Valvular Heart Disease II:The Aortic Valve

Laura Wexler, M.D.

475-6383

wexlerl@ucmail.uc.edu

Reference Sources for Valvular Heart Disease

Reading: Harrison, 14th Edition p 1311-1323

Computer:

Umedic: Aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation

Instructional Programs:

Heart Sounds and Murmurs

Case:An active 75 yo farmer comes to your office after experiencing a fainting spell while baling hay. The episode occurred without warning and he had no symptoms following the episode. However, on close questioning he admits to some breathlessness and vague chest heaviness with his usual heavy exertion over the past few months. He has been healthy all his life, doesn’t smoke and has not seen a doctor in 30 years. He served in the army in 1942; no abnormalities were reported during his induction physical.

Physical ExamRobust looking older man.

BP 135/90 P 68 bpm, regular RR-12 T-98.6 F

JVP 6 cm with normal “a” and “v” waves

Carotids: Difficult to palpate, delayed upstroke

Lungs: Clear

Heart: Palpation: Palpable “thrill” over the mid LSB. PMI 5 ICS, 2 cm lateral to the MCL. Palpable presystolic impulse followed by a sustained ventricular lift.

Auscultation: Loud S4. S1 is normal. A single S2 (P2) is heard at the upper left sternal border but no A2 is heard at the lower left sternal border. There is a 4/6 systolic ejection murmur (crescendo-decrescendo) heard best at the R 2nd interspace that radiates widely to the LSB, and to the neck. No diastolic murmurs.

Abdomen and extremities are unremarkable.

Aortic Stenosis

Aortic Stenosis: Etiology

Congenital bicuspid aortic valve

Rheumatic aortic valve disease

Calcific (senile) aortic stenosis

Norma Burns:Norma Burns:

Pathophysiology of Aortic Stenosis Left ventricular outflow obstruction

LV systolic pressure > aortic pressure

Concentric left ventricular hypertrophySustains high LV pressuresNormalizes wall stress (radius x pressure/wall thickness)Eventually results in impaired LV diastolic compliance

LA hypertrophy and enlargement Severe stenosis: Limits ability to increase stroke

volume on demand

Critical aortic stenosis = fixed cardiac output

Key Physical Findings in SevereAortic Stenosis

Carotid impulse: “parvus et tardus”

JVP: Prominent “a” wave

Heart: Systolic thrill Palpable presystolic impulse (S4)Sustained apical systolic impulseS4

Coarse late peaking systolic ejection murmur (may radiate to neck and/or LSB)

Attenuated/absent aortic component of S2

Natural History of Aortic Stenosis Long asymptomatic “latent” period “Cardinal” symptoms of severe aortic stenosis

DyspneaAnginaSyncope

Sudden death Left ventricular dilatation and contractile failure Endocarditis Arrhythmias

Ventricular tachycardiaConduction system diseaseAtrial fibrillation

Natural History of AS

Mechanisms of Dyspnea inAortic Stenosis

LVH diastolic dysfunction

Progressive LV dilation and contractile failure systolic dysfunction

Mechanisms of Anginal Chest Pain in

Aortic Stenosis Increased wall stress increased

myocardial O2 demand, exceeds ability to coronary flow to meet demand

Associated coronary artery disease

Mechanisms of Syncope in Aortic Stenosis

Fixed cardiac output: Vasodilation (exercise, vagal stimulation, drug induced), inability to augment CO, drop in cerebral perfusion pressure.

Heart block: Ca++ deposits in aortic ring encroach upon conduction tissue

Ventricular arrhythmias (LVH, ischemia)

Diagnostic Studies in Aortic Stenosis ECG: LVH with repolarization changes “strain

pattern” Chest X-Ray: Aortic root dilation

(aortic valve Ca++) Echo: Aortic valve thickening and restricted

motion Doppler: Gradient across aortic valve and aortic

valve area can be estimated from increased flow velocity across aortic valve

Cath: Measure gradient across aortic valve and calculate valve area

Aortic Stenosis

Treatment of Aortic Stenosis Mild to moderate asymptomatic aortic stenosis:

Close follow up: History and physical exam, serial echocardiograms

Endocarditis prophylaxis

Severe, symptomatic aortic stenosis (1 year survival 57%)Aortic valve replacement with either mechanical or bioprosthetic valve

- Ten year survival ~75%- Complications of prosthetic heart valves: infection, thromboembolism, mechanical

failure

Severe, symptomatic aortic stenosis NOT surgically treatable: Palliative option: aortic balloon valvuloplasty

CASE:

A 52 yo 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 or diabetes, doesn’t smoke, and takes no medications. A lipid profile done five years ago was reported to be “OK”.

Physical ExamBP - 145/45 P - 78 reg RR - 12 Temp:98.6F

Carotids: Very brisk with sharp collapse

JVP: 5 with normal ‘a’ and ‘v’ waves

Lungs: Clear

Heart: Palpation: PMI is enlarged (4fb), in the anterior axillary line

Auscultation: S1 normal, S2 soft. A 2/6 early peaking systolic ejection murmur at the upper RSB 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 overthe femoral arteries

Additional Testing

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). *

Major Causes of Aortic Regurgitation

Leaflet Dysfunction Aortic Root Dilation

Rheumatic fever Systemic hypertensionEndocarditis Dissecting aneurysmTrauma Aortitis (syphilis)Bicuspid aortic valve Reiter’s syndromeRheumatoid arthritis Ankylosing spondylitisMyxomatous degeneration Ehlers-DanlosAnkylosing spondylitis Osteogenesis imperfectaMarfan’s syndrome Pseudoxanthoma elasticumFenfluramine-phentermine Marfan’s syndromeAnnulo-aortic ectasia

Aortic regurgitation

Physical Findings in Aortic Regurgitation Wide pulse pressure: Bounding pulses Soft aortic second sound (A2) Early diastolic murmur (blowing) immediately

after A2

Upper RSB with root dilationMid to lower LSB with leaflet dysfunction

Systolic murmur at base (similar to aortic stenosis) Austin Flint murmur: mid to late diastolic

“rumble” at apex

*

Some Really Neat Physical Findings in Severe Chronic Aortic Regurgitation deMusset’s sign: Head bob with each systolic pulsation

Corrigans’s pulses: “Pistol shot” pulses over femoral artery

Mueller’s sign: Pulsation of the uvula

Duroziez’s sign: Systolic/diastolic bruit over femoral artery

Quincke’s pulses: Capillary pulsations seen in the nailbeds

Becker’s sign: Pulsation of retinal arteries and pupils

Hill’s sign: Popliteal BP exceeds brachial BP by > 60 mmHg

Acute vs. chronic aortic regurgitation

Pathophysiology of Chronic Aortic Regurgitation

Slowly progressive diastolic volume overload

Augmented stroke volume with rapid runoffIncreased systolic pressure with low diastolic pressure: wide pulse pressure

Progressive left ventricular dilation, some hypertrophy

Increased diastolic compliance with maintenance of normal diastolic pressures initially

Late systolic failure with reduced ejection fraction and CHF

Acute Aortic Regurgitation

Sudden diastolic volume overload without LV dilation:

- Acute elevation in left ventricular diastolic pressure pulmonary edema- Acute LV systolic failure hypotension

Provide inotropic support, vasodilator therapy if tolerated, urgent valve replacement.

Natural History of Chronic Aortic Regurgitation

Long asymptomatic phase; may be decades long. Left ventricular systolic dysfunction ( decline in

EF) NOTE!! LV dysfunction may occur in the absence of symptoms

Symptoms associated with LV dysfunction:- Exercise intolerance

- Dyspnea on exertion Angina (rare) Sudden death (rare)

Natural history of aortic regurgitation

Factors Influencing Severity ofAortic Regurgitation

Size of regurgitant orifice

Gradient across aortic valve in diastole (i.e. worse AR with high diastolic BP)

Duration of diastole

Management of Chronic Aortic Regurgitation

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)

Endocarditis prophylaxis Medical therapy:

Vasodilator therapy: reduces blood pressurereduces regurgitant volume

Delays need for aortic valve replacement Digoxin (enhance systolic function) Diuretics (reduce LA pressure) Do NOT slow heart rate! Aortic valve replacement with mechanical or bioprosthetic

valve

Criteria for Aortic Valve Replacement in Chronic Aortic Regurgitation

SymptomsCongestive heart failureDeclining exercise tolerance on exercise testingAngina

Anatomy, regardless of symptoms:Left ventricular dysfunction: EF <50%Progressive left ventricular dilation or decline in EF on serial studiesSevere dilation (echo): - Left ventricular diastolic dimension >75 mm

- Left ventricular systolic dimension >55 mmAortic root dimension >50 mm

Right Sided Valve Disease:Read Harrison, 14th Edition: Pages 1322-1323

Tricuspid stenosis

Tricuspid regurgitation

Pulmonic stenosis

Pulmonic regurgitation