Aortic stenosis causes

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Aortic Stenosis Microchapters

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Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Aortic Stenosis from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Cardiac Stress Test

Electrocardiogram

Chest X Ray

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MRI

Echocardiography

Cardiac Catheterization

Aortic Valve Area

Aortic Valve Area Calculation

Treatment

General Approach

Medical Therapy

Surgery

Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty

Transcatheter Aortic Valve Replacement (TAVR)

TAVR vs SAVR
Critical Pathway
Patient Selection
Imaging
Evaluation
Valve Types
TAVR Procedure
Post TAVR management
AHA/ACC Guideline Recommendations

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Prevention

Precautions and Prophylaxis

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Claudia P. Hochberg, M.D. [2], Abdul-Rahman Arabi, M.D. [3], Keri Shafer, M.D. [4], Priyamvada Singh, MBBS [5], Mohammed A. Sbeih, M.D. [6]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [7]

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 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

References

  1. 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
  2. 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.

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