Mitral stenosis overview: Difference between revisions
Line 6: | Line 6: | ||
Mitral [[stenosis]] is a [[valvular heart disease]] characterized by narrowing of the orifice of the [[mitral valve]] of the heart.<ref name="pmid16027271">{{cite journal |author=Carabello BA |title=Modern management of mitral stenosis |journal=Circulation |volume=112 |issue=3 |pages=432–7 |year=2005 |month=July |pmid=16027271 |doi=10.1161/CIRCULATIONAHA.104.532498 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=16027271}}</ref> In normal cardiac [[physiology]], the mitral valve opens during [[left ventricle | left ventricular]] [[diastole]], to allow blood to flow from the [[left atrium]] to the left ventricle. Blood flows in the proper direction because during this phase of the [[cardiac cycle]]; the pressure in the [[left ventricle]] is lower than the pressure in the [[left atrium]], and the blood flows down the [[pressure gradient]]. In the case of mitral stenosis, the valve does not open completely, and to transport the same amount of blood, the left atrium needs a higher pressure than normal to overcome the increased gradient. Mitral stenosis typically progresses slowly (over decades) from the initial signs of mitral stenosis to [[New York Heart Association Functional Classification|NYHA functional class]] II symptoms to the development of [[atrial fibrillation]] to the development of NYHA functional class III or IV symptoms. Once an individual develops NYHA class III or IV symptoms, the progression of the disease accelerates and the patient's condition deteriorates. Severe mitral stenosis (MS) is eventually lethal disease unless treated with vulvotomy or [[valve replacement]], it may progress to serious complications like [[pulmonary hypertension]], [[heart failure]] and death. Most of the cases are due to [[rheumatic heart disease]]. | Mitral [[stenosis]] is a [[valvular heart disease]] characterized by narrowing of the orifice of the [[mitral valve]] of the heart.<ref name="pmid16027271">{{cite journal |author=Carabello BA |title=Modern management of mitral stenosis |journal=Circulation |volume=112 |issue=3 |pages=432–7 |year=2005 |month=July |pmid=16027271 |doi=10.1161/CIRCULATIONAHA.104.532498 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=16027271}}</ref> In normal cardiac [[physiology]], the mitral valve opens during [[left ventricle | left ventricular]] [[diastole]], to allow blood to flow from the [[left atrium]] to the left ventricle. Blood flows in the proper direction because during this phase of the [[cardiac cycle]]; the pressure in the [[left ventricle]] is lower than the pressure in the [[left atrium]], and the blood flows down the [[pressure gradient]]. In the case of mitral stenosis, the valve does not open completely, and to transport the same amount of blood, the left atrium needs a higher pressure than normal to overcome the increased gradient. Mitral stenosis typically progresses slowly (over decades) from the initial signs of mitral stenosis to [[New York Heart Association Functional Classification|NYHA functional class]] II symptoms to the development of [[atrial fibrillation]] to the development of NYHA functional class III or IV symptoms. Once an individual develops NYHA class III or IV symptoms, the progression of the disease accelerates and the patient's condition deteriorates. Severe mitral stenosis (MS) is eventually lethal disease unless treated with vulvotomy or [[valve replacement]], it may progress to serious complications like [[pulmonary hypertension]], [[heart failure]] and death. Most of the cases are due to [[rheumatic heart disease]]. | ||
==Pathophysiology== | |||
Mitral stenosis ([[MS]]) is most commonly secondary to acute [[rheumatic fever]]. Generally, the initial [[valvulitis]] is associated with [[valvular]] [[regurgitation]] but over a period of 2 or more years, the [[commissures]] fuse and the valves thicken and calcify. The chordal supporting structure also calcifies and retracts. The result is the typical “fish mouth deformity”. 70% of the time; the mitral valve is involved in isolation, and 25% of the time; the [[aortic valve]] is involved as well. The [[tricuspid]] and [[pulmonic valve]]s are involved less commonly. Patients develop symptoms when the mitral vavle area is 2 to 2.5 cm<sup>2</sup>. | |||
==References== | ==References== |
Revision as of 15:34, 17 January 2013
Mitral Stenosis Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Mitral stenosis overview On the Web |
American Roentgen Ray Society Images of Mitral stenosis overview |
Risk calculators and risk factors for Mitral stenosis overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Mohammed A. Sbeih, M.D. [2]
Overview
Mitral stenosis is a valvular heart disease characterized by narrowing of the orifice of the mitral valve of the heart.[1] In normal cardiac physiology, the mitral valve opens during left ventricular diastole, to allow blood to flow from the left atrium to the left ventricle. Blood flows in the proper direction because during this phase of the cardiac cycle; the pressure in the left ventricle is lower than the pressure in the left atrium, and the blood flows down the pressure gradient. In the case of mitral stenosis, the valve does not open completely, and to transport the same amount of blood, the left atrium needs a higher pressure than normal to overcome the increased gradient. Mitral stenosis typically progresses slowly (over decades) from the initial signs of mitral stenosis to NYHA functional class II symptoms to the development of atrial fibrillation to the development of NYHA functional class III or IV symptoms. Once an individual develops NYHA class III or IV symptoms, the progression of the disease accelerates and the patient's condition deteriorates. Severe mitral stenosis (MS) is eventually lethal disease unless treated with vulvotomy or valve replacement, it may progress to serious complications like pulmonary hypertension, heart failure and death. Most of the cases are due to rheumatic heart disease.
Pathophysiology
Mitral stenosis (MS) is most commonly secondary to acute rheumatic fever. Generally, the initial valvulitis is associated with valvular regurgitation but over a period of 2 or more years, the commissures fuse and the valves thicken and calcify. The chordal supporting structure also calcifies and retracts. The result is the typical “fish mouth deformity”. 70% of the time; the mitral valve is involved in isolation, and 25% of the time; the aortic valve is involved as well. The tricuspid and pulmonic valves are involved less commonly. Patients develop symptoms when the mitral vavle area is 2 to 2.5 cm2.
References
- ↑ Carabello BA (2005). "Modern management of mitral stenosis". Circulation. 112 (3): 432–7. doi:10.1161/CIRCULATIONAHA.104.532498. PMID 16027271. Unknown parameter
|month=
ignored (help)