Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Valvular heart disease
Introduction
The burden of valvular heart disease in developed countries is steadily increasing with current estimates of an overall prevalence of 2.5% in the United States who have moderate or severe valvular disease, increasing to 13% prevalence in those older than 75 years of age. Since the overall incidence of valvular heart disease increases with age, the need for cardiac surgery or percutaneous valvular interventions has increased in aging populations. While significant advances have been made in recent years with regard to diagnosis and treatment options, these patients still face significant perioperative morbidity and mortality.
Valvular heart disease results in the development of hemodynamic changes on the left- and/or right-sided chambers that are initially tolerated well as a result of compensatory adaptations, but eventually lead to decompensation and thus symptom onset. An in-depth understanding of the pathophysiology and clinical progression of the disease is required by those caring for these patients to optimize perioperative care. Appropriate workup for patients with valvular heart disease includes a thorough history for evaluation of causes and symptoms, and assessment of the valvular pathology by physical examination along with appropriate noninvasive and invasive diagnostic tests to accurately quantify the severity of the valve dysfunction and associated pathologies, if present.
Degenerative valve disease is the most common form of valvular heart disease in Western countries whereas rheumatic heart disease (RHD) accounts for the majority of valvular pathology in developing countries. Aortic stenosis (AS) due to calcific disease and mitral regurgitation (MR) due to primary causes such as degenerative disease, or secondary causes such as ischemic heart disease, are the most commonly encountered valvular lesions in Western countries. Patients may present with both stenotic and regurgitant lesions affecting a single heart valve, or can have more than one affected. These lesions will produce pressure and/or volume overload within the heart chambers thus altering normal physiology. Anesthetic management requires an understanding of the likely effects of drug-induced changes to the cardiac rhythm, heart rate, preload, afterload, and myocardial contractility as well as the changes to systemic and pulmonary vascular resistance relative to the pathophysiology of the specific valvular lesion.
Stenotic vs regurgitant lesions
Each valvular lesion will impart unique hemodynamic consequences on the upstream and downstream heart chambers and/or vessels. The narrowed orifice of the affected valve obstructs blood flow across the valve, during systole in aortic and pulmonary valves, and diastole in mitral and tricuspid valves, which results in increased pressure proximal to the affected valve. As blood reaches the stenotic valve, there is flow convergence causing the blood to eject with increased velocity through the orifice with a simultaneous pressure drop and thus consequent increase in the pressure gradient across the valve. Valvular obstruction can be classified as either fixed, defined as a constant degree of obstruction to blood flow throughout the cardiac cycle as seen in patients with AS, or dynamic, defined as a variable degree of obstruction dependent on the phase of the cardiac cycle as seen in patients with hypertrophic obstructive cardiomyopathy.
Regurgitant lesions cause pathologies that result in volume overload that leads to chamber dilation and eccentric hypertrophy in the originating chamber. The affected chamber can initially compensate for this increased volume load, but eventually function declines once the compensatory mechanism is exhausted and irreversible failure subsequently occurs.
Multiple and mixed valvular heart disease are becoming increasingly prevalent conditions. The hemodynamic and clinical consequences of valvular heart lesions may be modulated by the presence of another concomitant stenotic or regurgitant lesion on the same valve, termed mixed valvular heart disease, or on another valve, termed multiple valvular heart disease . The consequences will depend on the complex interplay of several factors: the specific combination of the lesions present, the severity and timing of onset of each individual lesion, the loading conditions, and ventricular systolic and diastolic performance. Multiple valvular disease is most often acquired, and the most frequent associations are AS with aortic regurgitation (AR), AS with MR, and AR with MR.
Structural and functional response of left ventricle to pressure and/or volume overload
Valvular heart disease results in unique hemodynamic changes to the Left ventricle (LV). Despite the LV being a complex structure, it can only respond to these changes using three basic mechanisms: (1) activation of the Frank-Starling mechanism, (2) use of the adrenergic neurohormonal systems, and (3) chamber remodeling. Each of these processes has both beneficial and maladaptive effects, and the symptom onset will depend on their interplay.
The LV generates pressure and displaces a volume of blood into the systemic circulation. The three factors determining LV performance are the preload (venous return, end-diastolic volume), myocardial contractility (the force generated at any given end-diastolic volume), and afterload (aortic impedance and wall stress). The relationship between LV pressure generation and volume ejection can be expressed as a plot of LV pressure versus LV volume, better known as the Frank-Starling curve. In ventricles with normal cardiac function, there is a positive correlation between increased cardiac filling pressures and increased myocardial performance. As cardiac function declines, this relationship is shifted to the right and flattened so that further increases in the left heart filling pressures lead to minimal increases in cardiac output ( Fig. 6.1 ). Initial reductions in LV performance are then countered with activation of neurohumoral systems resulting in increased fluid retention, increasing both sarcomere length and contractility. While this response is initially compensatory, it will eventually transition to a maladaptive one as the sarcomere is overstretched and the number of cross bridges that can form is reduced linearly with increasing length. With diastolic dysfunction, there is also an upward shift in the end-diastolic pressure-volume relationship that occurs because a higher pressure is required to achieve the same volume.
LV remodeling is another important response to valvular heart disease. Remodeling is defined as a structural heart change that occurs to meet the increased demand due to increased hemodynamic load or neurohormonal activation. Stresses typically include pressure overload as seen in AS or volume overload as seen in regurgitant lesions. While initially remodeling is a compensatory measure, it will ultimately transition to worsening cardiac function with continued stress. The three general patterns of remodeling are (1) concentric LV remodeling that occurs in response to pressure overload, (2) eccentric LV hypertrophy due to volume overload, or (3) mixed hypertrophy that may occur due to mixed valvular lesions. Factors affecting the degree of remodeling include decreased contractility due to ischemia, increased vascular resistance, and neurohormonal activation.
Each valvular lesion will create its own unique set of loading conditions that will cause specific structural and functional changes to facilitate compensation. Faced with similar stressors and lesions, patients will exhibit significant differences in the compensatory response suggesting a great deal of modulation downstream from the initial mechanical signal. Ascertaining when these changes go from being compensatory to maladaptive is crucial in deciding when to intervene in valvular heart disease.
Evaluation of valvular heart disease
History should focus on questions designed to evaluate exercise tolerance, which will give an indication of cardiac reserve. Patients are generally classified according to the criteria established by the New York Heart Association (NYHA) ( Table 6.1 ). The presence of angina should also be screened for in the history, as this may occur even in the absence of coronary artery disease (CAD). This generally reflects increased myocardial oxygen demand due to ventricular hypertrophy where the metabolic demands of the thickened muscle mass may exceed the ability of even patent coronary arteries to deliver adequate amounts of oxygen, causing angina-type symptoms.
TABLE 6.1
New York Heart Association Functional Classification of Patients With Heart Disease
| Class | Description |
|---|---|
| I | Asymptomatic |
| II | Symptoms with ordinary activity but comfortable at rest |
| III | Symptoms with minimal activity but comfortable at rest |
| IV | Symptoms at rest |
Physical examination should focus on signs of heart failure, which can be left sided (i.e., pulmonary edema) and/or right sided (i.e., dependent edema or ascites). The presence of a heart murmur reflecting turbulent blood flow across the valve should also be detected and appreciated in a patient with clinically significant valvular heart disease. The character, location, intensity, and direction of radiation of a heart murmur provide clues to the location and severity of the valvular lesion.
The electrocardiogram (ECG) of a patient with valvular disease often exhibits characteristic changes that reflect either the direct insult or the compensatory remodeling from the primary lesion. Broad and notched P waves (P mitrale) suggest the presence of left atrial enlargement typical of mitral valve disease. LV and right ventricular (RV) hypertrophy can be diagnosed by the presence of left or right axis deviation and high voltage. Other common ECG findings include dysrhythmias, conduction abnormalities, and evidence of active ischemia or previous myocardial infarction.
The cornerstone of diagnosis of valvular heart disease is Doppler echocardiography ( Table 6.2 ). In addition to diagnosis, echocardiography can also be used to noninvasively monitor the lesion and help guide decision making for interventions. It is critical in determining the indication and timing of surgery as well as making intraoperative decisions about whether a valve should be repaired or replaced. Three-dimensional echocardiography is also rapidly being incorporated into the evaluation of patients with valvular heart disease and is becoming the standard of care in a multitude of circumstances, including assessing suitability of repair in mitral valve surgery and measurement of the LV outflow tract in patients with AS or the mitral area in patients with mitral stenosis (MS). Stress echocardiography can be of use in certain situations such as distinguishing true severe AS from pseudosevere and assessing LV flow reserve when the pressure gradient is low and LV ejection fraction is reduced.
TABLE 6.2
Utility of Echocardiography in the Evaluation of Valvular Heart Disease
| Determine significance of cardiac murmurs |
| Identify hemodynamic abnormalities associated with physical findings |
| Determine transvalvular pressure gradient |
| Determine valve area |
| Determine ventricular ejection fraction |
| Diagnose valvular regurgitation |
| Evaluate prosthetic valve function |
Cardiac catherization is currently recommended in situations where noninvasive evaluation is inconclusive or discordant with clinical findings. While most assessments, such as assessing the valve area using the Gorlin equation, are unaffected by valvular disease, other standardized techniques such as assessing cardiac output by either thermodilution or the Fick method must be interpreted with caution as disease states such as severe tricuspid regurgitation (TR) and low cardiac output can affect the accuracy of these results.
Computed tomography (CT) is increasingly used to assess the aortic valve calcium score when there is evidence of low-flow, low-gradient AS, and preserved LV ejection fraction. High calcium scores are consistent with an increase in the likelihood of severe AS. CT is also routinely used in procedural planning for patients undergoing transcatheter aortic valve replacement (TAVR) to size the LV outflow tract and determine the optimal size valve to implant.
Cardiac magnetic resonance imaging (MRI) is an evolving tool in the diagnosis of valvular heart disease. It has particular utility in the diagnosis of regurgitant lesions as well as measurement of ventricular volumes and systolic function. Cardiac MRI allows for accurate identification of serial changes in ventricular volumes, mass, and function. These changes reflect the global burden of the evolving valvular pathology and may have the potential to help determine the optimal time for surgical intervention.
Regardless of what method is used to evaluate patients with valvular heart disease, it is crucial to perform periodic evaluation of any patient with valvular heart disease. This is important because when patients start to develop symptoms, they will have a higher risk of perioperative adverse events. Performing periodic evaluation to track disease progression helps optimize timing of surgical intervention and thus improves perioperative outcomes.
Aortic stenosis
Etiology
Age-related degenerative AS is by far the most common cause among adults in the United States, while rheumatic heart disease is the most common worldwide. The prevalence of AS increases with advancing age, with over 30% of adults over age 65 years exhibiting some degree of aortic sclerosis, and 2% overall having severe grade valvular stenosis often requiring intervention. On histology, these valves appear thickened, inflamed, and calcified. This degenerative process of the aortic valve has been compared to atherosclerosis with endothelial dysfunction, lipid deposition, and oxidative changes that stimulate inflammation and lead to fibrosis and calcification. Risk factors for the development of calcific AS are similar to those of atherosclerosis and include systemic hypertension, hypercholesterolemia, diabetes mellitus, smoking, and male gender.
Bicuspid aortic valve (BAV) is the second most common cause for the development of AS in the United States and has a prevalence of 1% to 2%. The abnormal valve architecture makes the leaflets susceptible to constant low shear stress that over time leads to thickened and calcified leaflets that generally tend to occur in the fifth or sixth decade; trileaflet aortic valves rarely develop degenerative calcific AS before the sixth or seventh decade of life. Other pathologies associated with BAV include aortic root dilation, aortic coarctation, and AR.
RHD is characterized by fusion of the commissures between the leaflets, fibrosis, and calcification, with a resultant narrowing of the valve orifice. Rheumatic AS very commonly affects the mitral valve as well; as a result, most patients with rheumatic AS also have an isolated or combined mitral lesion, including stenosis or regurgitation. Other rarer causes of AS include metabolic diseases (i.e., Fabry disease), systemic lupus erythematous, or alkaptonuria.
Pathophysiology
The decrease in aortic valve area causes an obstruction to LV forward flow, which requires a compensatory increase in LV pressure to maintain stroke volume. The initial response to this increased pressure is concentric hypertrophy, which reduces wall stress as demonstrated by Laplace’s law of wall tension. The LV remodeling process can accommodate the pressure overload for many years before it eventually becomes maladaptive, and LV function begins to decline with chamber dilation and a reduction in cardiac output. A mean gradient of greater than 40 mm Hg or a valve area of less than 1 cm 2 is characteristic of severe disease. Cardiac output, requiring significant compensation already to remain normal at rest, may lack the cardiac reserve to rise in response to exercise. Angina may occur in these patients even in the absence of CAD. This is due to mismatch between a consistent supply of oxygen meeting the increased demand secondary to concentric LV hypertrophy and the increase in myocardial work necessary to offset the afterload produced by the stenotic valve. Myocardial ischemia can also result from compression of the subendocardial vessels by the increased LV pressure. Syncope may occur in these patients and is usually associated with exertion as exercise-induced vasodilation in the presence of an obstruction with a fixed cardiac output can result in hypotension and reduced cerebral perfusion.
Clinical manifestations and diagnosis
The onset of symptoms in patients with AS does not occur until late in the disease because the hypertrophied left ventricle can produce the elevated pressures necessary to maintain an adequate stroke volume. When symptoms do occur, this generally signifies severe disease and often heralds the need for intervention due to the significant mortality that is associated with untreated, severe AS.
The classic triad of symptoms associated with AS include exertional dyspnea, chest pain, and syncope. Dyspnea typically occurs as a result of diastolic dysfunction, caused by elevated LV filling pressures in the noncompliant, hypertrophied left ventricle. Chest pain and syncope occur due to a mismatch between myocardial oxygen supply and demand from the thickened myocardium and the inability to augment cardiac output through the stenotic valve. Symptoms related to LV failure are generally not present until the advanced stages of AS when it is associated with LV systolic dysfunction.
On physical examination, cardiac auscultation will reveal a characteristic systolic murmur that is best appreciated in the aortic area and may radiate to the neck, mimicking a carotid bruit. The intensity of the murmur does not necessarily correlate with the severity of the murmur. Pulsus parvus et tardus is another sign associated with AS in which palpation of the carotid pulse rises slowly to a delayed and sustained peak. While this physical finding is specific to AS, it is often difficult to appreciate in the elderly with stiffened arterial walls that can mask this finding. Other nonspecific findings include splitting of S 2 due to prolonged LV ejection across the stenotic valve and an audible S 4 at the apex reflecting LV hypertrophy.
Diagnostic investigations should begin with ECG, which may have evidence of LV hypertrophy and, in advanced cases, ST depression and T-wave inversion in the lateral leads. Chest radiograph may show a prominent ascending aorta due to post–stenotic aortic dilation, and aortic valve calcification may be identified on the lateral film.
Transthoracic echocardiography with Doppler examination is the test of choice for the diagnosis and monitoring of patients with AS. Key findings include whether it is a trileaflet or bileaflet aortic valve, thickening and calcification of the valvular leaflets with decreased mobility, LV hypertrophy, and LV systolic or diastolic dysfunction ( Fig. 6.2 A–B). Valve area and transvalvular pressure gradients can also be estimated with Doppler (see Fig. 6.2 C). Stress echocardiography may be required in a subset of patients with reduced LV function and low flow AS.
Cardiac catherization with invasive measurement of transvalvular gradients may be useful if there is a discrepancy between the clinical and echocardiographic findings. Coronary angiogram is also often indicated to detect for CAD in patients who are being considered for operative intervention due to its high prevalence in this population. CT is increasingly used to assess the aortic valve calcium score, which correlates well with the likelihood of severe AS.
Timing and type of intervention
Patients with AS have a long latent period in which the onset of symptoms is prevented by compensatory measures and survival is similar to patients without AS. However, once symptoms develop, survival declines dramatically with mortality approaching 75% within 3 years of symptom onset unless the aortic valve is replaced ( Fig. 6.3 ). Asymptomatic patients should be followed carefully for the development of symptoms and have serial echocardiograms to quantitatively monitor for deteriorating LV function. Risk stratification using a combination of serial echocardiography and additional testing to help determine the degree of AS may help to identify patients who would benefit from valve replacement before symptom onset.
Surgical aortic valve replacement (SAVR) and TAVR are the mainstays of treatment for severe AS. As clinical experience and evidence of good long-term outcomes is growing with TAVR, its use is steadily increasing over SAVR. The decision to proceed with SAVR or TAVR should be made on a case-by-case basis and involve a multidisciplinary heart valve team taking into account a multitude of factors: the patient’s life expectancy, frailty, comorbidities, specific anatomy, valves, and personal preferences. The type of treatment suitable for patients is often informed by their surgical risk as defined by the Society of Thoracic Surgeons Predicted Risk of Mortality (STS-PROM). In low-risk surgical patients, the decision between SAVR or TAVR is uncertain, and the decision to proceed with one over the other should be made based on individualized risk-benefit assessment. Current guidelines recommend TAVR over SAVR in low-risk surgical patients who meet all four of the following criteria: (1) age is over 65 years, (2) transfemoral TAVR is feasible, (3) aortic valve is trileaflet, and (4) absence of high-risk anatomic features such as adverse aortic root, low coronary ostia height, or LV outflow tract calcification. For patients who lack one or more of these four criteria, SAVR is preferred. In intermediate-risk patients, if TAVR is feasible and high anatomic features (i.e., adverse aortic root, low coronary ostia height, heavily calcified bicuspid aortic valve, and severe LV outflow tract calcification) are absent, TAVR is recommended. In high-risk patients, TAVR is the intervention of choice.
Medical therapy does not prevent the progression of AS, but it is useful in patients who are not suitable candidates for valve replacement. The therapy typically focuses on treatment of concurrent cardiovascular conditions along with prevention or treatment of superimposed diseases such as atrial fibrillation (Afib), CAD, and heart failure that often exacerbate the effects of valve obstruction. Optimal hemodynamic conditions should be maintained as much as possible, and any symptoms that develop should be treated promptly. Physical activity should be curtailed or even avoided in these patients. Medications that alter preload, contractility, and afterload should be used with caution.
Percutaneous aortic balloon valvotomy (PABV) is occasionally performed in adolescents and young adults with congenital, noncalcific AS. It is not routinely used as an intervention in adults with severe calcific AS because of high restenosis rates, embolic complications, and the potential development of AR. In rare cases, PABV may be used in patients with severe LV dysfunction and cardiogenic shock as a bridge to surgical intervention.
Intraoperative management
Patients with AS who are undergoing noncardiac surgery are at high risk for perioperative complications. An appropriate preoperative investigation should ascertain the severity of AS, and anesthetic management of these patients should include maintenance of sinus rhythm, a normal heart rate, and maintenance of adequate preload, afterload, and contractility ( Table 6.3 ).
TABLE 6.3
Anesthetic Considerations in Patients With Aortic Stenosis
| Maintain normal sinus rhythm |
| Avoid bradycardia or tachycardia |
| Avoid hypotension |
| Optimize intravascular fluid volume to maintain venous return and left ventricular filling |
Normal sinus rhythm should be preserved as much as possible because filling of the hypertrophic, noncompliant left ventricle depends significantly on the left atrial contraction during end diastole that is lost in conditions such as atrial fibrillation. Loss of atrioventricular synchrony will result in reduced LV filling and lead to a dramatic decrease in stroke volume and blood pressure. Avoiding both tachycardia and excessive bradycardia is important. With tachycardia, the decrease in diastolic filling time will result in inadequate oxygen delivery to the hypertrophied left ventricle. With bradycardia, the heart will have inadequate cardiac output as these patients cannot compensate by increasing stroke volume due to the stenotic valve.
Maintaining adequate preload with volume resuscitation is paramount as these patients are generally preload dependent; fluid boluses should be titrated according to either clinical assessment or ideally by a goal-directed method such as transesophageal echocardiography (TEE) or other invasive parameters. Hypotension should ideally be prevented or at least treated promptly with an α-adrenergic vasoconstrictor such as phenylephrine. This will increase the systemic vascular resistance (SVR) without the chronotropic side effects associated with other medications such as epinephrine or dobutamine. Avoiding doses of anesthetic agents that might cause significant depression of myocardial contractility such as high doses of propofol or volatile anesthetic agents is important in maintaining cardiac output.
General anesthesia is often selected in preference to epidural or spinal anesthesia because the sympathetic blockade produced by neuraxial anesthesia can lead to significant hypotension as a result of severely impaired preload. Induction of general anesthesia can be achieved with a combination of intravenous (IV) induction agents that do not decrease SVR or myocardial contractility such as opioids, benzodiazepines, and etomidate. Propofol can be utilized with caution at reduced doses in combination with other induction agents with prompt prevention or treatment of the anticipated drop in SVR. Maintenance of anesthesia is generally accomplished with a combination of volatile anesthetics and opioids.
Monitoring of patients with AS must include a five-lead ECG that can reliably detect cardiac arrhythmias and ischemia. The decision to proceed with invasive monitoring such as invasive arterial monitoring or TEE should be made based on severity of the disease and the complexity of the surgery.
Aortic regurgitation
Etiology
Aortic regurgitation (AR) occurs as a result of incomplete coaptation of the aortic valve leaflets in diastole and may be caused by disease processes that affect the aortic valve leaflets, aortic root, or both. Common causes of leaflet abnormalities include congenital abnormalities of the aortic valve (i.e., bicuspid valves), rheumatic disease, infective endocarditis, calcific degeneration, and myxomatous degeneration. Abnormalities of the aortic root include idiopathic aortic root dilatation, hypertension-induced annuloaortic ectasia, aortic dissection, Marfan syndrome, Ehlers-Danlos syndrome, or aortitis occurring as a result of syphilitic infection, rheumatoid arthritis, or ankylosing spondylitis. AR has also been described as a complication in patients undergoing PABV or TAVR. The majority of these lesions produce chronic AR, with slow, insidious LV dilatation. In contrast, acute AR is almost always a result of either infective endocarditis or aortic dissection.
Pathophysiology
The inability of the aortic valve leaflets to remain competent during diastole results in a portion of the LV stroke volume leaking back into the left ventricle from the aorta ( Fig. 6.4 A). This regurgitant volume results in increased LV end-diastolic volume and pressure. As a compensatory measure, the left ventricle responds with eccentric hypertrophy, with an increase in LV mass with normal relative wall thickness. The combination of LV eccentric hypertrophy along with LV chamber enlargement increases the total stroke volume. The magnitude of the regurgitant volume depends on the heart rate and SVR. The heart rate affects the time available for the regurgitant flow to occur, and the SVR impacts the pressure gradient across the aortic valve. Thus the regurgitant volume can be reduced by inducing tachycardia and peripheral vasodilation.
The LV remodeling that occurs due to the increase in LV pressure and volume overload is initially adaptive as the forward stroke volume and systemic blood flow are maintained with little to no change in filling pressures or cardiac output despite the regurgitation. Eventually as the lesion progresses, these adaptive measures will fail, and the ejection fraction and decline in forward flow results in symptom onset. The reduction in LV function that occurs in the advanced stages of AR often precedes symptom onset and should prompt intervention.
While patients with chronic AR have adequate time to develop compensatory measures to deal with the increased volume and pressure overload, this is not the case with acute AR. With acute AR, there is a sudden increase in LV volume and pressure, which typically results in coronary ischemia. Rapid deterioration can occur with impaired LV function leading to heart failure ( Fig. 6.4 ).
Clinical manifestations and diagnosis
Patients with chronic AR may remain asymptomatic for an extended period of time due to adequate compensation with adaptive mechanisms. Some patients may develop symptoms related to the increased LV size and stroke volume, experienced as an uncomfortable awareness of their heartbeat, particularly noticed when lying down, or head pounding due to increased stroke volume. Exertional dyspnea is usually an early symptom of decompensation and is related to the gradual decline in systolic function. More severe symptoms of heart failure such as orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema may develop without appropriate intervention. Angina may also occur even in the absence of CAD and often occurs at night, due to bradycardia with subsequent fall in the diastolic blood pressure and increased regurgitant volume. The drop in diastolic blood pressure reduces coronary perfusion pressure and results in angina-type symptoms.
Physical examination in patients with severe AR centers on examination of peripheral pulses, precordial inspection and palpation, and auscultation of the heart. Signs that are present due to AR are generally related to increased stroke volume. The arterial pulse rises sharply and collapses abruptly with a widened pulse pressure, known as the Corrigan pulse. A pistol shot pulse may be heard over the femoral arteries, known as Traube sign. Capillary pulsations can also be appreciated in the fingertips or lips, which is known as Quincke pulses. Palpation of the heart in chronic, severe AR reveals a heaving, laterally displaced LV impulse and an apical diastolic thrill. The murmur of AR is a high-pitched, blowing decrescendo murmur that is often loudest along the left sternal border. A low-pitched middiastolic rumble, known as the Austin Flint murmur, may be audible in severe AR due to the high-frequency fluttering of the anterior mitral valve leaflet caused by the AR jet.
In patients with chronic AR, there will be evidence of LV enlargement and hypertrophy on both the chest radiography and ECG. Echocardiography is the gold standard for diagnosis, evaluation, and surveillance of AR. Anatomic abnormalities of the aortic valve such as congenital abnormalities, leaflet perforations, or prolapse along with abnormalities of the aortic root and annulus can be identified on echocardiography. LV size, volume, and function can be easily measured, with Doppler interrogation used to assess the severity of regurgitation. To quantify the severity of AR, there are several methods available: (1) the Perry index, which measures the regurgitant jet width as a percentage of overall LV outflow tract width ( Fig.6.4 B) (2) regurgitant fraction, the percentage of stroke volume that returns to the left ventricle from the aorta during diastole; or (3) pressure half-time, the time it takes for the initial maximal pressure gradient in diastole to fall by 50% Fig. 6.4 C. In patients with severe AR, a rapid drop in the pressure gradient occurs. Cardiac catheterization can also be used in the assessment of AR, generally in patients with angina to rule out CAD as a cause.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here
