You are in: eMedicine Specialties > Radiology > CARDIAC Aortic RegurgitationArticle Last Updated: Sep 10, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI, Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine Vibhuti N Singh is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Florida Medical Association Coauthor(s): Rakesh K Sharma, MBBS, FACC, FACP, Interventional Cardiologist, The Heart and Vascular Institute of Florida; Navin C Nanda, MD, FACC, Director, Heart Station and Echocardiography Laboratories, Professor, Department of Internal Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham; Hanumanth K Reddy, MD, FACC, Clinical Professor of Medicine, St Louis University Medical School; Associate Chief, Department of Cardiovascular Services, Three Rivers Healthcare; Joel A Strom, MD, ME, Professor of Internal Medicine, Chemical and Biomedical Engineering, and Honors College, University of South Florida Editors: Justin D Pearlman, MD, PhD, ME, MA, Director of Dartmouth Advanced Imaging Center, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Robert M Steiner, MD, Professor of Radiology, Temple University School of Medicine, Clinical Professor of Radiology, Medical School of the University of Pennsylvania; Consulting Radiologist, Temple University Hospital, Temple University Children's Medical Center; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Clinical Assistant Professor of Radiology, University of Washington Medical School Author and Editor Disclosure Synonyms and related keywords: aortic regurgitation, aortic valvular regurgitation, aortic insufficiency, aortic valve insufficiency, aortic valvular insufficiency, valve regurgitation, valvular regurgitation, heart valve disease, aorta valve regurgitation, AR, aortic incompetence, AI, aortic valve disease, aortic root disease, rheumatic fever, aortic valve replacement, AVR INTRODUCTIONSection 2 of 12
  BackgroundAortic regurgitation affects 10% of all patients with valvular heart disease. It is characterized by an abnormal backward leakage of blood from the aorta into the left ventricle (LV) during the diastolic phase of the cardiac cycle. The disease process may involve the aortic valve cusps, the aortic root, or both.1, 2 Clinically, aortic regurgitation manifests itself in a wide variety of ways; it may be recognized in association with an asymptomatic heart murmur on physical examination, or it may manifest itself in symptoms of substantial LV dysfunction and heart failure. The diagnosis may be established through any of a number of noninvasive techniques. Echocardiography has emerged as the most important imaging modality in the diagnosis of aortic regurgitation; echocardiography is also useful in the determination of the causes and severity of aortic regurgitation, as well as in decisions as to management strategy. Treatment often depends on whether the regurgitation develops acutely or as a chronic disease. Patients with acute aortic regurgitation have a poor prognosis unless rapid surgical treatment is undertaken. Chronic aortic regurgitation may remain asymptomatic for years. The prognosis for asymptomatic patients is generally good, as compared with patients who have symptoms of LV dysfunction. Medical management is the initial choice. This treatment strategy involves the use of pharmacologic agents for afterload reduction, the treatment of symptoms, and prophylaxis against subacute bacterial endocarditis, as well as periodic echocardiographic assessment to monitor progression of aortic regurgitation. Aortic valve replacement is indicated in later stages before LV dysfunction sets in; however, determination of the exact timing of the procedure requires careful analysis of echocardiographic indices and, occasionally, cardiopulmonary exercise testing. The surgical outcome is usually good, with mortality rates of 3-8%. After valve replacement, the progression of heart failure stops in most patients; some patients experience positive remodeling and improvement in exertional capacity.3, 4 PathophysiologyChronic aortic regurgitation Aortic regurgitation represents a reflux of blood that has been ejected into the aorta back into the LV during the diastolic phase of each cardiac cycle. The LV receives blood from the left atrium at the same time. This results in volume overload of the LV, which over time, leads to structural and physiologic changes in the LV. The gradual structural change causes sizable LV enlargement — enlargement greater than that seen in any other form of heart disease. LV end-diastolic volume increases, but LV compliance often increases and LV end-diastolic pressure stays near normal. LV hypertrophy is minimal; it is of an eccentric variety known as hypertrophy in length. It is caused by replication of myocardial sarcomeres in series. Through such hypertrophy, systolic wall stress is maintained at normal levels, and the ratio of LV thickness to cavity radius remains normal. This adaptive response allows the LV to function as an effective low-compliance pump. As aortic regurgitation becomes severe, the regurgitant flow may exceed 20 L/min, with total LV output almost 30 L/min — a level seen only in trained endurance runners at maximal exercise. Ultimately, a persistent rise in preload and afterload in aortic regurgitation leads to myocardial dysfunction. LV end-diastolic volume increases disproportionately to the regurgitant amount. This process of decompensation may be gradual and may precede the onset of symptoms. With progressive LV decompensation, an increase in the pressure occurs in the left atrium, the pulmonary bed, the right ventricle, and the right atrium; cardiac output decreases, even at rest. It is crucial for the clinician to detect the onset of such LV dysfunction to avoid missing the optimal time for valve replacement. The extent and severity of aortic regurgitation depend on the size of the diastolic aortic valve opening, the diastolic gradient between the aortic and LV pressure, and the length of the diastolic period. During dynamic exercise, as the heart rate increases, the diastolic period tends to shorten, leading to a decrease in the amount of aortic regurgitation. The increased systolic output into the aorta and the diastolic blood reflux into the LV cause an increase in pulse pressure; manifestations include the Corrigan pulse and the Hill sign. Lower diastolic aortic pressure leads to a lower-pressure head in the coronary circulation, which may manifest as ischemia. The regurgitant jet may hit the anterior mitral cusp, causing reverse doming in diastole. Fast-moving blood produces a drop in pressure (ie, the Bernoulli effect), which can pull the anterior mitral leaflet and/or submitral chordae toward the outflow tract (systolic anterior motion [SAM]). The ascending aorta may progressively dilate in turn, leading to poorer aortic cusp coaptation and increasing regurgitation. Acute aortic regurgitation In contrast with chronic aortic regurgitation, in which the LV may adapt to the volume overload by becoming enlarged and hypertrophic, in acute aortic regurgitation, the LV is of normal dimension and compliance. In such cases, the stroke volume cannot increase adequately, and forward cardiac output declines. LV volumes remain small, and the pulse pressure decreases. To compensate for the low stroke volume, the heart rate increases sharply, and patients experience tachycardia. Rising LV end-diastolic pressure leads to early closure of the mitral valve, which protects the pulmonary vascular bed from the backward transmission of high pressure. However, it also reduces LV preload. Systolic pressure in the LV and aorta remains normal. FrequencyUnited StatesAortic regurgitation accounts for approximately 10% of all cases of valvular heart disease. Only 5% of patients with a bicuspid aortic valve develop aortic regurgitation as a primary problem. Myxomatous degeneration occurs in up to 15% of patients. Dilatation of the aortic root is common in cases of aortic regurgitation; such dilatation is associated with connective-tissue changes in the media. InternationalRheumatic fever accounts for most cases of aortic regurgitation worldwide. Mortality/MorbidityFor patients with aortic regurgitation, mortality and morbidity rates are greater or lesser, depending on whether the disease is acute in onset or is chronic. In the latter case, these rates vary in accordance with whether symptoms are present and, if so, how severe those symptoms are, as well as with the degree of LV dysfunction.
RaceAortic regurgitation has been described in all races. SexNo clear-cut sex predilection appears to exist in aortic regurgitation. Age
AnatomyCauses of aortic regurgitation Rheumatic heart disease still remains the most common cause of severe aortic regurgitation. Over the past several decades, however, diseases involving the aortic root are becoming more frequent. Causes of aortic regurgitation include the following:
Aortic cusp disease Aortic cusp disease leads to aortic regurgitation as a result of inadequate leaflet coaptation; such inadequate leaf coaptation is a result of the cusps shrinking or retracting because of inflammation. For example, in rheumatic fever, the cusps that are infiltrated by fibrous tissue gradually shrink, leading to regurgitation into the LV through a central opening. When the inflammatory process leads to fusion of the commissures, combined aortic stenosis and aortic regurgitation may occur. Other primarily valvular causes of aortic regurgitation Other primarily valvular causes of aortic regurgitation include the following:
Causes of aortic root disease Aortic root disease may result from dilatation of the ascending aorta, as well as from other processes. Aortic regurgitation secondary to severe dilatation of the ascending aorta is becoming more frequent than primary aortic cusp disease in patients operated on for isolated aortic regurgitation. Diseases that involve the aortic root include degenerative aortic dilatation in the elderly; cystic medial necrosis of the aorta in patients with Marfan syndrome; syphilitic aortitis; and dissection of the ascending aorta. Clinical DetailsClinical findings in chronic aortic regurgitationMost patients with aortic regurgitation are asymptomatic, and the diagnosis is made with the detection of a heart murmur during physical examination. Symptoms Although a heart murmur and heart failure may develop rapidly in patients with acute aortic regurgitation, patients with chronic regurgitation develop symptoms late in the course of the disease. Chronic regurgitation may be present for a decade before exertional dyspnea develops as its presenting symptom. Patients whose functional capacity is reduced to NYHA class III generally have underlying LV dysfunction. Heart pounding is another frequent symptom; chest pain occurs in 20% of the patients with aortic regurgitation. Concomitant coronary stenosis is also present in 20% of patients. Chest pain occurs less often in patients with aortic regurgitation than in patients with aortic stenosis; however, nocturnal angina, often accompanied by diaphoresis, may occur when the heart rate slows and arterial diastolic pressure falls to extremely low levels. Some patients with aortic regurgitation also report abdominal pain; it is presumed that such pain is secondary to splanchnic ischemia. Signs In severe chronic aortic regurgitation, a marked decrease in diastolic pressure occurs in conjunction with some increase in systolic blood pressure. As a result, the pulse pressure may become high, often greater than 80 mm Hg. In patients with this finding, determination of the exact diastolic blood pressure becomes difficult because the Korotkoff sounds remain audible all the way down to zero. The diastolic pressure is established at the point of muffling. On inspection, visible pulsations of the carotid artery are noticeable. Such pulsations are the result of a wide pulse pressure and rapid decrease; such pulsations may be transmitted to the adjacent tissues in the neck, causing pulsatile movements of the head (Musset sign), larynx (Oliver-Cardarelli sign), and uvula (Muller sign). Capillary pulsations over the lips and the ball of the fingertips may be visualized using light compression with a glass slide. The pulsations in the abdominal aorta may be visible in the suprarenal region. On palpation, the rapid arterial filling followed by an abrupt fall in the intraluminal pressure as a result of aortic regurgitation causes a water-hammer pulse (Corrigan pulse). Auscultation over the femoral arteries in patients with at least moderate aortic regurgitation exhibits a loud, early systolic sound, called a pistol-shot sound. On gentle compression of the femoral artery, one may hear a systodiastolic murmur (Duroziez sign). Precordial auscultation usually reveals a soft first heart sound (S1) and a loud S2. The latter becomes muffled as aortic regurgitation worsens. An S3 gallop is audible once LV dysfunction sets in. The characteristic murmur of chronic aortic regurgitation is a diastolic decrescendo murmur, which is best heard in the right second intercostal space. If the patient sits up and leans forward, the same murmur may be heard in the left third and fourth intercostal spaces. As the disease worsens, the length of the murmur increases; eventually, in the most severe cases, it is present throughout the entire diastolic period. Occasionally, the diastolic murmur of aortic regurgitation sounds musical, like a seagull cry or "dove coo" murmur. A concomitant systolic ejection murmur is almost always present; it results from an increase in turbulent flow through the aortic valve. Patients with severe aortic regurgitation sometimes exhibit a diastolic murmur at the apex (Austin Flint murmur), as a result of functional mitral stenosis. The anterior mitral leaflet closes early because the aortic regurgitation jet hits it in diastole. Clinical findings in acute aortic regurgitationBecause of the limited ability of the LV to handle acute severe aortic regurgitation, patients with acute disease generally have a sudden onset of symptoms, including heart failure with weakness, severe dyspnea, and hypertension. Angina is uncommon. The pulse pressure is generally not wide; therefore, the signs related to increased pulsation are lacking. The murmur of aortic regurgitation is shorter as well, and it ends in the middle of the diastolic interval. Also, because the mitral valve closes in diastole, no S1 is audible. Preferred ExaminationElectrocardiography In patients with chronic aortic regurgitation, electrocardiography usually shows a normal sinus rhythm; as the disease progresses, evidence of LV hypertrophy becomes apparent. Some patients may have a first-degree heart block. The presence of ST-segment depression and T-wave inversion is associated with an adverse prognosis. A bundle-branch block may develop in cases of advanced aortic regurgitation.5 Holter monitoring In patients with aortic regurgitation, 24-hour Holter monitoring may show complex ventricular arrhythmias. The severity of arrhythmias is proportional to the deterioration of LV function. Systolic time intervals For patients with chronic aortic regurgitation, carotid pulse tracing may exhibit rapid upstroke and the absence of a clear-cut incisura on the downstroke. Systolic intervals are rarely used at present. Chest radiography An enlarged cardiac silhouette is often the hallmark of a patient with significant aortic regurgitation. As aortic regurgitation becomes more severe, LV enlargement ensues, mainly in the transverse and caudal directions, leading to an increase in the cardiothoracic ratio. A cardiothoracic ratio in excess of 0.60 is associated with a diminished survival rate. Dilatation of the aorta, as well as aortic valvular calcification, is occasionally seen. Echocardiography Two-dimensional, color, and Doppler echocardiography have become preferred imaging techniques in the diagnosis and assessment of aortic regurgitation. With these modalities, the disease may be identified, and the severity and (in many instances) the etiology may be determined with high sensitivity and specificity. In addition, analysis of the LV function and end-diastolic dimension may be used to determine the optimal timing of valve surgery.5 Radioisotope study Radioisotope studies may occasionally be used to quantify the severity of AR. Likewise, the LV function may be assessed. Determination of preexercise and postexercise LV ejection fraction (LVEF) may often show a failure of the ejection fraction to increase during exercise; this is an indicator of early LV dysfunction. Generally, echocardiography has come to replace these tests; echocardiography has demonstrated reasonable reliability. Cardiopulmonary exercise testing Exercise capacity and maximal oxygen consumption may be measured to determine the onset of functional deterioration; subsequently, surveillance may aid in deciding the optimal time for surgical intervention. Cardiac catheterization and angiography Cardiac catheterization is used mainly for evaluating concomitant coronary artery disease before surgery. Noninvasive techniques have supplanted angiocardiography for the evaluation of aortic regurgitation. Limitations of TechniquesElectrocardiographic findings are generally nonspecific. Systolic intervals are no longer used in clinical practice. Chest radiographic findings of an increase in the cardiothoracic ratio may aid in the diagnosis, but such findings cannot of themselves be used to make a diagnosis. Echocardiography is pivotal to making the diagnosis of aortic regurgitation, as well as in determining its severity and the timing of surgery. Limitations, which are minimal, may include poor acoustic windows. Findings may be equivocal for determining the onset of LV dysfunction, in which case a radioisotope technique may be helpful. Certain patients may need to undergo cardiopulmonary exercise testing to determine the optimal time for valve replacement. DIFFERENTIALSSection 3 of 12
Ankylosing Spondylitis Aorta, Dissection Crohn Disease Osteogenesis Imperfecta Psoriatic Arthritis Other Problems To Be ConsideredMarfan syndrome
RADIOGRAPHSection 4 of 12
FindingsThe size of the heart is represented by the size of the cardiac shadow or silhouette seen on the chest radiograph. In patients with chronic aortic regurgitation, the size of the heart depends on both the severity and the duration of the regurgitation (see Image 5). In patients with aortic regurgitation, chest radiographs show cardiac enlargement, as manifested by an increase in the cardiothoracic ratio (ie, the diameter of the cardiac shadow divided by the diameter of the thoracic cavity). The LV is enlarged laterally and inferiorly. Therefore, the vertical diameter increases more prominently than the horizontal diameter. The left atrium may also be enlarged. Dilatation of the aortic root may be seen as well. In some patients with combined aortic stenosis and regurgitation, aortic valvular calcification may also be present. Linear calcifications in the wall of the ascending aorta may be seen in cases of syphilitic aortitis. Degree of ConfidenceRadiographic findings are nonspecific for aortic regurgitation. MRISection 5 of 12
FindingsMRI may be a valuable tool in the assessment of aortic regurgitation. MRI may be used if echo windows are poor. For instance, the lung may block echo views, and aortic root calcifications may produce echo image artifacts. Aortic regurgitation is easily detected with MRI by use of gradient recalled echo (GRE; FIESTA) sequences; regurgitation may be accurately quantified by use of dynamic 2-dimensional (2D) phase contrast. This method creates a series of images at the level of the aortic root that show the direction and speed of blood movement throughout the cardiac cycle. The forward and regurgitant volumes may be calculated more accurately with MRI than with sonography to compute regurgitant volume and regurgitant fraction. In patients with aortic regurgitation, MRI may still be helpful in cases in which the Doppler echocardiographic results are insufficient or are not consistent with the clinical data.6 Pulse sequences Recent technologic advances in MRI computer technologies have enabled the use of many pulse sequences for cardiac imaging. The 2 main pulse sequences may be classified as dark-blood and bright-blood techniques. In the dark-blood techniques, such as spin-echo (SE) and fast SE (FSE) imaging, the fast-flowing blood is black and of low intensity. This method is principally useful for delineating the structure of cardiac chambers and the lumens of blood vessels. In contrast, the bright-blood techniques, such as GRE sequences, depict flowing blood as white and of high intensity. This method can be used to determine gradients and flows. In some cases, the cause of the regurgitation may be inferred by examining SE images. Examples include aortoannular ectasia, aortic dissection, and endocarditis. Certain structural changes related to valvular regurgitation, such as LV enlargement, may also be demonstrated on SE images. Blood has high signal intensity on cine GE images. An abnormal flow pattern caused by aortic regurgitation creates dephasing of the spins in a voxel, causing signal loss, or flow void. This is better demonstrated with longer echo time (TE). Cine GE images enable quantitative assessment of aortic regurgitation on the basis of the area and the length of the signal void. Aortic regurgitation is best seen on a coronal plane as a signal void extending from the aortic valve into the LV during diastole. Fast cine GE imaging may be used to measure ventricular and stroke volumes and to calculate the regurgitant fraction (regurgitant volume divided by LV stroke volume). Imaging planes The imaging planes for MRI of the thorax are the 3 orthogonal planes: transverse, sagittal, and coronal. Because the cardiac axes are not parallel to the body axes, planes parallel and orthogonal to cardiac axes (short axis and long axis of the heart) are used for cardiac imaging. Velocity-encoded MRI Velocity-encoded MRI is the best way to calculate LV and right ventricular stroke volumes and to quantify the aortic regurgitant fraction. This technique may be used to measure the blood flow in the ascending aorta and the pulmonary artery or to display phase shift. Fixed areas appear gray, whereas blood flow in a forward and a backward direction along a flow-encoding axis appears bright and dark, respectively. These findings permit the estimation of antegrade and retrograde flow, which may also be color coded. Curves of flow versus time during cardiac cycle are then plotted. The area of the curve beneath the baseline indicates the regurgitant volume; the area above the baseline represents the stroke volume. The regurgitant fraction may then be calculated. Degree of ConfidenceCine GE images with measurements such as the area and depth of signal void provide only a semiquantitative assessment of the severity of aortic regurgitation. The signal void is generally traced manually; it may vary, depending on the image display settings. This method has limitations because the display of signal void may vary, inasmuch as it is affected by the difference in TE, display parameters, and even physiologic factors, such as variance in LV volume and pressure. Cine GE is not a determinant of MRI confidence. In addition, 2D phase-contrast analysis does not rely on the assumptions commonly used with echo Doppler study, and it produces reliable model-independent measurements. However, arrhythmias, electrocardiographic gating problems, and obesity may reduce MRI quality. Good-quality MRI offers a high degree of confidence, but with gating or other problems, the confidence level may be low. False Positives/NegativesThere is essentially never a false-positive MRI. The display of the signal void on cine GE images depends on several technical parameters, such as display parameters, including window level and window width; flip angle; and, most importantly, the TE. With a short TE, the signal void may even disappear, whereas with a long TE, it tends to show up well. This dependency must be taken into account, and the TE should be kept long. One way to decrease the acquisition time by a factor of 2 or 3 is to use segmentation of k space, depending on the heart rate. 2D phase-contrast imaging may produce a false-negative result if the parameters are set incorrectly (few temporal bins, low velocity sensitivity, or velocity aliasing) or if gating is poor. Simple GE imaging may produce a false-negative result if MRIs are acquired with only a short TE, but this is much less of an issue with GRE. ULTRASOUNDSection 6 of 12
FindingsEchocardiography Echocardiography is generally the most important diagnostic imaging study for evaluating patients with aortic regurgitation. The presence or absence of regurgitation is reliably established by means of Doppler echocardiography. However, quantification of the severity is difficult, and it requires integration of several M-mode, 2D, and Doppler indices; no one index alone has proved reliable.7, 8, 9, 10, 5 M-mode echocardiography M-mode echocardiograph shows diastolic fluttering of the anterior mitral leaflet (AML), which is a finding of diagnostic significance. It results from the aortic regurgitation jet hitting the AML, and may be seen in cases of aortic regurgitation of even mild degree. In severe cases, the AML may fully close from the impact of the jet; this finding may serve as an indication for valve surgery. Diastolic flutter of the interventricular septum may also be seen in some patients. Aortic root and LV dimensions are increased. M-mode echocardiography may show systolic anterior motion of the anterior mitral valve leaflet or chordae. 2D echocardiography The structural integrity of the aortic valve leaflet, the LV outflow tract, and the aortic root may be examined in detail in several planes by means of 2D echocardiography. Often, the cause of aortic regurgitation may be determined from these images. For example, the presence of aortic valve vegetation, a flail aortic leaflet, aortic cusp retraction and shortening, or aortic root abnormalities are discernible with reasonable ease. Determination of LV dimensions and systolic function is central to the decision regarding the timing of surgery. Some of the echocardiographic indices that represent indications for surgery include dilatation of the LV beyond 70 mm in diastole or beyond 55 mm in systole; a fractional shortening of less than 25%; and progressive dilation of the LV of 1.0 cm or more over a 12-month period. Color-flow imaging Aortic regurgitation may be quantified in terms of its severity by color-flow and Doppler echocardiography. Color-flow imaging may display the regurgitant jet in various planes. Whereas the size and depth of the jet is only poorly correlated with the severity of aortic regurgitation, measurement of the width or the cross-sectional area of the regurgitant jet as a ratio of the total width or cross-sectional area of the outflow tract is more reliable (see Images 1-3). Aortic regurgitation may be classified as mild, moderate, or severe on the basis of whether the width of the regurgitant jet occupies less than 20%, 20-40%, or more than 40% of the total width of the LV outflow tract, respectively. Another way of estimating the severity of regurgitation is by examining the regurgitant color-flow Doppler jet, which involves measuring the linear distance the jet travels into the LV cavity, or by mapping the area of the color jet. Doppler echocardiography By using continuous-wave Doppler imaging from the apex, the actual velocity of the regurgitant flow may be recorded. A relatively flat slope of velocity and pressure decay indicates mild aortic regurgitation, whereas a steep slope of velocity decay over the diastolic pressure curve (rapid deceleration or short pressure half-time) indicates severe disease. A pressure half-time value of the aortic regurgitation jet of greater than 450 ms indicates mild regurgitation; one less than 250 ms indicates severe regurgitation. Often, the continuity equation may be used to calculate the regurgitant volume. Retrograde flow should be assessed in the descending aorta. Small, retrograde, early diastolic signals are normal in the descending thoracic or abdominal aorta. However, any degree of holodiastolic retrograde flow indicates severe aortic regurgitation. Degree of ConfidenceThe degree of confidence is high. In the assessment of the severity of aortic regurgitation with color-flow Doppler techniques, the measurements depend on imaging the jet in its minor axis. An eccentric jet that crosses across the outflow tract results in a finding that is disproportionate to the jet's true dimension. Transesophageal echocardiography often provides more accurate visualization of the true direction and size of the regurgitant jet. False Positives/NegativesDoppler echo imaging may produce a false-positive result if continuous Doppler wave, a side lobe, or a distant multiple pulsed wave picks up a similar flow pattern (eg, from a resistive VSD). Doppler echo sonography may produce a false-negative result if the valve is not studied thoroughly at varied angles and if the regurgitant jet is angulated or is off-center (as may occur, eg, from a leaflet perforation). NUCLEAR MEDICINESection 7 of 12
FindingsRadioisotope techniques, especially first-pass multiple-gated acquisition (MUGA) scanning, may be used to determine the LVEF. Such techniques may also be used to assess the severity of aortic regurgitation. In patients who are minimally symptomatic or asymptomatic, an evaluation of LVEF before and after dynamic exercise may provide valuable clues regarding the onset of the early stages of LV dysfunction. In patients in whom myocardial dysfunction begins to develop, the ejection fraction does not increase after exercise. Degree of ConfidenceThe degree of confidence is moderate. Often, patients have LV dysfunction, but the studies may not show that the ejection fraction does not increase during exercise. ANGIOGRAPHYSection 8 of 12
FindingsInvasive evaluation of moderate to severe degrees of aortic regurgitation may be indicated when clinical deterioration appears to have begun, as evidenced by progressive symptoms; by an increase in the cardiothoracic ratio on the chest radiograph; by ST-T changes on electrocardiography; and by a fractional shortening of <25% on the echocardiogram, in conjunction with an end-diastolic LV diameter of >7 cm. Angiography helps in determining the presence of concomitant coronary artery disease, which may be found in 20% of patients (see Image 4). Hemodynamic arterial tracings typically show greatly increased pulse pressure. In cases of severe aortic regurgitation, the aortic and LV pressures tend to equalize at end diastole. A regurgitant fraction may be calculated by using green dye. A regurgitant fraction of <0.3 represents mild regurgitation, whereas a fraction of >0.5 represents severe regurgitation. An overall LVEF of <50% is of prognostic value; such a finding has been found to be predictive of greater postoperative mortality and a failure to recover cardiac pump function. Degree of ConfidenceThe degree of confidence is high. In the current era of thorough echocardiographic evaluation, the need for cardiac catheterization has diminished tremendously. Often, the only indication for performing catheterization in patients with chronic aortic regurgitation is the need to rule out the presence of significant coronary stenosis in patients older than 40 years. False Positives/NegativesFalse-positive and false-negative results are infrequent. A false-positive result may occur because of ectopy or because of the catheter's interfering with valve closure. A false-negative result may occur because of ectopy and/or outflow tract obstruction. INTERVENTIONSection 9 of 12
No percutaneous treatment modality is applicable to the treatment of aortic regurgitation. Prompt surgical treatment is recommended for symptomatic patients and patients with acute aortic regurgitation. The central aim in recommending valve replacement surgery is the preservation of LV function. In contrast, the outlook for asymptomatic patients is generally excellent for a number of years. Therefore, aortic valve replacement is deferred as long as the patient has good exercise tolerance, an ejection fraction of 50% or greater, and an LV end-diastolic diameter of under 7 cm. In asymptomatic patients with normal LVEF, close follow-up at 6-month intervals is recommended. Aortic valve replacement surgery should be undertaken if the LV end-diastolic dimension increases to greater than 7 cm, if the end-systolic diameter becomes 5.5 cm or more, and if the fractional shortening decreases to less than 25%. Medical/Legal Pitfalls
Special Concerns
FURTHER READINGSection 10 of 12
Guidelines on the management of valvular heart disease. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
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