Medication Summary
Treatment of valvular aortic stenosis is interventional. Medical treatment in aortic stenosis essentially is reserved for patients who have complications of the disorder, such as heart failure, infective endocarditis, hypertension, or arrhythmias.
The medical treatment options are limited in symptomatic patients with aortic stenosis who are not candidates for surgery. In patients with pulmonary congestion, cautious use of digitalis, diuretics, and angiotensin-converting enzyme (ACE) inhibitors might be attempted, whereas beta-blockers might be used if the predominant symptom is angina.
Antibiotic prophylaxis for the prevention of bacterial endocarditis is no longer recommended in patients with valvular aortic stenosis.[27]
Beta-Adrenergic Receptor Blockers
Class Summary
The medical treatment options are limited in symptomatic patients with aortic stenosis who are not candidates for surgery. Beta-blockers may be used if the predominant symptom is angina.
Esmolol (Brevibloc)
Esmolol is an ultra–short-acting that selectively blocks beta1-receptors with little or no effect on beta2-receptor types. It is particularly useful in patients with elevated arterial pressure, especially if surgery is planned.
Metoprolol (Lopressor, Toprol XL)
Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During intravenous (IV) administration, carefully monitor blood pressure (BP), heart rate, and electrocardiogram (ECG).
Cardiac Glycoside
Class Summary
Cardiac glycosides slow AV nodal conduction primarily by increasing vagal tone. Patients with aortic stenosis who are not candidates for surgery and present with pulmonary congestion may be treated with digoxin. Digoxin can also be used as an inotropic agent to control the ventricular rate in patients with atrial fibrillation.
Digoxin (Lanoxin)
Digoxin enhances myocardial contractility by inhibition of Na+/K+ ATPase, a cell membrane enzyme that extrudes sodium and brings potassium into the myocyte. The resulting increase in intracellular sodium stimulates the sodium-calcium exchanger in the cell membrane, which extrudes sodium and brings in calcium, leading to an increase in intracellular calcium in the sarcoplasmic reticulum of cardiac cells, thereby increasing the contractility of myocytes.
Loop Diuretics
Class Summary
Loop diuretics act on the ascending limb of the loop of Henle, inhibiting the reabsorption of sodium and chloride. Prehospital and emergency department management is focused on acute exacerbations of the symptoms of aortic stenosis. A patient presenting with uncontrolled heart failure should be treated supportively with loop diuretics.
Furosemide (Lasix)
Furosemide increases the excretion of water by interfering with the chloride-binding co-transport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule.
Bumetanide (Bumex)
Bumetanide increases the excretion of water by interfering with chloride-binding co-transport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in the ascending loop of Henle. These effects increase urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs following administration, renal vascular resistance decreases, and renal blood flow is enhanced.
Angiotensin-converting Enzyme (ace) Inhibitor
Class Summary
These agents are competitive inhibitors of angiotensin-converting enzyme (ACE). They reduce angiotensin II levels, thus decreasing aldosterone secretion.
Captopril (Capoten)
Captopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Enalapril (Vasotec)
Enalapril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It helps control blood pressure and proteinuria. Enalapril decreases pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance.
Opioid Analgesics
Class Summary
Opioid analgesics such as morphine act by binding to opioid receptors on neurons distributed throughout the nervous system and immune system. They can also help patient anxiety, distress, and dyspnea.
Morphine sulfate (MS Contin, Astramorph, Avinza)
Morphine is a drug of choice for analgesia due to reliable and predictable effects and safety profile. A patient presenting with uncontrolled heart failure due to aortic stenosis should be treated supportively with morphine.
Tzemos N, Therrien J, Yip J, Thanassoulis G, Tremblay S, Jamorski MT, et al. Outcomes in adults with bicuspid aortic valves. JAMA. Sep 17 2008;300(11):1317-25. [Medline].
Hughes BR, Chahoud G, Mehta JL. Aortic stenosis: is it simply a degenerative process or an active atherosclerotic process?. Clin Cardiol. Mar 2005;28(3):111-4. [Medline].
Roberts WC, Vowels TJ, Ko JM. Comparison of interpretations of valve structure between cardiac surgeon and cardiac pathologist among adults having isolated aortic valve replacement for aortic valve stenosis (+/- aortic regurgitation). Am J Cardiol. Apr 15 2009;103(8):1139-45. [Medline].
Townsend CM, et al. Sabiston Textbook of Surgery. 18th ed. Saunders; 2008:1841-1844..
Kerstjens-Frederikse WS, Du Marchie Sarvaas GJ, et al. Left ventricular outflow tract obstruction: should cardiac screening be offered to first-degree relatives?. Heart. Aug 2011;97(15):1228-32. [Medline].
Lancellotti P, Magne J, Donal E, et al. Clinical outcome in asymptomatic severe aortic stenosis insights from the new proposed aortic stenosis grading classification. J Am Coll Cardiol. Jan 17 2012;59(3):235-43. [Medline].
Jander N, Minners J, Holme I, et al. Outcome of patients with low-gradient "severe" aortic stenosis and preserved ejection fraction. Circulation. Mar 1 2011;123(8):887-95. [Medline].
Tintinalli JE, Kelen GD, Stapczynski JS, eds. Valvular emergencies. In: 6th ed. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill; 2004:54.
Rodrigues Tda R, Sternick EB, Moreira Mda C. Epilepsy or syncope? An analysis of 55 consecutive patients with loss of consciousness, convulsions, falls, and no EEG abnormalities. Pacing Clin Electrophysiol. Jul 2010;33(7):804-13. [Medline].
Topol EJ, Califf RM, et al, eds. Aortic valve disease. In: Textbook of Cardiovascular Medicine. Section Two. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2007:Chap 23.
[Guideline] Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing Committee to Revise the 1998 guidelines for the management of patients with valvular heart disease) developed in collaboration with the Society of Cardiovascular Anesthesiologists endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol. Aug 1 2006;48(3):e1-148. [Medline].
Zamorano JL, Badano LP, Bruce C, et al. EAE/ASE recommendations for the use of echocardiography in new transcatheter interventions for valvular heart disease. Eur Heart J. Sep 2011;32(17):2189-214. [Medline].
Piérard LA, Lancellotti P. Stress testing in valve disease. Heart. Jun 2007;93(6):766-72. [Medline]. [Full Text].
Messika-Zeitoun D, Aubry MC, Detaint D, Bielak LF, Peyser PA, Sheedy PF, et al. Evaluation and clinical implications of aortic valve calcification measured by electron-beam computed tomography. Circulation. Jul 20 2004;110(3):356-62. [Medline].
Shah RG, Novaro GM, Blandon RJ, Whiteman MS, Asher CR, Kirsch J. Aortic valve area: meta-analysis of diagnostic performance of multi-detector computed tomography for aortic valve area measurements as compared to transthoracic echocardiography. Int J Cardiovasc Imaging. Aug 2009;25(6):601-9. [Medline].
Bergler-Klein J. Natriuretic peptides in the management of aortic stenosis. Curr Cardiol Rep. Mar 2009;11(2):85-93. [Medline].
Bergler-Klein J, Klaar U, Heger M, Rosenhek R, Mundigler G, Gabriel H, et al. Natriuretic peptides predict symptom-free survival and postoperative outcome in severe aortic stenosis. Circulation. May 18 2004;109(19):2302-8. [Medline].
Brown DW, Dipilato AE, Chong EC, Gauvreau K, McElhinney DB, Colan SD, et al. Sudden unexpected death after balloon valvuloplasty for congenital aortic stenosis. J Am Coll Cardiol. Nov 30 2010;56(23):1939-46. [Medline].
Agarwal A, Kini AS, Attanti S, Lee PC, Ashtiani R, Steinheimer AM, et al. Results of repeat balloon valvuloplasty for treatment of aortic stenosis in patients aged 59 to 104 years. Am J Cardiol. Jan 1 2005;95(1):43-7. [Medline].
Rahimtoola SH. Choice of prosthetic heart valve in adults an update. J Am Coll Cardiol. Jun 1 2010;55(22):2413-26. [Medline].
[Best Evidence] Stassano P, Di Tommaso L, Monaco M, Iorio F, Pepino P, Spampinato N, et al. Aortic valve replacement: a prospective randomized evaluation of mechanical versus biological valves in patients ages 55 to 70 years. J Am Coll Cardiol. Nov 10 2009;54(20):1862-8. [Medline].
Leon MB, Smith CR, Mack M, Miller DC, Moses JW, Svensson LG, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. Oct 21 2010;363(17):1597-607. [Medline].
Clavel, MA, et al. Comparison Between Transcatheter and Surgical Prosthetic Valve Implantation in Patients With Severe Aortic Stenosis and Reduced Left Ventricular Ejection Fraction. Circulation. Nov 9 2010Vol;. 122 No.19.
Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med. Jun 9 2011;364(23):2187-98. [Medline].
Daneault B, Kirtane AJ, Kodali SK, et al. Stroke associated with surgical and transcatheter treatment of aortic stenosis: a comprehensive review. J Am Coll Cardiol. Nov 15 2011;58(21):2143-50. [Medline].
[Guideline] Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. May 21 2003;289(19):2560-72. [Medline].
[Guideline] Nishimura RA, Carabello BA, Faxon DP, et al. ACC/AHA 2008 Guideline Update on Valvular Heart Disease: Focused Update on Infective Endocarditis: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology. August 2008;52:676-85. [Medline].
Moura LM, Ramos SF, Zamorano JL, Barros IM, Azevedo LF, Rocha-Gonçalves F, et al. Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis. J Am Coll Cardiol. Feb 6 2007;49(5):554-61. [Medline].
Chan KL, Teo K, Dumesnil JG, Ni A, Tam J. Effect of Lipid lowering with rosuvastatin on progression of aortic stenosis: results of the aortic stenosis progression observation: measuring effects of rosuvastatin (ASTRONOMER) trial. Circulation. Jan 19 2010;121(2):306-14. [Medline].
Rossebo AB, Pedersen TR, Boman K, et al. Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. N Engl J Med. Sep 25 2008;359(13):1343-56. [Medline].
Cowell SJ, Newby DE, Prescott RJ, et al. A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. N Engl J Med. Jun 9 2005;352(23):2389-97. [Medline].
[Guideline] Wann LS, Curtis AB, Ellenbogen KA, et al. 2011 ACCF/AHA/HRS Focused Update on the Management of Patients With Atrial Fibrillation (Update on Dabigatran): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. Mar 15 2011;123(10):1144-50. [Medline]. [Full Text].
[Best Evidence] Bagur R, Webb JG, Nietlispach F, Dumont E, De Larochellière R, Doyle D, et al. Acute kidney injury following transcatheter aortic valve implantation: predictive factors, prognostic value, and comparison with surgical aortic valve replacement. Eur Heart J. Apr 2010;31(7):865-74. [Medline]. [Full Text].
Eltchaninoff H, Prat A, Gilard M et al,. Transcatheter aortic valve implantation: early results of the FRANCE (FRench Aortic National CoreValve and Edwards) registry. Eur Heart Jl. 2011;32:191–197.
Lefevre T, Kappetein AP, Wolner E, et al. One year follow-up of the multi-centre European PARTNER transcatheter heart valve study. Eur Heart Jl. 2011;32:148–157.
Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. Oct 21 2010;363(17):1597-607. [Medline].
Prasad Y, Bhalodkar NC. Aortic sclerosis--a marker of coronary atherosclerosis. Clin Cardiol. Dec 2004;27(12):671-3. [Medline].
[Best Evidence] Rosenhek R, Zilberszac R, Schemper M, Czerny M, Mundigler G, Graf S, et al. Natural history of very severe aortic stenosis. Circulation. Jan 5 2010;121(1):151-6. [Medline].
Tamburino C, Capodanno D, Ramondo A, Petronio AS, Ettori F, Santoro G, et al. Incidence and predictors of early and late mortality after transcatheter aortic valve implantation in 663 patients with severe aortic stenosis. Circulation. Jan 25 2011;123(3):299-308. [Medline].
Zahn R, Gerckens U, EGrube E et al. Transcatheter aortic valve implantation: first results from a multi-centre real-world registry. Eur Heart Jl. 2011;32:198–204.
Zajarias A, Cribier AG. Outcomes and safety of percutaneous aortic valve replacement. J Am Coll Cardiol. May 19 2009;53(20):1829-36. [Medline].
- Table 1. Common Causes of Aortic Stenosis Among Patients Requiring Surgery
- Table 2. ACC/AHA Recommendations for Echocardiography (Imaging, Spectral, and Color Doppler) in Aortic Stenosis
- Table 3. Criteria for Determining Severity of Aortic Stenosis
- Table 4. Recommendations for Cardiac Catheterization in Aortic Stenosis
- Table 5. Recommendations for Aortic Valve Replacement in Aortic Stenosis
| Age < 70 years (n=324) | Age >70 years (n=322) |
| Bicuspid AV (50%) Postinflammatory (25%) Degenerative (18%) Unicommissural (3%) Hypoplastic (2%) Indeterminate (2%) | Degenerative (48%) Bicuspid (27%) Postinflammatory (23%) Hypoplastic (2%) |
| Indication | Class |
| Diagnosis and assessment of severity of aortic stenosis | I |
| Assessment of LV size, function, and/or hemodynamics | I |
| Reevaluation of patients with known aortic stenosis with changing symptoms or signs | I |
| Assessment of changes in hemodynamic severity and ventricular function in patients with known aortic stenosis during pregnancy | I |
| Reevaluation of asymptomatic patients with severe aortic stenosis | I |
| Reevaluation of asymptomatic patients with mild to moderate aortic stenosis and evidence of LV dysfunction or hypertrophy | IIa |
| Routine reevaluation of asymptomatic adult patients with mild aortic stenosis who have stable physical signs and normal LV size and function | III |
| Severity | Mean gradient (mm Hg) | Aortic valve area (cm2) |
| Mild | < 25 | >1.5 |
| Moderate | 25-40 | 1-1.5 |
| Severe | >40 | < 1 (or < 0.5 cm2/m2 body surface area) |
| Critical | >80 | < 0.5 |
| Indication | Class |
| Coronary angiography before aortic valve replacement in patients at risk for coronary artery disease | I |
| Assessment of severity of aortic stenosis in symptomatic patients when aortic valve replacement is planned or when noninvasive tests are inconclusive or a discrepancy exists in the clinical findings regarding the severity of aortic stenosis or the need for surgery | I |
| Coronary angiography before aortic valve replacement in patients for whom a pulmonary autograft (Ross procedure) is contemplated and the origin of the coronary arteries was not identified by noninvasive tests | I |
| With infusion of dobutamine, can be useful for evaluation of patients with low-flow/low-gradient aortic stenosis and LV dysfunction | IIa |
| Not recommended for hemodynamic measurements for assessment of aortic stenosis severity when noninvasive techniques are adequate and concord with clinical findings | III |
| Not recommended for hemodynamic measurements for assessment of LV function and aortic stenosis severity in asymptomatic patients | III |
| Indication | Class |
| Symptomatic patients with severe aortic stenosis | I |
| Patients with severe aortic stenosis undergoing coronary artery bypass surgery | I |
| Patients with severe aortic stenosis undergoing surgery on the aorta or other heart valves | I |
| Patients with severe aortic stenosis and LV systolic dysfunction (ejection fraction < 0.50) | I |
| Patients with moderate aortic stenosis undergoing coronary artery bypass surgery or surgery on the aorta or other heart valves | IIa |
| Patients with mild aortic stenosis undergoing coronary artery bypass surgery when there is evidence that progression may be rapid, such as moderate-to-severe valve calcification | IIb |
| Asymptomatic patients with severe aortic stenosis and abnormal response to exercise (eg, hypotension) | IIb |
| Asymptomatic patients with severe aortic stenosis and a high likelihood of rapid progression (based on age, calcification, and coronary artery disease) or if surgery might be delayed at the time of symptom onset | IIb |
| Asymptomatic patients with extremely severe aortic stenosis (valve area less than 0.6 cm2, mean gradient greater than 60 mm Hg, and jet velocity greater than 5 m per second) if the patient’s expected operative mortality is 1% or less | IIb |
| AVR is not useful for prevention of sudden death in asymptomatic patients with none of the findings listed under asymptomatic patients with severe aortic stenosis | III |
Print
