Approach

AR is usually detected on clinical exam with a diastolic murmur, or incidentally during echocardiogram evaluation for other causes. ECG, chest x-ray, and echocardiogram are routinely performed for all patients with features of AR.

Acute AR: clinical presentation

The patient can present with sudden onset of pulmonary edema and hypotension or in cardiogenic shock. Patients may also present with signs and symptoms of myocardial ischemia or aortic root dissection.[1] When valvular regurgitation is acute, many of the characteristic findings of chronic AR are absent and the severity of the problem may be underestimated. For example, during the physical exam, no increase in left ventricular (LV) size may be detected and the diastolic murmur may be short and/or soft due to diastolic pressure equilibrium between aorta and ventricle occurring before the end of diastole. Pulse pressure may not be increased due to reduced systolic pressure.[2]

Signs and symptoms of pulmonary edema

  • Dyspnea

  • Pink frothy sputum

  • Pale and sweaty

  • Basal lung crepitations

  • Wheeze (cardiac asthma).

Signs and symptoms of cardiogenic shock

  • Pale and/or cyanotic, cool to touch with mottled extremities

  • Evidence of hypoperfusion with altered mental status and decreased urine output

  • Rapid and faint peripheral pulses

  • Jugular venous distension

  • Third and fourth heart sounds may be present

  • Arrhythmias

  • Dyspnea.

Myocardial ischemia, due to decreased perfusion pressure in acute severe AR, classically presents with central crushing chest pain radiating to the jaw or left arm. Aortic root dissection classically presents with chest pain radiating to the back.

Acute AR: investigation and imaging

ECG

  • Determines any arrhythmias and the rate of tachycardia. It will also rule out or diagnose myocardial ischemia or infarction.

Chest x-ray

  • May not show cardiomegaly, which is a characteristic finding for chronic AR. There may be evidence of pulmonary edema with bilateral basal shadowing, pleural effusions at costophrenic angles, and fluid in the lung fissures.

Transthoracic echocardiogram

  • One of the best noninvasive diagnostic tests to evaluate the valvular diseases.[16]

  • Confirms the presence and severity of the valvular regurgitation, assesses LV size (which is usually normal) and systolic function, and determines a cause.

Transoesophageal echocardiogram

  • Performed if aortic root dissection is suspected: classically, patients have chest pain that radiates to the back.[1]

Chronic AR: clinical symptoms

Patients have a protracted course and remain asymptomatic for decades. LV systolic dysfunction often precedes the development of symptoms. Patients may remain asymptomatic with normal exercise tolerance even with chronic severe AR due to LV compensation.

Initial symptoms may include uncomfortable awareness of the pounding heart when lying on the left side, due to closer contact of the enlarged LV with the chest wall.[10] Palpitations occur frequently, secondary to premature ventricular contractions. These symptoms may persist for years before exercise intolerance occurs. With progressive systolic dysfunction, patients will complain of typical symptoms of congestive heart failure including fatigue, weakness, orthopnea, and paroxysmal nocturnal dyspnea.[17]

Uncommonly, patients may complain of angina without coronary artery disease (CAD) at rest or with exercise. Myocardial ischemia can result in interstitial fibrosis, which further deteriorates LV systolic function. Syncope and sudden cardiac death are rare.

Chronic AR: clinical signs

Pulse

  • Arterial pulse shows rapid rise and a quick collapse (Corrigan pulse or water hammer pulse) resulting in widened pulse pressure >50 mmHg.

  • There are multiple eponymous peripheral hemodynamic signs associated with a bounding pulse and systolic hypertension of chronic severe AR. The sensitivity and specificity of these signs in diagnosing AR is low and should be used only as supportive evidence.[18]

Apical impulse

  • Diffuse, hyperdynamic,and shifted inferiorly and leftward.

  • A systolic thrill may be palpable over the base of the heart or suprasternal notch due to increased stroke volume.

Murmurs

  • The murmur of AR is a high-pitched early diastolic, decrescendo blowing sound, which is heard best with the diaphragm of the stethoscope just after A2.[19] The murmur is usually soft and can be accentuated with the patient sitting up, leaning forward, and holding his or her breath at the end of expiration.

  • The murmur due to valvular cause is best heard at the third and fourth intercostal space at the left sternal border. Regurgitation due to aortic dilation resulting from dissection or aneurysm is best heard at the second to third right intercostal space. Maneuvers that increase arterial pressure, such as squatting, accentuate the murmur, while inhalation of amyl nitrate or Valsalva, which lower arterial pressure, decreases the intensity of the murmur.

  • Moderate to severe AR is sometimes associated with an ejection systolic flow murmur after S1 due to the flow of increased stroke volume across a nonstenotic aortic valve. The murmur is an early peaking, crescendo-decrescendo systolic sound, best heard at the second right intercostal space, and can be differentiated from an aortic stenosis murmur by the absence of an ejection click.

    Aortic regurgitation (severe)
    Aortic regurgitation (severe)

    Auscultation sounds: Aortic regurgitation (severe)

  • Another murmur that is often associated with severe AR is the Austin Flint murmur. It is a soft, rumbling, mid to late diastolic murmur heard best at the apex. It is produced by the abutment of an aortic regurgitant jet against the LV endocardium.[20] An Austin Flint murmur is distinguished from the murmur of mitral stenosis by the absence of an opening snap and loud S1.

Heart sounds

  • Chronic AR is also associated with changes in heart sounds. S1 may be due to early coaptation of the mitral valve leaflets from increased end-diastolic pressure. With increasing severity of AR, end-diastolic pressure can rise steeply above left atrial pressure causing even diastolic closure of the mitral valve.

  • LV dysfunction can result in S3 gallop or occasionally S4 due to LV hypertrophy. Inadequate closure of the aortic valve in severe AR may cause a soft A2 or even absent A2.

    Third heart sound gallop
    Third heart sound gallop

    Auscultation sounds: Third heart sound gallop

    Fourth heart sound gallop
    Fourth heart sound gallop

    Auscultation sounds: Fourth heart sound gallop

    ​​

Chronic AR: imaging and investigations

Physical signs are not specific enough to judge the severity of the AR. Echocardiography should be performed for evaluation of symptomatic and asymptomatic chronic AR. If the echocardiogram is of insufficient quality, radionuclide angiography or magnetic resonance imaging (MRI) can be ordered to evaluate the valvular abnormality.

ECG

  • Normal early in the disease but shows left axis deviation in chronic AR supporting LV volume overload. May also show signs of conduction abnormalities.[1]

Chest x-ray

  • Cardiomegaly is a characteristic finding in chronic AR.

Echocardiogram

  • For asymptomatic patients with chronic AR, the diagnosis can be established using a good-quality echocardiogram, and no further diagnostic testing is required.[1] This test allows visualization of the origin of the regurgitant jet and its width, and detection of the cause of aortic valve pathology. A transthoracic echocardiogram is usually adequate, but a transesophageal echocardiogram can be used if the quality of the transthoracic echocardiogram is inadequate.[1][21]​​

  • Two-dimensional echocardiography helps in evaluating the valvular anatomy and the impact of volume overload on the ventricular size and function. M-mode imaging indirectly assesses the AR by detecting premature closure of the mitral valve and diastolic fluttering of the anterior mitral leaflet from the regurgitant aortic jet.

  • Doppler echocardiography is the most specific technique used for detecting the severity of regurgitation. Several indices are used to assess severity. Color flow Doppler provides visualization of the origin of the regurgitant jet and its width. There are several pulsed and continuous wave Doppler methods that give clues to the severity of AR. These include color flow, pulsed wave, and continuous wave Doppler.

Exercise testing

  • In chronic severe AR, if the patient's physical activity is minimal or symptoms are equivocal, exercise testing is helpful to assess the functional status and symptomatic response.[1]

Cardiac catheterization, angiography, or MRI

  • In asymptomatic patients with chronic AR, if the quality of the echocardiogram is inadequate to assess LV function, radionuclide angiography or MRI can be used.[1][22]

  • In cases of acute AR, right and left heart catheterization shows severe elevations of LV end-diastolic pressure and pulmonary capillary wedge pressure (PCWP) due to sudden volume overloading of normal-sized LV. LV end-diastolic pressure is often much higher than PCWP because of early closure of the mitral valve.

  • Angiography is also used to evaluate coronary anatomy in patients with high risk for CAD and who will be undergoing aortic valve replacement/repair. In this setting, men aged >35 years, premenopausal women aged >35 years with risk factors for CAD, and postmenopausal women should undergo coronary angiography.

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