![]() Left ventricular structural derangements in chronic aortic regurgitation progress in proportion to the degree of regurgitant volume a normal or hyperdynamic left ventricle in the presence of severe features suggest that the valvulopathy is acute 3,7. effective regurgitant orifice area ≥0.30 cm 2.Various parameters are used in order to determine severity, such as 3,7: Features which may be suggestive on 2D echocardiography include failure of valvular coaptation, flail or prolapsed leaflets, and, when chronic, progressive left ventricular dilation. Ultrasound: echocardiographyĮchocardiography is useful for evaluating the cause of aortic regurgitation, either valvular or due to root disease, for assessing the regurgitant volume, and for assessing the left ventricle 3,7. Furthermore, if the aortic regurgitation is due to aortic root disease, then aneurysmal dilation may be noted 1. Variable appearance on chest radiographs depending on stage and severity of the disease 1. In chronic severe aortic regurgitation, the apex may be displaced to the left on posterior-anterior projections, and there may be signs of congestive heart failure 1. during transcatheter aortic valve implantation) calcific aortic stenosis), bacterial infective endocarditis, prolapse, quadricuspid aortic valve, ankylosing spondylitis, syphilitic aortitis, radiation-induced heart disease, etc.Īcute aortic regurgitation is less common, but also exists, with specific causes 2,3: valvular: rheumatic heart disease, calcific aortic valve disease (i.e.Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta, etc.), aortic dissection, Takayasu arteritis, syphilitic aortitis, etc. root disease: hypertension, congenital bicuspid aortic valve, connective tissue disorders (e.g. ![]() Predisposing factors or causes of chronic aortic regurgitation can broadly be divided into being due to root disease or due to intrinsic valvulopathy, although there is overlap 2,3: It is at this point where patients manifest clinical features of heart failure 2,3. This adaptive mechanism is able to compensate for even severe aortic regurgitation, however, eventually fails and the end-diastolic volume becomes too large and the ejection fraction and forward (rather than ‘total’) stroke volume both fall 2,3. This results in systolic hypertension, accounting for the wide pulse pressure, and aortic and arterial pressures rapidly falling during late systole and diastole, accounting for the timing of the murmur and the various eponymous signs 2,3. Patients with chronic aortic regurgitation compensate for the leakage into the left ventricle by increasing total stroke volume (this is the forward ‘true’ stroke volume in addition to the volume leaking) ejected by the left ventricle through dilation and hypertrophy of the left ventricle 2,3. A detailed discussion of these rare signs is beyond the scope of this article. Occasionally the murmur heard may be holodiastolic, reflecting increased disease severity, and there may be an additional mid-diastolic Austin Flint murmur heard at the apex, attributed to the regurgitant jet striking the anterior mitral valve leaflet 1-3.Īortic regurgitation is also infamously associated with a number of eponymous signs, all of which are now rare due to the decreased incidence of syphilitic aortitis 2,5,6. Clinical examination classically reveals a widened pulse pressure, pulsus bisferiens , a volume loaded (‘thrusting’) apex beat, and a decrescendo early diastolic murmur (the Key-Hodgkin murmur) that is heard on praecordial auscultation 1-4. Clinical presentationĪlthough chronic aortic regurgitation can be asymptomatic, even in reasonably severe disease, it eventually leads to left-predominant clinical features of heart failure such as dyspnea and angina 1-3. Aortic regurgitation occurs slightly more in males, and the incidence increases progressively after the age of 50 years 1.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |