LV dysfunction = < 3.5% per yearRate of sudden death = less than 0.2% per yearIn asymptomatic patients with decreased EF, rate of progression to symptoms = >25% per year.In symptomatic patients, mortality rate = >10% per year.Again, the strongest predictors of outcome are echocardiographic parameters (EF and LV end-systolic dimension), underscoring the crucial role of serial echocardiography in the management of patients with severe AR.

Aortic regurgitation

1.
Pratap Sagar Tiwari,Resident, Internal Medicine, NGMC
2.
• Anatomy ofAortic valve/variants • Aortic Regurgitation • Aortic Stenosis
3.
The AV islocated betwn the LVOT and the ascending aorta. It forms the centerpiece of t heart and closely approximates many other important cardiac structures; specifically, th PV anteriorly, MV posterolaterally, and TV posteromedially.[1] Ref: 1. Anderson RH. Clinical anatomy of the aortic root. Heart. Dec 2000;84(6):670-3.
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Picture ref: AndersonRH. Clinical anatomy of the aortic root. Heart. Dec 2000;84(6):670-3.
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Picture reference: AndersonRH. Clinical anatomy of the aortic root. Heart. Dec 2000;84(6):670-3.
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Bicuspid aortic valve •Bicuspid aortic valves are the most common cardiac valvular anomaly, occurring in 1- 2% of the general population. • It is twice as common in males as in females.[1] Ref: 1. Tzemos N, Therrien J, Yip J et al (September 2008). "Outcomes in adults with bicuspid aortic valves". JAMA 300 (11): 1317–1325
7.
• AR isa condition due to inadequate closure of the aortic valve leaflets leading to abnormal retrograde flow of blood through the aortic valve during cardiac diastole. • It can be induced either by damage to and dysfunction of the aortic valve leaflets or by distortion or dilatation of the aortic root and ascending aorta • In the developing world, the most common cause of AR is rheumatic heart disease. However, in developed countries, AR is most often due to aortic root dilation or a congenital bicuspid aortic valve .[1] Ref: 1. Maurer G. Aortic regurgitation. Heart. Jul 2006;92(7):994-1000.
8.
Leaflet abnormalities Aortic rootor ascending aorta Rheumatic fever Systemic hypertension Endocarditis Aortitis (eg, syphilis) Trauma Reactive arthritis Bicuspid aortic valve Ankylosing spondylitis Rheumatoid arthritis Trauma/ Dissecting aneurysm Myxomatous degeneration Osteogenesis imperfecta Ankylosing spondylitis Marfan syndrome/ EDS Acromegaly Inflammatory bowel disease AR is seen more commonly in men than in women. As in the Framingham study, AR was 13% of men versus 8.5% of women.[1] The greater prevalence of AR in men may reflect, in the male preponderance of underlying conditions such as Marfan syndrome[2] or bicusp valve[3] . Ref: 1. Singh JP, Evans JC, et al. Prevalence and clinical determinants of mitral, tricuspid, and AR (the Framingham Heart Study). Am J Cardiol. Mar 15 1999;83(6 2. Keane MG, Pyeritz RE. Medical management of Marfan syndrome. Circulation. May 27 2008;117(21):2802-13. 3. Ortiz JT, Shin DD, Rajamannan NM. Approach to the patient with bicuspid AVand ascending aorta aneurysm. Curr Treat Options Cardiovasc Med. Dec 200
9.
Law of laplace ↑LV Volume LV Hypertrophy
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Sudden large regurgitantvolume imposed on LV of normal size with normal compliance 1. Rapid ↑ LVEDP and ↑ LAP 2. LV attempts to maintain CO with ↑HR and ↑ Contractility Attempts to maintain forward SV/CO may be inadequate Cardiogenic Shock ↓ Forward SV/CO Pulmonary edema ↑ LVEDP and ↑ LAP Angina ↓ Coronary perfusion ↑demand myocardial O2
11.
Regurgitant Volume Load CompensatoryMechanisms: 1. ↑LV dilatation ↑ LVED vol and ↑chamber compliance 2. ↑ LV hypertrophy Decompensation Steadily increasing regurgitant volume load Further ventricular dilatation  ↑ wall stress Inability to continue further hypertrophy Contractile dysfunction  ↓ EF/SV/CO CHF symptoms Due to both congestion and ↓ CO Angina ↓ Coronary perfusion pressure & marked LVH
12.
deMusset's sign A headbob occurring with each cardiac cycle Mueller's sign Systolic pulsations of the uvula. Becker's sign Visible pulsations of the retinal arteries and pupils. Quincke's pulses visible Capillary pulsations in the nailbeds after holding the tip of the nail. Duroziez's sign A systolic and diastolic bruit heard when the femoral artery is partially compressed.to and fro murmur Traube's sign A pistol shot murmur (systolic and diastolic sounds) heard over the femoral arteries. Mayne's sign More than a 15 mmHg decrease in DBP with arm elevation from the value obtained with the arm in the standard position. Hill's sign Popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg. Rosenbach's sign Systolic pulsations of the liver. Gerhard's sign Systolic pulsations of the spleen.
13.
• The diastolicmurmur of AR begins immediately after A2 . • It is high pitched, often blowing in quality, and may be sustained in intensity or decrescendo. • It may be soft and barely audible, often appreciated only when the patient is sitting up, leaning forward, and holding his or her breath in expiration.
14.
• Patients witha longer diastolic murmur, a displaced left ventricular impulse, a wide pulse pressure, and the peripheral findings of a wide pulse pressure are considered to have severe AR. Note: When the Diastolic murmur of AR is louder in the 3rd /4th RICS than in the 3/4th LICS ,the AR is likely to result from Aortic root dilatation than deformitiy of leaflets alone. Ref: ACC/AHA Guidelines 2006
15.
• In areview of the literature, the presence of an early diastolic murmur, as heard by a cardiologist, was the most useful finding for establishing the presence of AR (positive likelihood ratio 8.8 [ie, the odds of AR are increased 8.8 fold]) and its absence the most useful finding for eliminating the presence of AR (negative likelihood ratio 0.2 to 0.3 [ie, the odds of disease are reduced by a factor of 0.2 to 0.3]) .[1] Ref: 1. Choudhry NK, Etchells EE. The rational clinical examination. Does this patient have aortic regurgitation? JAMA 1999; 281:2231
16.
• Laboratory testingin patients with aortic regurgitation should be guided by the clinical scenario. • For example, in patients with AR due to suspected infective endocarditis, peripheral blood counts and cultures may help clarify the diagnosis and identify the causative organism. • Specific serologic tests may assist in the diagnosis of rheumatological causes.
17.
• Aortic valvestructure and morphology (bileaflet versus trileaflet, flail, thickening) • Presence of vegetations • Severity of AR • Color Doppler jet width • Vena contracta width • Regurgitant volume, fraction, and orifice area • Premature closure of the mitral valve (seen in severe AR) • Associated lesions of the aorta, including dilation, aneurysm, dissection • LV structure and function • LV hypertrophy and dilation • EF and end-systolic dimension are key determinants of outcome
18.
MILD MOD SEVERE Structural parameters Left ventricularsize N N or dilated Dilated, except acute AR Aortic leaflets N or abnormal N or abnormal Abnormal/flail, or wide coaptation defect Color Doppler jet width Central jet, width <25 percent of LVOT Central jet, width 25 to 65 percent of LVOT Central jet width >65 percent of LVOT Doppler vena contracta width <3 mm 3 to 6 mm >6 mm Doppler parameters Quantitative parameters Regurgitant volume <30 mL/beat 30 to 59 mL/beat ≥60 mL/beat Regurgitant fraction <30 percent 30 to 49 percent ≥50 percent Regurgitant orifice area <0.10 cm2 0.10 to 0.29 cm2 ≥0.30 cm2 Severe chronic AR is typically a/w c/f including a longer diastolic murmur, a displaced LVI, a wide PP, and the peripheral findings of
19.
References: 1. ACC/AHA 2006guidelines 2. Gaasch WH, Andrias CW, Levine HJ. Chronic aortic regurgitation: the effect of aortic valve replacement on left ventricular volume, mass and function. Circulation 1978; 58:82 3. Schuler G, Peterson KL, Johnson AD, et al. Serial noninvasive assessment of left ventricular hypertrophy and function after surgical correction of AR. Am J Cardiol 1979; 44: 4. Borow KM, Green LH, Mann T, et al. End-systolic volume as a predictor of postoperative LVperformance in volume overload from valvular regurgitation. Am J Med 1980; 68: 5. Henry WL, Bonow RO, et al. Observations on the optimum time for operative intervention for AR. Evaluation of the results of AVR in symptomatic patients. Circulation 1980; 6. Kumpuris AG, Quinones MA, Waggoner AD, et al. Importance of preoperative hypertrophy, wall stress and end-systolic dimension as echocardiographic predictors of norma of left ventricular dilatation after valve replacement in chronic aortic insufficiency. Am J Cardiol 1982; 49:1091. 7. Gaasch WH, Carroll JD, Criscitiello MG. Chronic AR: prognostic value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio. J Am Coll Cardiol 19 8. Stone PH, Clark RD, Goldschlager N, et al. Determinants of prognosis of patients with aortic regurgitation who undergo aortic valve replacement. J Am Coll Cardiol 1984; 3:1 9. Bonow RO, Rosing DR, McIntosh CL, et al. The natural history of asymptomatic patients with aortic regurgitation and normal left ventricular function. Circulation 1983; 68:509 10. Bonow RO, Lakatos E. Serial long-term assessment of the natural history of asymptomatic patients with chronic AR and normal left ventricular systolic function. Circulation 11. Siemienczuk D, Greenberg B, Morris C, et al. Chronic aortic insufficiency: factors associated with progression to aortic valve replacement. Ann Intern Med 1989; 110:587.
21.
Class I indicationsfor CC under current ACC/AHA guidelines include the following:[1] • Assessment of coronary anatomy prior to aortic valve surgery in patients with risk factors for coronary artery disease. Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. .
22.
Class IIa -The weight of evidence or opinion is in favor of efficacy of the following test patients with AR in the above settings. Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with VHD.
23.
• In acutesevere AR, surgical intervention is usually indicated, but the patient may be supported medically with dobutamine to augment cardiac output and shorten diastole and sodium nitroprusside to reduce afterload in hypertensive patients. • In chronic severe AR, vasodilator therapy may be used in select conditions to reduce afterload in patients with systolic hypertension to minimize wall stress and optimize LV function; in normotensive patients, vasodilator therapy is not likely to reduce regurgitant volume (preload) significantly and thus may not be of Ref: 1. Bekeredjian R, Grayburn PA. Valvular heart disease: aortic regurgitation. Circulation. Jul 5 2005;112(1):125-34. clinical benefit.[1]
24.
• The acuteadministration of Na Nitoprusside , hydralazine, nifedipine or felodipine ↓PVR and results in an immediate augmentation in forward CO and a ↓ in regurgitant volume. • With nitroprusside and hydralazine ,these acute hemodynamic changes lead to a consistent ↓in EDV and an ↑in EF. References: 1. Miller RR, Vismara LA, .Afterload reduction therapy with nitroprusside in severe AR: improved cardiac performance and reduced regurgitant volume. AmJ Cardiol 976;38:564–7 2. Greenberg BH, DeMots H. Beneficial effects of hydralazine on rest and exercise hemodynamics in patients with chronic severe aortic insufficiency. Circulation 1980;62:49–55 3. FiorettiP, BenussiB.Afterload reduction with nifedipine in aortic insufficiency. AmJ Cardiol 1982;49:1728–32
25.
• Reduced EDVand ↑EF have also been observed in small number of pts receiving long term oral therapy with hydralazine and nifedipine for a period of 1-2 yrs. With nifedipine these effects are A/W ↓ in LV mass.[1,2] • Reduced BP with enalapril and quinapril has been A/W ↓ in EDV and mass but no change in EF.[3,4] References: 1. Scognamiglio R, Fasoli G. Long-term nifedipine unloading therapy in asymptomatic patients with chronic severe AR. J Am Coll Cardiol 1990; 16:424–9. 2. Greenberg B, Massie B, et al. Long-term vasodilator therapy of chronic AI: a randomized double-blinded, placebo-controlled clinical trial. Circulation 1988;7 3. Lin M, Chiang HT,etal.Vasodilator therapy in chronic asymptomatic AR: enalapril versus hydralazine therapy. J Am Coll Cardiol 1994;24:1046–53. 4. Schon HR, Dorn R. Effects of 12 months quinapril therapy in asymptomatic patients with chronic AR. J Heart Valve Dis 1994;3:500–9.
26.
• Indicated forlong-term therapy in patients with chronic, severe AR and symptoms of LV dysfunction but who are not candidates for surgery.( CLASS I: LOE-b) • Is reasonable for short-term therapy in patients with severe LV dysfunction and HF symptoms to improve their hemodynamic profile before proceeding with surgery.(CLASS IIa: LOE-c) • Is acceptable for long-term therapy in asymptomatic patients with severe AR and LV dilation with normal Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/A EF. (CLASS IIb: LOE-b) guidelines for the management of patients with valvular heart disease. Note: LOE = Level of Evidence
27.
• Antibiotic prophylaxisprior to dental procedures is no longer routinely recommended for all patients with AR under current ACC/AHA guidelines.[1] Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/A 2006 guidelines for the management of patients with valvular heart disease
28.
• Surgical treatmentof AR usually requires replacement of the diseased valve with a prosthetic valve, although valve-sparing repair is increasingly possible with advances in surgical technique and technology.
29.
• Patient issymptomatic. • Patient is asymptomatic, with a resting EF of ≤ 55%. • Patient is asymptomatic, with LV dilation (LV end-systolic dimension >55 mm). Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC 2006 guidelines for the management of patients with valvular heart disease.
30.
• For patientsundergoing AV replacement, careful consideration should be given to the relative risks and benefits of mechanical vs bioprosthetic valves. • Mechanical valves : more durable but require long-term anticoagulation with warfarin due to increased risk of thrombosis. • Bioprosthetic valves carry a greater risk of long-term deterioration and risk of reoperation but avoid the need for long-term warfarin.[1] Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/A 2006 guidelines for the management of patients with valvular heart disease. .
31.
• Inpatient careis required for most patients with acute severe aortic regurgitation (AR), particularly with symptoms or evidence of hemodynamic decompensation.
32.
ESD EDD Stable Dimension Incresing Dimension <45 mm <60 mm Evaluate 6-12 mn Repeat Echo in 12 mnth 3mnth 3 mnth 45-50 mm 60-70 mm Evaluate 6 mn Repeat Echo in 12 mnth 3 mnth 3 mnth 50-55 mm 70-75 mm Evaluate in 6 mn Repeat Echo 6 mnth 3 mnth 3 mnth >55 mm > 75 mm Surgery
33.
• Left untreated,acute severe AR is likely to lead to considerable morbidity and mortality from either the underlying cause (typically infective endocarditis or aortic dissection) or from hemodynamic decompensation of the LV. • Potential complications in patients with chronic severe AR include progressive LV dysfunction and dilation, CHF, MI, arrhythmia, and sudden death.
34.
The prognosis forpatients with severe AR depends on the presence or absence of LV dysfunction and symptoms, as follows:[1] • In asymptomatic patients with normal EF 1. Rate of progression to symptoms &/or LVD = < 6% per yr 2. Rate of progression to asymptomatic LVD = < 3.5% per yr 3. Rate of sudden death = less than 0.2% per yr • In asymptomatic patients with decreased EF, rate of progression to symptoms = >25% per year. • In symptomatic patients, mortality rate = >10% per yr. The strongest predictors of outcome are echocardiographic parameters (EF and LV end-systolic dimension). Ref: 1. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease.
35.
References: 1. 2008 updateon ACC/AHA 2006 Guideline on VHD. 2. Harrison’s Principle of Internal Medicine ,18th ed. 3. Washington manual; Cardiology Subspeciality Consult ,2nd ed. 4. Cardiology Secrets by Glenn L Levine, 3rd ed. 5. Uptodate 19.1 .Last literature review sep 30 2011. 6. Emedicine “ 7. Mayo Clinic

Editor's Notes

#4 The normal human heart contains 4 valves that regulate blood flow into and out of the heart. The aortic and pulmonic valves are known as the semilunar valves, whereas the tricuspid and mitral valves are referred to as the atrioventricular valves. All the valves are trileaflet, with the exception of the mitral valve, which has 2 leaflets. All 4 cardiac valves are surrounded by fibrous tissue forming partial or complete valvular rings, or annuli. These annuli join the fibrous skeleton of the heart and helps anchoring and supporting the valvular structures.The AV is located betwn the LVOT and the ascending aorta. It forms the centerpiece of the heart and closely approximates many other important cardiac structures; specifically, the pulmonic valve anteriorly, mitral valve posterolaterally, and tricuspid valve posteromedially.[1]
#5 The aortic valve functions to prevent the regurgitation of blood from the aorta into the left ventricle during ventricular diastole and to allow the appropriate flow of blood—the cardiac output—from the left ventricle into the aorta during ventricular systole. The aortic valve has 3 principle components: the annulus, cusps, and commissures.
#6 The aortic valve annulus is a collagenous structure lying at the level of the junction of the aortic valve and the ventricular septum.This area is also referred to as the aortic ring and serves to provide structural support to the aortic valve complex. There are 3 aortic valve cusps, each half-moon shaped or semilunar in appearance CONTAIN aortic sinuses and as it is named after the italian anatomist antoniovalsalva ,these aortic sinuses are also called sinus of valsalva. Their association with the respective coronary ostia identifies them: left, right, and posterior (or noncoronary). In the normal human heart, the left and right coronary arteries originate from the left and right aortic sinuses, 91% and 93% of the time, respectively.The rim of each valve cusp is slightly thicker than the cusp body and is known as the lunula. The lunulae of adjacent cusps slightly overlap each other at the time of valve closure, serving a role of increased valve support .The small spaces between each cusp's attachment point are called the aortic valve commissures .
#7 A bicuspid aortic valve (BAV) is most commonly a congenital condition of the aortic valve where two of the aortic valvular leaflets fuse during development resulting in a valve that is bicuspid instead of the normal tricuspid configuration.Bicuspid aortic valves are the most common cardiac valvular anomaly, occurring in 1- 2% of the general population. It is twice as common in males as in females.[1]In many cases, a bicuspid aortic valve will cause no problems.[4] However BAV may become calcified later in life, which may lead to varying degrees of severity of aortic stenosis or If the leaflets do not close correctly, aortic regurgitation can occur.The other uncommon variants can be unicuspid or quadricuspid.Pathophysiologic VariantsUnicuspid aortic valveUnicuspid aortic valve is a congenital valvular defect with an incidence of 0.02% in the general population. It is commonly associated with clinically significant aortic stenosis, usually manifesting during the third decade of life. All valves are unicommissural with the posterior commissural attachment. The free edge of the valve extends from the single commissure without further communication with the aorta. An estimated 50% of individuals with unicuspid aortic valve have associated ascending aortic dilatation. This is a rare cardiac anomaly but should be suspected in patients presenting at a young age with clinically significant aortic stenosis.[5, 9, 10]Bicuspid aortic valveBicuspid aortic valve is the most common congenital cardiac anomaly, occurring in 1-2% of the population, with a 2:1 male predominance. Evidence exists of familial clustering, with the incidence as high as 10% in some families. Bicuspid aortic valve may be clinically silent but can lead to early development of aortic stenosis or aortic insufficiency, most commonly in the fifth and sixth decades of life. Conditions associated with bicuspid aortic valve include patent ductusarteriosus,Williams syndrome, Turner syndrome, and coarctation of the aorta. Of clinical importance is the association of aortic root dilatation and ascending aortic aneurysm.[5, 11]Quadricuspid aortic valveQuadricuspid aortic valve (QAV), first described in 1862 by Balington, is a rare congenital valvular abnormality that affects both the pulmonic and aortic valves in a 10:1 ratio. The incidence of QAV is estimated at 0.0125–0.033% in the general population. Seven different subtypes of QAV have been identified, with the most common being 3 cusps of equal size with a fourth smaller cusp.QAV most commonly occurs as an isolated defect but has been associated with patent ductusarteriosus, Ehlers-Danlos syndrome, hypertrophic obstructive cardiomyopathy, and subaortic stenosis. Aortic valvular insufficiency is commonly observed in QAV. It occurs secondary to a central orifice formed from malcoaptation of the 4 valvular leaflets. In a small case series, 56% of subjects with QAV had significant valvular insufficiency, with a mean age at presentation of 46 years.[12, 13]
#8 AR is a condition due to inadequate closure of the aortic valve leaflets leading to abnormal retrograde flow of blood through the aortic valve during cardiac diastole.
#9 AR may be caused by either valvular or aortic root pathology. Valvular abnormalities that may result in AR include bicuspid aortic valve (the most common congenital cause), rheumatic fever, infective endocarditis, collagen vascular diseases, and degenerative aortic valve disease.Abnormalities of the ascending aorta, in the absence of valve pathology, may also cause AR, such as may occur with longstanding uncontrolled hypertension, Marfan syndrome, idiopathic aortic dilation, syphilitic aortitis, giant cell arteritis, Takayasu arteritis, ankylosing spondylitis, Whipple disease, and other spondyloarthropathies.The absence of a wide pulse pressure and of the characteristic arterial auscultatory signs of chronic AR in patients with acute AR is thought to be due to the much higher LV end-diastolic pressure (LVEDP) in the acute form. The acute development of a severe aortic valvular leak causes a much higher LVEDP in the normal-sized LV of patients with acute AR. Patients with chronic AR commonly have a dilated LV with increased compliance capable of accommodating large blood volumes without a significant rise of LVEDP.
#10 To understand the pathophysiology of condition like aortic regurgitation ,it is important to understand the law of laplace.As stated by Laplace law: left ventricular (LV) wall stress is directly proportional to the cavity pressure and inversely proportional to wall thickness. Due to the added regurgitantvol there is increase in lv volume that leads to An elevation in LV cavity pressure and it causes an increase in wall stress. If a hypertrophic response occurs, increasing thickness can return wall stress to normal. All forms of AR produce a similar hemodynamic abnormality. The inability of the aortic valve leaflets to remain closed or coapted during diastole results in a portion of the left ventricular stroke volume leaking back from the aorta into the left ventricle. The added volume of regurgitant blood produces an increase in left ventricular end-diastolic volume and that results in an elevation of wall stress. The heart responds with compensatory increase in wall thickness ,so that increasing thickness can return wall stress to normal.THIS compensatory myocardial hypertrophy occurs in chornic AR.The combination of hypertrophy and chamber enlargement raises the total stroke volume. AND also as we remember the starlings law ie the increase in lvedvie the preload results in increased stretching of the myocytes leading to increased contractility. The net effect is that forward stroke volume and hence cardiac output are initially maintained or the ef can even be supra normal despite the regurgitant lesion. Thus, the heart initially adapts well to chronic AR, functioning as a very efficient and compliant high output pump.
#11 But there is a slight different scenario in case of acute ar that can result from conditions like Endocarditis in which there occurs valve destruction and leaflet perforation or Aortic dissection or Traumatic rupture of the valve leaflets or even Iatrogenic ar that results during aortic balloon valvotomy..these all can result in acute ar . in chronic AR, the LV may undergo a series of adaptive changes over course of time but in cases of acute AR, the LV does not have time to dilate in response to the volume load.with acute AR the regurgitant volume fills a small ventricle that has not had time to dilate, resulting in an acute increase in left ventricular diastolic pressure and leading to increased LAP.Lv may attempt to maintain co with increase hr and contractility but usually becomes inadequate And results in a fall in forward cardiac output. The decline in forward stroke volume may be exacerbated by a shortening of diastolic filling time due to the combination of early closure of the mitral valve (due to high end diastolic pressures) and tachycardia (caused by a decrease in forward flow and cardiac output). The net effect is often profound hypotension and cardiogenic shock.As a result of rapidly increased LV end-diastolic pressure ,The elevated left ventricular end-diastolic pressure leads to elevated left atrial and pulmonary venous pressures .As pressure increases throughout the pulmonary circuit, the patient develops dyspnea and pulmonary edema. And correlating clinically ,unlike chronic ar , left ventricular stroke volume and diastolic filling volume are not increased with acute regurgitation.wide pulse pressure is may not be present and thereby the peripheral signs of wide pulse pressure are also not present. The pulse pressure is normal or may be reduced, but the pulse is usually weak, thready, and rapid. The cardiac apex is generally not displaced and is not hyperdynamic.Aortic dissection should always be suspected in patients with AR and chest or back pain. If aortic dissection is the cause, an inequality of pulses and blood pressure between the left and right arms may be observed. However, this finding may not be appreciated in the setting of profound hypotensionCardiac auscultation — Acute AR alters the quality of most of the heart sounds:due to the elevated lvdiastolicpresuure that close the mitral valve prematurely can result in reduced intensity of first heart sound.which can occasionally be heard in mid-diastole.The aortic component of S2 is often soft, while P2 is usually increased, reflecting pulmonary hypertension.An S3 is frequently heard but an S4 is absent.In contrast to the high pitched holodiastolic decrescendo murmur of chronic AR, the murmur with acute AR is a low pitched early diastolic murmur beginning after S2 .The murmur, however, may not be heard, especially when the diastolic gradient between the aorta and left ventricle lessens. A systolic murmur resulting from the increased volume of blood crossing the aortic valve may be heard, but is usually not loud. The combination of a soft systolic and a low-pitched diastolic murmur often produces a "to-and-fro" murmur at the cardiac base in acute AR.
#12 In chronic AR, the volume overload of the left ventricle is associated with a gradual increase in left ventricular size that maintains a normal forward cardiac output despite the regurgitant valve flow; left ventricular diastolic pressures remain normal.The resulting hypertrophy is necessary to accommodate the increased wall tension and stress that results from LV dilation .The combination of hypertrophy and chamber enlargement raises the total stroke volume .The net effect is that forward stroke volume and hence cardiac output are initially maintained despite the regurgitant lesion. although the LV vol is increased ,end diastolic pressure remains normal due to this ventricular complaince. Thus the heart initially adapts well to chronic ar functioning as a very efficient and compliant high output pump. As said During the early phases of chronic AR, the LV ejection fraction (EF) is normal or even increased (due to the increased preload and the Frank-Starling mechanism). Patients may remain asymptomatic during this period. As AR progresses, Eventually, the LV reaches its maximal diameter and diastolic pressure begins to rise, resulting in symptoms (dyspnea) that may be worse during exercise. Increasing LV end-diastolic pressure may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia, necrosis, and apoptosis. Patients with AR may remain asymptomatic for decades, even if there is progressive ventricular dilatation. If, however, there is a large regurgitant volume, the patient may complain of symptoms related to the increased mass of the enlarged left ventricle. These include:A sense of pounding and an uncomfortable awareness of the heartbeat. These symptoms are especially pronounced when lying down or lying on the left side which brings the left ventricular apex closer to the chest wall, augmenting the sensation during systolic contraction.Palpitations due to tachycardia or premature beats. The latter cause a compensatory pause and postextrasystolic potentiation with a further sense of variable cardiac motion by the patient.Symptoms of left-sided heart failure (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and eventual pulmonary edema) occur in the presence of left ventricular dysfunction.Physical examination — The physical examination in patients with chronic AR is often dramatic and frequently establishes the diagnosis without the need for laboratory testing. Both examination of the peripheral pulses and auscultation of the heart are important. The increased stroke volume results in abrupt distension of the peripheral arteries and an elevation in systolic pressure. Regurgitation back into the left ventricle then leads to a rapid fall in pressure with quick collapse of the arteries and a low diastolic pressure which may approach zero in severe disease.The net effect is a wide pulse pressure, which is manifested on examination as a "water hammer" or Corrigan pulse. This finding may be best appreciated by palpation of the radial or brachial arteries (exaggerated by raising the arm) or the carotid pulses. Other findings are associated with a hyperdynamic pulse:deMusset's sign — A head bob occurring with each cardiac cycle ..heart beat.Corrigan pulse :rapid carotid upstroke followed by arterial collapseTraube's sign — A pistol shot murmur (systolic and diastolic sounds) heard over the femoral arteries.Duroziez's sign — A systolic and diastolic bruit heard when the femoral artery is partially compressed.to and fro murmurQuincke's pulses —visible Capillary pulsations in the nailveds after holding the tip of the nail.Mueller's sign — Systolic pulsations of the uvula.Becker's sign — Visible pulsations of the retinal arteries and pupils.Hill's sign — Popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg.Mayne's sign — More than a 15 mmHg decrease in diastolic blood pressure with arm elevation from the value obtained with the arm in the standard position.Rosenbach's sign — Systolic pulsations of the liver.Gerhard's sign — Systolic pulsations of the spleen.Although all of these clinical signs have been described as ancillary findings useful in the diagnosis of AR, there are few published studies that have assessed the predictive value of any of these findings [5]. Exaggerated or bounding pulses and these physical signs are not specific for AR, since they can be seen in any condition associated with a marked increase in stroke volume and a hyperdynamic circulation. Included in this group are sympathetic hyperactivity, anemia, fever, pregnancy, thyrotoxicosis, large arteriovenous fistula, patent ductusarteriosus, and severe bradycardia. Severe mitral regurgitation also can cause rapid rising arterial pulses, but the pulse pressure is not increased.The combination of left ventricular enlargement and forceful systolic function results in the apical impulse being displaced laterally and inferiorly and being diffuse and hyperdynamic. A prominent pulsation (and occasionally a thrill) may be felt at the sternal notch due to concurrent dilatation of the ascending aorta.
#13 Sherman sign ; prominently located and palpated dorsalispedis pulseLandolfi sign: alternating constriction and dilatation of pupilDuroziez sign: systolic portion of murmur was caused by forward flow into the lower extremity and the diastolic segment was caused by aortic regurgitation towards the heart.Seagull murmur: it is murmur with musical qualities such as that heard occasionally in aortic insufficiency. A sea gull cry murmur is defined as a murmur imitating the cooing sound of a seagull.this type of murmur is typically characterised by a music timbre and a high frequency and may occur as a result of various valve disease.it is usually described as a sign of tight calcific aortic stenosis when the murmur high frequency components are transmitted to the lower left sternal border and the cardiac apex during most of the systole (gallavardin phenomenon).in this condition,the typical harsh timbre of the ejective murmur tends to assume a musical high pitched quality ,resembling that of mitral regurgitation which may be reminiscent of the cry of a seagull. A protodiastolic murmur with similar characteristics ,typically in decrescendo ,may occur in severe AR particularly when the flow presents high velocities. However, a seagulls cry murmur may also be the sign of MR or prolapse. Similarly the muscial and holosystolic sound reflects the presence of high frequency components due to high velocities of reflow.
#14 On palpation, the point of maximal impulse may be diffuse or hyperdynamic but is often displaced inferiorly and toward the axilla. Chronic AR is associated with changes in the heart sounds and a distinctive murmur. The heart sounds typically have the following characteristics. S1 may be soft, often reflecting a long PR intervalS2 is variable; it may be soft, absent, or singleA2 is often soft or absent while P2 may be normal, but obscured by the diastolic murmurA systolic ejection sound may be due to abrupt aortic distension caused by the large stroke volumeA third heart sound (S3 gallop) is heard when left ventricular function is severely depressedThe diastolic murmur of AR begins immediately after A2 . It is high pitched, often blowing in quality, and may be sustained in intensity or decrescendo. It may be soft and barely audible, often appreciated only when the patient is sitting up, leaning forward, and holding his or her breath in expiration.The intensity of the murmur does not correlate well with the severity of AR. However, the timing and duration of the murmur may be helpful.In mild AR, the murmur occurs only in early diastole and is blowing.As the regurgitation becomes more severe, the murmur extends through more of diastole, may become holodiastolic and is often rougher in quality. Patients with a longer diastolic murmur, a displaced left ventricular impulse, a wide pulse pressure, and the peripheral findings of a wide pulse pressure are considered to have severe AR.The intensity of the murmur can also be affected by certain maneuvers. As examples, the murmur increases with squatting and decreases with the Valsalva maneuver. The site at which the murmur is best heard varies with the cause. The murmur is heard best along the left sternal border, at the third and fourth intercostal space, when AR is due to valvular disease. In contrast, when the diastolic murmur of ar is louder in the 3rd /4thRics than in the 3/4thLics ,the ar is likely to result from aortic root dilatation than deformitiy of leaflets alone.A systolic murmur can be heard in many patients. It typically resembles the ejection type of murmur heard in aortic stenosis, ie, a crescendo-decrescendo harsh murmur beginning after S1. This murmur does not necessarily reflect concurrent aortic stenosis, since the increased ejection rate and large stroke volume across the aortic valve can lead to a "functional" stenosis. A second type of diastolic murmur (the Austin Flint murmur) may also be appreciated. volume.An Austin Flint murmur may be present at the cardiac apex in severe AR and is a low-pitched, mid-diastolic rumbling murmur due to blood jets from the AR striking the anterior leaflet of the mitral valve, which results in premature closure of the mitral leaflets.Distinguishing features from mitral stenosis include the absence of both a loud S1 and an opening snap of the mitral valve.However, the physical findings are not sufficiently reliable and echocardiography is typically used to assess severity.In very severe regurgitation with ventricular decompensation, the murmur may become soft or even absent. This change in character reflects the near equivalence of aortic diastolic and left ventricular end-diastolic pressures which markedly diminishes regurgitant flow. A similar situation can occur when AR is acute and the left ventricular end-diastolic pressure is very high.
#16 Discovery of a diastolic murmur is essential for the diagnosis of AR. In a review of the literature, the presence of an early diastolic murmur, as heard by a cardiologist, was the most useful finding for establishing the presence of AR (positive likelihood ratio 8.8 [ie, the odds of AR are increased 8.8 fold]) and its absence the most useful finding for eliminating the presence of AR (negative likelihood ratio 0.2 to 0.3 [ie, the odds of disease are reduced by a factor of 0.2 to 0.3]) [6].
#17 Laboratory testing in patients with aortic regurgitation (AR) should be guided by the clinical scenario. For example, in patients with AR due to suspected infective endocarditis, peripheral blood counts and cultures may help clarify the diagnosis and identify the causative organism. Specific serologic tests may assist in the diagnosis of rheumatological causes. Laboratory assessment of renal and hepatic function may play an important role in determining a patient's eligibility for certain vasodilator or other drug therapy.
#18 Echocardiography is part of the standard evaluation of patients with ARTransthoracic echocardiography should be performed in all patients with suspected AR, and periodically in patients with confirmed AR of significant severity.and it is of class I b recommendation acc to acc/aha 2006 guideline. Echocardiography is a highly accurate test in AR, with sensitivity and specificity well in excess of 90%. In addition, echocardiographic parameters are used to determine the optimal timing of surgery in many cases.[5]Important echocardiographic findings in AR include the following:Aortic valve structure and morphology (bileaflet versus trileaflet, flail, thickening)Presence of vegetations or nodules (may require transesophageal echocardiography in selected cases)Quantitative measurements of regurgitantvolume,fraction and orifice area assessed .Transeesophageal echo is done To clarify whether there is bicuspid valve if unclear on tteBetter sensitivity and specificity for aortic dissection than tteClarify whether there is endocarditis or root abscess if unclear on tteBetter visualisation of av in pt with prosthetic avSeverity of ARColor Doppler jet width (the vena contracta width is usually >65% of the width of the left ventricular outflow tract in severe AR)Vena contracta widthRegurgitant volume, fraction, and orifice areaPremature closure of the mitral valve (seen in severe AR) and opening of the aortic valve (with severely elevated LV end-diastolic pressure)Pressure half-time (usually < 300-350 ms with significant AR)Associated lesions of the aorta, including dilation, aneurysm, dissection, or ectasiaLV structure and functionLV hypertrophy and dilationEF and end-systolic dimension are key determinants of outcomeSurgery recommended if EF is ≤ 55% or if end-systolic dimension is >55 mm[5]
#19 Standard chest radiography shows cardiomegaly due to the dilatation of the left ventricle, which enlarges in an inferior and leftward direction. The ascending aorta (and often the aortic arch or knob) are typically markedly dilated.Left atrial enlargement does not occur unless there is significant left ventricular dysfunction. Apart from evidence of structural abnormalities (aortic dilation, ) The chest radiograph shows may also show stage of functional compromise (pulmonary edema).Electrocardiography findings are nonspecific The electrocardiogram (ECG) reflects the adaptive changes that occur in the left ventricle as a result of the volume overload.may include evidence of the following:LV hypertrophyLeft axis deviationLeft atrial enlargementLV volume overload pattern (prominent Q waves in leads I, aVL, and V3 to V6 and relatively small r waves in V1)LV conduction defects (typically late in the disease process)Exercise treadmill testing may be used to guide recommendations for surgical therapy in patients with chronic severe AR and equivocal symptoms.[5] However, the role of stress echocardiography in patients with AR remains uncertain, and further studies may be needed before it can be recommended for routine clinical use.[21]
#20 Stages and course — Data from patients undergoing aortic valve replacement, in addition to clinical information, has been used to develop criteria for the definition of compensated and decompensated stages of chronic AR (table 3) [8,10-16].An LV end-diastolic dimension less than 65 mm and an LVEF >55 percent indicate a compensated stage.An LV end-systolic volume greater than 60 mL/m2, an LV end-systolic dimension greater than 50 mm, or an LVEF <50 percent usually indicates serious depression of LV systolic function (decompensated stage).The nature of the transition from a compensated to a decompensated stage is poorly understood and the definitions of these stages have not been validated in a prospective fashion. Thus, they should only be used as general guidelines in a decision analysis that includes all other clinical data and patient preferences. Nevertheless, this information has been useful in defining limits that are predictive of the future need for aortic valve replacement [17,18].For example, one report included serial studies in 77 asymptomatic patients with moderate to severe AR [9]. Most patients had LV enlargement but all had normal LV systolic function. During a mean follow-up duration of 49 months, there were no deaths but 12 underwent surgery because of the development of symptoms and/or LV dysfunction. By life table analysis, the percent of patients not requiring surgery was 90 percent at three years, 81 percent at five years, and 75 percent at seven years.Thus, asymptomatic patients with moderate to severe AR and a normal LVEF at baseline require aortic valve replacement at the rate of approximately 4 percent per year. Similar findings were noted in a later study [10].The prognosis is not as good in asymptomatic patients with LV dysfunction. As many as two-thirds of such patients develop symptoms and require surgery within three years [11].One factor that may play a role in the progression of left ventricular dysfunction is vascular adaptation. In some patients, total arterial elastance, determined by measuring left ventricular pressure and left ventricular volumes during different loading conditions, decreases to maximize left ventricular work and to maintain performance [20]. However, in other patients, elastance increases, enhancing afterload excess and leading to a reduction in left ventricular work and pump performance; this is most apparent in those with depressed left ventricular contractility.
#22 Cardiac catheterization is not always required in all patients with chronic AR but may provide extremely valuable clinical information, especially in patients who are contemplating surgery. Class I indications for cardiac catheterization under current American College of Cardiology/American Heart Association guidelines include the following:[5]Assessment of coronary anatomy prior to aortic valve surgery in patients with risk factors for coronary artery diseaseAssessment of severity of AR, LV function, or aortic root size when noninvasive tests are inconclusive or discordant with clinical findingsAortic angiography, which may be performed during a cardiac catheterization procedure, may provide useful information regarding the severity of the patient's AR. Traditional angiographic grading is as follows:Mild (1+): A small amount of contrast enters the left ventricle during diastole and clears with each systole.Moderate AR (2+): Contrast enters the LV with each diastole, but the LV chamber is less dense than the aorta.Moderately severe AR (3+): The LV chamber is equal in density with the ascending aorta.Severe AR (4+): Complete, dense opacification of the LV chamber occurs on the first beat and the LV is more densely opacified than the ascending aorta.An intraaortic balloon pump is contraindicated because inflation of the balloon in diastole will worsen the severity of AR.
#24 The role of medical therapy in pt with ar is limited.In acute severe aortic regurgitation (AR), surgical intervention is usually indicated, but the patient may be supported medically with dobutamine to augment cardiac output and shorten diastole and sodium nitroprusside to reduce afterload in hypertensive patients.In chronic severe AR, vasodilator therapy may be used in select conditions to reduce afterload in patients with systolic hypertension to minimize wall stress and optimize LV function; in normotensive patients, vasodilator therapy is not likely to reduce regurgitant volume (preload) significantly and thus may not be of clinical benefit.[22]Therapy with vasodilating agents is designed to improve forward sv and reduce the regurgitantcolume.these effects should translate into reductio n in lvedv,wall stress, and afterload ,resulting in preservation of lv systolic function and reduction in lv mass.The acute administration of sodium nitoprusside ,hydralazine,nifedipine or felodipine reduces peripheral vascular resistance and results in and immediate augmentation in forward cardiac output and a decrease in regurgitant volume.With nitroprusside and hydralazine ,these acute hemodynamic changes lead to a consistent reduction in edv and an increase in ef.Reduced edv and increased ef have also been observed in small number of patients receiving long term oral therapy with hydralazine and nifedipine for a period of 1 to 2 years.withnifedipine these effects are associated with a reduction in left ventricular mass.Reduced bp with enalapril and quinapril has been associated with decrease in edv and mass but no change in ejection fraction.
#25 Therapy with vasodilating agents is designed to improve forward sv and reduce the regurgitantcolume.these effects should translate into reductio n in lvedv,wall stress, and afterload ,resulting in preservation of lv systolic function and reduction in lv mass.The acute administration of sodium nitoprusside ,hydralazine,nifedipine or felodipine reduces peripheral vascular resistance and results in and immediate augmentation in forward cardiac output and a decrease in regurgitant volume.With nitroprusside and hydralazine ,these acute hemodynamic changes lead to a consistent reduction in edv and an increase in ef.Reduced edv and increased ef have also been observed in small number of patients receiving long term oral therapy with hydralazine and nifedipine for a period of 1 to 2 years.withnifedipine these effects are associated with a reduction in left ventricular mass.Reduced bp with enalapril and quinapril has been associated with decrease in edv and mass but no change in ejection fraction.
#26 Reduced edv and increased ef have also been observed in small number of patients receiving long term oral therapy with hydralazine and nifedipine for a period of 1 to 2 years.withnifedipine these effects are associated with a reduction in left ventricular mass.Reduced bp with enalapril and quinapril has been associated with decrease in edv and mass but no change in ejection fraction.
#27 The current American College of Cardiology/American Heart Association (ACC/AHA) guidelines say the following about vasodilator therapy:Vasodilator therapy is indicated for long-term therapy in patients with chronic, severe AR and symptoms of LV dysfunction but who are not candidates for surgery.Vasodilator therapy is reasonable for short-term therapy in patients with severe LV dysfunction and heart failure symptoms to improve their hemodynamic profile before proceeding with surgery.Vasodilator therapy is acceptable for long-term therapy in asymptomatic patients with severe AR and LV dilation with normal EF.COntraindicatedLong-term therapy in asymptomatic patients with less than severe AR (mild to mod)and normal EFLong-term therapy in asymptomatic patients with LV dysfunction who are otherwise candidates for surgeryLong-term therapy in symptomatic patients with less than severe LV dysfunction who are candidates for surgery
#28 Although diuretics, nitrates, and digoxin are sometimes used to help control symptoms in patients with AR, not enough data in the clinical literature justify routinely recommending or discouraging these therapies. Also, no data support drug therapy of any class in patients with less than severe AR.[5]Antibiotic prophylaxis prior to dental procedures is no longer routinely recommended for all patients with AR under current ACC/AHA guidelines.[5]However, select patient groups for whom prophylactic antibiotic therapy prior to dental procedures may be reasonable include the following:Patients with prosthetic material in their hearts (such as artificial valves or valves repaired with prosthetic material)Patients with prior infective endocarditis.Patients with the following forms of congenital heart disease (CHD):Cyanotic CHD that is incompletely or not repaired (including patients with palliative shunts and conduits)Repaired CHD using prosthetic material, for the first 6 months post-procedurally (ie, prior to endothelialization of the material)Repaired CHD but at risk of inhibited endothelialization (ie, with residual defects at or adjacent to the site of the prosthetic material)Patients following cardiac transplantation who have valve regurgitation due to a structurally abnormal valve
#29 Surgical treatment of AR usually requires replacement of the diseased valve with a prosthetic valve, although valve-sparing repair is increasingly possible with advances in surgical technique and technology.
#30 Under current ACC/AHA guidelines[5] , aortic valve surgery is recommended for patients with chronic severe AR under the following circumstances:Patient is symptomaticPatient is asymptomatic, with a resting EF of ≤ 55%Patient is asymptomatic, with LV dilation (LV end-systolic dimension >55 mm)Additional circumstances in which aortic valve surgery may be reasonable include the following:Patient has moderate AR and is undergoing coronary artery bypass surgery or other surgery involving the ascending aortaPatient has severe AR with no symptoms, normal EF, and less severe LV dilation (LV end-systolic dimension >50 mm or LV end-diastolic dimension >70 mm) if the patient experiences (1) progressive LV dilation on serial imaging studies; (2) deteriorating exercise tolerance, or (3) abnormal hemodynamic responses to exercise, such as inability to augment blood pressure during a treadmill studyOngoing improvements in surgical technique and technology have enabled many patients with even severe LV dysfunction to undergo surgery (rather than cardiac transplantation).[23]In patients undergoing aortic valve surgery for bicuspid aortic valve disease who also have a dilated or aneurysmal ascending aorta with a diameter of >4.5 cm, concurrent aortic root repair or replacement is indicated.Aortic valve surgery is generally not indicated in asymptomatic patients with normal EF and less LV dilation (LV end-systolic dimension < 50 mm or LV end-diastolic dimension < 70 mm)
#31 For patients undergoing aortic valve replacement, careful consideration should be given to the relative risks and benefits of mechanical versus bioprosthetic valves. Traditionally, mechanical valves have been thought to be more durable but require long-term anticoagulation with warfarin due to increased risk of thrombosis, whereas bioprosthetic valves carry a greater risk of long-term deterioration and risk of reoperation but avoid the need for long-term warfarin.[24] In some cases, a clear choice is apparent (eg, a homografts is often preferred to a mechanical valve in the setting of active infective endocarditis).While further discussion is beyond the scope of this article, the reader is referred to the current ACC/AHA guidelines, which include major criteria for aortic valve selection as well as recommendations for antithrombotic therapy (including aspirin for all prosthetic valve recipients along with long-term anticoagulation with warfarin for selected patients).[5]
#32 Inpatient care is required for most patients with acute severe aortic regurgitation (AR), particularly with symptoms or evidence of hemodynamic decompensation. Patients with chronic severe AR may be followed as inpatients or outpatients, depending on the stage of their disease and severity of their symptoms and LV dysfunction.
#33 Asymptomatic patients with chronic severe AR require ongoing clinical surveillance with periodic echocardiography because in many cases, significant LV dysfunction may arise even before the patient becomes symptomatic.The recommended frequency of clinical evaluation is based on the stability of the left ventricular end-systolic dimensions (ESD) and end-diastolic dimensions (EDD) as listed below. After the initial study, clinical evaluation and repeat echocardiogram are recommended in 3 months. Subsequent follow-up is based on the results of the 2 evaluations.For patients with ESD < 45 mm or EDD < 60 mm and stable dimensions, clinical evaluation is recommended every 6-12 months and repeat echocardiography is recommended every 12 months.For patients with ESD < 45 mm or EDD < 60 mm and increasing dimensions, clinical evaluation and repeat echocardiography are recommended in 3 months.For patients with ESD 45-50 mm or EDD 60-70 mm and stable dimensions, clinical evaluation is recommended every 6 months and repeat echocardiography is recommended every 12 months.For patients with ESD 45-50 mm or EDD 60-70 mm and increasing dimensions, clinical evaluation and repeat echocardiography are recommended in 3 months.For patients with ESD 50-55 mm or EDD 70-75 mm and stable dimensions, clinical evaluation and repeat echocardiography are recommended every 6 months.For patients with ESD 50-55 mm or EDD 70-75 mm and increasing dimensions, clinical evaluation and repeat echocardiography are recommended in 3 months.For patients with ESD >55 mm or EDD >75 mm, surgery is recommended.
#34 Left untreated, acute severe AR is likely to lead to considerable morbidity and mortality from either the underlying cause (typically infective endocarditis or aortic dissection) or from hemodynamic decompensation of the LV.Potential complications in patients with chronic severe AR include progressive LV dysfunction and dilation, congestive heart failure, myocardial ischemia, arrhythmia, and sudden death. Additional complications may arise as a result of the patient's underlying condition (such as aortic root dissection in a patient with a bicuspid aortic valve and a severely dilated aortic root
#35 The prognosis for patients with severe AR depends on the presence or absence of LV dysfunction and symptoms, as follows:[5]In asymptomatic patients with normal EFRate of progression to symptoms or LV dysfunction = < 6% per yearRate of progression to asymptomatic LV dysfunction = < 3.5% per yearRate of sudden death = less than 0.2% per yearIn asymptomatic patients with decreased EF, rate of progression to symptoms = >25% per year.In symptomatic patients, mortality rate = >10% per year.Again, the strongest predictors of outcome are echocardiographic parameters (EF and LV end-systolic dimension), underscoring the crucial role of serial echocardiography in the management of patients with severe AR.

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