Aortic regurgitation overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.
Please Join in Editing This Page and Apply to be an Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [3] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Overview of Aortic Insufficiency
Aortic Insufficiency refers to retrograde or backwards flow of blood from the aorta into the left ventricle during diastole[1] [2] [3] [4].
Etiology
- Aortic valve disease:
- Rheumatic fever causes retraction of the cusps with resultant mixed aortic stenosis and aortic insufficiency with involvement of mitral valve disease.
- Infective endocarditis
- Traumatic aortic rupture following blunt chest trauma or deceleration injury.
- Congenital bicuspid aortic valve associated with increased risk of aortic dissection which then leads to aortic insufficiency.
- Dopamine agonists[3][5][6]
- Aortic root disease:
- Hypertension
- Aortic dissection
- Marfan syndrome
- HLA B-27 positive conditions : Psoriatic arthritis ; Ankylosing spondylitis ; Reiter's syndrome
- Giant cell arteritis
- Syphilitic aortitis
Pathophysiology
In acute aortic insufficiency, there is sudden decrease in stroke volume and subsequent increase in left ventricular end diastolic volume thereby causing decrease cardiac output with resultant reflex tachycardia. The sharply rising high left ventricular end diastolic pressure and reflex tachycardia causes profound hypotension and cardiogenic shock. Initially, the rising left ventricle end diastolic pressure causes early closure of mitral valve during diastole thereby preventing backward blood flow. But in severe cases, the rapidly rising left ventricular end diastolic pressure equalizes with the aortic end-diastolic pressure leading to backward flow of blood progressing towards development of pulmonary edema.
In chronic aortic insufficiency, initially the left ventricle remains complaint, thereby compensates for increased left ventricular end diastolic volume by progressive left ventricular dilatation and left ventricular hypertrophy, which maintains normal ratio of wall thickness to the cavity radius, thereby maintaining normal wall stress. Overtime, when the left ventricular hypertrophy fails to keep up with chronic volume overload, end systolic wall stress rises and at this point the left ventricle fails and results in left ventricle decompensation causing reduction in the left ventricular wall compliance with resultant congestive heart failure.
Diagnosis
The most common test used for the evaluation of the severity of aortic insufficiency is the echocardiogram, which can provide two-dimensional views of the regurgitant jet, and allow measurement of the velocity and volume of the jet.
Treatment
Aortic insufficiency can be treated either medically or surgically, depending on the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction.
In general, acute aortic insufficiency should be treated surgically with aortic valve replacement if there are no contraindications. Chronic aortic insufficiency is managed with vasodilators such as ACE inhibitors or hydralazine to reduce the afterload. Indications for surgery include heart failure failure with a reduced ejection fraction.
References
- ↑ Connolly HM, Crary JL, McGoon MD; et al. (1997). "Valvular heart disease associated with fenfluramine-phentermine". N. Engl. J. Med. 337 (9): 581–8. doi:10.1056/NEJM199708283370901. PMID 9271479.
- ↑ Weissman NJ (2001). "Appetite suppressants and valvular heart disease". Am. J. Med. Sci. 321 (4): 285–91. doi:10.1097/00000441-200104000-00008. PMID 11307869.
- ↑ 3.0 3.1 Schade R, Andersohn F, Suissa S, Haverkamp W, Garbe E (2007). "Dopamine agonists and the risk of cardiac-valve regurgitation". N. Engl. J. Med. 356 (1): 29–38. doi:10.1056/NEJMoa062222. PMID 17202453.
- ↑ Zanettini R, Antonini A, Gatto G, Gentile R, Tesei S, Pezzoli G (2007). "Valvular heart disease and the use of dopamine agonists for Parkinson's disease". N. Engl. J. Med. 356 (1): 39–46. doi:10.1056/NEJMoa054830. PMID 17202454.
- ↑ Rothman RB, Baumann MH, Savage JE, Rauser L, McBride A, Hufeisen SJ, Roth BL (2000). "Evidence for possible involvement of 5-HT(2B) receptors in the cardiac valvulopathy associated with fenfluramine and other serotonergic medications". Circulation. 102 (23): 2836–41. PMID 11104741. Retrieved 2011-03-28. Unknown parameter
|month=ignored (help) - ↑ Waller EA, Kaplan J, Heckman MG (2005). "Valvular heart disease in patients taking pergolide". Mayo Clinic Proceedings. Mayo Clinic. 80 (8): 1016–20. PMID 16092580. Retrieved 2011-03-28. Unknown parameter
|month=ignored (help)