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  • Valvular Heart Disease II: The Aortic Valve Laura Wexler, M.D.Case: An active 75 year old farmer comes to your office after experiencing a faintingspell while bailing hay. The episode occurred without warning and he had no symptomsfollowing the episode. However, on close questioning he admits to some breathlessnessand vague chest heaviness with his usual heavy exertion over the past few months. Hehas been healthy all his life, doesn’t smoke and has not seen a doctor in 30 years. Heserved in the army in 1942; no abnormalities were reported during his induction physical. On exam he is a robust looking older man. Blood pressure is 135/90, pulse68/min and regular, respiratory rate 12, and temperature 98.6°F. JVP is 6 cm withnormal “a” and “v” waves. Carotids are difficult to palpate, and there is a delayedupstroke. Lungs are clear. Heart palpation reveals a palpable “thrill” over the mid LSB.PMI is in the 5th ICS, 2 cm lateral to the MCL. There is a palpable presystolic impulsefollowed by a sustained ventricular lift. On auscultation, there is loud S4. S1 is normal. Asingle S2 (P2) is heard at the upper left sternal border but no A2 is heard at the lower leftsternal border. There is a 4/6 systolic ejection murmur (crescendo-decrescendo) heardbest at the R 2nd interspace but radiating widely to the LSB, and to the neck. No diastolicmurmurs are heard. Abdomen and extremities are unremarkable.A. Aortic Stenosis 1. Etiology of aortic stenosis a. Congenital bicuspid aortic valve b. Rheumatic aortic valve disease c. Calcific (senile) aortic stenosis 2. Pathophysiology of aortic stenosis a. Left ventricular outflow obstruction i. Left ventricular systolic pressure > aortic pressure b. Concentric left ventricular hypertrophy i. Enables LV to generate the systolic pressures required to eject through the narrowed aortic valve. ii. Normalizes wall stress (radius x pressure/wall thickness) iii. Eventually results in impaired LV diastolic compliance c. LA hypertrophy and enlargement d. Severe stenosis : Impaired ability to increase stroke volume on demand e. Critical aortic stenosis – fixed cardiac output…LV is unable to increase stroke volume on demand. 3. Key physical findings of severe aortic stenosis a. Carotid impulse “parvus et tardus” (low volume and delayed upstroke). b. JVP : Prominent “a” wave (atrium contracting into stiff, hypertrophied LV). c. Heart
  • Valvular Heart Disease II: The aortic valvePage 2 i.Systolic thrill ii.Palpable presystolic impulse (S4) iii.Sustained apical systolic impulse iv. Loud S4 v. Harsh, late peaking systolic ejection murmur (may radiate to neck and/or LSB) vi. Attenuated/absent aortic component of S2 (aortic leaflets become thickened and immobilized) 4. Natural history of aortic stenosis a. Long asymptomatic “latent” period b. “Cardinal” symptoms of severe/critical aortic stenosis i. dyspnea ii. angina iii. syncope c. Sudden death d. Progressive LV hypertrophy followed by transition to LV failure with dilation and depressed ejection fraction. e. Endocarditis f. Arrhythmias i. ventricular tachycardia ii. conduction system disease (progressive calcification of aortic ring iii. atrial fibrillation 5. Mechanisms of dyspnea in aortic stenosis a. LVH → diastolic dysfunction b. Progressive LV dilatation and contractile failure → systolic dysfunction. 6. Mechanisms of anginal chest pain in aortic stenosis a. Increased wall stress → increased myocardial O2 demand, exceeds ability of coronary flow to meet demand. b. Associated coronary artery disease. 7. Mechanisms of syncope in aortic stenosis. a. With vasodilation (exercise, vagal stimulation, drug induced), LV is unable to augment stroke volume… results in drop in cerebral perfusion pressure. b. Heart block bradycardia: Ca++ deposits in aortic ring encroach upon conduction tissue. c. Ventricular arrhythmias (LVH, ischemia). 8. Diagnostic studies in aortic stenosis: a. ECG – LVH with repolarization changes “strain pattern” b. Chest X-ray – aortic root dilatation (aortic valve Ca++) c. Echo – aortic valve thickening and restricted motion
  • Valvular Heart Disease II: The aortic valvePage 3 d. Doppler – gradient across aortic valve and aortic valve area can be estimated from increased flow velocity across aortic valve e. Cath – measure gradient across aortic valve and calculate valve area. 9. Treatment of aortic stenosis a. Mild to moderate asymptomatic aortic stenosis. i. Close follow-up – periodic history and physical exam, serial echocardiograms. ii. Endocarditis prophylaxis. b. Severe, symptomatic aortic stenosis (1 year survival 57%) i. Aortic valve replacement with either mechanical or bioprosthetic valve 1. Ten year survival ~ 75% 2. Complications of prosthetic heart valves: infection, thromboembolism, mechanical failure c. Severe, symptomatic aortic stenosis NOT surgically treatable: palliative option: aortic balloon valvuloplasty CASE: A 52 year old salesman is referred to you for evaluation of a heart murmur. He had applied for a pilot’s license and was denied because of the murmur. He is asymptomatic and physically active. He denies chest pain, dyspnea or dizzy spells and gives no history of a murmur being mentioned during his last physical exam five years ago. He has no family history of heart disease. He has never had high blood pressure, abnormal lipids, or diabetes, doesn’t smoke, and takes no medications. On physical exam his blood pressure is 145/45, pulse 78 and regular, respiratory rate 12 and temperature 98.6°F. Carotids – very brisk and full with sharp collapse. JVP 5 cm with normal ‘a’ and ‘v’ waves. Lungs are clear. Heart palpation – PMI is enlarged (4fb), displaced to the anterior axillary line. On auscultation S1 is normal, S2 soft. A 2/6 early peaking systolic ejection murmur at the RUSB, and a 3/6 holodiastolic blowing murmur, heard best at the lower LSB when you ask the patient to hold his breath in expiration and lean forward. There is a different 2/6 low-pitched diastolic murmur at the apex. Pulses are all very prominent and brisk; audible pulse over the femoral arteries. Diagnostic studies: ECG: LVH with massive voltage in the lateral precordial leads (V4-V6) Chest X-ray: Large heart, predominant left ventricular enlargement. No congestive heart failure. Echo: Marked left ventricular dilation, estimated EF 65%. The end diastolic dimension is 65 mm and the end diastolic dimension is 55 mm. Aortic valve: bicuspid and thickened. Doppler: Severe aortic regurgitation. The aorta is slightly enlarged (4.2 mm) View slide
  • Valvular Heart Disease II: The aortic valvePage 4 B. Aortic Regurgitation 1. Major causes of aortic regurgitation a. Leaflet dysfunction i. Rheumatic fever ii. Endocarditis iii. Trauma iv. Bicuspid aortic valve v. Rheumatoid arthritis vi. Myxomatous degeneration vii. Ankylosing spondylitis viii. Marfan’s syndrome ix. Fenfluramine-phentermine x. Annulo-aortic ectasia b. Aortic root dilatation i. Systemic hypertension ii. Dissecting aneurysm iii. Aortitis (syphilis) iv. Reiter’s syndrome v. Ankylosing spondylitis vi. Ehlers-Danlos vii. Osteogenesis imperfecta viii. Pseudoxanthoma elasticum ix. Marfan’s syndrome 2. Physical findings in aortic regurgitation a. Wide pulse pressure b. Bounding pulses c. Soft aortic second sound (A2) d. Early diastolic murmur (blowing) immediately after A2 i. Upper RSB with root dilatation ii. Mid to lower LSB with leaflet dysfunction e. Early peaking systolic murmur at base (similar to mild aortic stenosis… caused by abnormally high volume (normal diastolic filling plus regurgitant volume) ejected across the aortic valve. f. Austin Flint murmur: mid to late diastolic “rumble” at apex (regurgitant jet flowing across aortic valve in diastole pushes anterior mitral leaflet partially closed…thus restricting path of incoming blood from the LA to LV. 3. Some really neat physical findings in severe chronic aortic regurgitation: a. deMusset’s sign – head bob with each systolic pulsation b. Corrigan’s pulses – “pistol shot” pulses over femoral artery c. Mueller’s sign – pulsation of the uvula d. Duroziez’s sign – systolic/diastolic bruit over femoral artery e. Quincke’s pulses – capillary pulsations seen in the nailbeds f. Becker’s sign – pulsation of retinal arteries and pupils View slide
  • Valvular Heart Disease II: The aortic valvePage 5 g. Hill’s sign – popliteal blood pressure exceed brachial blood pressure by > 60 mmHg 4. Pathophysiology of chronic aortic regurgitation. a. Slowly progressive diastolic volume overload. b. Augmented stroke volume with rapid runoff. i. Increased systolic pressure with low diastolic pressure: wide pulse pressure. c. Progressive left ventricular dilation, some hypertrophy. Initial supernormal ejection fraction as LV is able to handle increased stroke volume. d. Initially increased diastolic compliance with maintenance of normal diastolic pressures in face of increased LV diastolic volume. e. Late systolic failure with reduced ejection fraction and CHF. 5. Pathophysiology of acute aortic regurgitation (e.g., damage from endocarditis, blunt chest trauma). a. Sudden diastolic volume overload without LV dilation. i. Acute elevation in left ventricular diastolic pressure → pulmonary edema. ii. Acute LV systolic failure → hypotension. b. Provide inotropic support, vasodilator therapy if tolerated, urgent valve replacement. 6. Natural history of chronic aortic regurgitation. a. Long asymptomatic phase; may be decades long b. Left ventricular systolic dysfunction (decline in ejection fraction) i. NOTE: Initially, LV dysfunction may occur in the absence of symptoms. c. Symptoms associated with LV dysfunction: i. Exercise intolerance. ii. Dyspnea on exertion. d. Angina (rare) e. Sudden death (rare) 7. Factors influencing severity of aortic regurgitation. a. Size of regurgitant orifice. b. Gradient across aortic valve in diastole (i.e. worse AR with high aortic diastolic pressure). c. Duration of diastole (the slower the HR, the longer the diastolic period and the greater the volume of regurgitant blood).
  • Valvular Heart Disease II: The aortic valvePage 6 8. Management of chronic aortic regurgitation. a. Close follow-up of left ventricular size and function with serial echocardiograms (every few years with mild AR, every 6-12 months with severe AR). b. Endocarditis prophylaxis. c. Medical therapy. i. Vasodilator therapy – reduces diastolic blood pressure → reduced regurgitant volume. Delays need for aortic valve replacement. ii. Digoxin (enhance systolic function). iii. Diuretics (reduce LA pressure). d. Aortic valve replacement with mechanical or bioprosthetic valve. 9. Criteria for aortic valve replacement in chronic aortic regurgitation a. Symptoms i. Congestive heart failure ii. Declining exercise tolerance on exercise testing iii. Angina b. Anatomy, regardless of symptoms i. Left ventricular dysfunction: EF <50% ii. Progressive left ventricular dilation or decline in ejection fraction on serial studies iii. Severe dilation (echo) 1. Left ventricular diastolic dimension > 75 mm 2. Left ventricular systolic dimension > 55 mm iv. Aortic root dimension > 50 mm 10. Right sided valve disease (Harrison, 14th Edition: Pages 1322-1323) a. Tricuspid stenosis b. Tricuspid regurgitation c. Pulmonic stenosis d. Pulmonic regurgitation 11. References for valvular heart disease a. Reading i. Harrison, 14th Edition, p 1311-1323 b. Computer i. Umedic: aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation ii. Instructional programs 1. Heart Sounds and Murmurs
  • Valvular Heart Disease II: The aortic valvePage 7