Aortic regurgitation overview
Resident Survival Guide |
Aortic Regurgitation Microchapters |
Diagnosis |
---|
Treatment |
Acute Aortic regurgitation |
Chronic Aortic regurgitation |
Special Scenarios |
Case Studies |
Aortic regurgitation overview On the Web |
American Roentgen Ray Society Images of Aortic regurgitation overview |
Risk calculators and risk factors for Aortic regurgitation overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.; Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.
Overview
Aortic insufficiency refers to the retrograde or backward flow of blood from the aorta into the left ventricle during diastole.[1][2][3][4]
Pathophysiology
In aortic insufficiency (AI), when the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve is not able to completely close. This causes a leaking of blood from the aorta into the left ventricle. This means that some of the blood that was already ejected from the heart is regurgitating back into the heart. The percentage of blood that regurgitates back through the aortic valve due to AI is known as the regurgitant fraction. For instance, if an individual with AI has a stroke volume of 100ml and during ventricular diastole 25ml regurgitates back through the aortic valve, the regurgitant fraction is 25%. This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore an increase in the pulse pressure (systolic pressure - diastolic pressure). Thus, physical examination will reveal a bounding pulse, especially in the radial artery.[5][6]
Causes
Aortic insufficiency can be an acute illness or a chronic illness and the causes differ depending upon the acuity of the disease. In general, aortic insufficiency is due to abnormalities of the aortic valve itself or the aortic root. Aortic regurgitation secondary to dilation of the ascending aorta has overtaken the valvular aortic disease as the most common cause of aortic regurgitation.It can also occur after surgical valve placement. [7][8]
Epidemiology and Demographics
The prevalence of aortic regurgitation varies with age, geographic location, and gender.[9] Aortic insufficiency is unusual before the age of 50 and then increases progressively later in life.[10] Aortic regurgitation is more commonly seen in men as compared to women.[11][12]Worldwide the most common cause of aortic insufficiency is the rheumatic heart disease, particularly in the Asia, the Middle East, and the North Africa. In the United States, senile degenerative calcific aortic valve disease and bicuspid aortic valve disease are the most common causes.[8]
Risk Factors
In the past, the most common risk factor for aortic valvular disease had been the rheumatic fever, with subsequent fibrosis of the scarred valve then leading to retraction of the aortic valve cusps and prevention of their apposition during diastole. In the modern era, a more common risk factor for acquired aortic regurgitation is degenerative disease of the aorta and aortic valve in which case there is calcification and fibrosis of the cusps. Infective endocarditis remains an important risk factor and cause of aortic insufficiency. Congenital conditions such as congenital bicuspid aortic valve or a ventricular septal defect can also result in aortic insufficiency. Patients with bicuspid aortic valve are at increased risk of developing aortic dissection.[5][13]
Natural History, Complications and Prognosis
In acute aortic insufficiency symptoms of heart failure often develop acutely. Chronic aortic insufficiency is usually insidious and progressive and the patient may remain asymptomatic for years. Once left ventricular dilation and left ventricular failure occur, dyspnea on exertion and exercise intolerance begin to occur. Later symptoms such as angina, syncope, and other symptoms of heart failure are present. There are two main parameters that reflect the overall outcome in patients with aortic insufficiency: ejection fraction (the lower the ejection fraction, the poorer the outcome) and end systolic diameter. Left ventricular dysfunction develops in patients with aortic insufficiency after decades of the onset of the symptoms. This lag period is longer than that of mitral regurgitation.[7]
Diagnosis
History and Symptoms
The symptoms of acute aortic regurgitation (AR) include dyspnea, chest pain (when aortic dissection is the cause of AR), weakness, and symptoms of congestive heart failure. Chronic AR may be without symptoms for several years until there is a decrease in the stroke volume and cardiac output due to heart failure progression. Symptoms of chronic aortic insufficiency include exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and palpitations.[14]
Physical Examination
A patient with suspected aortic insufficiency may have an early diastolic heart murmur which is usually a high-pitched sound best heard at the left sternal border. An ejection systolic 'flow' murmur may also be present. The apex beat is typically displaced down and to the left. A patient with chronic aortic insufficiency may present with signs of congestive heart failure. Other significant findings on physical exam include:[15]
- Bounding pulses may be present.
- Head nodding (de Musset's sign) - rhythmic nodding or bobbing of the head in synchrony with the beating of the heart.
- Capillary pulsations (Quincke's sign) - pulsation of arteriolar and venous plexuses of the nail bed causing alternate blanching and flushing.
- Corrigan's pulse - A rapid upstroke and collapse of the carotid artery pulse.
- Duroziez's sign - 'pistol' shot sounds (audible diastolic murmur heard over the femoral artery)
- Early diastolic murmur best heard in the right second intercostal space. The murmur may be soft in acute AR.
- S3 and S4 may be heard.
Cardiac Stress Test
A cardiac stress test (CST) is an evaluation modality used in cardiology in which the ability of the heart to respond to stress, either actually induced by exercise or stimulated by pharmacologic agents, is measured in a controlled clinical setting. CST for chronic aortic insufficiency is reasonable for assessment of functional capacity and symptomatic response in patients with a history of equivocal symptoms.[15]
Electrocardiogram
Electrocardiographic abnormalities in the patient with aortic insufficiency include left ventricular hypertrophy and left axis deviation.[15]
Chest X Ray
Chest x ray findings associated with aortic insufficiency may include left ventricular enlargement, cardiomegaly, prominent aortic root with valvular calcification, prosthetic valve dis-lodgement, or aortic dilation. If aortic insufficiency is severe, signs of pulmonary edema may also be present.[15]
Echocardiography
The echocardiogram is the single most useful diagnostic imaging study in the diagnosis and ongoing surveillance of the severity of aortic insufficiency. Echocardiography allows for serial assessment of left ventricular volumes which can be critical in determining the timing of aortic valve replacement. Echocardiography is used to assess the following parameters: end-diastolic diameter, end systolic diameter, and ejection fraction.[16]Aortic valve replacement should be performed if the LVEF is ≤ 55% or if left ventricular end-systolic dimension is > 55mm.
Cardiac MRI
Cardiac MRI may be used for assessing individuals with valvular heart disease in which evaluation of valvular stenosis, regurgitation, para- or perivalvular masses, perivalvular complications of infectious processes, or prosthetic valve disease are needed. CMR may be useful in identifying serial changes in LV volumes or mass in patients with valvular dysfunction. For patients with suboptimal echocardiograms showing aortic regurgitation, radionuclide angiography or magnetic resonance imaging is indicated to assess left ventricular volume and function at rest. CMR can also be used to determine the severity of AR in patients with suboptimal echocardiograms.[14][17][18][19]
Cardiac Catheterization
Although echocardiography is now the primary imaging modality used to evaluate aortic insufficiency, cardiac catheterization is often performed in patients with aortic insufficiency primarily to assess for the presence of epicardial coronary artery disease prior to surgical aortic valve replacement.[14]Aortography can also be performed to assess the severity of aortic insufficiency. The presence or absence of an aortic dissection can be evaluated. Left ventricular function (hemodynamics), size, and systolic function (ejection fraction) can also be evaluated.[15]
Treatment
Aortic insufficiency can be treated either medically with vasodilators or surgically with aortic valve replacement, depending upon the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction. Nitroprusside and ionotropes can be used to maintain blood pressure. Treatment options that are contraindicated include intra aortic balloon pump, pressors, and beta blockers (except in aortic dissection, where beta blockers can be used cautiously).[15]
Acute Aortic Insufficiency
Patients with acute severe aortic insufficiency are usually managed with emergency aortic valve replacement or repair. However, they can be stabilized medically before surgery with vasodilators.
Chronic Aortic Insufficiency
In the management of chronic aortic insufficiency, the left ventricular size and function should be monitored closely along with the exercise tolerance of the patient. If the patient develops heart failure symptoms and the disease starts to be symptomatic, then aortic valve replacement or valve repair is indicated. Annual echocardiographic studies are indicated in all patients with significant aortic insufficiency. Vasodilators such as ACE inhibitors, nifedipine, sodium nitroprusside, and hydralazine may slow the rate of progression of aortic insufficiency. The greatest benefit of medical therapy is in symptomatic patients and for those with heart failure symptoms due to advanced disease, but in general, they have a limited role in aortic insufficiency because symptomatic cases should be treated with valve replacement if the patient is a good candidate for surgery. Warfarin and long-term anticoagulation is not recommended in aortic insufficiency if there are no other indications for anticoagulation.[20]
Special Scenarios
Pregnancy
Isolated aortic insufficiency in pregnant patients can be managed with combination of diuretics and vasodilators.[21] ACE inhibitors are contraindicated in pregnancy. Patients with signs and symptoms of left ventricular failure should be monitored throughout labor and delivery with strict attention to volume status and blood pressure.
Young Adults
Congenital aortic insufficiency rarely occurs alone and is often associated with aortic stenosis or ventricular septal defect. It may occasionally be observed in adolescents and young adults with a bicuspid aortic valve, discrete subaortic obstruction, or prolapse of one of the aortic cusp into a ventricular septal defect. Turner syndrome, osteogenesis imperfecta, tetralogy of Fallot, and truncus arteriosus are other congenital disorders that are associated with aortic insufficiency in young patients. Rheumatic heart disease is one of the important causes for acquired aortic insufficiency in young patients in developing countries. It can also occur following an episode of infective endocarditis or as a consequence of attempts to relieve aortic stenosis by either balloon valvuloplasty or surgical valvulotomy, or when the pulmonary artery is relocated in the aortic position during repair of transposition of great vessels.[15]
End-stage Renal Disease
Aortic insufficiency in patients with end stage renal disease can be due to either valvular calcification or infective endocarditis.
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.
- ↑ 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.
- ↑ 5.0 5.1 Okafor I, Raghav V, Midha P, Kumar G, Yoganathan A (2016). "The hemodynamic effects of acute aortic regurgitation into a stiffened left ventricle resulting from chronic aortic stenosis". Am J Physiol Heart Circ Physiol. 310 (11): H1801–7. doi:10.1152/ajpheart.00161.2016. PMID 27106040.
- ↑ Devlin WH, Petrusha J, Briesmiester K, Montgomery D, Starling MR (1999). "Impact of vascular adaptation to chronic aortic regurgitation on left ventricular performance". Circulation. 99 (8): 1027–33. PMID 10051296.
- ↑ 7.0 7.1 Phan K, Haswell JM, Xu J, Assem Y, Mick SL, Kapadia SR; et al. (2016). "Percutaneous transcatheter interventions for aortic insufficiency in continuous-flow left ventricular assist device patients: A systematic review and meta-analysis". ASAIO J. doi:10.1097/MAT.0000000000000447. PMID 27676407.
- ↑ 8.0 8.1 Enriquez-Sarano M, Tajik AJ (2004). "Clinical practice. Aortic regurgitation". N Engl J Med. 351 (15): 1539–46. doi:10.1056/NEJMcp030912. PMID 15470217.
- ↑ Singh JP, Evans JC, Levy D, Larson MG, Freed LA, Fuller DL, Lehman B, Benjamin EJ (1999). "Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study)". The American Journal of Cardiology. 83 (6): 897–902. PMID 10190406. Retrieved 2011-12-27. Unknown parameter
|month=
ignored (help) - ↑ Tomsic A, Li WW, van Paridon M, Bindraban NR, de Mol BA (2016). "Infective Endocarditis of the Aortic Valve with Anterior Mitral Valve Leaflet Aneurysm". Tex Heart Inst J. 43 (4): 345–9. doi:10.14503/THIJ-15-5322. PMC 4979397. PMID 27547149.
- ↑ Klodas E, Enriquez-Sarano M, Tajik AJ, Mullany CJ, Bailey KR, Seward JB (1997). "Optimizing timing of surgical correction in patients with severe aortic regurgitation: role of symptoms". J Am Coll Cardiol. 30 (3): 746–52. PMID 9283535.
- ↑ Dujardin KS, Enriquez-Sarano M, Schaff HV, Bailey KR, Seward JB, Tajik AJ (1999). "Mortality and morbidity of aortic regurgitation in clinical practice. A long-term follow-up study". Circulation. 99 (14): 1851–7. PMID 10199882.
- ↑ Fedak PW, Verma S, David TE, Leask RL, Weisel RD, Butany J (2002). "Clinical and pathophysiological implications of a bicuspid aortic valve". Circulation. 106 (8): 900–4. PMID 12186790. Retrieved 2011-03-28. Unknown parameter
|month=
ignored (help) - ↑ 14.0 14.1 14.2 Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA; et al. (2014). "2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". J Am Coll Cardiol. 63 (22): e57–185. doi:10.1016/j.jacc.2014.02.536. PMID 24603191.
- ↑ 15.0 15.1 15.2 15.3 15.4 15.5 15.6 Bonow RO, Carabello B, de Leon AC, Edmunds LH, Fedderly BJ, Freed MD; et al. (1998). "ACC/AHA Guidelines for the Management of Patients With Valvular Heart Disease. Executive Summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease)". J Heart Valve Dis. 7 (6): 672–707. PMID 9870202.
- ↑ Grinstein J, Kruse E, Sayer G, Fedson S, Kim GH, Sarswat N; et al. (2016). "Novel echocardiographic parameters of aortic insufficiency in continuous-flow left ventricular assist devices and clinical outcome". J Heart Lung Transplant. 35 (8): 976–85. doi:10.1016/j.healun.2016.05.009. PMID 27373822.
- ↑ Gabriel RS, Renapurkar R, Bolen MA, Verhaert D, Leiber M, Flamm SD; et al. (2011). "Comparison of severity of aortic regurgitation by cardiovascular magnetic resonance versus transthoracic echocardiography". Am J Cardiol. 108 (7): 1014–20. doi:10.1016/j.amjcard.2011.05.034. PMID 21784393.
- ↑ Goffinet C, Kersten V, Pouleur AC, le Polain de Waroux JB, Vancraeynest D, Pasquet A; et al. (2010). "Comprehensive assessment of the severity and mechanism of aortic regurgitation using multidetector CT and MR". Eur Radiol. 20 (2): 326–36. doi:10.1007/s00330-009-1544-x. PMID 19652976.
- ↑ Debl K, Djavidani B, Buchner S, Heinicke N, Fredersdorf S, Haimerl J; et al. (2008). "Assessment of the anatomic regurgitant orifice in aortic regurgitation: a clinical magnetic resonance imaging study". Heart. 94 (3): e8. doi:10.1136/hrt.2006.108720. PMID 17686805.
- ↑ Salem DN, O'Gara PT, Madias C, et al. Valvular and structural heart disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; 133:593S
- ↑ Sheikh F, Rangwala S, DeSimone C, Smith HS, O'Leary AM (1995). "Management of the parturient with severe aortic incompetence". Journal of Cardiothoracic and Vascular Anesthesia. 9 (5): 575–7. PMID 8547563. Retrieved 2011-03-25. Unknown parameter
|month=
ignored (help)