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78-Year-Old-Woman With Dyspnea on Exertion Chad W. McRee, MD; Jordan C. Ray, MD; and Brian P. Shapiro, MD
A
78-year-old woman presented to her physician with dyspnea on exertion that had progressed over the previous several months, particularly with activities such as climbing stairs. She reported no symptoms of fever, chills, cough, chest pain, lightheadedness, dizziness, palpitations, syncope, paroxysmal nocturnal dyspnea, orthopnea, or unexplained weight gain. Her medical history included hypertension, hyperlipidemia, paroxysmal atrial fibrillation, heart failure (HF) with preserved ejection fraction, and severe chronic obstructive pulmonary disease (COPD). She had no history of coronary artery disease (CAD). Results of a pharmacological stress test 1 year previously were unremarkable. Allergies included penicillin-related anaphylaxis. Medications included niacin and inhaled fluticasone-salmeterol and tiotropium. Her surgical, social, and family histories were unremarkable. On physical examination, the patient could speak in full sentences with unlabored breathing. Her body mass index (calculated as the weight in kilograms divided by the height in meters squared) was 19 kg/m2. Vital signs included a temperature of 36.5 C, pulse rate of 69 beats/min, blood pressure of 160/84 mm Hg, respiratory rate of 16 breaths/min, and oxygen saturation of 95% while breathing room air. The patient appeared her stated age and in no acute distress. Cardiac examination revealed a regular heart rate and rhythm with no rubs or heaves. A 2/6 late-peaking, systolic murmur at the right upper sternal border was transmitted to the carotid arteries and encroached on the second heart sound. A soft S4 was present. The carotid pulse was delayed with low amplitude and upstroke. The point of maximal impulse was nondisplaced but enlarged. Jugular venous pressure was normal. Her lungs were clear on auscultation bilaterally, and abdominal examination revealed no abnormalities. There was no evidence of clubbing, cyanosis, or edema of the lower extremities.
1. In view of the initial findings, which one of the following is the most likely diagnosis? a. Aortic stenosis (AS) b. Severe mitral regurgitation c. CAD d. COPD with severe tricuspid regurgitation and right-sided HF e. Atrial fibrillation
See end of article for correct answers to questions. Resident in Internal Medicine, Mayo School of Graduate Medical Education, Jacksonville, FL (C.W.M., J.C.R.); Advisor to residents and Consultant in Cardiovascular Diseases, Mayo Clinic, Jacksonville, FL (B.P.S.).
This patient presented with a systolic ejection murmur best heard at the right upper sternal border in the second intercostal space radiating to the carotid arteries, which is most consistent with AS.1,2 Severe mitral regurgitation classically presents with a holosystolic, blowing murmur radiating to the back and axilla.1,2 Although this patient has cardiac risk factors, normal results on a recent stress test and the lack of angina make CAD less likely.3 Chronic obstructive pulmonary disease affects pulmonary vasculature and can lead to development of ventricular dysfunction, pulmonary hypertension, tricuspid regurgitation, and cor pulmonale.4 However, COPD with severe tricuspid regurgitation and right-sided HF presents with findings of a pansystolic murmur best heard along the left lower sternal border in the fifth intercostal space with elevated jugular venous pressure, ascites, and peripheral edema,4 which are absent in this patient. Atrial fibrillation can be asymptomatic or present with an irregularly irregular rhythm and palpitations. Although HF with preserved ejection fraction predisposes this patient to dysrhythmias such as atrial fibrillation, the clinical examination findings are more consistent with AS.1,2 The patient was informed that her symptoms and cardiac examination findings were most consistent with AS. She was anxious to know what could be done to help improve her symptoms. Further diagnostic work-up was pursued to determine the most appropriate treatment.
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2. Which one of the following is the best initial diagnostic test to evaluate this patient’s aortic stenosis? a. Cardiovascular magnetic resonance imaging (CMR) b. Cardiac computed tomographic angiography c. Exercise stress test d. Cardiac catheterization e. 2-Dimensional and Doppler transthoracic echocardiography The initial evaluation of patients with dyspnea on exertion consists of a comprehensive history and physical examination, a complete blood cell count, serum electrolyte panel, chest radiography, and 12-lead electrocardiography. Although CMR provides excellent image quality and visualization of tissue characteristics, it is used in highly selected situations in which traditional testing is inadequate or equivocal and thus would not be the best answer.1,2,5,6 Computed tomography can evaluate AS primarily by assessing valve calcifications; however, it is considered a complementary imaging modality to traditional testing. Computed tomographic angiography can be used before percutaneous intervention in planning the access route and valve sizing. However, radiation exposure and the use of iodinated contrast media limit its use.1,2,6 Exercise stress testing can be useful in evaluating patients who present with symptoms of angina or dyspnea on exertion, but given our patient’s recent normal stress test results, clinically important CAD would be less likely.3 Cardiac catheterization is used to assess aortic valve area and mean gradient as well as for confirmation when echocardiographic findings are equivocal. It is invasive and often unnecessary to establish the diagnosis.1,2,6 Doppler TTE should be the initial diagnostic test in the evaluation of suspected AS.1,2,6 It can assess the presence and severity of AS and sequelae of left ventricular hypertrophy, left atrial enlargement, diastolic dysfunction, and pulmonary hypertension.1,2,6 Laboratory studies yielded the following results (reference ranges shown parenthetically): hemoglobin, 13.7 g/dL (12.0-15.5 g/dL); white blood cells, 4.9 109/L (3.5-10.5 109/L); platelet count, 229 109/L (150-450 109/L); potassium, 4.7 mmol/L (3.6-5.2 mmol/L); serum urea nitrogen, 12 mg/dL (6-21 mg/dL); e110
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and creatinine, 0.9 mg/dL (0.6-1.1 mg/dL). Chest radiography revealed hyperinflated lungs and a normal cardiac silhouette with no evidence of pleural effusion. Pulmonary function test results were consistent with severe obstruction, with a forced expiratory volume in the first second of expiration of 45%. Electrocardiography revealed normal sinus rhythm and left ventricular hypertrophy. Although TTE proved technically difficult because of poor acoustic windows, it revealed normal left ventricular systolic function and chamber size with concentric left ventricular hypertrophy, grade 2 diastolic dysfunction without regional wall motion abnormalities, and moderate left atrial enlargement. The calculated ejection fraction was 61%. The calculated aortic valve area was 1.25 cm2 with a mean gradient of 28 mm Hg, consistent with moderate stenosis. Trivial mitral, tricuspid, and pulmonary valve regurgitation were present. In this patient, clinical and imaging findings are inconsistent in grading the severity of her valvulopathy. The TTE findings in this patient suggested moderate AS, whereas the physical examination findings were more consistent with severe stenosis. 3. Given the physical examination and TTE findings, which one of the following is the best next step? a. Proceed with aortic valve replacement (AVR) b. Repeat TTE with Doppler c. Medical therapy with vasodilators d. CMR e. Cardiac catheterization Management of AS is based on severity and symptoms. Moderate stenosis is managed with medical therapy targeting comorbid conditions, and severe stenosis is managed with AVR.1,2,6 Aortic valve replacement is indicated in patients with severe AS. Given the conflicting clinical and echocardiographic findings, it is important to confirm the stenosis severity before intervention. In addition to physical examination, the severity can be assessed by TTE with Doppler using aortic valve peak velocity, aortic valve area, or mean gradient. Often the examination and TTE findings are concordant. However, TTE may underestimate severity because of technical limitations regarding patient
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body habitus, underlying pulmonary disease, incomplete Doppler interrogation of the aortic valve, or low stroke volume.1,6 Repeating the same diagnostic test would unlikely yield different results and is not the best next step. Medical therapy may be indicated in patients with AS who do not meet criteria for AVR but not until valve severity is determined.1,2,6,7 If physical examination and imaging findings conflict, cardiac catheterization should be pursued for definitive diagnosis.1,6 The patient underwent cardiac catheterization, which revealed an aortic valve area of 0.85 cm2 and a mean gradient of 48 mm Hg.
conventional surgical replacement of her valve. She elected to undergo TAVR, which resulted in improvement in her overall symptoms and quality of life. Approximately 1 year after TAVR, the patient is scheduled for a root canal procedure.
4. Which one of the following is the most appropriate treatment for this patient? a. Medical therapy with nitroglycerin b. Surgical AVR with or without aortic root enlargement c. Transcatheter AVR (TAVR) d. Balloon valvuloplasty e. Hospice or palliative care consultation
This patient has a prosthetic valve and requires antimicrobial prophylaxis before her dental procedure.8 The American Heart Association recommends that patients with highest risk of adverse outcomes from infective endocarditis receive prophylaxis before dental procedures with risk of bleeding.8 Conditions include the presence of a prosthetic valve or cardiac device, valvulopathy in cardiac transplant recipients, the first 6 months after congenital heart disease repair, unrepaired cyanotic congenital heart disease, history of endocarditis, or presence of palliative conduits or shunts.8 Amoxicillin is a penicillin derivative and would be inappropriate given this patient’s previous anaphylactic reaction. Cephalexin is a firstgeneration cephalosporin, and although data on the cross-reactivity of penicillin and cephalosporins is limited, current guidelines recommend that they not be used in patients with a history of penicillin-induced anaphylaxis.8 Vancomycin is not included in recommendations for antimicrobial prophylaxis before dental procedures.8 Clindamycin is the appropriate choice in a patient who has a penicillin allergy.8 Because the presence of a prosthetic valve is one of the indications for infective endocarditis prophylaxis, no prophylaxis would be inappropriate.8
In patients with severe AS, vasodilators such as nitroglycerin can cause severe hypotension and should be used with caution because reduction in systemic vascular resistance can increase the valve gradient.1,6 Symptomatic patients with severe AS or those with ventricular dysfunction should undergo AVR.1,2,6,7 This patient meets criteria for severe AS with high transvalvular aortic gradient and decreased valve area and should undergo evaluation for valve replacement. Surgical AVR remains the criterion standard in the absence of contraindications.1,6,7 With this patient’s age, severe COPD, and a calculated Society of Thoracic Surgeons (STS) risk score of 9.4%, she is not a safe candidate for surgical valve replacement. Valvuloplasty can be diagnostic and can assess the contribution of valvular dysfunction to the patient’s dyspnea. However, valvuloplasty should only be performed in patients who are hemodynamically unstable or as a bridge to AVR.1 Transcatheter AVR is a newer option for patients with high operative risk and is the most appropriate management for our patient.1,6,7 Hospice or palliative care consultation is inappropriate because the patient is a candidate for TAVR. The patient was apprised of her condition and told that it would not be safe to perform Mayo Clin Proc. n November 2014;89(11):e109-e113 www.mayoclinicproceedings.org
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5. Which one of the following prophylactic antibiotic regimens is most appropriate before the procedure? a. Amoxicillin b. Cephalexin c. Vancomycin d. Clindamycin e. No prophylaxis is needed
DISCUSSION Degenerative aortic valve disease is the most common valvulopathy in the Western Hemisphere and commonly affects individuals older than 55 years of age.9 The normal aortic valve is composed of 3 mobile leaflets that form an opening that is 3 to 4 cm2. Aortic stenosis is progressive, with declining aortic valve area
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of approximately 0.10 to 0.12 cm2 per year.1,2,6,9 This decline induces a gradual increase in obstruction and elevated transvalvular gradients.1,2,6,9 Typical symptoms that develop with disease progression include light-headedness, dizziness, exertional dyspnea, angina, or palpitations.1,2,6,9 Prognosis is related to severity and symptoms.1,2,6,9 Those with severe AS and symptoms of angina and syncope or those with signs of HF have the worst prognosis, and urgent evaluation and intervention should be pursued.2 Physical examination reveals a harsh, crescendo-decrescendo systolic ejection murmur heard at the right second intercostal space or left sternal border that radiates to the carotid arteries but can be diminished in severe COPD, and as the severity progresses, the peak of the murmur shifts later into systole.1,2,6,9 Carotid palpation reveals decreased amplitude and delayed upstroke, but this symptom can be absent in the elderly and in those with advanced atherosclerosis.1,2,6 The initial diagnostic test is TTE, which can confirm the diagnosis and grade the severity.1,2,6 However, echocardiography has limitations and can underestimate the transvalvular gradient, especially in those with declining ventricular function. On rare occasions, patients may require hemodynamic catheterization with measurement of the transaortic gradient and area calculation.1,2,6,7 The severity of AS can be categorized as mild, moderate, or severe on the basis of valve area and mean gradient. Aortic valve area classifications are 1.9 to 1.5 cm2 for mild, 1.5 to 1.0 cm2 for moderate, and less than 1.0 cm2 for severe disease. Mean gradient classifications are mild, less than 25 mm Hg; moderate, 25 to 40 mm Hg; and severe, greater than 40 mm Hg.1,6 Mild to moderate AS may be treated initially with conservative medical management, best accomplished with angiotensin-converting enzyme inhibitors and b-blockers.10 However, no medical therapy has been shown to slow the progression of AS. Treatment should also include management of comorbid conditions such as atrial fibrillation, CAD, and hypertension.7,10 All patients with AS and symptoms of exertional dyspnea, angina, syncope, ventricular dysfunction with an ejection fraction of less than 50%, or a dilated ascending aorta diameter of more than 45 mm should be referred to a cardiologist.1,2,6,7 Severe AS should be treated e112
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with valve replacement via conventional surgical approaches or less invasive TAVR.1,2,6,7 Because both approaches have complex risks and benefits, a new model referred to as the heart care team has been suggested. The goal is to provide patient-centered information and education from a multispecialty group of surgeons, interventional and general cardiologists, and the patient’s primary physician.11 Currently, TAVR is indicated for individuals with severe AS who are considered to be highrisk candidates for surgical replacement. This includes those with porcelain aorta, previous extensive mediastinal radiation, friable aortic atheromas, and severe pulmonary disease. Risk caclulators such as the STS risk score and EUROscore (European System for Cardiac Operative Risk Evaluation) are readily available online, and their use in the evaluation of severe AS is encouraged.7 The American College of Cardiology/American Heart Association consider an STS score greater than 8% to indicate high risk for surgical replacement.11 Transcatheter AVR is a less invasive procedure but not without risks. The PARTNER (Placement of Aortic Transcatheter Valve) trial compared TAVR with conventional surgical replacement and found a stroke risk of 5.5% vs 2.4%, respectively. However, after 2 years, stroke risk equalized between the 2 groups.7 Although there was a higher stroke risk in the TAVR group, this risk was counterbalanced with an increased mortality in high risk patients receiving surgical AVR. Other complications inherent to valve replacements include major vascular complications (eg, dissection, vessel rupture), bleeding, acquired conduction abnormalities leading to pacemaker placement, and dysrhythmias such as atrial fibrillation.1,6,7 Currently, TAVR is indicated for individuals with severe AS who are considered poor candidates for surgical replacement, including those with porcelain aorta, previous extensive mediastinal radiation, friable aortic atheromas, severe pulmonary disease, or high risk scores calculated by STS and EUROscore.7 Finally, although no study to date has documented a benefit in infective endocarditis prophylaxis before dental procedures, it is recommended that antimicrobial prophylaxis be provided to patients with any type of surgical or transvascular prosthetic valve replacement with the caveat that the effect is still unknown.8
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Correspondence: Address to Brian P. Shapiro, MD, Division of Cardiovascular Diseases, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32223 ([email protected]).
REFERENCES 1. Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease (version 2012): the Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2012;33(19):2451-2496. 2. Manning WJ. Asymptomatic aortic stenosis in the elderly: a clinical review. JAMA. 2013;310(14):1490-1497. 3. Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/ AATS/PCNA/SCAI/STS Guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2012;60(24):e44-e164. 4. Gupta NK, Agrawal RK, Srivastav AB, Ved ML. Echocardiographic evaluation of heart in chronic obstructive pulmonary disease patient and its co-relation with the severity of disease. Lung India. 2011;28(2):105-109. 5. Debl K, Djavidani B, Seitz J, et al. Planimetry of aortic valve area in aortic stenosis by magnetic resonance imaging. Invest Radiol. 2005;40(10):631-636.
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6. Baumgartner H, Hung J, Bermejo J, et al; American Society of Echocardiography; European Association of Echocardiography. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice [published correction appears in J Am Soc Echocardiogr. 2009;22(5):442]. J Am Soc Echocardiogr. 2009;22(1):1-23. 7. Holmes DR Jr, Mack MJ, Kaul S, et al. 2012 ACCF/AATS/ SCAI/STS expert consensus document on transcatheter aortic valve replacement. J Am Coll Cardiol. 2012;59(13): 1200-1254. 8. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association; a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group [published correction appears in Circulation. 2007;116(15):e376e377]. Circulation. 2007;116(15):1736-1754. 9. Spaccarotella C, Mongiardo A, Indolfi C. Pathophysiology of aortic stenosis and approach to treatment with percutaneous valve implantation. Circ J. 2011;75(1):11-19. 10. Grimard BH, Larson JM. Aortic stenosis: diagnosis and treatment. Am Fam Physician. 2008;78(6):717-724. 11. Holmes DR Jr, Rich JB, Zoghbi WA, Mack MJ. The heart team of cardiovascular care. J Am Coll Cardiol. 2013;61(9):903-907.
CORRECT ANSWERS: 1. a. 2. e. 3. e. 4. c. 5. d
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78-Year-Old-Woman With Dyspnea on Exertion Chad W. McRee, MD; Jordan C. Ray, MD; and Brian P. Shapiro, MD
A
78-year-old woman presented to her physician with dyspnea on exertion that had progressed over the previous several months, particularly with activities such as climbing stairs. She reported no symptoms of fever, chills, cough, chest pain, lightheadedness, dizziness, palpitations, syncope, paroxysmal nocturnal dyspnea, orthopnea, or unexplained weight gain. Her medical history included hypertension, hyperlipidemia, paroxysmal atrial fibrillation, heart failure (HF) with preserved ejection fraction, and severe chronic obstructive pulmonary disease (COPD). She had no history of coronary artery disease (CAD). Results of a pharmacological stress test 1 year previously were unremarkable. Allergies included penicillin-related anaphylaxis. Medications included niacin and inhaled fluticasone-salmeterol and tiotropium. Her surgical, social, and family histories were unremarkable. On physical examination, the patient could speak in full sentences with unlabored breathing. Her body mass index (calculated as the weight in kilograms divided by the height in meters squared) was 19 kg/m2. Vital signs included a temperature of 36.5 C, pulse rate of 69 beats/min, blood pressure of 160/84 mm Hg, respiratory rate of 16 breaths/min, and oxygen saturation of 95% while breathing room air. The patient appeared her stated age and in no acute distress. Cardiac examination revealed a regular heart rate and rhythm with no rubs or heaves. A 2/6 late-peaking, systolic murmur at the right upper sternal border was transmitted to the carotid arteries and encroached on the second heart sound. A soft S4 was present. The carotid pulse was delayed with low amplitude and upstroke. The point of maximal impulse was nondisplaced but enlarged. Jugular venous pressure was normal. Her lungs were clear on auscultation bilaterally, and abdominal examination revealed no abnormalities. There was no evidence of clubbing, cyanosis, or edema of the lower extremities.
1. In view of the initial findings, which one of the following is the most likely diagnosis? a. Aortic stenosis (AS) b. Severe mitral regurgitation c. CAD d. COPD with severe tricuspid regurgitation and right-sided HF e. Atrial fibrillation
See end of article for correct answers to questions. Resident in Internal Medicine, Mayo School of Graduate Medical Education, Jacksonville, FL (C.W.M., J.C.R.); Advisor to residents and Consultant in Cardiovascular Diseases, Mayo Clinic, Jacksonville, FL (B.P.S.).
This patient presented with a systolic ejection murmur best heard at the right upper sternal border in the second intercostal space radiating to the carotid arteries, which is most consistent with AS.1,2 Severe mitral regurgitation classically presents with a holosystolic, blowing murmur radiating to the back and axilla.1,2 Although this patient has cardiac risk factors, normal results on a recent stress test and the lack of angina make CAD less likely.3 Chronic obstructive pulmonary disease affects pulmonary vasculature and can lead to development of ventricular dysfunction, pulmonary hypertension, tricuspid regurgitation, and cor pulmonale.4 However, COPD with severe tricuspid regurgitation and right-sided HF presents with findings of a pansystolic murmur best heard along the left lower sternal border in the fifth intercostal space with elevated jugular venous pressure, ascites, and peripheral edema,4 which are absent in this patient. Atrial fibrillation can be asymptomatic or present with an irregularly irregular rhythm and palpitations. Although HF with preserved ejection fraction predisposes this patient to dysrhythmias such as atrial fibrillation, the clinical examination findings are more consistent with AS.1,2 The patient was informed that her symptoms and cardiac examination findings were most consistent with AS. She was anxious to know what could be done to help improve her symptoms. Further diagnostic work-up was pursued to determine the most appropriate treatment.
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2. Which one of the following is the best initial diagnostic test to evaluate this patient’s aortic stenosis? a. Cardiovascular magnetic resonance imaging (CMR) b. Cardiac computed tomographic angiography c. Exercise stress test d. Cardiac catheterization e. 2-Dimensional and Doppler transthoracic echocardiography The initial evaluation of patients with dyspnea on exertion consists of a comprehensive history and physical examination, a complete blood cell count, serum electrolyte panel, chest radiography, and 12-lead electrocardiography. Although CMR provides excellent image quality and visualization of tissue characteristics, it is used in highly selected situations in which traditional testing is inadequate or equivocal and thus would not be the best answer.1,2,5,6 Computed tomography can evaluate AS primarily by assessing valve calcifications; however, it is considered a complementary imaging modality to traditional testing. Computed tomographic angiography can be used before percutaneous intervention in planning the access route and valve sizing. However, radiation exposure and the use of iodinated contrast media limit its use.1,2,6 Exercise stress testing can be useful in evaluating patients who present with symptoms of angina or dyspnea on exertion, but given our patient’s recent normal stress test results, clinically important CAD would be less likely.3 Cardiac catheterization is used to assess aortic valve area and mean gradient as well as for confirmation when echocardiographic findings are equivocal. It is invasive and often unnecessary to establish the diagnosis.1,2,6 Doppler TTE should be the initial diagnostic test in the evaluation of suspected AS.1,2,6 It can assess the presence and severity of AS and sequelae of left ventricular hypertrophy, left atrial enlargement, diastolic dysfunction, and pulmonary hypertension.1,2,6 Laboratory studies yielded the following results (reference ranges shown parenthetically): hemoglobin, 13.7 g/dL (12.0-15.5 g/dL); white blood cells, 4.9 109/L (3.5-10.5 109/L); platelet count, 229 109/L (150-450 109/L); potassium, 4.7 mmol/L (3.6-5.2 mmol/L); serum urea nitrogen, 12 mg/dL (6-21 mg/dL); e110
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and creatinine, 0.9 mg/dL (0.6-1.1 mg/dL). Chest radiography revealed hyperinflated lungs and a normal cardiac silhouette with no evidence of pleural effusion. Pulmonary function test results were consistent with severe obstruction, with a forced expiratory volume in the first second of expiration of 45%. Electrocardiography revealed normal sinus rhythm and left ventricular hypertrophy. Although TTE proved technically difficult because of poor acoustic windows, it revealed normal left ventricular systolic function and chamber size with concentric left ventricular hypertrophy, grade 2 diastolic dysfunction without regional wall motion abnormalities, and moderate left atrial enlargement. The calculated ejection fraction was 61%. The calculated aortic valve area was 1.25 cm2 with a mean gradient of 28 mm Hg, consistent with moderate stenosis. Trivial mitral, tricuspid, and pulmonary valve regurgitation were present. In this patient, clinical and imaging findings are inconsistent in grading the severity of her valvulopathy. The TTE findings in this patient suggested moderate AS, whereas the physical examination findings were more consistent with severe stenosis. 3. Given the physical examination and TTE findings, which one of the following is the best next step? a. Proceed with aortic valve replacement (AVR) b. Repeat TTE with Doppler c. Medical therapy with vasodilators d. CMR e. Cardiac catheterization Management of AS is based on severity and symptoms. Moderate stenosis is managed with medical therapy targeting comorbid conditions, and severe stenosis is managed with AVR.1,2,6 Aortic valve replacement is indicated in patients with severe AS. Given the conflicting clinical and echocardiographic findings, it is important to confirm the stenosis severity before intervention. In addition to physical examination, the severity can be assessed by TTE with Doppler using aortic valve peak velocity, aortic valve area, or mean gradient. Often the examination and TTE findings are concordant. However, TTE may underestimate severity because of technical limitations regarding patient
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body habitus, underlying pulmonary disease, incomplete Doppler interrogation of the aortic valve, or low stroke volume.1,6 Repeating the same diagnostic test would unlikely yield different results and is not the best next step. Medical therapy may be indicated in patients with AS who do not meet criteria for AVR but not until valve severity is determined.1,2,6,7 If physical examination and imaging findings conflict, cardiac catheterization should be pursued for definitive diagnosis.1,6 The patient underwent cardiac catheterization, which revealed an aortic valve area of 0.85 cm2 and a mean gradient of 48 mm Hg.
conventional surgical replacement of her valve. She elected to undergo TAVR, which resulted in improvement in her overall symptoms and quality of life. Approximately 1 year after TAVR, the patient is scheduled for a root canal procedure.
4. Which one of the following is the most appropriate treatment for this patient? a. Medical therapy with nitroglycerin b. Surgical AVR with or without aortic root enlargement c. Transcatheter AVR (TAVR) d. Balloon valvuloplasty e. Hospice or palliative care consultation
This patient has a prosthetic valve and requires antimicrobial prophylaxis before her dental procedure.8 The American Heart Association recommends that patients with highest risk of adverse outcomes from infective endocarditis receive prophylaxis before dental procedures with risk of bleeding.8 Conditions include the presence of a prosthetic valve or cardiac device, valvulopathy in cardiac transplant recipients, the first 6 months after congenital heart disease repair, unrepaired cyanotic congenital heart disease, history of endocarditis, or presence of palliative conduits or shunts.8 Amoxicillin is a penicillin derivative and would be inappropriate given this patient’s previous anaphylactic reaction. Cephalexin is a firstgeneration cephalosporin, and although data on the cross-reactivity of penicillin and cephalosporins is limited, current guidelines recommend that they not be used in patients with a history of penicillin-induced anaphylaxis.8 Vancomycin is not included in recommendations for antimicrobial prophylaxis before dental procedures.8 Clindamycin is the appropriate choice in a patient who has a penicillin allergy.8 Because the presence of a prosthetic valve is one of the indications for infective endocarditis prophylaxis, no prophylaxis would be inappropriate.8
In patients with severe AS, vasodilators such as nitroglycerin can cause severe hypotension and should be used with caution because reduction in systemic vascular resistance can increase the valve gradient.1,6 Symptomatic patients with severe AS or those with ventricular dysfunction should undergo AVR.1,2,6,7 This patient meets criteria for severe AS with high transvalvular aortic gradient and decreased valve area and should undergo evaluation for valve replacement. Surgical AVR remains the criterion standard in the absence of contraindications.1,6,7 With this patient’s age, severe COPD, and a calculated Society of Thoracic Surgeons (STS) risk score of 9.4%, she is not a safe candidate for surgical valve replacement. Valvuloplasty can be diagnostic and can assess the contribution of valvular dysfunction to the patient’s dyspnea. However, valvuloplasty should only be performed in patients who are hemodynamically unstable or as a bridge to AVR.1 Transcatheter AVR is a newer option for patients with high operative risk and is the most appropriate management for our patient.1,6,7 Hospice or palliative care consultation is inappropriate because the patient is a candidate for TAVR. The patient was apprised of her condition and told that it would not be safe to perform Mayo Clin Proc. n November 2014;89(11):e109-e113 www.mayoclinicproceedings.org
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5. Which one of the following prophylactic antibiotic regimens is most appropriate before the procedure? a. Amoxicillin b. Cephalexin c. Vancomycin d. Clindamycin e. No prophylaxis is needed
DISCUSSION Degenerative aortic valve disease is the most common valvulopathy in the Western Hemisphere and commonly affects individuals older than 55 years of age.9 The normal aortic valve is composed of 3 mobile leaflets that form an opening that is 3 to 4 cm2. Aortic stenosis is progressive, with declining aortic valve area
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of approximately 0.10 to 0.12 cm2 per year.1,2,6,9 This decline induces a gradual increase in obstruction and elevated transvalvular gradients.1,2,6,9 Typical symptoms that develop with disease progression include light-headedness, dizziness, exertional dyspnea, angina, or palpitations.1,2,6,9 Prognosis is related to severity and symptoms.1,2,6,9 Those with severe AS and symptoms of angina and syncope or those with signs of HF have the worst prognosis, and urgent evaluation and intervention should be pursued.2 Physical examination reveals a harsh, crescendo-decrescendo systolic ejection murmur heard at the right second intercostal space or left sternal border that radiates to the carotid arteries but can be diminished in severe COPD, and as the severity progresses, the peak of the murmur shifts later into systole.1,2,6,9 Carotid palpation reveals decreased amplitude and delayed upstroke, but this symptom can be absent in the elderly and in those with advanced atherosclerosis.1,2,6 The initial diagnostic test is TTE, which can confirm the diagnosis and grade the severity.1,2,6 However, echocardiography has limitations and can underestimate the transvalvular gradient, especially in those with declining ventricular function. On rare occasions, patients may require hemodynamic catheterization with measurement of the transaortic gradient and area calculation.1,2,6,7 The severity of AS can be categorized as mild, moderate, or severe on the basis of valve area and mean gradient. Aortic valve area classifications are 1.9 to 1.5 cm2 for mild, 1.5 to 1.0 cm2 for moderate, and less than 1.0 cm2 for severe disease. Mean gradient classifications are mild, less than 25 mm Hg; moderate, 25 to 40 mm Hg; and severe, greater than 40 mm Hg.1,6 Mild to moderate AS may be treated initially with conservative medical management, best accomplished with angiotensin-converting enzyme inhibitors and b-blockers.10 However, no medical therapy has been shown to slow the progression of AS. Treatment should also include management of comorbid conditions such as atrial fibrillation, CAD, and hypertension.7,10 All patients with AS and symptoms of exertional dyspnea, angina, syncope, ventricular dysfunction with an ejection fraction of less than 50%, or a dilated ascending aorta diameter of more than 45 mm should be referred to a cardiologist.1,2,6,7 Severe AS should be treated e112
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with valve replacement via conventional surgical approaches or less invasive TAVR.1,2,6,7 Because both approaches have complex risks and benefits, a new model referred to as the heart care team has been suggested. The goal is to provide patient-centered information and education from a multispecialty group of surgeons, interventional and general cardiologists, and the patient’s primary physician.11 Currently, TAVR is indicated for individuals with severe AS who are considered to be highrisk candidates for surgical replacement. This includes those with porcelain aorta, previous extensive mediastinal radiation, friable aortic atheromas, and severe pulmonary disease. Risk caclulators such as the STS risk score and EUROscore (European System for Cardiac Operative Risk Evaluation) are readily available online, and their use in the evaluation of severe AS is encouraged.7 The American College of Cardiology/American Heart Association consider an STS score greater than 8% to indicate high risk for surgical replacement.11 Transcatheter AVR is a less invasive procedure but not without risks. The PARTNER (Placement of Aortic Transcatheter Valve) trial compared TAVR with conventional surgical replacement and found a stroke risk of 5.5% vs 2.4%, respectively. However, after 2 years, stroke risk equalized between the 2 groups.7 Although there was a higher stroke risk in the TAVR group, this risk was counterbalanced with an increased mortality in high risk patients receiving surgical AVR. Other complications inherent to valve replacements include major vascular complications (eg, dissection, vessel rupture), bleeding, acquired conduction abnormalities leading to pacemaker placement, and dysrhythmias such as atrial fibrillation.1,6,7 Currently, TAVR is indicated for individuals with severe AS who are considered poor candidates for surgical replacement, including those with porcelain aorta, previous extensive mediastinal radiation, friable aortic atheromas, severe pulmonary disease, or high risk scores calculated by STS and EUROscore.7 Finally, although no study to date has documented a benefit in infective endocarditis prophylaxis before dental procedures, it is recommended that antimicrobial prophylaxis be provided to patients with any type of surgical or transvascular prosthetic valve replacement with the caveat that the effect is still unknown.8
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RESIDENTS’ CLINIC
Correspondence: Address to Brian P. Shapiro, MD, Division of Cardiovascular Diseases, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32223 ([email protected]).
REFERENCES 1. Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease (version 2012): the Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2012;33(19):2451-2496. 2. Manning WJ. Asymptomatic aortic stenosis in the elderly: a clinical review. JAMA. 2013;310(14):1490-1497. 3. Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/ AATS/PCNA/SCAI/STS Guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2012;60(24):e44-e164. 4. Gupta NK, Agrawal RK, Srivastav AB, Ved ML. Echocardiographic evaluation of heart in chronic obstructive pulmonary disease patient and its co-relation with the severity of disease. Lung India. 2011;28(2):105-109. 5. Debl K, Djavidani B, Seitz J, et al. Planimetry of aortic valve area in aortic stenosis by magnetic resonance imaging. Invest Radiol. 2005;40(10):631-636.
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6. Baumgartner H, Hung J, Bermejo J, et al; American Society of Echocardiography; European Association of Echocardiography. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice [published correction appears in J Am Soc Echocardiogr. 2009;22(5):442]. J Am Soc Echocardiogr. 2009;22(1):1-23. 7. Holmes DR Jr, Mack MJ, Kaul S, et al. 2012 ACCF/AATS/ SCAI/STS expert consensus document on transcatheter aortic valve replacement. J Am Coll Cardiol. 2012;59(13): 1200-1254. 8. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association; a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group [published correction appears in Circulation. 2007;116(15):e376e377]. Circulation. 2007;116(15):1736-1754. 9. Spaccarotella C, Mongiardo A, Indolfi C. Pathophysiology of aortic stenosis and approach to treatment with percutaneous valve implantation. Circ J. 2011;75(1):11-19. 10. Grimard BH, Larson JM. Aortic stenosis: diagnosis and treatment. Am Fam Physician. 2008;78(6):717-724. 11. Holmes DR Jr, Rich JB, Zoghbi WA, Mack MJ. The heart team of cardiovascular care. J Am Coll Cardiol. 2013;61(9):903-907.
CORRECT ANSWERS: 1. a. 2. e. 3. e. 4. c. 5. d
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