Aortic Stenosis Clinical Presentation

Updated: Mar 23, 2017
  • Author: Xiushui (Mike) Ren, MD; Chief Editor: Terrence X O'Brien, MD, MS, FACC  more...
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Presentation

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 one of the classic triad of chest pain, heart failure, and syncope. [1]

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.

Results from the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study revealed that in patients with aortic stenosis without diabetes or known renal or cardiovascular disease, persistent or new-onset asymmetric interventricular septum hypertrophy was associated with a higher incidence of ischemic cardiovascular events than in those without asymmetric interventricular septum hypertrophy. [13]

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. [14]

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 [15] ) 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.

Patientts with bicuspid valve have an increased incidence of aortic root dilatation (25-40% of patients) and aortic dissection.

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 the aortic valve with delayed 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 and mobile valve leaflets, 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 venous "a" wave (Bernheim effect).

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