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J Am Coll Cardiol, 2006; 48:1-148, doi:10.1016/j.jacc.2006.05.021 © 2006 by the American College of Cardiology Foundation |
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Table of contents |
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 Top Table of contents Preamble1. Introduction2. General principles3. Specific valve lesionsAPPENDIX 1. Author Relationships...APPENDIX 2. External Peer...APPENDIX 3. Abbreviation ListReferences |
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APPENDIX 1......e121
APPENDIX 2......e122
APPENDIX 3......e124
REFERENCES......e124
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Preamble |
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TopTable of contentsPreamble1. Introduction2. General principles3. Specific valve lesionsAPPENDIX 1. Author Relationships...APPENDIX 2. External Peer...APPENDIX 3. Abbreviation ListReferences |
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The American College of Cardiology (ACC) and the American Heart Association (AHA) have jointly engaged in the production of such guidelines in the area of cardiovascular disease since 1980. This effort is directed by the ACC/AHA Task Force on Practice Guidelines, whose charge is to develop, update, or revise practice guidelines for important cardiovascular diseases and procedures. Writing committees are charged with the task of performing an assessment of the evidence and acting as an independent group of authors to develop and update written recommendations for clinical practice.
Experts in the subject under consideration are selected from both organizations to examine subject-specific data and write guidelines. The process includes additional representatives from other medical practitioner and specialty groups where appropriate. Writing committees are specifically charged to perform a formal literature review, weigh the strength of evidence for or against a particular treatment or procedure, and include estimates of expected health outcomes where data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that might influence the choice of particular tests or therapies are considered, as well as frequency of follow-up. When available, information from studies on cost will be considered; however, review of data on efficacy and clinical outcomes will be the primary basis for preparing recommendation in these guidelines.
The ACC/AHA Task Force on Practice Guidelines makes every effort to avoid any actual, potential, or perceived conflicts of interest that might arise as a result of an outside relationship or personal interest of a member of the writing committee. Specifically, all members of the writing committee and peer reviewers of the document are asked to provide disclosure statements of all such relationships that might be perceived as real or potential conflicts of interest. Writing committee members are also strongly encouraged to declare a previous relationship with industry that might be perceived as relevant to guideline development. If a writing committee member develops a new relationship with industry during his or her tenure, he or she is required to notify guideline staff in writing. The continued participation of the writing committee member will be reviewed. These statements are reviewed by the parent task force, reported orally to all members of the writing panel at each meeting, and updated and reviewed by the writing committee as changes occur. Please refer to the methodology manual for the ACC/AHA guideline writing committees for further description and the relationships with industry policy, available on ACC and AHA World Wide Web sites (http://www.acc.org/clinical/manual/manual_introltr.htm and http://circ.ahajournals.org/manual). See Appendix 1 for a list of writing committee member relationships with industry and Appendix 2 for a listing of peer reviewer relationships with industry that are pertinent to this guideline.
These practice guidelines are intended to assist healthcare providers in clinical decision making by describing a range of generally acceptable approaches for the diagnosis, management, and prevention of specific diseases or conditions. These guidelines attempt to define practices that meet the needs of most patients in most circumstances. These guideline recommendations reflect a consensus of expert opinion after a thorough review of the available, current scientific evidence and are intended to improve patient care. If these guidelines are used as the basis for regulatory/payer decisions, the ultimate goal is quality of care and serving the patient’s best interests. The ultimate judgment regarding care of a particular patient must be made by the healthcare provider and patient in light of all of the circumstances presented by that patient. There are circumstances in which deviations from these guidelines are appropriate.
The "ACC/AHA 2006 Guideline for the Management of Patients With Valvular Heart Disease" was approved for publication by the ACC Foundation (ACCF) board of trustees in May 2006 and the AHA Science Advisory and Coordinating Committee in May 2006. The executive summary and recommendations are published in the August 1, 2006 issue of the Journal of the American College of Cardiology and the August 1, 2006 issue of Circulation. The full-text guideline is e-published in the same issues of each journal and is posted on the World Wide Web sites of the ACC (www.acc.org) and the AHA (www.americanheart.org). The guidelines will be reviewed annually by the ACC/AHA Task Force on Practice Guidelines and will be considered current unless they are updated, revised, or sunsetted and withdrawn from distribution. Copies of the full text and the executive summary are available from both organizations.
Sidney C. Smith, Jr., MD, FACC, FAHA, Chair, ACC/AHA Task Force on Practice Guidelines
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1. Introduction |
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TopTable of contentsPreamble1. Introduction2. General principles3. Specific valve lesionsAPPENDIX 1. Author Relationships...APPENDIX 2. External Peer...APPENDIX 3. Abbreviation ListReferences |
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During the past 2 decades, major advances have occurred in diagnostic techniques, the understanding of natural history, and interventional cardiology and surgical procedures for patients with valvular heart disease. These advances have resulted in enhanced diagnosis, more scientific selection of patients for surgery or catheter-based intervention versus medical management, and increased survival of patients with these disorders. The information base from which to make clinical management decisions has greatly expanded in recent years, yet in many situations, management issues remain controversial or uncertain. Unlike many other forms of cardiovascular disease, there is a scarcity of large-scale multicenter trials addressing the diagnosis and treatment of patients with valvular disease from which to derive definitive conclusions, and the information available in the literature represents primarily the experiences reported by single institutions in relatively small numbers of patients.
The 1998 Committee on Management of Patients With Valvular Heart Disease reviewed and compiled this information base and made recommendations for diagnostic testing, treatment, and physical activity. For topics for which there was an absence of multiple randomized, controlled trials, the preferred basis for medical decision making in clinical practice (evidence-based medicine), the committee’s recommendations were based on data derived from single randomized trials or nonrandomized studies or were based on a consensus opinion of experts. The current writing committee was charged with revising the guidelines published in 1998. The committee reviewed pertinent publications, including abstracts, through a computerized search of the English literature since 1998 and performed a manual search of final articles. Special attention was devoted to identification of randomized trials published since the original document. A complete listing of all publications covering the treatment of valvular heart disease is beyond the scope of this document; the document includes those reports that the committee believes represent the most comprehensive or convincing data that are necessary to support its conclusions. However, evidence tables were updated to reflect major advances over this time period. Inaccuracies or inconsistencies present in the original publication were identified and corrected when possible. Recommendations provided in this document are based primarily on published data. Because randomized trials are unavailable in many facets of valvular heart disease treatment, observational studies and, in some areas, expert opinions form the basis for recommendations that are offered.
All of the recommendations in this guideline revision were converted from the tabular format used in the 1998 guideline to a listing of recommendations that has been written in full sentences to express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document, would still convey the full intent of the recommendation. It is hoped that this will increase the readers’ comprehension of the guidelines. Also, the level of evidence, either A, B, or C, for each recommendation is now provided.
Classification of recommendations and level of evidence are expressed in the ACC/AHA format as follows:
In addition, the weight of evidence in support of the recommendation is listed as follows:
The schema for classification of recommendations and level of evidence is summarized in Figure 1, which also illustrates how the grading system provides an estimate of the size of the treatment effect and an estimate of the certainty of the treatment effect.
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This document was reviewed by 2 official reviewers nominated by the ACC; 2 official reviewers nominated by the AHA; 1 official reviewer from the ACC/AHA Task Force on Practice Guidelines; reviewers nominated by the Society of Cardiovascular Anesthesiologists, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons (STS); and individual content reviewers, including members of the ACCF Cardiac Catheterization and Intervention Committee, ACCF Cardiovascular Imaging Committee, ACCF Cardiovascular Surgery Committee, AHA Endocarditis Committee, AHA Cardiac Clinical Imaging Committee, AHA Cardiovascular Intervention and Imaging Committee, and AHA Cerebrovascular Imaging and Intervention Committee.
1.2 Scope of the Document. The guidelines attempt to deal with general issues of treatment of patients with heart valve disorders, such as evaluation of patients with heart murmurs, prevention and treatment of endocarditis, management of valve disease in pregnancy, and treatment of patients with concomitant coronary artery disease (CAD), as well as more specialized issues that pertain to specific valve lesions. The guidelines focus primarily on valvular heart disease in the adult, with a separate section dealing with specific recommendations for valve disorders in adolescents and young adults. The diagnosis and management of infants and young children with congenital valvular abnormalities are significantly different from those of the adolescent or adult and are beyond the scope of these guidelines.
This task force report overlaps with several previously published ACC/AHA guidelines about cardiac imaging and diagnostic testing, including the guidelines for the clinical use of cardiac radionuclide imaging (1), the clinical application of echocardiography (2), exercise testing (3), and percutaneous coronary intervention (4). Although these guidelines are not intended to include detailed information covered in previous guidelines on the use of imaging and diagnostic testing, an essential component of this report is the discussion of indications for these tests in the evaluation and treatment of patients with valvular heart disease.
The committee emphasizes the fact that many factors ultimately determine the most appropriate treatment of individual patients with valvular heart disease within a given community. These include the availability of diagnostic equipment and expert diagnosticians, the expertise of interventional cardiologists and surgeons, and notably, the wishes of well-informed patients. Therefore, deviation from these guidelines may be appropriate in some circumstances. These guidelines are written with the assumption that a diagnostic test can be performed and interpreted with skill levels consistent with previously reported ACC training and competency statements and ACC/AHA guidelines, that interventional cardiological and surgical procedures can be performed by highly trained practitioners within acceptable safety standards, and that the resources necessary to perform these diagnostic procedures and provide this care are readily available. This is not true in all geographic areas, which further underscores the committee’s position that its recommendations are guidelines and not rigid requirements.
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2. General principles |
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TopTable of contentsPreamble1. Introduction2. General principles3. Specific valve lesionsAPPENDIX 1. Author Relationships...APPENDIX 2. External Peer...APPENDIX 3. Abbreviation ListReferences |
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Often, more than 1 of these factors is operative (5–7).
A heart murmur may have no pathological significance or may be an important clue to the presence of valvular, congenital, or other structural abnormalities of the heart (8). Most systolic heart murmurs do not signify cardiac disease, and many are related to physiological increases in blood flow velocity (9). In other instances, a heart murmur may be an important clue to the diagnosis of undetected cardiac disease (e.g., valvular aortic stenosis [AS]) that may be important even when asymptomatic or that may define the reason for cardiac symptoms. In these situations, various noninvasive or invasive cardiac tests may be necessary to establish a firm diagnosis and form the basis for rational treatment of an underlying disorder. Echocardiography is particularly useful in this regard, as discussed in the "ACC/AHA/ASE 2003 Guidelines for the Clinical Application of Echocardiography" (2). Diastolic murmurs virtually always represent pathological conditions and require further cardiac evaluation, as do most continuous murmurs. Continuous "innocent" murmurs include venous hums and mammary souffles.
The traditional auscultation method of assessing cardiac murmurs has been based on their timing in the cardiac cycle, configuration, location and radiation, pitch, intensity (grades 1 through 6), and duration (5–9). The configuration of a murmur may be crescendo, decrescendo, crescendo-decrescendo (diamond-shaped), or plateau. The precise times of onset and cessation of a murmur associated with cardiac pathology depend on the period of time in the cardiac cycle in which a physiologically important pressure difference between 2 chambers occurs (5–9). A classification of cardiac murmurs is listed in Table 1.
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Midsystolic (systolic ejection) murmurs, often crescendo-decrescendo in configuration, occur when blood is ejected across the aortic or pulmonic outflow tracts. The murmurs start shortly after S1, when the ventricular pressure rises sufficiently to open the semilunar valve. As ejection increases, the murmur is augmented, and as ejection declines, it diminishes.
In the presence of normal semilunar valves, this murmur may be caused by an increased flow rate such as that which occurs with elevated cardiac output (e.g., pregnancy, thyrotoxicosis, anemia, and arteriovenous fistula), ejection of blood into a dilated vessel beyond the valve, or increased transmission of sound through a thin chest wall. Most innocent murmurs that occur in children and young adults are midsystolic and originate either from the aortic or pulmonic outflow tracts. Valvular, supravalvular, or subvalvular obstruction (stenosis) of either ventricle may also cause a midsystolic murmur, the intensity of which depends in part on the velocity of blood flow across the narrowed area. Midsystolic murmurs also occur in certain patients with functional mitral regurgitation (MR) or, less frequently, tricuspid regurgitation (TR). Echocardiography is often necessary to separate a prominent and exaggerated (grade 3) benign midsystolic murmur from one due to valvular AS.
Early systolic murmurs are less common; they begin with the first sound and end in midsystole. An early systolic murmur is often due to TR that occurs in the absence of pulmonary hypertension, but it also occurs in patients with acute MR. In large ventricular septal defects with pulmonary hypertension and small muscular ventricular septal defects, the shunting at the end of systole may be insignificant, with the murmur limited to early and midsystole.
Late systolic murmurs are soft or moderately loud, high-pitched murmurs at the left ventricular (LV) apex that start well after ejection and end before or at S2. They are often due to apical tethering and malcoaptation of the mitral leaflets due to anatomic and functional changes of the annulus and ventricle. Late systolic murmurs in patients with midsystolic clicks result from late systolic regurgitation due to prolapse of the mitral leaflet(s) into the left atrium. Such late systolic murmurs can also occur in the absence of clicks.
Early diastolic murmurs begin with or shortly after S2, when the associated ventricular pressure drops sufficiently below that in the aorta or pulmonary artery. High-pitched murmurs of aortic regurgitation (AR) or pulmonic regurgitation due to pulmonary hypertension are generally decrescendo, consistent with the rapid decline in volume or rate of regurgitation during diastole. The diastolic murmur of pulmonic regurgitation without pulmonary hypertension is low to medium pitched, and the onset of this murmur is slightly delayed because regurgitant flow is minimal at pulmonic valve closure, when the reverse pressure gradient responsible for the regurgitation is minimal. Such murmurs are common late after repair of tetralogy of Fallot.
Middiastolic murmurs usually originate from the mitral and tricuspid valves, occur early during ventricular filling, and are due to a relative disproportion between valve orifice size and diastolic blood flow volume. Although they are usually due to mitral or tricuspid stenosis, middiastolic murmurs may also be due to increased diastolic blood flow across the mitral or tricuspid valve when such valves are severely regurgitant, across the normal mitral valve (MV) in patients with ventricular septal defect or patent ductus arteriosus, and across the normal tricuspid valve in patients with atrial septal defect. In severe, chronic AR, a low-pitched, rumbling diastolic murmur (Austin-Flint murmur) is often present at the LV apex; it may be either middiastolic or presystolic. An opening snap is absent in isolated AR.
Presystolic murmurs begin during the period of ventricular filling that follows atrial contraction and therefore occur in sinus rhythm. They are usually due to mitral or tricuspid stenosis. A right or left atrial myxoma may cause either middiastolic or presystolic murmurs similar to tricuspid or mitral stenosis (MS).
Continuous murmurs arise from high- to low-pressure shunts that persist through the end of systole and the beginning of diastole. Thus, they begin in systole, peak near S2, and continue into all or part of diastole. There are many causes of continuous murmurs, but they are uncommon in patients with valvular heart disease (5–9).
2.1.2.1 Dynamic Cardiac Auscultation
Attentive cardiac auscultation during dynamic changes in cardiac hemodynamics often enables the observer to deduce the correct origin and significance of a cardiac murmur (10–13). Changes in the intensity of heart murmurs during various maneuvers are indicated in Table 2.
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Conversely, many asymptomatic children and young adults with grade 2/6 midsystolic murmurs and no other cardiac physical findings need no further workup after the initial history and physical examination (Fig. 2). A particularly important group is the large number of asymptomatic older patients, many with systemic hypertension, who have midsystolic murmurs, usually of grade 1 or 2 intensity, related to sclerotic aortic valve leaflets; flow into tortuous, noncompliant great vessels; or a combination of these findings. Such murmurs must be distinguished from those caused by more significant degrees of aortic valve thickening, calcification, and reduced excursion that result in milder or greater degrees of valvular AS. The absence of LV hypertrophy on the electrocardiogram (ECG) may be reassuring, but echocardiography is frequently necessary. Aortic sclerosis can be defined by focal areas of increased echogenicity and thickening of the leaflets without restriction of motion and a peak velocity of less than 2.0 m per second. The recognition of aortic valve sclerosis may prompt the initiation of more aggressive programs of coronary heart disease prevention. In patients with AS, it is difficult to assess the rate and severity of disease progression on the basis of auscultatory findings alone.
2.1.3 Electrocardiography and Chest Roentgenography
Although echocardiography usually provides more specific and often quantitative information about the significance of a heart murmur and may be the only test needed, the ECG and chest X-ray are readily available and may have been obtained previously. The absence of ventricular hypertrophy, atrial enlargement, arrhythmias, conduction abnormalities, prior myocardial infarction, and evidence of active ischemia on the ECG provides useful negative information at a relatively low cost. Abnormal ECG findings in a patient with a heart murmur, such as ventricular hypertrophy or a prior infarction, should lead to a more extensive evaluation that includes echocardiography (Fig. 2).
Posteroanterior and lateral chest roentgenograms often yield qualitative information on cardiac chamber size, pulmonary blood flow, pulmonary and systemic venous pressure, and cardiac calcification in patients with cardiac murmurs. When abnormal findings are present on chest X-ray, echocardiography should be performed (Fig. 2). A normal chest X-ray and ECG are likely in asymptomatic patients with isolated midsystolic murmurs, particularly in younger age groups, when the murmur is grade 2 or less in intensity and heard along the left sternal border (16–18). Routine ECG and chest radiography are not recommended in this setting.
2.1.4 Echocardiography
Class I
Class IIa
Class III
Echocardiography with color flow and spectral Doppler evaluation is an important noninvasive method for assessing the significance of cardiac murmurs. Information regarding valve morphology and function, chamber size, wall thickness, ventricular function, pulmonary and hepatic vein flow, and estimates of pulmonary artery pressures can be readily integrated.
Although echocardiography can provide important information, such testing is not necessary for all patients with cardiac murmurs and usually adds little but expense in the evaluation of asymptomatic younger patients with short grade 1 to 2 midsystolic murmurs and otherwise normal physical findings. At the other end of the spectrum are patients with heart murmurs for whom transthoracic echocardiography proves inadequate. Depending on the specific clinical circumstances, transesophageal echocardiography, cardiac magnetic resonance, or cardiac catheterization may be indicated for better characterization of the valvular lesion.
It is important to note that Doppler ultrasound devices are very sensitive and may detect trace or mild valvular regurgitation through structurally normal tricuspid and pulmonic valves in a large percentage of young, healthy subjects and through normal left-sided valves (particularly the MV) in a variable but lower percentage of patients (16,19–22).
General recommendations for performing echocardiography in patients with heart murmurs are provided. Of course, individual exceptions to these indications may exist.
2.1.5 Cardiac Catheterization
Cardiac catheterization can provide important information about the presence and severity of valvular obstruction, valvular regurgitation, and intracardiac shunting. It is not necessary in most patients with cardiac murmurs and normal or diagnostic echocardiograms, but it provides additional information for some patients in whom there is a discrepancy between the echocardiographic and clinical findings. Indications for cardiac catheterization for hemodynamic assessment of specific valve lesions are given in Section 3, "Specific Valve Lesions," in these guidelines. Specific indications for coronary angiography to screen for the presence of CAD are given in Section 10.2.
2.1.6 Exercise Testing
Exercise testing can provide valuable information in patients with valvular heart disease, especially in those whose symptoms are difficult to assess. It can be combined with echocardiography, radionuclide angiography, and cardiac catheterization. It has a proven track record of safety, even among asymptomatic patients with severe AS. Exercise testing has generally been underutilized in this patient population and should constitute an important component of the evaluation process.
2.1.7 Approach to the Patient
The evaluation of the patient with a heart murmur may vary greatly depending on many of the considerations discussed above (23,24). These include the timing of the murmur in the cardiac cycle, its location and radiation, and its response to various physiological maneuvers (Table 2). Also of importance is the presence or absence of cardiac and noncardiac symptoms and other findings on physical examination that suggest the murmur is clinically significant (Fig. 2).
Patients with diastolic or continuous heart murmurs not due to a cervical venous hum or a mammary souffle during pregnancy are candidates for echocardiography. If the results of echocardiography indicate significant heart disease, further evaluation may be indicated. An echocardiographic examination is also recommended for patients with apical or left sternal edge holosystolic or late systolic murmurs, for patients with midsystolic murmurs of grade 3 or greater intensity, and for patients with softer systolic murmurs in whom dynamic cardiac auscultation suggests a definite diagnosis (e.g., hypertrophic cardiomyopathy).
Echocardiography is also recommended for patients in whom the intensity of a systolic murmur increases during the Valsalva maneuver, becomes louder when the patient assumes the upright position, and decreases in intensity when the patient squats. These responses suggest the diagnosis of either hypertrophic obstructive cardiomyopathy or MV prolapse (MVP). Additionally, further assessment is indicated when a systolic murmur increases in intensity during transient arterial occlusion, becomes louder during sustained handgrip exercise, or does not increase in intensity either in the cardiac cycle that follows a premature ventricular contraction or after a long R-R interval in patients with atrial fibrillation. The diagnosis of MR or ventricular septal defect in these circumstances is likely.
In many patients with grade 1 or 2 midsystolic murmurs, an extensive workup is not necessary. This is particularly true for children and young adults who are asymptomatic, have an otherwise normal cardiac examination, and have no other physical findings associated with cardiac disease.
However, echocardiography is indicated in certain patients with grade 1 or 2 midsystolic murmurs, including patients with symptoms or signs consistent with infective endocarditis, thromboembolism, heart failure, myocardial ischemia/infarction, or syncope. Echocardiography also usually provides an accurate diagnosis in patients with other abnormal physical findings, including widely split second heart sounds, systolic ejection sounds, and specific changes in intensity of the systolic murmur during certain physiological maneuvers (Table 2).
Although echocardiography is an important test for patients with a moderate to high likelihood of a clinically important cardiac murmur, it must be re-emphasized that trivial, minimal, or physiological valvular regurgitation, especially affecting the mitral, tricuspid, or pulmonic valves, is detected by color flow imaging techniques in many otherwise normal patients, including many patients who have no heart murmur at all (16,19–22). This observation must be considered when the results of echocardiography are used to guide decisions in asymptomatic patients in whom echocardiography was used to assess the significance of an isolated murmur.
Very few data address the cost-effectiveness of various approaches to the patient undergoing medical evaluation of a cardiac murmur. Optimal auscultation by well-trained examiners who can recognize an insignificant midsystolic murmur with confidence (by dynamic cardiac auscultation as indicated) results in less frequent use of expensive additional testing to define murmurs that do not indicate cardiac pathology.
Characteristics of innocent murmurs in asymptomatic adults that have no functional significance include the following:
Such murmurs are especially common in high-output states such as anemia and pregnancy (25,26). When the characteristic features of individual murmurs are considered together with information obtained from the history and physical examination, the correct diagnosis can usually be established (24). In patients with ambiguous clinical findings, the echocardiogram can often provide a definite diagnosis, rendering a chest X-ray and/or ECG unnecessary.
In the evaluation of heart murmurs, the purposes of echocardiography are to
Throughout these guidelines, treatment recommendations will often derive from specific echocardiographic measurements of LV size and systolic function. Accuracy and reproducibility are critical, particularly when applied to surgical recommendations for asymptomatic patients with MR or AR. Serial measurements over time, or reassessment with a different imaging technology (radionuclide ventriculography or cardiac magnetic resonance), are often helpful for counseling individual patients. Lastly, although handheld echocardiography can be used for screening purposes, it is important to note that its accuracy is highly dependent on the experience of the user. The precise role of handheld echocardiography for the assessment of patients with valvular heart disease has not been elucidated.
As valuable as echocardiography may be, the basic cardiovascular physical examination is still the most appropriate method of screening for cardiac disease and will establish many clinical diagnoses. Echocardiography should not replace the cardiovascular examination but can be useful in determining the cause and severity of valvular lesions, particularly in older and/or symptomatic patients.
2.2 Valve Disease Severity Table. Classification of the severity of valve disease in adults is listed in Table 4 (27). The classification for regurgitant lesions is adapted from the recommendations of the American Society of Echocardiography (27). For full recommendations of the American Society of Echocardiography, please refer to the original document. Subsequent sections of the current guidelines refer to the criteria in Table 4 (27) to define severe valvular stenosis or regurgitation.
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2.3.1 Endocarditis Prophylaxis
Class I
Prophylaxis against infective endocarditis is recommended for the following patients:
Class III
Prophylaxis against infective endocarditis is not recommended for the following patients:
*Patients with MVP without regurgitation require additional clinical judgment. Indications for antibiotic prophylaxis in MVP are discussed in Section 3.5.2. Patients who do not have MR but who do have echocardiographic evidence of thickening and/or redundancy of the valve leaflets, and especially men 45 years of age or older, may be at increased risk for infective endocarditis (30). Additionally, approximately one third of patients with MVP without MR at rest may have exercise-induced MR (31). Some patients may exhibit MR at rest on one occasion and not on another. There are no data available to address this latter issue, and at present, the decision must be left to clinical judgment, taking into account the nature of the invasive procedure, the previous history of endocarditis, and the presence or absence of valve thickening and/or redundancy.
Infective endocarditis is a serious illness associated with significant morbidity and mortality. Its prevention by the appropriate administration of antibiotics before procedures expected to produce bacteremia merits serious consideration. Experimental studies suggest that endothelial damage leads to platelet and fibrin deposition and the formation of a nonbacterial thrombotic endocardial lesion. In the presence of bacteremia, the organisms may adhere to these lesions and multiply within the platelet-fibrin complex, leading to an infective vegetation (30,32). Valvular and congenital abnormalities, especially those that result in abnormal high-velocity jet streams, can damage the endothelial lining and predispose to platelet aggregation and fibrin deposition at those sites, which are thus at higher risk for bacterial colonization.
Several issues must be considered in generating recommendations for endocarditis prophylaxis (33). The rationale for antimicrobial prophylaxis is based on the following:
The following evidence raises questions about the value of prophylaxis:
In view of these issues, and until the AHA’s recommendations have been revised, the committee continues to recommend that the risk of endocarditis in patients with pre-existing cardiac disorders be classified as relatively high, moderate, or low, as determined primarily by the underlying cardiac disorder (28).
Various dental and surgical procedures are associated with varying degrees and frequencies of bacteremia. The frequency of bacteremia is highest with dental and oral procedures, intermediate with procedures that involve the genitourinary tract, and lowest with gastrointestinal procedures (33). Recommendations for endocarditis prophylaxis, as determined by dental, surgical, and other procedures, are listed in Tables 5 through 8
(28). Anecdotal reports of infective endocarditis complicating body piercing and tattoo application underscore the changing nature of this disease.
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2.3.2 Rheumatic Fever Prophylaxis
2.3.2.1 General Considerations
Rheumatic fever is an important cause of valvular heart disease. In the United States (and Western Europe), cases of acute rheumatic fever have been uncommon since the 1970s. However, starting in 1987, an increase in cases has been observed (43,44). With the enhanced understanding of the causative organism, group A beta hemolytic streptococcus, its rheumatogenicity is attributed to the prevalence of M-protein serotypes of the offending organism. This finding has resulted in the development of kits that allow rapid detection of group A streptococci with specificity greater than 95% and more rapid identification of their presence in upper respiratory infection. Because the test has a low sensitivity, a negative test requires throat culture confirmation (44). Prompt recognition and treatment comprise primary rheumatic fever prevention. For patients who have had a previous episode of rheumatic fever, continuous antistreptococcal prophylaxis is indicated for secondary prevention.
2.3.2.2 Primary Prevention
Rheumatic fever prevention and treatment guidelines have been established previously by the AHA (Table 9) (45).
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Patients who have had an episode of rheumatic fever are at high risk of developing recurrent episodes of acute rheumatic fever. Patients who develop carditis are especially prone to similar episodes with subsequent attacks. Secondary prevention of rheumatic fever recurrence is thus of great importance. Continuous antimicrobial prophylaxis has been shown to be effective. Anyone who has had rheumatic fever with or without carditis (including patients with MS) should receive prophylaxis for recurrent rheumatic fever. The 1995 AHA guidelines for secondary prevention are shown in Table 10, and the 1995 AHA guidelines for duration of secondary prevention are shown in Table 11 (45).
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In 2003 the ACC/AHA Task Force on Practice Guidelines recently provided a list of suggested phrases to use when writing recommendations. All recommendations in this guideline have been written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document (including headings above sets of recommendations), would still convey the full intent of the recommendation. It is hoped that this will increase readers’ comprehension of the guidelines and will allow queries at the individual recommendation level.