Aortic stenosis medical therapy: Difference between revisions
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===Lipid Lowering Drugs=== | ===Lipid Lowering Drugs=== | ||
Hypertension is common in patients with AS, may be a risk factor for AS, and adds to the total pressure overload on the LV in combination with valve obstruction. Concern that antihypertensive medications might result in a decrease in cardiac output has not been corroborated in studies of medical therapy, including 2 small RCTs, likely because AS does not result in “fixed” valve obstruction until late in the disease process. In 1616 patients with asymptomatic AS in the SEAS (Simvastatin Ezetimibe in Aortic Stenosis) study, hypertension (n=1340) was associated with a 56% higher rate of ischemic cardiovascular events and a 2-fold higher mortality rate (both P<0.01) than those seen in normotensive patients with AS, although no impact on progression of valve stenosis leading to symptoms requiring AVR was seen. Medical therapy for hypertension follows standard guidelines, starting at a low dose and gradually titrating upward as needed to achieve blood pressure control. There are no studies addressing specific antihypertensive medications in patients with AS, but diuretics may reduce stroke volume, particularly if the LV chamber is small at baseline. In theory, ACE inhibitors may be advantageous because of the potential beneficial effects on LV fibrosis, in addition to control of hypertension. Consideration should be given to a higher target blood pressure for patients with AS than is recommended for the general population, but this is an underexplored area, and further data are needed before a different target blood pressure can be recommended for patients with AS.1–3,9–13 | |||
2. | |||
Concurrent CAD is common in patients with AS, and all patients should be screened and treated for hypercholesterolemia, with GDMT used for primary and secondary prevention of CAD. In RCTs of statin therapy for mild to moderate AS, although aortic valve event rates were not reduced, the rate of ischemic events was reduced by about 20% in the statin therapy group even though these patients did not meet standard criteria for statin therapy.4–6,14,15 | |||
3. | |||
In patients undergoing TAVI, observational and registry data show that those who were treated 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%. When stratified by LVEF, having a prescription for a renin–angiotensin system inhibitor, versus no prescription, was associated with a lower 1-year mortality rate among patients with preserved LVEF but not among those with reduced LVEF.7,8,16,17 | |||
4. | |||
Despite experimental models and retrospective clinical studies suggesting that lipid-lowering therapy with a statin might prevent disease progression of calcific AS, 3 large well-designed RCTs failed to show a benefit, either in terms of changes in hemodynamic severity or in clinical outcomes, in patients with mild to moderate valve obstruction. Thus, at the time of publication, there are no data to support the use of statins for prevention of progression of AS | |||
More rapid progression of aortic stenosis has been associated with traditional risk factors for [[atherosclerosis]]. Based on the similarities that exist between [[calcific aortic stenosis]] and [[atherosclerosis]] in terms of their pathological features and risk factors, there has been a substantial interest to modify the progression of calcific aortic stenosis with the administration of cholesterol lowering agents such as [[statins]]. Although a number of small, [[observational studies]] have demonstrated an association between low cholesterol levels and decreased progression of aortic stenosis,<ref>{{cite journal |author=Moura LM, Ramos SF, Zamorano JL, ''et al'' |title=Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis |journal=J. Am. Coll. Cardiol. |volume=49 |issue=5 |pages=554-61 |year=2007 |pmid=17276178 |doi=10.1016/j.jacc.2006.07.072}}</ref> randomized clinical trials have failed to corroborate the effect of statin on halting the progression of calcific aortic stenosis.<ref name="pmid18765433">{{cite journal| author=Rossebø AB, Pedersen TR, Boman K, Brudi P, Chambers JB, Egstrup K et al.| title=Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. | journal=N Engl J Med | year= 2008 | volume= 359 | issue= 13 | pages= 1343-56 | pmid=18765433 | doi=10.1056/NEJMoa0804602 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18765433 }} </ref><ref name="pmid15944423">{{cite journal| author=Cowell SJ, Newby DE, Prescott RJ, Bloomfield P, Reid J, Northridge DB et al.| title=A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. | journal=N Engl J Med | year= 2005 | volume= 352 | issue= 23 | pages= 2389-97 | pmid=15944423 | doi=10.1056/NEJMoa043876 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15944423 }} </ref><ref name="pmid20048204">{{cite journal| author=Chan KL, Teo K, Dumesnil JG, Ni A, Tam J, ASTRONOMER Investigators| title=Effect of Lipid lowering with rosuvastatin on progression of aortic stenosis: results of the aortic stenosis progression observation: measuring effects of rosuvastatin (ASTRONOMER) trial. | journal=Circulation | year= 2010 | volume= 121 | issue= 2 | pages= 306-14 | pmid=20048204 | doi=10.1161/CIRCULATIONAHA.109.900027 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20048204 }} </ref> Nevertheless, many patients with AS have concomitant atherosclerotic disease which require [[statin]] therapy. | More rapid progression of aortic stenosis has been associated with traditional risk factors for [[atherosclerosis]]. Based on the similarities that exist between [[calcific aortic stenosis]] and [[atherosclerosis]] in terms of their pathological features and risk factors, there has been a substantial interest to modify the progression of calcific aortic stenosis with the administration of cholesterol lowering agents such as [[statins]]. Although a number of small, [[observational studies]] have demonstrated an association between low cholesterol levels and decreased progression of aortic stenosis,<ref>{{cite journal |author=Moura LM, Ramos SF, Zamorano JL, ''et al'' |title=Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis |journal=J. Am. Coll. Cardiol. |volume=49 |issue=5 |pages=554-61 |year=2007 |pmid=17276178 |doi=10.1016/j.jacc.2006.07.072}}</ref> randomized clinical trials have failed to corroborate the effect of statin on halting the progression of calcific aortic stenosis.<ref name="pmid18765433">{{cite journal| author=Rossebø AB, Pedersen TR, Boman K, Brudi P, Chambers JB, Egstrup K et al.| title=Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. | journal=N Engl J Med | year= 2008 | volume= 359 | issue= 13 | pages= 1343-56 | pmid=18765433 | doi=10.1056/NEJMoa0804602 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18765433 }} </ref><ref name="pmid15944423">{{cite journal| author=Cowell SJ, Newby DE, Prescott RJ, Bloomfield P, Reid J, Northridge DB et al.| title=A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. | journal=N Engl J Med | year= 2005 | volume= 352 | issue= 23 | pages= 2389-97 | pmid=15944423 | doi=10.1056/NEJMoa043876 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15944423 }} </ref><ref name="pmid20048204">{{cite journal| author=Chan KL, Teo K, Dumesnil JG, Ni A, Tam J, ASTRONOMER Investigators| title=Effect of Lipid lowering with rosuvastatin on progression of aortic stenosis: results of the aortic stenosis progression observation: measuring effects of rosuvastatin (ASTRONOMER) trial. | journal=Circulation | year= 2010 | volume= 121 | issue= 2 | pages= 306-14 | pmid=20048204 | doi=10.1161/CIRCULATIONAHA.109.900027 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20048204 }} </ref> Nevertheless, many patients with AS have concomitant atherosclerotic disease which require [[statin]] therapy. | ||
Revision as of 03:09, 29 June 2022
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Resident Survival Guide |
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Aortic Stenosis Microchapters |
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Diagnosis |
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Treatment |
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Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty |
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Transcatheter Aortic Valve Replacement (TAVR) |
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Case Studies |
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Aortic stenosis medical therapy On the Web |
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American Roentgen Ray Society Images of Aortic stenosis medical therapy |
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Directions to Hospitals Treating Aortic stenosis medical therapy |
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Risk calculators and risk factors for Aortic stenosis medical therapy |
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
Lipid Lowering Drugs
Hypertension is common in patients with AS, may be a risk factor for AS, and adds to the total pressure overload on the LV in combination with valve obstruction. Concern that antihypertensive medications might result in a decrease in cardiac output has not been corroborated in studies of medical therapy, including 2 small RCTs, likely because AS does not result in “fixed” valve obstruction until late in the disease process. In 1616 patients with asymptomatic AS in the SEAS (Simvastatin Ezetimibe in Aortic Stenosis) study, hypertension (n=1340) was associated with a 56% higher rate of ischemic cardiovascular events and a 2-fold higher mortality rate (both P<0.01) than those seen in normotensive patients with AS, although no impact on progression of valve stenosis leading to symptoms requiring AVR was seen. Medical therapy for hypertension follows standard guidelines, starting at a low dose and gradually titrating upward as needed to achieve blood pressure control. There are no studies addressing specific antihypertensive medications in patients with AS, but diuretics may reduce stroke volume, particularly if the LV chamber is small at baseline. In theory, ACE inhibitors may be advantageous because of the potential beneficial effects on LV fibrosis, in addition to control of hypertension. Consideration should be given to a higher target blood pressure for patients with AS than is recommended for the general population, but this is an underexplored area, and further data are needed before a different target blood pressure can be recommended for patients with AS.1–3,9–13 2. Concurrent CAD is common in patients with AS, and all patients should be screened and treated for hypercholesterolemia, with GDMT used for primary and secondary prevention of CAD. In RCTs of statin therapy for mild to moderate AS, although aortic valve event rates were not reduced, the rate of ischemic events was reduced by about 20% in the statin therapy group even though these patients did not meet standard criteria for statin therapy.4–6,14,15 3. In patients undergoing TAVI, observational and registry data show that those who were treated 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%. When stratified by LVEF, having a prescription for a renin–angiotensin system inhibitor, versus no prescription, was associated with a lower 1-year mortality rate among patients with preserved LVEF but not among those with reduced LVEF.7,8,16,17 4. Despite experimental models and retrospective clinical studies suggesting that lipid-lowering therapy with a statin might prevent disease progression of calcific AS, 3 large well-designed RCTs failed to show a benefit, either in terms of changes in hemodynamic severity or in clinical outcomes, in patients with mild to moderate valve obstruction. Thus, at the time of publication, there are no data to support the use of statins for prevention of progression of AS
More rapid progression of aortic stenosis has been associated with traditional risk factors for atherosclerosis. Based on the similarities that exist between calcific aortic stenosis and atherosclerosis in terms of their pathological features and risk factors, there has been a substantial interest to modify the progression of calcific aortic stenosis with the administration of cholesterol lowering agents such as statins. Although a number of small, observational studies have demonstrated an association between low cholesterol levels and decreased progression of aortic stenosis,[3] randomized clinical trials have failed to corroborate the effect of statin on halting the progression of calcific aortic stenosis.[4][5][6] Nevertheless, many patients with AS have concomitant atherosclerotic disease which require statin therapy.
Antihypertensive Drugs
A large number of patients with aortic stenosis have concomitant hypertension. Hypertension in aortic stenosis patients should be treated according to the guidelines.[7][8][9]
- Beta blockers and angiotensin-converting enzyme inhibitors are generally safe for asymptomatic patients with preserved left ventricular systolic function.
- Diuretics should be administered cautiously to avoid dehydration, hypovolemia and a significant reduction in cardiac output. Diuretics should be avoided among patients with a left ventricle of a small size.
Vasodilators
Extreme care should be taken to avoid excess vasodilation in the patient with critical aortic stenosis which could precipitate a downward spiral of low forward output, impaired subendocardial perfusion, ischemia and further reduction in forward output.[10]
- Vasodilators might be used to stabilize patients with acute severe decompensated aortic stenosis with heart failure of NYHA class IV while awaiting urgent AVR. The patient's hemodynamic status must be monitored closely.
- Nitroglycerin is helpful in relieving angina pectoris symptoms but should be used cautiously to avoid hypotension and excess vasodilation.
Sodium Restriction
If the patient has hypertension or symptoms of heart failure, the patient should be placed on sodium restriction.[11]
Contraindicated Medications
Severe Aortic Stenosis is considered an absolute contraindication to the use of following medications.[12][13]
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.
- ↑ Moura LM, Ramos SF, Zamorano JL; et al. (2007). "Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis". J. Am. Coll. Cardiol. 49 (5): 554–61. doi:10.1016/j.jacc.2006.07.072. PMID 17276178.
- ↑ Rossebø AB, Pedersen TR, Boman K, Brudi P, Chambers JB, Egstrup K; et al. (2008). "Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis". N Engl J Med. 359 (13): 1343–56. doi:10.1056/NEJMoa0804602. PMID 18765433.
- ↑ Cowell SJ, Newby DE, Prescott RJ, Bloomfield P, Reid J, Northridge DB; et al. (2005). "A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis". N Engl J Med. 352 (23): 2389–97. doi:10.1056/NEJMoa043876. PMID 15944423.
- ↑ Chan KL, Teo K, Dumesnil JG, Ni A, Tam J, ASTRONOMER Investigators (2010). "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. 121 (2): 306–14. doi:10.1161/CIRCULATIONAHA.109.900027. PMID 20048204.
- ↑ "2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary". Retrieved 4 March 2014.
- ↑ "2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary". Retrieved 4 March 2014.
- ↑ "2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary". Retrieved 4 March 2014.
- ↑ Khot UN, Novaro GM, Popović ZB, Mills RM, Thomas JD, Tuzcu EM; et al. (2003). "Nitroprusside in critically ill patients with left ventricular dysfunction and aortic stenosis". N Engl J Med. 348 (18): 1756–63. doi:10.1056/NEJMoa022021. PMID 12724481.
- ↑ Chung ML, Park L, Frazier SK, Lennie TA (2016). "Long-Term Adherence to Low-Sodium Diet in Patients With Heart Failure". West J Nurs Res. doi:10.1177/0193945916681003. PMID 27903829.
- ↑ Lindstrom, Eric J., and CRNA Ahmed F. Attaallah. "Novel Use of Clevidipine for Intraoperative Blood Pressure Management in Patients With Pheochromocytoma." AANA Journal 84.5 (2016): 343.
- ↑ Cruz JE, Thomas Z, Lee D, Moskowitz DM, Nemeth J (2016). "Therapeutic Interchange of Clevidipine For Sodium Nitroprusside in Cardiac Surgery". P T. 41 (10): 635–639. PMC 5047001. PMID 27757002.