Aortic Regurgitation

Author: Stanley S Wang, MD, JD, MPH; Chief Editor: Richard A Lange, MD

Background
Aortic regurgitation (AR) is the abnormal retrograde flow of blood through the aortic valve during cardiac diastole. AR may be caused by either valvular or aortic root pathology. Valvular abnormalities that may result in AR include bicuspid aortic valve (the most common congenital cause), rheumatic fever, infective endocarditis, collagen vascular diseases, and degenerative aortic valve disease. Abnormalities of the ascending aorta, in the absence of valve pathology, may also cause AR, such as may occur with longstanding uncontrolled hypertension, Marfan syndrome, idiopathic aortic dilation, cystic medial necrosis, senile aortic ectasia and dilation, syphilitic aortitis, giant cell arteritis, Takayasu arteritis, ankylosing spondylitis, Whipple disease, and other spondyloarthropathies.

Pathophysiology
AR causes a volume load of the left ventricle (LV); in diastole, the LV fills antegrade from the left atrium and retrograde from the aorta through the leaky aortic valve. The pathophysiology depends upon whether the AR is acute or chronic. In acute AR, the LV does not have time to dilate in response to the volume load, whereas in chronic AR, the LV may undergo a series of adaptive (and maladaptive) changes.
Acute aortic regurgitation

Acute AR of significant severity leads to increased blood volume in the LV during diastole. The LV does not have sufficient time to dilate in response to the sudden increase in volume. As a result, LV end-diastolic pressure increases rapidly, causing an increase in pulmonary venous pressure. As pressure increases throughout the pulmonary circuit, the patient develops dyspnea and pulmonary edema. In severe cases, heart failure may develop and potentially deteriorate to cardiogenic shock. Early surgical intervention should be considered (particularly if AR is due to aortic dissection, in which case surgery should be performed immediately).
Chronic aortic regurgitation

Chronic AR causes gradual left ventricular (LV) volume overload that leads to a series of compensatory changes, including LV enlargement and eccentric hypertrophy. LV dilation occurs through addition of sarcomeres in series (resulting in longer myocardial fibers) as well as rearrangement of myocardial fibers. As a result, the LV becomes larger and more compliant, with greater capacity to deliver a large stroke volume that can compensate for the regurgitant

volume. The resulting hypertrophy is necessary to accommodate the increased wall tension and stress that results from LV dilation (Laplace law). During the early phases of chronic AR, the LV ejection fraction (EF) is normal or even increased (due to the increased preload and the Frank-Starling mechanism). Patients may remain asymptomatic during this period. As AR progresses, LV enlargement surpasses preload reserve on the Frank-Starling curve with the EF falling to normal and then subnormal levels. The LV end-systolic volume rises and is a sensitive indicator of progressive myocardial dysfunction. Eventually, the LV reaches its maximal diameter and diastolic pressure begins to rise, resulting in symptoms (dyspnea) that may be worse during exercise. Increasing LV end-diastolic pressure may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia, necrosis, and apoptosis. Grossly, the LV gradually transforms from an elliptical to a spherical configuration.

Epidemiology
Frequency United States

Worldwide, rheumatic heart disease is the most common cause of AR. In the United States, congenital and degenerative valve abnormalities are most common, with the age of detection peaking at 40-60 years. Estimates of the prevalence of AR of any severity range from 2-30%, but only 5-10% of patients with AR have severe disease, resulting in an overall prevalence of severe AR of less than 1% in the general population.[1] In the Framingham study (with an original cohort of 5,209 patients aged 28-62 y and an additional cohort of 5,124 patients), AR of any severity was found in 13% of men and 8.5% of women.[2] Prevalence and severity both increased with age; when stratified by decades of life, AR of moderate or greater severity was seen in less than 1% in all strata younger than 70 years.
International

The prevalence of AR internationally is not well known. However, the international prevalence of underlying conditions has been described elsewhere. For example, rheumatic heart disease remains highly prevalent in many Asian, Middle Eastern, and North African countries.[3]
Mortality/Morbidity

Acute severe AR carries a very high short-term rate of morbidity and mortality owing to the imposition of a greatly increased regurgitant volume upon a relatively noncompliant LV. Increased LV end-diastolic pressure leads to elevated left atrial and pulmonary pressures with resulting pulmonary edema, as well as decreased coronary perfusion gradients potentially causing myocardial ischemia and even sudden cardiac death. In most cases, early (if not emergent) surgical intervention is warranted.

Chronic severe AR tends to follow a more gradual clinical course that is typically characterized initially by a long, relatively asymptomatic period. However, once symptoms ensue, the patient's clinical status may deteriorate relatively rapidly. Thus, current guidelines recommend surgical intervention before symptoms develop, usually based on echocardiographic parameters. With conservative (medical) management of chronic severe AR, the linearized yearly rates of major events have been estimated as follows:[4]

Death from any cause, 4.7% Congestive heart failure, 6.2% Aortic valve surgery, 14.6%

The presence of symptoms predicted yearly mortality risk, as follows:

Asymptomatic, 2.8% NYHA Class I, 3.0% NYHA Class II, 6.3% NYHA Class III-IV, 24.6%

Although these types of data suggest that a symptom-triggered approach to surgical intervention may be feasible, multiple studies have shown that the most important predictors of mortality (and of postoperative LV function) are not symptoms but 2 crucial echocardiographic parameters: LV ejection fraction and LV end-systolic dimension.[5]
Race

The prevalence of AR appears to be similar across racial populations in the United States, although internationally there is significant variation in the prevalence of predisposing conditions such as rheumatic heart disease.[3]
Sex

Aortic regurgitation is seen more commonly in men than in women. As discussed above in the Framingham cohort, AR was found in 13% of men versus 8.5% of women.[2] The greater prevalence of AR in men may reflect, in part, the male preponderance of underlying conditions such as Marfan syndrome[6] or bicuspid aortic valve[7] .
Age

In general, the prevalence and severity of AR increase with age, although severe chronic AR is uncommon before aged 70 years.[2] However, there are many exceptions to this observation. Patients with bicuspid aortic valve and especially Marfan syndrome tend to present much earlier.[6, 7]

Clinical Presentation

History
Acute aortic regurgitation

The typical presentation of acute severe aortic regurgitation (AR) includes sudden, severe shortness of breath, rapidly developing heart failure, and chest pain if myocardial perfusion pressure is decreased or an aortic dissection is present. Because the LV is non-compliant in acute cases, the LV end-diastolic pressure is high resulting in a smaller diastolic gradient across the aortic valve and, in some cases, a short or minimal diastolic murmur on examination. Cases may be fulminant and lead to cardiogenic shock. Early surgical intervention is recommended in cases due to infective endocarditis, and emergent intervention is warranted in cases due to aortic dissection.
Chronic aortic regurgitation

Patients with chronic AR often have a long-standing asymptomatic period that may last for several years. A compensatory tachycardia may develop to maintain a large forward stroke volume, resulting in a decreased diastolic filling period. As a result, patients may be asymptomatic even with exercise. Over time, chronic volume overload eventually leads to LV dysfunction as the LV dilates. Significant deterioration of LV function may begin prior to the development of symptoms in up to one-fourth of patients, highlighting the importance of periodic echocardiographic surveillance.[5] Among patients with asymptomatic LV dysfunction, more than one-fourth develop symptoms within 1 year. Once symptoms arise, cardiac function usually worsens more rapidly and mortality may exceed 10% per year. Symptoms of chronic severe AR include the following:

Palpitations, often described as the sensation of having forceful heart beats, due to widened pulse pressure with hyperdynamic circulation Shortness of breath, which may not worsen with exertion in the early stages due to compensatory tachycardia with shortened diastole Chest pain, if LV end-diastolic pressure compromises coronary perfusion pressure gradients Sudden cardiac death, although this is uncommon (< 0.2%/y) in asymptomatic patients with preserved LV function

Physical
Many classical physical examination findings have been described in patients with chronic severe AR. However, these findings may be minimally present (if at all) in patients with acute severe AR. Manifestations of chronic severe AR are often the result of widened pulse pressure (ie, an exaggerated difference between systolic and diastolic blood pressure) because (1) of elevated stroke volume during systole and (2) the incompetent aortic valve allows the diastolic pressure

within the aorta to fall significantly. Diastolic pressures are often lower than 60 mm Hg with pulse pressures (ie, the difference between the systolic and diastolic pressure) often exceeding 100 mm Hg, although younger patients with more compliant vessels may have a less widened pulse pressure. Many physical examination findings have associated eponyms.

Becker sign - Visible systolic pulsations of the retinal arterioles Corrigan pulse ("water-hammer" pulse) - Abrupt distention and quick collapse on palpation of the peripheral arterial pulse de Musset sign - Bobbing motion of the patient's head with each heartbeat Hill sign - Popliteal cuff systolic blood pressure 40 mm Hg higher than brachial cuff systolic blood pressure Duroziez sign - Systolic murmur over the femoral artery with proximal compression of the artery, and diastolic murmur over the femoral artery with distal compression of the artery Mller sign - Visible systolic pulsations of the uvula Quincke sign - Visible pulsations of the fingernail bed with light compression of the fingernail Traube sign ("pistol-shot" pulse) - Booming systolic and diastolic sounds auscultated over the femoral artery

On palpation, the point of maximal impulse may be diffuse or hyperdynamic but is often displaced inferiorly and toward the axilla. Peripheral pulses are prominent or bounding. Auscultation may reveal an S3 gallop if LV dysfunction is present. The murmur of AR occurs in diastole, usually as a high-pitched sound that is loudest at the left sternal border. The duration of the murmur correlates better with the severity of AR than the loudness of the murmur. A functional systolic flow murmur may also be present because of increased stroke volume, although concurrent aortic stenosis may also be present. An Austin Flint murmur may be present at the cardiac apex in severe AR and is a low-pitched, mid-diastolic rumbling murmur due to blood jets from the AR striking the anterior leaflet of the mitral valve, which results in premature closure of the mitral leaflets. In many cases, physical examination also reveals findings relating to the underlying cause. For example, there may be various embolic phenomena in patients with AR due to infective endocarditis or skeletal features suggestive of Marfan syndrome or a spondyloarthropathy if AR is due to these conditions.

Causes
Acute aortic regurgitation

Infective endocarditis may lead to destruction or perforation of the aortic valve leaflet. A bulky vegetation can also interfere with proper coaptation of the valve leaflets or cause lead to frank prolapse or disruption of a leaflet (flail leaflet). In acute ascending aortic dissection (type A), the retrograde proximal dissection undermines the suspensions of the aortic valve leaflets. Varying levels of aortic valve malcoaptation and prolapse occur. Prosthetic valve malfunction can lead to AR. Chest trauma may lead to a tear in the ascending aorta and disruption of the aortic valve support apparatus.

Chronic aortic regurgitation

Bicuspid aortic valve is the most common congenital lesion of the human heart and leads more commonly to progressive aortic stenosis, but is also the most common cause of isolated AR requiring aortic valve surgery. In addition, an associated aortopathy may be present, resulting in aortic dilation and/or dissection that worsens the AR.[8] Connective tissue disorders, including Marfan syndrome, Ehlers-Danlos syndrome, floppy aortic valve, aortic valve prolapse, sinus of Valsalva aneurysm, and aortic annular fistula can all lead to significant AR. Certain weight loss medications, such as fenfluramine and dexfenfluramine (commonly referred to as Phen-Fen), may induce degenerative valvular changes that result in chronic AR. Rheumatic fever was a common cause of AR in the first half of the 20th century but has become less common in the United States, although it remains prevalent in some immigrant populations. Fibrotic changes cause thickening and retraction of the aortic valve leaflets, resulting in central valvular regurgitation. Leaflet fusion may occur, resulting in concurrent aortic stenosis. Associated rheumatic mitral valve disease is almost always present. Ankylosing spondylitis often causes an aortitis that most frequently involves the aortic root with associated AR.[9] Further extension of the subaortic fibrotic process into the intraventricular septum may result in conduction system disease. Coronary and more distal aortic abnormalities are also seen in this condition. Behcet disease rarely causes cardiac complications (< 5% of patients) but potential findings include proximal aortitis with AR as well as coronary artery disease.[10] Giant cell arteritis is a systemic vasculitis that typically affects the extracranial branches of the carotid artery but may also cause aortic inflammation and AR (as well as coronary artery disease and LV dysfunction.[11] Rheumatoid arthritis uncommonly causes granulomatous nodules to form within the aortic valve leaflets and, in rare cases, this may lead to clinical AR, although it is more commonly an incidental finding postmortem.[12] Systemic lupus erythematosus can cause valvular fibrosis and consequent dysfunction, including AR.[13] Lupus is also associated with Libman-Sacks endocarditis, resulting in sterile verrucous valvular vegetations that can cause AR.[14, 15] Takayasu arteritis can produce an aortitis in addition to aortic valve (and coronary) involvement. The aortitis may increase the risk of prosthetic valve detachment, leading some to advocate for concurrent aortic root replacement in patients undergoing valve surgery.[16] Whipple disease has been reported in the literature in association with AR or aortic valve endocarditis.[17]

Differential Diagnoses

Mitral Stenosis Pulmonic Regurgitation Tricuspid Stenosis

Workup

Laboratory Studies
Laboratory testing in patients with aortic regurgitation (AR) should be guided by the clinical scenario. For example, in patients with AR due to suspected infective endocarditis, peripheral blood counts and cultures may help clarify the diagnosis and identify the causative organism. Specific serologic tests may assist in the diagnosis of rheumatological causes. Laboratory assessment of renal and hepatic function may play an important role in determining a patient's eligibility for certain vasodilator or other drug therapy.

Imaging Studies

Transthoracic echocardiography should be performed in all patients with suspected AR, and periodically in patients with confirmed AR of significant severity. Echocardiography is a highly accurate test in AR, with sensitivity and specificity well in excess of 90%. In addition, echocardiographic parameters are used to determine the optimal timing of surgery in many cases.[5] Important echocardiographic findings in AR include the following: o Aortic valve structure and morphology (bileaflet versus trileaflet, flail, thickening) o Presence of vegetations or nodules (may require transesophageal echocardiography in selected cases) o Severity of AR Color Doppler jet width (the vena contracta width is usually >65% of the width of the left ventricular outflow tract in severe AR) Vena contracta width Regurgitant volume, fraction, and orifice area Premature closure of the mitral valve (seen in severe AR) and opening of the aortic valve (with severely elevated LV end-diastolic pressure) Pressure half-time (usually < 300-350 ms with significant AR) o Associated lesions of the aorta, including dilation, aneurysm, dissection, or ectasia o LV structure and function LV hypertrophy and dilation EF and end-systolic dimension are key determinants of outcome [5] Surgery recommended if EF is 55% or if end-systolic dimension is >55 mm Standard chest radiography may show evidence of structural abnormalities (aortic dilation, prosthetic valve dislodgement, aortic valvular calcification) or functional compromise (pulmonary edema, cardiomegaly). Radionuclide imaging may provide complementary clinical information, including AR regurgitant fraction and LV/RV stroke volume ratio (often >2 in severe AR). Cardiac computed tomography (CT) and magnetic resonance imaging (MRI) have not yet achieved widespread adoption in the management of AR, although support in the literature is increasing for the potential clinical use of these imaging techniques.[18, 19, 20]

Other Tests

Electrocardiography findings are nonspecific but may include evidence of the following: o LV hypertrophy

Left axis deviation Left atrial enlargement LV volume overload pattern (prominent Q waves in leads I, aVL, and V3 to V6 and relatively small r waves in V1) o LV conduction defects (typically late in the disease process) Exercise treadmill testing may be used to guide recommendations for surgical therapy in patients with chronic severe AR and equivocal symptoms.[5] However, the role of stress echocardiography in patients with AR remains uncertain, and further studies may be needed before it can be recommended for routine clinical use.[21]

o o o

Procedures

Cardiac catheterization is not always required in all patients with chronic AR but may provide extremely valuable clinical information, especially in patients who are contemplating surgery. Class I indications for cardiac catheterization under current American College of Cardiology/American Heart Association guidelines include the following:[5] o Assessment of coronary anatomy prior to aortic valve surgery in patients with risk factors for coronary artery disease o Assessment of severity of AR, LV function, or aortic root size when noninvasive tests are inconclusive or discordant with clinical findings Aortic angiography, which may be performed during a cardiac catheterization procedure, may provide useful information regarding the severity of the patient's AR. Traditional angiographic grading is as follows: o Mild (1+): A small amount of contrast enters the left ventricle during diastole and clears with each systole. o Moderate AR (2+): Contrast enters the LV with each diastole, but the LV chamber is less dense than the aorta. o Moderately severe AR (3+): The LV chamber is equal in density with the ascending aorta. o Severe AR (4+): Complete, dense opacification of the LV chamber occurs on the first beat and the LV is more densely opacified than the ascending aorta. Intra-aortic balloon counterpulsation is contraindicated in patients with severe AR.

Histologic Findings
Histological valvular findings in patients with AR depend on the cause of the patient's AR. Patient with congenital abnormalities can usually be easily characterized noninvasively or grossly at the time of surgery or during pathological inspection. Aortic root dilatation may be present in up to 25% of patients with AR due to bicuspid valve. Many patients with a bicuspid aortic valve have concurrent aortopathy including connective tissue and cellular abnormalities that predispose to aortic dilation, aneurysm, and dissection.[8]
Treatment & Management

Medical Care
In acute severe aortic regurgitation (AR), surgical intervention is usually indicated, but the patient may be supported medically with dobutamine to augment cardiac output and shorten diastole and sodium nitroprusside to reduce afterload in hypertensive patients. In chronic severe AR, vasodilator therapy may be used in select conditions to reduce afterload in patients with systolic hypertension to minimize wall stress and optimize LV function; in normotensive patients, vasodilator therapy is not likely to reduce regurgitant volume (preload) significantly and thus may not be of clinical benefit.[22] The current American College of Cardiology/American Heart Association (ACC/AHA) guidelines say the following about vasodilator therapy:

Vasodilator therapy is indicated for long-term therapy in patients with chronic, severe AR and symptoms of LV dysfunction but who are not candidates for surgery. Vasodilator therapy is reasonable for short-term therapy in patients with severe LV dysfunction and heart failure symptoms to improve their hemodynamic profile before proceeding with surgery. Vasodilator therapy is acceptable for long-term therapy in asymptomatic patients with severe AR and LV dilation with normal EF.

However, under the current guidelines, vasodilator therapy is not indicated for the following:

Long-term therapy in asymptomatic patients with less than severe AR and normal EF Long-term therapy in asymptomatic patients with LV dysfunction who are candidates for surgery Long-term therapy in symptomatic patients with less than severe LV dysfunction who are candidates for surgery

Although diuretics, nitrates, and digoxin are sometimes used to help control symptoms in patients with AR, not enough data in the clinical literature justify routinely recommending or discouraging these therapies. Also, no data support drug therapy of any class in patients with less than severe AR.[5] Antibiotic prophylaxis prior to dental procedures is no longer routinely recommended for all patients with AR under current ACC/AHA guidelines.[5] However, select patient groups for whom prophylactic antibiotic therapy prior to dental procedures may be reasonable include the following:

Patients with prosthetic material in their hearts (such as artificial valves or valves repaired with prosthetic material) Patients with prior infective endocarditis Patients with the following forms of congenital heart disease (CHD): o Cyanotic CHD that is incompletely or not repaired (including patients with palliative shunts and conduits) o Repaired CHD using prosthetic material, for the first 6 months post-procedurally (ie, prior to endothelialization of the material)

Repaired CHD but at risk of inhibited endothelialization (ie, with residual defects at or adjacent to the site of the prosthetic material) Patients following cardiac transplantation who have valve regurgitation due to a structurally abnormal valve

Surgical Care
Surgical treatment of AR usually requires replacement of the diseased valve with a prosthetic valve, although valve-sparing repair is increasingly possible with advances in surgical technique and technology. Under current ACC/AHA guidelines[5] , aortic valve surgery is recommended for patients with chronic severe AR under the following circumstances:

Patient is symptomatic Patient is asymptomatic, with a resting EF of 55% Patient is asymptomatic, with LV dilation (LV end-systolic dimension >55 mm)

Additional circumstances in which aortic valve surgery may be reasonable include the following:

Patient has moderate AR and is undergoing coronary artery bypass surgery or other surgery involving the ascending aorta Patient has severe AR with no symptoms, normal EF, and less severe LV dilation (LV end-systolic dimension >50 mm or LV end-diastolic dimension >70 mm) if the patient experiences (1) progressive LV dilation on serial imaging studies; (2) deteriorating exercise tolerance, or (3) abnormal hemodynamic responses to exercise, such as inability to augment blood pressure during a treadmill study

Ongoing improvements in surgical technique and technology have enabled many patients with even severe LV dysfunction to undergo surgery (rather than cardiac transplantation).[23] In patients undergoing aortic valve surgery for bicuspid aortic valve disease who also have a dilated or aneurysmal ascending aorta with a diameter of >4.5 cm, concurrent aortic root repair or replacement is indicated. Aortic valve surgery is generally not indicated in asymptomatic patients with normal EF and less LV dilation (LV end-systolic dimension < 50 mm or LV end-diastolic dimension < 70 mm).
Mechanical versus bioprosthetic aortic valve

For patients undergoing aortic valve replacement, careful consideration should be given to the relative risks and benefits of mechanical versus bioprosthetic valves. Traditionally, mechanical valves have been thought to be more durable but require long-term anticoagulation with warfarin due to increased risk of thrombosis, whereas bioprosthetic valves carry a greater risk of longterm deterioration and risk of reoperation but avoid the need for long-term warfarin.[24] In some

cases, a clear choice is apparent (eg, a homografts is often preferred to a mechanical valve in the setting of active infective endocarditis). While further discussion is beyond the scope of this article, the reader is referred to the current ACC/AHA guidelines, which include major criteria for aortic valve selection as well as recommendations for antithrombotic therapy (including aspirin for all prosthetic valve recipients along with long-term anticoagulation with warfarin for selected patients).[5]

Consultations

Cardiologist Cardiothoracic surgeon

Diet
No specific dietary recommendations exist pertaining purely to AR. However, for patients with hypertension or hypervolemia (including peripheral edema or other heart failure symptoms), salt restriction may provide significant clinical benefit.

Activity
Current recommendations regarding activity in patients with AR is based mostly on expert opinion as there is a paucity of clinical trial data, including no convincing evidence to suggest that even strenuous periodic exercise worsens LV function in patients with AR. Patients who are asymptomatic and have normal EF may safely participate in normal daily activities as well mild exercise and some forms of competitive exercise. However, isometric exercise is discouraged. The short-term safety of more vigorous exercise (such as with competitive athletics) may be estimated through the use of stress testing at a comparable level of exertion, but the long-term effects of such exercise is not known.
Medication

Medication Summary
Vasodilator therapy may be considered under the conditions described above. Many classes of vasodilators have been studied, with long-term hydralazine or nifedipine therapy being associated with higher EF and less LV dilation in smaller trials, but a less consistent association has been found for enalapril and quinapril.[5] Historically, beta-blocker therapy has been discouraged in patients with severe AR because heart rate reduction could prolong diastole, thus worsening AR. However, beta-blockers have been shown to produce beneficial neuroendocrine alterations in patients with heart failure. A recent observational study has suggested that beta-blocker therapy is associated with a significant

survival benefit in patients with severe AR[25] , spurring hope that further investigation may confirm this finding and allow its translation into a clinically meaningful recommendation.

Angiotensin-converting enzyme inhibitors

Class Summary

Competitive inhibitors of angiotensin-converting enzyme (ACE). Reduce angiotensin II levels, decreasing aldosterone secretion.
View full drug information Enalapril (Vasotec)

ACE-I produces a small increase in EF and significant decrease in LV volume and mass. Effective vasodilator therapy requires adjustment of dosage to achieve a decrease in arterial pressure.

Calcium channel blockers

Class Summary

Inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.
View full drug information Nifedipine (Procardia)

Produces significant fall in arterial pressure, reduces LV volume and mass, increases EF, and delays need for AVR in asymptomatic patients with severe AR and normal LV systolic function. Effective vasodilator therapy requires adjustment of dosage to decrease arterial pressure.

Cardiac glycosides
Class Summary

Inhibit sodium-potassium ATPase. Inhibition of the enzyme leads to an increase in the intracellular concentration of sodium and calcium. Vagomimetic action leads to reduced activity of sympathetic nervous system.
View full drug information

Digoxin (Lanoxin)

Pharmacologic consequences include an increase in the force and velocity of myocardial systolic contraction (positive inotropic action) and slowing of the heart rate and decreased conduction velocity through the AV node (vagomimetic effect). Use in patients with heart failure is associated with 25% reduction in the frequency of hospitalization for heart failure. Use is not associated with mortality benefit.

Diuretics
Class Summary

Increase urine flow. These agents are ion transport inhibitors that decrease the reabsorption of sodium at different sites in the nephron. Diuretics have major clinical uses in managing disorders involving abnormal fluid retention (edema) or in treating hypertension, in which their diuretic action causes decreased blood volume.
View full drug information Furosemide (Lasix)

Like torsemide and bumetanide, is a potent loop diuretic. Compared to all other classes of diuretics, these drugs have the highest efficacy in mobilizing sodium and chloride from the body. Loop diuretics inhibit the Na+, K+, and Cl- cotransport in the ascending limb of the loop of Henle. Furosemide and other loop diuretics are indicated in treatment of edema associated with CHF, cirrhosis of the liver, and renal disease, including nephrotic syndrome. May be used to treat hypertension alone or in combination with other antihypertensive agents.

Direct-acting adrenergic agonists

Class Summary

Act directly on alpha- and beta-receptors, producing effects similar to those that occur following stimulation of sympathetic nerves or release of the hormone epinephrine from the adrenal medulla.
View full drug information Dobutamine (Dobutrex)

Synthetic direct-acting catecholamine and beta-receptor agonist. Increases cardiac contractility and output in CHF. At therapeutic dose, mainly an inotropic agent, while producing comparatively mild chronotropic and vasodilative effects. As compared to other

sympathomimetic drugs, does not significantly increase myocardial oxygen demands, which is its major advantage compared to other direct-acting catecholamines.
Follow up

Further Inpatient Care

Inpatient care is required for most patients with acute severe aortic regurgitation (AR), particularly with symptoms or evidence of hemodynamic decompensation. Patients with chronic severe AR may be followed as inpatients or outpatients, depending on the stage of their disease and severity of their symptoms and LV dysfunction.

Further Outpatient Care

Asymptomatic patients with chronic severe AR require ongoing clinical surveillance with periodic echocardiography because in many cases, significant LV dysfunction may arise even before the patient becomes symptomatic. The recommended frequency of clinical evaluation is based on the stability of the left ventricular end-systolic dimensions (ESD) and end-diastolic dimensions (EDD) as listed below. After the initial study, clinical evaluation and repeat echocardiogram are recommended in 3 months. Subsequent follow-up is based on the results of the 2 evaluations.

For patients with ESD < 45 mm or EDD < 60 mm and stable dimensions, clinical evaluation is recommended every 6-12 months and repeat echocardiography is recommended every 12 months. For patients with ESD < 45 mm or EDD < 60 mm and increasing dimensions, clinical evaluation and repeat echocardiography are recommended in 3 months. For patients with ESD 45-50 mm or EDD 60-70 mm and stable dimensions, clinical evaluation is recommended every 6 months and repeat echocardiography is recommended every 12 months. For patients with ESD 45-50 mm or EDD 60-70 mm and increasing dimensions, clinical evaluation and repeat echocardiography are recommended in 3 months. For patients with ESD 50-55 mm or EDD 70-75 mm and stable dimensions, clinical evaluation and repeat echocardiography are recommended every 6 months. For patients with ESD 50-55 mm or EDD 70-75 mm and increasing dimensions, clinical evaluation and repeat echocardiography are recommended in 3 months. For patients with ESD >55 mm or EDD >75 mm, surgery is recommended.

Inpatient & Outpatient Medications

Vasodilator therapy may be used on an inpatient or outpatient basis under the conditions listed above as recommended under current ACC/AHA guidelines. All patients with artificial heart valves should receive antibiotic prophylaxis prior to dental procedures. For antithrombotic therapy, all patients with artificial heart valves should receive daily aspirin, and many should also receive oral anticoagulation therapy with warfarin according to the ACC/AHA guidelines.[5]

Transfer
For patients who are hospitalized for severe AR in facilities without appropriate cardiovascular and surgical expertise, transfer may be justified to optimize clinical outcomes. For outpatients with stable but severe AR, longitudinal care by a cardiologist with appropriate expertise is recommended.

Deterrence/Prevention
Recommendations regarding exercise and antibiotic prophylaxis have been discussed above.

Complications
Left untreated, acute severe AR is likely to lead to considerable morbidity and mortality from either the underlying cause (typically infective endocarditis or aortic dissection) or from hemodynamic decompensation of the LV. Potential complications in patients with chronic severe AR include progressive LV dysfunction and dilation, congestive heart failure, myocardial ischemia, arrhythmia, and sudden death. Additional complications may arise as a result of the patient's underlying condition (such as aortic root dissection in a patient with a bicuspid aortic valve and a severely dilated aortic root).

Prognosis
The prognosis for patients with severe AR depends on the presence or absence of LV dysfunction and symptoms, as follows:[5]

In asymptomatic patients with normal EF o Rate of progression to symptoms or LV dysfunction = < 6% per year o Rate of progression to asymptomatic LV dysfunction = < 3.5% per year o Rate of sudden death = less than 0.2% per year In asymptomatic patients with decreased EF, rate of progression to symptoms = >25% per year. In symptomatic patients, mortality rate = >10% per year.

Again, the strongest predictors of outcome are echocardiographic parameters (EF and LV endsystolic dimension), underscoring the crucial role of serial echocardiography in the management of patients with severe AR.

Patient Education
The current ACC/AHA guidelines for valvular heart disease, including for AR, are available to the public online for free.[5] Additionally, educational and support organizations exist for many of the underlying conditions, such as National Marfan Foundation and Bicuspid Aortic Foundation.