Aortic stenosis pathophysiology: Difference between revisions
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{{ | {{Aortic stenosis}} | ||
{{CMG}} | {{CMG}} | ||
'''Associate Editors-In-Chief:''' Claudia P. Hochberg, M.D. [mailto:chochber@bidmc.harvard.edu]; [[User:Abdarabi|Abdul-Rahman Arabi, M.D.]] [mailto:abdarabi@yahoo.com]; [[User:KeriShafer|Keri Shafer, M.D.]] [mailto:kshafer@bidmc.harvard.edu] | '''Associate Editors-In-Chief:''' Claudia P. Hochberg, M.D. [mailto:chochber@bidmc.harvard.edu]; [[User:Abdarabi|Abdul-Rahman Arabi, M.D.]] [mailto:abdarabi@yahoo.com]; [[User:KeriShafer|Keri Shafer, M.D.]] [mailto:kshafer@bidmc.harvard.edu]; [[Priyamvada Singh|Priyamvada Singh, MBBS]] [[mailto:psingh@perfuse.org]] | ||
'''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [[mailto:kfeeney@perfuse.org]] | |||
==Overview== | |||
Aortic stenosis results in left ventricule overloading, where a pressure gradient exists between the left ventricule and aorta. This gradient can influence the functional integrity of the surrounding mitral valve. [[left ventricular hypertrophy|Hypertrophy]] is a common complication associated with aortic stenosis. | |||
==Pathophysiology== | ==Pathophysiology== | ||
When the aortic valve becomes | When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta.<ref name=Lilly>{{cite book | author = Lilly LS (editor) | title = Pathophysiology of Heart Disease | edition = 3rd ed. | publisher = Lippincott Williams & Wilkins | year = 2003 | id = ISBN 0-7817-4027-4 }}</ref> The more constricted the valve, the higher the gradient between the LV and the aorta. For instance, with a mild AS, the gradient may be 20 [[mmHg]]. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted to the aorta will only be 120 mmHg. So, while a [[Sphygmomanometer|blood pressure cuff]] may measure a normal [[systole|systolic]] [[blood pressure]], the actual pressure generated by the LV would be considerably [[hypertension|higher]]. | ||
In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased [[afterload]] caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the [[myocardium]] (muscle) of the LV undergoes [[left ventricular hypertrophy|hypertrophy]] (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened. | In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased [[afterload]] caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the [[myocardium]] (muscle) of the LV undergoes [[left ventricular hypertrophy|hypertrophy]] (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened. | ||
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{{reflist|2}} | {{reflist|2}} | ||
[[Category:DiseaseState]] | [[Category:DiseaseState]] | ||
[[Category:Signs and symptoms]] | [[Category:Signs and symptoms]] | ||
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[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Congenital heart disease]] | [[Category:Congenital heart disease]] | ||
[[Category:Mature chapter]] | |||
[[es:Estenosis aórtica]] | [[es:Estenosis aórtica]] | ||
[[fr:Rétrécissement aortique]] | [[fr:Rétrécissement aortique]] | ||
[[pl:Stenoza Aortalnej]] | [[pl:Stenoza Aortalnej]] | ||
[[pt:Estenose aórtica]] | [[pt:Estenose aórtica]] | ||
[[ro:Stenoza Aortică]] | [[ro:Stenoza Aortică]] | ||
[[tr:Aort darlığı]] | [[tr:Aort darlığı]] | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} |
Revision as of 14:52, 25 July 2011
Aortic Stenosis Microchapters |
Diagnosis |
---|
Treatment |
Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty |
Transcatheter Aortic Valve Replacement (TAVR) |
Case Studies |
Aortic stenosis pathophysiology On the Web |
American Roentgen Ray Society Images of Aortic stenosis pathophysiology |
Directions to Hospitals Treating Aortic stenosis pathophysiology |
Risk calculators and risk factors for Aortic stenosis pathophysiology |
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]]
Assistant Editor-In-Chief: Kristin Feeney, B.S. [[6]]
Overview
Aortic stenosis results in left ventricule overloading, where a pressure gradient exists between the left ventricule and aorta. This gradient can influence the functional integrity of the surrounding mitral valve. Hypertrophy is a common complication associated with aortic stenosis.
Pathophysiology
When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta.[1] The more constricted the valve, the higher the gradient between the LV and the aorta. For instance, with a mild AS, the gradient may be 20 mmHg. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted to the aorta will only be 120 mmHg. So, while a blood pressure cuff may measure a normal systolic blood pressure, the actual pressure generated by the LV would be considerably higher.
In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased afterload caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the myocardium (muscle) of the LV undergoes hypertrophy (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened.
References
- ↑ Lilly LS (editor) (2003). Pathophysiology of Heart Disease (3rd ed. ed.). Lippincott Williams & Wilkins. ISBN 0-7817-4027-4.