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Aortic Stenosis Clinical Presentation

  • Author: Xiushui (Mike) Ren, MD; Chief Editor: Richard A Lange, MD, MBA  more...
 
Updated: Nov 10, 2014
 

History

Aortic stenosis usually has an asymptomatic latent period of 10-20 years. During this time, the LV outflow obstruction and the pressure load on the myocardium gradually increase. Symptoms develop gradually. Exertional dyspnea is the most common initial complaint, even in patients with normal LV systolic function, and it often relates to abnormal LV diastolic function. In addition, patients may develop exertional chest pain, effort dizziness or lightheadedness, easy fatigability, and progressive inability to exercise. Ultimately, patients experience the classic triad of chest pain, heart failure, and syncope.[2]

Chest pain

Angina pectoris in patients with aortic stenosis is typically precipitated by exertion and relieved by rest. Thus, it may resemble angina from coronary artery disease.

Heart failure

Heart failure symptoms (ie, paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion, and shortness of breath) may be due to systolic dysfunction from afterload mismatch, ischemia, or a separate cardiomyopathic process. Alternatively, diastolic dysfunction from LV hypertrophy or ischemia may also result in heart failure symptoms.

Syncope

Syncope from aortic stenosis often occurs upon exertion when systemic vasodilatation in the presence of a fixed forward stroke volume causes the arterial systolic blood pressure to decline. It also may be caused by atrial or ventricular tachyarrhythmias.

Syncope at rest may be due to transient ventricular tachycardia, atrial fibrillation, or (if calcification of the valve extends into the conduction system) atrioventricular block. Another cause of syncope is abnormal vasodepressor reflexes due to increased LV intracavitary pressure (vasodepressor syncope).

Syncope may be accompanied by convulsions.[13]

Patients with aortic stenosis may have a higher incidence of nitroglycerin-induced syncope than does the general population. Always consider aortic stenosis as a possible etiology for a patient who demonstrates particular hemodynamic sensitivity to nitrates.

Other manifestations

Gastrointestinal bleeding due to angiodysplasia (ie, Heyde syndrome[14] ) or other vascular malformations is present at a higher than expected frequency in patients with calcific aortic stenosis. These malformations usually resolve following aortic valve surgery.

Patients may present with manifestations of infective endocarditis (ie, fever, fatigue, anorexia, back pain, and weight loss). The risk of infective endocarditis is higher in younger patients with mild valvular deformity than in older patients with degenerated calcified aortic valves, but it can occur in either population. It can occur in patients of any age with hospital-acquired Staphylococcus aureus bacteremia.

Calcific aortic stenosis rarely may cause emboli of calcium to various organs, including the heart, kidney, and brain.

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Physical Examination

In severe aortic stenosis, the carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude, and gradual downslope (pulsus parvus et tardus). However, in elderly individuals with rigid carotid vessels, this sign may not be present. A lag time may be present between the apical impulse and the carotid impulse.

Systolic hypertension can coexist with aortic stenosis. However, a systolic blood pressure higher than 200 mm Hg is rare in patients with critical aortic stenosis.

Pulsus alternans can occur in the presence of LV systolic dysfunction. The jugular venous pulse may show prominent a waves reflecting reduced right ventricular compliance consequent to hypertrophy of the interventricular septum.

A hyperdynamic LV is unusual and suggests concomitant aortic regurgitation or mitral regurgitation.

S1 is usually normal or soft. The aortic component of the second heart sound, A2, is usually diminished or absent, because the aortic valve is calcified and immobile and/or the aortic ejection is prolonged and it is obscured by the prolonged systolic ejection murmur. The presence of a normal or accentuated A2 speaks against the presence of severe aortic stenosis.

Paradoxical splitting of the S2 also occurs, resulting from late closure of A2. P2 may also be accentuated in the presence of secondary pulmonary hypertension.

An ejection click is common in children and young adults with congenital aortic stenosis, but it is rare in elderly individuals with acquired calcific aortic stenosis, in whom the cusps become immobile and severely calcified. This sound occurs approximately 40-60 milliseconds after the onset of S1 and is frequently heard best along the mid to lower left sternal border; it is often well transmitted to the apex and may be confused with a split S1.

A prominent S4 can be present and is due to forceful atrial contraction into a hypertrophied left ventricle. The presence of an S4 in a young patient with aortic stenosis indicates significant aortic stenosis, but with aortic stenosis in an elderly person, this is not necessarily true.

Systolic murmur

The classic crescendo-decrescendo systolic murmur of aortic stenosis begins shortly after the first heart sound. The intensity increases toward midsystole, then decreases, and the murmur ends just before the second heart sound. It is generally a rough, low-pitched sound that is best heard at the second intercostal space in the right upper sternal border. It is harsh at the base and radiates to 1 or both carotid arteries.

In elderly persons with calcific aortic stenosis, however, the murmur may be more prominent at the apex, because of radiation of its high-frequency components (Gallavardin phenomenon). This may lead to its misinterpretation as a murmur of mitral regurgitation. Accentuation of the aortic stenosis murmur following a long R-R interval (as in atrial fibrillation or following a premature beat) distinguishes it from the mitral regurgitation murmur, which usually does not change.

The intensity of the systolic murmur does not correspond to the severity of aortic stenosis; rather, the timing of the peak and the duration of the murmur corresponds to the severity of aortic stenosis. The more severe the stenosis, the longer the duration of the murmur and the more likely it peaks at late systole.

The murmur of valvular aortic stenosis is augmented upon squatting or following a premature beat; the murmur intensity is reduced during Valsalva strain. This is contrary to what occurs with hypertrophic obstructive cardiomyopathy, in which a Valsalva maneuver increases the intensity of the murmur.

When the left ventricle fails and cardiac output falls, the aortic stenosis murmur becomes softer and may be barely audible. Atrial fibrillation with short R-R intervals can also decrease the murmur intensity or make it inaudible.

Other findings

A high-pitched, diastolic blowing murmur may be present if the patient has associated aortic regurgitation.

Rarely, right ventricular failure with systemic venous congestion, hepatomegaly, and edema precede LV failure. This is probably due to the bulging of the interventricular septum into the right ventricle, with impedance in filling, elevated jugular venous pressure, and a prominent a wave (Bernheim effect).

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Contributor Information and Disclosures
Author

Xiushui (Mike) Ren, MD Cardiologist, The Permanente Medical Group; Associate Director of Research, Cardiovascular Diseases Fellowship, California Pacific Medical Center

Xiushui (Mike) Ren, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Society of Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Acknowledgements

Jerry Balentine, DO Professor of Emergency Medicine, New York College of Osteopathic Medicine; Executive Vice President, Chief Medical Officer, Attending Physician in Department of Emergency Medicine, St Barnabas Hospital

Jerry Balentine, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American College of Physician Executives, American Osteopathic Association, and New York Academy of Medicine

Disclosure: Nothing to disclose.

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Daniel P Lombardi, DO Clinical Assistant Professor, New York College of Osteopathic Medicine; Attending Physician, Associate Department Director and Program Director, Department of Emergency Medicine, St Barnabas Hospital

Daniel P Lombardi, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

John A McPherson, MD, FACC, FAHA, FSCAI Associate Professor of Medicine, Division of Cardiovascular Medicine, Director of Cardiovascular Intensive Care Unit, Vanderbilt Heart and Vascular Institute

John A McPherson, MD, FACC, FAHA, FSCAI is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Society for Cardiac Angiography and Interventions, Society of Critical Care Medicine, and Tennessee Medical Association

Disclosure: Abbott Vascular Corp. Consulting fee Consulting

Bekir H Melek, MD, FACC Assistant Professor of Clinical Medicine, Department of Medicine, Section of Cardiology, Tulane University School of Medicine

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

James V Talano, MD, MM, FACC Director of Cardiovascular Medicine, SWICFT Institute

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Stenotic aortic valve (macroscopic appearance).
Table 1. Common Causes of Aortic Stenosis Among Patients Requiring Surgery
Age < 70 years (n=324) Age >70 years (n=322)
Bicuspid AV (50%)



Postinflammatory (25%)



Degenerative (18%)



Unicommissural (3%)



Hypoplastic (2%)



Indeterminate (2%)



 



Degenerative (48%)



Bicuspid (27%)



Postinflammatory (23%)



Hypoplastic (2%)



Table 2. ACC/AHA Recommendations for Echocardiography (Imaging, Spectral, and Color Doppler) in Aortic Stenosis
Indication Class
Diagnosis and assessment of severity of aortic stenosis I
Assessment of LV size, function, and/or hemodynamics I
Reevaluation of patients with known aortic stenosis with changing symptoms or signs I
Assessment of changes in hemodynamic severity and ventricular function in patients with known aortic stenosis during pregnancy I
Reevaluation of asymptomatic patients with severe aortic stenosis I
Reevaluation of asymptomatic patients with mild to moderate aortic stenosis and evidence of LV dysfunction or hypertrophy IIa
Routine reevaluation of asymptomatic adult patients with mild aortic stenosis who have stable physical signs and normal LV size and function III
Table 3. Criteria for Determining Severity of Aortic Stenosis
Severity Mean gradient (mm Hg) Aortic valve area (cm2)
Mild < 25 >1.5
Moderate 25-40 1-1.5
Severe >40 < 1



(or < 0.5 cm2/m2 body surface area)



Critical >80 < 0.5
Table 4. Recommendations for Cardiac Catheterization in Aortic Stenosis
Indication Class
Coronary angiography before aortic valve replacement in patients at risk for coronary artery disease I
Assessment of severity of aortic stenosis in symptomatic patients when aortic valve replacement is planned or when noninvasive tests are inconclusive or a discrepancy exists in the clinical findings regarding the severity of aortic stenosis or the need for surgery I
Coronary angiography before aortic valve replacement in patients for whom a pulmonary autograft (Ross procedure) is contemplated and the origin of the coronary arteries was not identified by noninvasive tests I
With infusion of dobutamine, can be useful for evaluation of patients with low-flow/low-gradient aortic stenosis and LV dysfunction IIa
Not recommended for hemodynamic measurements for assessment of aortic stenosis severity when noninvasive techniques are adequate and concord with clinical findings III
Not recommended for hemodynamic measurements for assessment of LV function and aortic stenosis severity in asymptomatic patients III
Table 5. Recommendations for Aortic Valve Replacement in Aortic Stenosis
Indication Class
Symptomatic patients with severe aortic stenosis I
Patients with severe aortic stenosis undergoing coronary artery bypass surgery I
Patients with severe aortic stenosis undergoing surgery on the aorta or other heart valves I
Patients with severe aortic stenosis and LV systolic dysfunction (ejection fraction < 0.50) I
Patients with moderate aortic stenosis undergoing coronary artery bypass surgery or surgery on the aorta or other heart valves IIa
Patients with mild aortic stenosis undergoing coronary artery bypass surgery when there is evidence that progression may be rapid, such as moderate-to-severe valve calcification IIb
Asymptomatic patients with severe aortic stenosis and abnormal response to exercise (eg, hypotension) IIb
Asymptomatic patients with severe aortic stenosis and a high likelihood of rapid progression (based on age, calcification, and coronary artery disease) or if surgery might be delayed at the time of symptom onset IIb
Asymptomatic patients with extremely severe aortic stenosis (valve area less than 0.6 cm2, mean gradient greater than 60 mm Hg, and jet velocity greater than 5 m per second) if the patient’s expected operative mortality is 1% or less IIb
AVR is not useful for prevention of sudden death in asymptomatic patients with none of the findings listed under asymptomatic patients with severe aortic stenosis III
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