Aortic stenosis causes: Difference between revisions
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{{Aortic stenosis}} | {{Aortic stenosis}} | ||
{{CMG}}; '''Associate Editors-In-Chief:''' | {{CMG}}; '''Associate Editors-In-Chief:''' [[User:Mohammed Sbeih|Mohammed A. Sbeih, M.D.]] [mailto:msbeih@perfuse.org]; '''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [mailto:kfeeney@perfuse.org] | ||
==Overview== | ==Overview== | ||
Aortic stenosis can be categorized under two methods of causation: '''acquired''' and '''congenital'''. Research regarding the influence of preventative therapies on causation is mixed. More research is needed specifically looking at cholesterol lowering interventions and their role on disease onset. | Aortic stenosis can be categorized under two methods of causation: '''acquired''' and '''congenital'''. Research regarding the influence of preventative therapies on causation is mixed. More research is needed specifically looking at cholesterol lowering interventions and their role on disease onset. | ||
==Frequency of Underlying Causes of Aortic Stenosis== | |||
In the Euro Heart Survey on [[Valvular Heart Disease]], the etiology of aortic stenosis was: | |||
#[[Degenerative]]-calcific 81.9% | |||
#[[Rheumatic]] 11.2% | |||
#[[Congenital]] 5.6% | |||
#Post-[[endocarditis]] 1.3% | |||
Aortic stenosis is most commonly caused by age-related progressive calcification of the normal tricuspid aortic valve (>50% of cases). Other causes include calcification of a congenital [[bicuspid aortic valve]] (30-40% of cases) and [[acute rheumatic fever]] (less than 10% of cases) <ref name=uas>VOC=VITIUM ORGANICUM CORDIS, a compendium of the Department of Cardiology at Uppsala Academic Hospital. By Per Kvidal September 1999, with revision by Erik Björklund May 2008</ref>. | Aortic stenosis is most commonly caused by age-related progressive calcification of the normal tricuspid aortic valve (>50% of cases). Other causes include calcification of a congenital [[bicuspid aortic valve]] (30-40% of cases) and [[acute rheumatic fever]] (less than 10% of cases) <ref name=uas>VOC=VITIUM ORGANICUM CORDIS, a compendium of the Department of Cardiology at Uppsala Academic Hospital. By Per Kvidal September 1999, with revision by Erik Björklund May 2008</ref>. | ||
Revision as of 00:44, 9 April 2012
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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 causes On the Web |
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American Roentgen Ray Society Images of Aortic stenosis causes |
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Risk calculators and risk factors for Aortic stenosis causes |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Mohammed A. Sbeih, M.D. [2]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [3]
Overview
Aortic stenosis can be categorized under two methods of causation: acquired and congenital. Research regarding the influence of preventative therapies on causation is mixed. More research is needed specifically looking at cholesterol lowering interventions and their role on disease onset.
Frequency of Underlying Causes of Aortic Stenosis
In the Euro Heart Survey on Valvular Heart Disease, the etiology of aortic stenosis was:
- Degenerative-calcific 81.9%
- Rheumatic 11.2%
- Congenital 5.6%
- Post-endocarditis 1.3%
Aortic stenosis is most commonly caused by age-related progressive calcification of the normal tricuspid aortic valve (>50% of cases). Other causes include calcification of a congenital bicuspid aortic valve (30-40% of cases) and acute rheumatic fever (less than 10% of cases) [1].
Normal valves have three leaflets (tricuspid), but some valves have two leafs (bicuspid). Typically, aortic stenosis due to calcification of a bicuspid valve appears earlier, in the 40s and 50s, whereas that due to calcification of a normal valve appears later, in the 70s and 80s. Hypertension, diabetes mellitus, hyperlipoproteinemia and uremia may speed up the process [1].
Since calcific aortic stenosis shares many pathological features and risk factors with atherosclerosis, and as atherosclerosis may be prevented and/or reversed by cholesterol lowering agents, there has been interest in attempting to modify the course of calcific aortic stenosis by cholesterol lowering with statin drugs. Although a number of small, observational studies demonstrated an association between lowered cholesterol and decreased progression, and even regression, of calcific aortic stenosis. A large randomized clinical trial, published in 2005, failed to find any predictable effect of cholesterol lowering on calcific aortic stenosis. Researchers in 2007 study conversely demonstrated a slowing of aortic stenosis with the statin rosuvastatin [2]. More research is necessary to further clarify the specific mechanisms of disease onset and the influence of interventional methodologies on overall causation.
Complete Differential Diagnosis for the Causes of Aortic Stenosis
| Cardiovascular | Age-induced calcification of normal tricuspid aortic valve 'wear and tear' (around the 7th or 8th decade of life), atherosclerosis (normal tricuspid valve becomes rigid with age, usually stenosis develops over age 70 and it is rarely severe), congenital bicuspid aortic valve (it is twice as common in men, there is slow increase in stenosis -progressive sclerosis- and as individuals age, calcification of the aortic valve may occur and result in stenosis, this occurs in the 40s and 50s in case of bicuspid valve), prosthetic aortic valve, rheumatic fever (slowly progressive stenosis), subacute bacterial endocarditis. |
| Chemical / poisoning | No underlying causes |
| Dermatologic | No underlying causes |
| Drug Side Effect | No underlying causes |
| Ear Nose Throat | No underlying causes |
| Endocrine | No underlying causes |
| Environmental | Radiation. |
| Gastroenterologic | No underlying causes |
| Genetic | 1/3rd of supravalvular aortic stenosis cases are transmitted as an autosomal dominant trait as 60% of patients with supravalvular obstruction have williams syndrome (supravalvular obstruction, intellectual impairment and facial abnormalities). |
| Hematologic | No underlying causes. |
| Iatrogenic | Radiation treatment to the chest. |
| Infectious Disease | Bacterial endocarditis in which the vegetations may favor increase risk of stenosis. |
| Musculoskeletal / Ortho | No underlying causes |
| Neurologic | No underlying causes |
| Nutritional / Metabolic | No underlying causes |
| Obstetric/Gynecologic | No underlying causes |
| Oncologic | No underlying causes. |
| Opthalmologic | No underlying causes |
| Overdose / Toxicity | No underlying causes |
| Psychiatric | No underlying causes |
| Pulmonary | No underlying causes |
| Renal / Electrolyte | No underlying causes |
| Rheum / Immune / Allergy | rheumatic fever (slowly progressive stenosis). |
| Sexual | No underlying causes |
| Trauma | No underlying causes |
| Urologic | No underlying causes |
| Miscellaneous | No underlying causes |
Differential Diagnosis of the Causes of Aortic Stenosis
- Age-induced calcification of normal tricuspid aortic valve 'wear and tear'.
- Atherosclerosis.
- Congenital bicuspid aortic valve.
- Infective endocarditis.
- Aortic valve annular calcification.
- Prosthetic Aortic valve.
- Radiation treatment to the chest.
- Rheumatic fever (slowly progressive stenosis).
- Subacute bacterial endocarditis.
- williams syndrome, autosomal dominant trait that cause supravalvular aortic valve obstruction.
References
- ↑ 1.0 1.1 VOC=VITIUM ORGANICUM CORDIS, a compendium of the Department of Cardiology at Uppsala Academic Hospital. By Per Kvidal September 1999, with revision by Erik Björklund May 2008
- ↑ 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.