Critical Care Medicine

Aortic incompetence, Aortic regurgitation

Aortic incompetence

Synonym

Aortic regurgitation

1. Description of the problem

What every clinician needs to know

Aortic regurgitation (AR), also known as aortic insufficiency (AI), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during diastole, from the aorta into the left ventricle.

AR can be due to abnormalities of either the aortic valve or the aortic root. About half of the cases of AI are due to the aortic root dilatation, which is idiopathic in more than 80% of cases, but may result from aging, syphilitic aortitis, osteogenesis imperfecta, aortic dissection, Behçet's disease, reactive arthritis and systemic hypertension. In about 15% of cases, the bicuspid aortic valve is the cause. Another 15% of cases are due to retraction of the cusps as part of post-inflammatory processes of endocarditis in rheumatic fever and various collegen-vascular diseases.

AI has been linked to the use of some medications, specifically medications containing fenfluramine or dexfenfluramine isotopes and dopamine agonists. Other potential causes that affect the valve directly include Marfan's syndrome, Ehlers-Danlos syndrome, ankylosing spondylitis and systemic lupus erythematosus. In acute cases of AI, the main causes are infective endocarditis, aortic dissection, rupture of a congenital valve fenestration and traumatic rupture of the valve leaflets. Iatrogenic causes include aortic balloon valvotomy or a failed surgical valve repair or replacement.

Clinical features

AI causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart. All forms of AR produce a similar hemodynamic abnormality. The inability of the aortic valve leaflets to remain closed or coapted during diastole results in a portion of the left ventricular stroke volume leaking back from the aorta into the left ventricle. The added volume of regurgitant blood produces an increase in left ventricular end-diastolic volume and an elevation in wall stress. The heart responds with compensatory myocardial hypertrophy.

The pressure overload (due to elevated pulse pressure and the systemic effects of neuroendocrine hormones) causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the increased left ventricular systolic pressures associated with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant fraction.

An additional factor that plays a role in left ventricular performance is vascular adaptation. One study found that in some patients, total arterial elastance, determined by measuring left ventricular pressure and left ventricular volumes during different loading conditions, decreases to maximize left ventricular work and maintain performance, while in other patients elastance increases, enhancing afterload excess and leading to a reduction in left ventricular work and pump performance. This is most apparent in those with impaired left ventricular contractility.

The combination of hypertrophy and chamber enlargement raises the total stroke volume. The net effect is that forward stroke volume and hence cardiac output are initially maintained despite the regurgitant lesion. Although left ventricular volume is increased, end-diastolic pressure remains normal due to an increase in ventricular compliance. Thus, the heart initially adapts well to chronic AR, functioning as a very efficient and compliant high-output pump.

Symptoms

Patients with AR usually remain asymptomatic for decades, even if there is progressive ventricular dilatation. If, however, there is a large regurgitant volume, the patient may complain of symptoms related to the increased mass of the enlarged left ventricle, which include:

  • A sense of pounding and an uncomfortable awareness of the heartbeat, especially when lying down or lying on the left side, which brings the left ventricular apex closer to the chest wall, augmenting the sensation during systolic contraction.

  • Atypical chest pain induced by a mechanical interaction between the heart and the chest wall.

  • Angina pectoris.

  • Palpitations due to tachycardia or premature beats.

Symptoms of left-sided heart failure (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea and eventual pulmonary edema) occur in the presence of left ventricular dysfunction.

Physical examination

The physical examination in patients with chronic AR is often dramatic and frequently establishes the diagnosis without the need for laboratory testing. Both examination of the peripheral pulses and auscultation of the heart are important.

The murmur of chronic AI is typically described as early diastolic and decrescendo, which is best heard at the aortic area when the patient is seated and leans forward with breath held in expiration.

The increased stroke volume results in abrupt distention of the peripheral arteries and an elevation in systolic pressure. Regurgitation back into the left ventricle then leads to a rapid fall in pressure with quick collapse of the arteries and a low diastolic pressure, which may approach zero in severe disease.

The net effect is a wide pulse pressure, which is manifested on examination as a "water hammer" or Corrigan pulse. This finding may be best appreciated by palpation of the radial or brachial arteries (exaggerated by raising the arm) or the carotid pulses. Other findings are associated with a hyperdynamic pulse:

  • deMusset's sign — a head nodding in time with each heartbeat.

  • Traube's sign — a pistol shot pulse (systolic and diastolic sounds) heard over the femoral arteries.

  • Duroziez's sign — a systolic and diastolic bruit heard when the femoral artery is partially compressed.

  • Quincke's pulses — capillary pulsations in the fingertips or lips.

  • Mueller's sign — systolic pulsations of the uvula.

  • Becker's sign — visible pulsations of the retinal arteries and pupils.

  • Hill's sign — popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg.

  • Mayne's sign — greater than 15 mmHg decrease in diastolic blood pressure with arm elevation from the value obtained with the arm in the standard position.

  • Rosenbach's sign — systolic pulsations of the liver.

  • Gerhard's sign — systolic pulsations of the spleen.

Unfortunately, none of the above putative signs of AI is of utility in making the diagnosis, but they may help as pointers. What is of value is hearing a diastolic murmur itself, whether or not the above signs are present.

Although all of these clinical signs have been described as ancillary findings useful in the diagnosis of AR, few published studies have assessed the predictive value of any of these findings. Exaggerated or bounding pulses and these physical signs are not specific for AR, since they can be seen in sympathetic hyperactivity, anemia, fever, pregnancy, thyrotoxicosis, large arteriovenous fistula, patent ductus arteriosus and severe bradycardia.

The combination of left ventricular enlargement and forceful systolic function results in the apical impulse being displaced laterally and inferiorly and being diffuse and hyperdynamic. A prominent pulsation (and occasionally a thrill) may also be felt at the sternal notch.

Key management points

AI can be treated either medically or surgically, depending on the acuteness of presentation, the symptoms and signs associated with the disease process and the degree of left ventricular dysfunction.

Surgical treatment is controversial in asymptomatic patients but has been recommended if the ejection fraction falls to 50% or below, in the face of progressive and severe left ventricular dilatation, or with symptoms or abnormal response to exercise testing. For both groups of patients, surgery before the development of worsening ejection fraction/LV dilatation is expected to reduce the risk of sudden death and is associated with lower peri-operative mortality. Also, surgery is optimally performed immediately in acute cases.

Medical treatment

Medical therapy of chronic AI that is stable and asymptomatic involves the use of vasodilators. Small trials have shown a short-term benefit in the use of ACE inhibitors or angiotensin receptor blockers, nifedipine and hydralazine in improving left ventricular wall stress, ejection fraction and mass. The use of these vasodilators is indicated only in individuals who suffer from hypertension in addition to AI.

The goal in using these pharmacological agents is to decrease the afterload so that the left ventricle is somewhat spared. The regurgitant fraction may not change significantly, since the gradient between the aortic and left ventricular pressures is usually fairly low at the initiation of treatment.

Other rather conservative medical treatments for stable and asymptomatic cases include diuretics, digoxin and calcium blockers, and avoiding very strenuous activity. In addition, endocarditis prophylaxis is indicated before dental, gastrointestinal or genitourinary procedures. In mild to moderate cases, echocardiography and cardiac stress test should be followed up every 1-2 years. In severe moderate/severe cases, echocardiography with cardiac stress testing should be performed every 3-6 months.

Surgical treatment

The surgical treatment of choice at this time is an aortic valve replacement. This is currently an open-heart procedure, requiring the individual to be placed on cardiopulmonary bypass. In the case of severe acute AI, all individuals should undergo surgery if there are no absolute contraindications for surgery. Individuals with bacteremia with aortic valve endocarditis should not wait for treatment with antibiotics to take effect, given the high mortality associated with the acute AI.

Instead, replacement with an aortic valve homograft should be performed if feasible. A percutaneous approach to aortic valve replacement is now feasible, but the main experience has been in the treatment of aortic stenosis.

2. Emergency Management

The treatment of acute severe AR is emergency aortic valve replacement. If there is any delay in surgery, stabilization may be attempted in the ICU using intravenous vasodilators such as nitroprusside and possibly inotropic agents such as dopamine or dobutamine in an attempt to enhance forward flow and lower left ventricular end-diastolic pressure. An intra-aortic balloon pump is contraindicated because inflation of the balloon in diastole will worsen the severity of AR.

A related issue is the management of acute mild AR. When due to an aortic dissection, the AR is repaired at the time of surgery for the dissection. When due to endocarditis, antibiotic therapy alone may be sufficient unless the patient has another indication for valve replacement.

The surgical approach depends upon the cause of AR, ranging from a composite valve and root replacement for aortic dissection to valve repair for a ruptured fenestration.

ACC/AHA Guideline Summary: Indications for aortic valve replacement or repair (AVR) in chronic aortic regurgitation

Class I

  • Symptomatic patients with severe chronic AR, irrespective of left ventricular ejection fraction (LVEF).

  • If the presence of symptoms in patients with severe chronic AR is equivocal, the development of symptoms during an exercise test.

  • Asymptomatic patients with severe chronic AR and an LVEF 50% or below at rest.

  • Patients with severe chronic AR who undergo coronary artery bypass graft surgery (CABG) or surgery on the aorta or other heart valves.

Class IIa

  • Asymptomatic patients with severe chronic AR and a normal LVEF (LVEF above 50%) who have severe left ventricular dilatation (end-diastolic dimension greater than 75 mm or end-systolic dimension greater than 55 mm). Lower threshold values can be considered for patients of small stature.

Class IIb

  • Patients with moderate chronic AR who undergo CABG or surgery on the ascending aorta.

  • Asymptomatic patients with severe chronic AR and an LVEF greater than 50% in whom the end-diastolic dimension is greater than 70 mm or the end-systolic dimension is greater than 50 mm, and there is evidence of progressive left ventricular dilatation, declining exercise tolerance or an abnormal hemodynamic response to exercise.

Class III

  • Asymptomatic patients with mild, moderate or severe chronic AR and an LVEF greater than 50% at rest in whom the degree of left ventricular dilatation is not moderate or severe (end-diastolic dimension below 70 mm or end-systolic dimension below 50 mm).

ACC/AHA guideline summary: Indications for aortic valve repair or replacement (AVR) in adolescents or young adults with chronic aortic regurgitation (AR)

Class I

  • Severe AR with symptoms of angina, syncope or dyspnea on exertion.

  • Asymptomatic severe AR with a left ventricular ejection fraction (LVEF) below 50% on serial studies separated by 1-3 months.

  • Asymptomatic severe AR with progressive left ventricular enlargement to an end-diastolic dimension greater than 4 standard deviations greater than normal.

  • Coronary angiography before aortic valve surgery when a pulmonary autograft (Ross procedure) is considered when the origin of the coronary arteries was not identified by noninvasive testing.

Class IIb

  • Asymptomatic adolescents with severe AR who also have moderate aortic stenosis (peak left ventricle-to-peak aortic gradient greater than 40 mmHg at cardiac catheterization).

  • Asymptomatic adolescents with severe AR who develop ST depression or T-wave inversion over the left precordium.

3. Diagnosis

Transthoracic echocardiography

The most common test used to evaluate the severity of AI is transthoracic echocardiography, which can provide two-dimensional views of the regurgitant jet, allow measurement of velocity using Doppler and estimate jet volume.

The findings in severe aortic regurgitation, based on the 2006 American College of Cardiology/American Heart Association guidelines, include:

  • An AI color jet width greater than 65% of the left ventricular outflow tract (LVOT) diameter (may not be true if the jet is eccentric).

  • Doppler vena contracta width greater than 0.6 cm.

  • The pressure half-time of the regurgitant jet is less than 250 msec.

  • Early termination of the mitral inflow (due to increase in LV pressure due to the AI).

  • Holodiastolic flow reversal in the descending aorta.

  • Regurgitant volume greater than 60 ml.

  • Regurgitant fraction greater than 50%.

  • Regurgitant orifice area greater than 0.3 cm2.

  • Increased left ventricular size.

In acute AR, echocardiography may show early closure of the mitral valve.

Chest X-ray

Chest X-Ray can assist in making the diagnosis, showing left ventricular hypertrophy and dilated aorta.

ECG

ECG typically indicates left ventricular hypertrophy.

Cardiac catheterization

Cardiac catheterization assists in assessing the severity of regurgitation and any left ventricular dysfunction.

ACC/AHA guideline summary: Diagnosis and initial evaluation of aortic regurgitation

Class I

Echocardiography

1. To confirm the diagnosis and to estimate the severity of acute or chronic AR.

2. To determine the cause of chronic AR, including assessment of valve morphology and the size and morphology of the aortic root.

3. To determine left ventricular function and detect left ventricular hypertrophy and left ventricular dimensions or volumes in chronic AR.

4. Among patients with an enlarged aortic root, to assess both AR and the severity of aortic dilatation.

5. Among asymptomatic patients with chronic AR, to periodically reevaluate left ventricular size and function.

6. To reassess mild, moderate, or severe AR in patients who have new or changing symptoms.

Radionuclide angiography or magnetic resonance imaging

1. For the initial and follow-up assessment of left ventricular volume and function at rest when echocardiography is suboptimal.

Cardiac catheterization

1. With aortic root angiography and measurement of left ventricular pressure to assess the severity of AR, left ventricular function and aortic root size when noninvasive tests are inconclusive or provide discrepant results from clinical findings.

Class IIa

Exercise stress testing in chronic AR

1. To assess functional capacity and symptom response in patients with a history of equivocal symptoms.

2. To assess symptoms and functional capacity prior to participation in athletic activity.

Magnetic resonance imaging

1. To assess the severity of AR when echocardiography is not satisfactory.

Class IIb

Exercise stress testing with radionuclide angiography

1. To assess left ventricular function in asymptomatic or symptomatic patients with chronic AR.

Class III

Cardiac catheterization

1. When noninvasive tests are adequate and consistent with clinical findings and coronary angiography is not required.

2. In asymptomatic patients in whom noninvasive tests are adequate.

Table I gives information about the severity of AR in adults.

Table I.

Severity of AR in adults
Mild Moderate Severe
Structural parameters
Left ventricular size Normal Normal or dilated Dilated, except acute AR
Aortic leaflets Normal or abnormal Normal or abnormal Abnormal/flail, or wide coaptation defect
Doppler parameters
Color Doppler jet width Central jet, width <25% of LVOT Central jet, width 25-65% of LVOT Central jet, width >65% of LVOT
Doppler vena contracta width <3 mm 3-6 mm >6 mm
Quantitative parameters
Regurgitant volume <30 mL/beat 30-59 mL/beat ≥60 mL/beat
Regurgitant fraction <30% 30-49% ≥50%
Regurgitant orifice area <0.10 cm 2 0.10-0.29 cm 2 ≥0.30 cm 2

Table II gives information about echocardiographic stages of chronic AR.

Table II.

Echocardiographic stages of chronic AR
Compensated Transitional Decompensated*
Dimensions
End-diastolic dimension (mm) <60 60-70 >75
End-systolic dimension (mm) <45 45-50 >55
Volumes
End-diastolic volume (mL/m 2) <120 130-160 >170
End-systolic volume (ml/m 2) <50 50-60 >60
Left ventricular function
Ejection fraction (percent) >55 51-55 ≤50
Fractional shortening (percent) >32 30-31 <29

Signs and symptoms and the investigations described above, especially transthoracic echocardiography, are usually enough to diagnose AR; however, it's important to differentiate acute and chronic AR.

In chronic AR, the volume overload of the left ventricle is associated with a gradual increase in left ventricular size that maintains a normal forward cardiac output despite the regurgitant valve flow; left ventricular diastolic pressures remain normal. In contrast, with acute AR the regurgitant volume fills a small ventricle that has not had time to dilate, resulting in an acute increase in left ventricular diastolic pressure and a fall in forward cardiac output.

So acute AR commonly presents catastrophically with sudden cardiovascular collapse. Other presenting symptoms are related to the cause of acute AR (e.g. signs and symptoms of endocarditis or aortic dissection). However, in some cases, acute AR is the first clue suggesting one of these diagnoses. Aortic dissection should always be suspected in patients with AR and chest or back pain.

Many of the characteristic findings of chronic AR are less prominent or absent on physical examination and imaging in patients with acute AR.

Table III gives the differential diagnosis.

Table III.

The most common test used for diagnosis and evaluation of the severity of AI is transthoracic echocardiography, which can provide two-dimensional views of the regurgitant jet, allow measurement of velocity using Doppler and estimate jet volume.

4. Specific Treatment

AI can be treated either medically or surgically, depending on the acuteness of presentation, the symptoms and signs associated with the disease process and the degree of left ventricular dysfunction.

Surgical treatment is controversial in asymptomatic patients but has been recommended if the ejection fraction falls to 50% or below in the face of progressive and severe left ventricular dilatation, or with symptoms or abnormal response to exercise testing. For both groups of patients, surgery before the development of worsening ejection fraction/LV dilatation is expected to reduce the risk of sudden death and is associated with lower peri-operative mortality. Also, surgery is optimally performed immediately in acute cases.

Medical treatment

Medical therapy of chronic AI that is stable and asymptomatic involves the use of vasodilators. Small trials have shown a short-term benefit in the use of ACE inhibitors or angiotensin receptor blockers, nifedipine and hydralazine in improving left ventricular wall stress, ejection fraction and mass. The use of these vasodilators is indicated only in individuals who suffer from hypertension in addition to AI.

The goal in using these pharmacological agents is to decrease the afterload so that the left ventricle is somewhat spared. The regurgitant fraction may not change significantly, since the gradient between the aortic and left ventricular pressures is usually fairly low at the initiation of treatment. Other rather conservative medical treatments for stable and asymptomatic cases include diuretics, digoxin, and calcium blockers and avoiding very strenuous activity. In addition, endocarditis prophylaxis is indicated before dental, gastrointestinal or genitourinary procedures.

In mild to moderate cases, echocardiography and cardiac stress testing should be followed up every 1-2 years. In severe moderate/severe cases, echocardiography with cardiac stress testing should be performed every 3-6 months.

Surgical treatment

The surgical treatment of choice at this time is an aortic valve replacement. This is currently an open-heart procedure, requiring the individual to be placed on cardiopulmonary bypass.

In the case of severe acute AI, all individuals should undergo surgery if there are no absolute contraindications for surgery. Individuals with bacteremia with aortic valve endocarditis should not wait for treatment with antibiotics to take effect, given the high mortality associated with severe acute AI. Instead, replacement with an aortic valve homograft should be performed if feasible. A percutaneous approach to aortic valve replacement is now feasible, but the main experience has been in the treatment of aortic stenosis.

Ongoing treatment

Vasodilators such as nifedipine and ACE inhibitors may influence LV size and function and slow the rate of progression of AR. The evidence of benefit is greatest in symptomatic patients with significant LV dilation.

Other forms of medical therapy, other than vasodilators, have a limited role in AR because symptomatic patients should be treated with valve replacement. For those patients who develop symptoms of heart failure but are not candidates for surgery, therapy is similar to that for other causes of heart failure (e.g. digoxin for symptoms, diuretics for fluid control, ACE inhibitors and/or angiotensin II receptor blockers to improve survival).

There is a relative contraindication to beta blockers in patients with AR because slowing the heart rate may increase the regurgitant volume by prolonging diastole. Similar concerns about excess slowing of the ventricular rate also apply to rate control with atrioventricular nodal blockers in the infrequent patients who develop atrial fibrillation.

There is one setting in which beta blockers may be considered. The 2006 ACC/AHA guidelines on the management of valvular heart disease concluded that beta blocker therapy was reasonable in patients with bicuspid aortic valves who have an aortic root diameter greater than 40 mm and do not have moderate or severe AR.

With respect to warfarin therapy, long-term anticoagulation is not recommended unless there are other indications for anticoagulation.

ACC/AHA guideline summary: Vasodilator therapy in aortic regurgitation (AR)

Class I - There is evidence and/or general agreement that vasodilator therapy is indicated in patients with AR in the following setting:

For chronic therapy in severe AR associated with symptoms or left ventricular dysfunction when surgery is not recommended due to other cardiac or extracardiac factors.

Class IIa - The weight of evidence or opinion is in favor of usefulness of vasodilator therapy in patients with AR in the following setting:

For short-term hemodynamic improvement in patients with symptoms of severe heart failure and severe left ventricular dysfunction before undergoing aortic valve replacement.

Class IIb - The efficacy of vasodilator therapy in patients with AR is less well established in the following setting:

For chronic therapy in severe asymptomatic AR with left ventricular dilatation but normal left ventricular systolic function.

Class III - There is evidence and/or general agreement that vasodilator therapy is not useful and may be harmful in patients with AR in the following settings:

For chronic therapy in mild to moderate asymptomatic AR with normal left ventricular systolic function.

For chronic therapy in patients who are otherwise candidates for aortic valve replacement, including asymptomatic patients with left ventricular systolic dysfunction and symptomatic patients with either normal left ventricular function or mild to moderate left ventricular systolic dysfunction.

Aortic valve replacement or repair is indicated in asymptomatic patients with chronic severe AR who have reliable evidence of LV systolic dysfunction (LVEF below 50%). In addition, aortic valve replacement is suggested in asymptomatic patients if LVEF is greater than 50% and LV end-systolic dimension is greater than 55 mm, or LV end-diastolic dimension is greater than 75 mm.

  • Surgery should be considered in asymptomatic patients who show progressive LV enlargement, particularly if the end-diastolic dimension exceeds 70 mm, the systolic dimension approaches 50 mm, or the ejection fraction approaches 50%.

  • Alternatively, vasodilator therapy can be used to reduce the hemodynamic burden and possibly delay the need for surgery. Many such patients will need surgery within the ensuing years, but the original decision on medical versus surgical therapy should be made in conjunction with the patient's wishes and expectations.

  • Evidence of LV systolic dysfunction (ie, LVEF below 50%, not merely LV enlargement) indicates that the patient may be entering a decompensated stage.

For patients who develop symptoms of heart failure but are not candidates for surgery, therapy is similar to that for other causes of heart failure.

5. Disease monitoring, follow-up and disposition

The prognosis of patients with severe AR is determined largely by symptom status and by left ventricular size and function.

The natural history of chronic AR is mostly based upon data from nine series with a total of 593 patients followed for a mean of 6.6 years (Table IV).

Table IV.

Natural history of chronic AR
Asymptomatic patients with normal left ventricular (LV) systolic function
Progression to symptoms and/or LV dysfunction <6%/year
Progression to symptoms, LV dysfunction, or death
According to LV end-systolic dimension
>50 mm 19%/year
40-50 mm 6%/year
<40 mm 0%/year
Progression to asymptomatic LV dysfunction <3.5%/year
Sudden death <0.2%/year
Asymptomatic patients with LV systolic dysfunction
Progression to cardiac symptoms >25%/year
Symptomatic patients
Mortality rate >10%/year

The association of symptoms of heart failure with prognosis was illustrated by a report from the Mayo Clinic of 246 patients with severe or moderately severe AR who were managed conservatively. Those with New York Heart Association class III or IV heart failure had an annual mortality of 25%, while those with class II heart failure had an annual mortality of 6%.

In addition to symptom status, prognosis in patients with AR is assessed by measurements of LV size and function, usually by echocardiography, as recommended by the 2006 ACC/AHA valvular guidelines. Evaluation of LV size and function is important because there is not a necessary correlation between these parameters and symptoms. In one report of 450 patients, for example, 28% of patients with an LVEF below 35% were asymptomatic, a value not significantly different from the 37% of patients with an LVEF 50% or higher who were asymptomatic.

Today, with the help of above-described investigations, in addition to clinical examination, it's easy to diagnose AR.

  • Patients with AR should have an initial echocardiogram with periodic follow-up examinations.

  • Exercise testing may be helpful for assessing functional capacity and symptom response when symptoms are equivocal or prior to participation in athletics.

  • Cardiac catheterization with angiography or radionuclide ventriculography is indicated if there is uncertainty about the functional state of the ventricle or the presence of associated disease (e.g. coronary artery disease).

  • The clinical examination, exercise tolerance, and LV size and function are monitored closely in patients with chronic AR who are not yet candidates for surgery. In the absence of symptoms, management decisions are largely based upon serial measurements of LV size and function.

  • Annual echocardiographic studies are indicated in all patients with clinically significant AR. Less-frequent studies may be indicated if the LV size and function remain stable over several years of follow-up.

Pathophysiology

AI causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart. All forms of AR produce a similar hemodynamic abnormality. The inability of the aortic valve leaflets to remain closed or coapted during diastole results in a portion of the left ventricular stroke volume leaking back from the aorta into the left ventricle. The added volume of regurgitant blood produces an increase in left ventricular end-diastolic volume and an elevation in wall stress. The heart responds with compensatory myocardial hypertrophy.

The pressure overload (due to elevated pulse pressure and the systemic effects of neuroendocrine hormones) causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the increased left ventricular systolic pressures associated with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant fraction.

An additional factor that plays a role in left ventricular performance is vascular adaptation. One study found that in some patients, total arterial elastance, determined by measuring left ventricular pressure and left ventricular volumes during different loading conditions, decreases to maximize left ventricular work and maintain performance, while in other patients elastance increases, enhancing afterload excess and leading to a reduction in left ventricular work and pump performance; this is most apparent in those with impaired left ventricular contractility.

The combination of hypertrophy and chamber enlargement raises the total stroke volume. The net effect is that forward stroke volume and hence cardiac output are initially maintained despite the regurgitant lesion. Although left ventricular volume is increased, end-diastolic pressure remains normal due to an increase in ventricular compliance. Thus, the heart initially adapts well to chronic AR, functioning as a very efficient and compliant high-output pump.

Epidemiology

AR is not as common as aortic stenosis and mitral regurgitation. An analysis from the Framingham Heart Study showed a prevalence of 13% in men and 8.5% in women, with most being trace or mild; a prevalence of 15.6% was reported in African-Americans. Prevalence increases with age in both genders.

Of asymptomatic people older than 55, 13% have moderate or severe echocardiographic AR, with a total prevalence of 29% (including mild AR). A prospective multicenter epidemiological study of healthy young adults aged 23-35 years revealed a prevalence of AR of 1.3%. There was no difference in the prevalence on the basis of gender or race.

Prognosis

The risk of death in individuals with AI, dilated ventricle and normal ejection fraction who are asymptomatic is about 0.2% per year. Risk increases if the ejection fraction decreases or if the individual develops symptoms.

Special considerations for nursing and allied health professionals.

N/A

What's the evidence?

Webb, JG, Wood, DA. "Current status of transcatheter aortic valve replacement". J Am Coll Cardiol. vol. 60. 2012 Aug 7. pp. 483-92.

Choo, WS, Steeds, RP. "Cardiac imaging in valvular heart disease". Br J Radiol. vol. 84. 2011 Dec. pp. S245-57.

Latsios, G, Tousoulis, D, Androulakis, E, Papageorgiou, N, Synetos, A, Tsioufis, C, Toutouzas, K, Stefanadis, C. "Monitoring calcific aortic valve disease: the role of biomarkers". Curr Med Chem.. vol. 19. 2012. pp. 2548-54.

Hartog, AW, Franken, R, Zwinderman, AH, Groenink, M, Mulder, BJ. "Current and future pharmacological treatment strategies with regard to aortic disease in Marfan syndrome". Expert Opin Pharmacother. vol. 13. 2012 Jul. pp. 1543-62.

Firstenberg, MS, Sai-Sudhakar, CB, Anyanwu, A. "Valvular disease in patients requiring long-term left ventricular assist devices: pathophysiology and therapeutic options". Expert Rev Cardiovasc Ther. vol. 10. 2012 Feb. pp. 205-13.

Huffmyer, J, Tashjian, J, Raphael, J, Jaeger, JM. "Management of the patient for transcatheter aortic valve implantation in the perioperative period". Semin Cardiothorac Vasc Anesth. vol. 16. 2012 Mar. pp. 25-40.

Myerson, SG. "Heart valve disease: investigation by cardiovascular magnetic resonance". J Cardiovasc Magn Reson. vol. 14. 2012 Jan 19. pp. 7.

Falk, V. "Valvular disease in 2011: Breakthrough for intervention?". Nat Rev Cardiol. vol. 9. 2011 Dec 20. pp. 77-8.

Yuan, SM. "The anatomopathology of bicuspid aortic valve". Folia Morphol (Warsz). vol. 70. 2011 Nov. pp. 217-27.

Chen, RS, Bivens, MJ, Grossman, SA. "Diagnosis and management of valvular heart disease in emergency medicine". Emerg Med Clin North Am. vol. 29. 2011 Nov. pp. 801-10, vii.

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