Aortic stenosis medical therapy
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Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Mohammed A. Sbeih, M.D. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Usama Talib, BSc, MD [4] Assistant Editor-In-Chief: Kristin Feeney, B.S. [5]; Rim Halaby, M.D. [6]
Overview
While medical therapy may improve the symptoms of patients with aortic stenosis (AS), medical therapy does not prolong life expectancy. Aortic valve replacement (AVR) remains the definitive treatment of symptomatic aortic stenosis and it improves both the symptoms and life expectancy of patients with aortic stenosis. When pharmacological therapies are used, extreme caution must be taken in the administration of vasodilators as excess vasodilation may lead to hypotension, a reduction in perfusion pressure to the heart, a further decline in cardiac output and further hypotension. This downward spiral can be fatal and must be avoided at all costs.[1][2]
Medical Therapy
- Hypertension is common in patients with AS, may be a risk factor for AS, and increases the total pressure overload on the left ventricle in combination with valve obstruction.[3][4][5]
- 2 small RCTs have not confirmed that antihypertensive medications may reduce the cardiac output because AS does not result in fixed valve obstruction until late stage in the disease.
- The study of asymptomatic AS showed the association of hypertension with higher rate of ischemic cardiovascular events and a 2-fold higher mortality rate ) than normotensive patients with AS. However, impact on progression of valve stenosis leading to symptoms requiring AVR was not observed.
- Medical therapy for hypertension is based on the standard guidelines, initiating at a low dose and gradually titrated upward as needed to controlling of blood pressure.
- There are no studies considering specific antihypertensive medications in patients with AS, but diuretics may reduce stroke volume, particularly if the LV chamber is small at baseline.
- The advantages of ACE inhibitors including beneficial effects on LV fibrosis, control of hypertension.[6]
- Target blood pressure should be considered higher for patients with AS than is recommended for the general population.
- Concurrent coronary artery disease is common in patients with AS, and screening of all patients is recommended for hypercholesterolemia, for primary and secondary prevention of CAD.
- In RCTs of statin therapy for mild to moderate AS, the rate of ischemic events was reduced by about 20% in the statin therapy group. Howerer, aortic valve event rates were not reduced.
- In patients undergoing TAVI, treatment with renin–angiotensin system blocker therapy after the procedure had a lower 1-year mortality rate than those not treated with renin–angiotensin system blocker therapy, with a relative risk reduction of about 20% to 50% and an absolute risk reduction between 2.4% and 5.0%.
- Use of renin–angiotensin system inhibitor, was associated with a lower 1-year mortality rate among patients with preserved LVEF but not among those with reduced LVEF.
- 3 large well-designed RCTs failed to show a benefit of statins for prevention of progression of AS in terms of hemodynamic severity or clinical outcomes.
References
- ↑ Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA; et al. (2008). "ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines on the Management of Adults With Congenital Heart Disease). Developed in Collaboration With the American Society of Echocardiography, Heart Rhythm Society, International Society for Adult Congenital Heart Disease, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons". J Am Coll Cardiol. 52 (23): e1–121. doi:10.1016/j.jacc.2008.10.001. PMID 19038677.
- ↑ Otto CM (2006). "Valvular aortic stenosis: disease severity and timing of intervention". J Am Coll Cardiol. 47 (11): 2141–51. doi:10.1016/j.jacc.2006.03.002. PMID 16750677.
- ↑ Nazarzadeh M, Pinho-Gomes AC, Smith Byrne K, Canoy D, Raimondi F, Ayala Solares JR, Otto CM, Rahimi K (August 2019). "Systolic Blood Pressure and Risk of Valvular Heart Disease: A Mendelian Randomization Study". JAMA Cardiol. 4 (8): 788–795. doi:10.1001/jamacardio.2019.2202. PMC 6624812 Check
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value (help). PMID 31290937. - ↑ Nielsen OW, Sajadieh A, Sabbah M, Greve AM, Olsen MH, Boman K, Nienaber CA, Kesäniemi YA, Pedersen TR, Willenheimer R, Wachtell K (August 2016). "Assessing Optimal Blood Pressure in Patients With Asymptomatic Aortic Valve Stenosis: The Simvastatin Ezetimibe in Aortic Stenosis Study (SEAS)". Circulation. 134 (6): 455–68. doi:10.1161/CIRCULATIONAHA.115.021213. PMID 27486164.
- ↑ Briand M, Dumesnil JG, Kadem L, Tongue AG, Rieu R, Garcia D, Pibarot P (July 2005). "Reduced systemic arterial compliance impacts significantly on left ventricular afterload and function in aortic stenosis: implications for diagnosis and treatment". J Am Coll Cardiol. 46 (2): 291–8. doi:10.1016/j.jacc.2004.10.081. PMID 16022957.
- ↑ O'Brien KD, Zhao XQ, Shavelle DM, Caulfield MT, Letterer RA, Kapadia SR, Probstfield JL, Otto CM (April 2004). "Hemodynamic effects of the angiotensin-converting enzyme inhibitor, ramipril, in patients with mild to moderate aortic stenosis and preserved left ventricular function". J Investig Med. 52 (3): 185–91. doi:10.1136/jim-52-03-33. PMID 15222408.