Aortic stenosis overview
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The aortic valve ensures that the blood moves forward from the left ventricle into the aorta and that it does not leak backwards during diastole. When functioning appropriately, the aortic valve does not impede the flow of blood between the left ventricle and the aorta and it does not leak. Under some circumstances, the aortic valve becomes narrower than normal impeding the flow of blood. This is known as aortic valve stenosis, or aortic stenosis, often abbreviated as AS.
Aortic stenosis can be classified broadly into two main categories: acquired and congenital. Further classification can be applied based on the origin of the stenosis such as acquired rheumatic, congenital bicuspid, congenital subaortic, congenital subvalvular, and congenital supravalvular aortic stenosis.
Aortic stenosis is the progressive narrowing of the aortic valve. Calcific aortic stenosis, in particular, is an active atherosclerotic pathology where inflammation, fibrosis and calcification are involved in the progressive narrowing of the effective aortic valve area in the absence of any commissural fusion. In contrast, rheumatic aortic stenosis is due to fusion of the commissures with valvular scarring and calcification. Aortic stenosis causes an impedance to the antegrade blood flow not only at the level of the aortic valve itself, but also at the subvalvular (below the aortic valve) or supravalvular (above the aortic valve) levels. As a result, chronic pressure overload develops in the left ventricle. The left ventricle undergoes hypertrophy as an initial adaptive mechanism to overcome the increased afterload. This compensatory mechanism ends up being maladpative by causing apoptosis of the hypertrophied myocytes and subsequent heart failure. Hence, aortic stenosis is a progressive valvular disease which progression depends mainly on the degree of the narrowing of the aortic valve as well as on the maladaptive ventricular wall response.
The frequency of causes of aortic stenosis varies depending on the age of the patient. Bicuspid valve is the most common cause of aortic stenosis in people below 50 years of age whereas calcified tricuspid valve is more common in older patients.
Differentiating Aortic Stenosis from other Disorders
Aortic stenosis must be differentiated from other cardiac or pulmonary causes of dyspnea, weakness, and dizziness. Furthermore, if there is left ventricular outflow tract obstruction, it is critical to identify whether the obstruction is subvalvular, valvular or supravalvular or due to hypertrophic cardiomyopathy (HOCM).
Epidemiology and Demographics
Aortic stenosis primarily affects older adults and the majority of cases are due to calcific degeneration. Aortic stenosis tends to affect approximately 2% of patients over the age of 65, 3% of patients over the age of 75, and 4% of patients over the age 85.
The most common risk factor for the subsequent development of aortic stenosis is congenital bicuspid aortic valve. Rheumatic fever is another risk factor for the subsequent development of aortic stenosis (rheumatic heart disease). Risk factors that may speed up the progression of degenerative calcific aortic stenosis include: hypertension, diabetes mellitus, hyperlipoproteinemia, uremia and smoking.
Natural History, Complications and Prognosis
Left untreated, aortic valve stenosis can lead to angina, syncope, congestive heart failure, atrial fibrillation, endocarditis, and sudden cardiac death. Surgical treatment of aortic stenosis also carries risks and potential complications that include vascular complications and mitral valve injury.
History and Symptoms
The main symptoms of aortic stenosis include angina, syncope and congestive heart failure. Left untreated, the average survival is 5 years after the onset of angina, 3 years after the onset of syncope, and 1 year after the onset of congestive heart failure.  Other symptoms include dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea.
Aortic stenosis is most often diagnosed when it is asymptomatic and can sometimes be detected during routine examination of the heart and circulatory system. The major signs include pulsus parvus et tardus (a slow-rising, small volume carotid pulse), a lag time between apical and carotid impulses, and a distinct systolic ejection murmur.
Cardiac Stress Test
Chest X-ray may be used as a diagnostic tool in the evaluation of aortic stenosis. Findings associated with aortic stenosis include left ventricular hypertrophy and calcification of the aortic valve.
Computed tomography can be helpful as a diagnostic tool in conditions where the echocardiographic findings are inconclusive.
Magnetic resonance imaging is rarely used in the diagnosis of aortic stenosis, except in rare cases where the echocardiographic findings are inconclusive. There is a signal void where the high velocity jet exits the aortic valve.
Echocardiography is the best non-invasive test to evaluate the aortic valve anatomy and function. It is indicated in the case of presence of symptoms suggestive of valvular problems or in the case of detection of a systolic murmur with a grade greater than 3/6. Doppler echocardiography allows the measurement of the maximum jet velocity and can be used to estimate the effective orifice area of the aortic valve as well as the gradient across the aortic valve using the modified Bernoulli equation (gradient = 4 x velocity2). The flow must be constant, so as the velocity increases, the valve area decreases proportionally. Attention to technical details is important as they may lead to underestimation of the severity of the aortic stenosis. Echocardiography can also be used to assess the severity of left ventricular hypertrophy.
Left and right heart catheterization as well as angiography may be useful in the assessment of the patient prior to aortic valve replacement surgery. In addition, asymptomatic patients with aortic stenosis should undergo cardiac catherization when echocardiographic findings are inconsistent with the clinical findings.
Aortic Valve Area
The aortic valve area is the size of the orifice for blood to flow from the left ventricle to the aorta. The aortic valve area is reduced in aortic stenosis, and the aortic valve area is the metric that is used to gauge the need for aortic valve replacement surgery. The pressure gradient across a narrowed aortic valve cannot be used to gauge the need for valve replacement as the gradient may be low in patients with impaired left ventricular function.
Aortic Valve Area Calculation
The calculation of the aortic valve area is an indirect method used to determine the area of the aortic valve. The calculated aortic valve orifice area is currently one of the measures for evaluating the severity of aortic stenosis. An aortic valve having an area less than 0.8 cm² is considered to be severe aortic stenosis.
There are many ways to calculate the aortic valve area. The most commonly used methods involve measurements taken during echocardiography. For interpretation of these values, the aortic valve area is generally divided by the body surface area.
Once a patient becomes symptomatic with aortic stenosis, aortic valve replacement should be performed as long as the patient can tolerate surgery and has no co-morbidities. If severe left ventricular dysfunction is present in the setting of aortic stenosis, it is of utmost importance to differentiate between true severe aortic stenosis and pseudo-severe aortic stenosis as these two entities have different pathophysiologies and different outcomes after aortic valve replacement. Medical therapy reduces symptoms but does not prolong life. If a patient has extensive co-morbidities, transcatheter aortic valve implantation can be considered. Aortic valvuloplasty can be considered in those patients who are too sick for surgery or transcatheter aortic valve implantation.
While medical therapy may improve the symptoms of patients with aortic stenosis, medical therapy does not prolong life expectancy. Aortic valve replacement remains the definitive treatment for symptomatic aortic stenosis and it improves both the symptoms and life expectancy of the patients. When pharmacological therapies are used, extreme caution must be taken in the administration of vasodilators as an excess in vasodilation may lead to hypotension, a reduction in perfusion pressure to the heart, a further decline in cardiac output and further hypotension. This vicious circle can be fatal and must be avoided at all costs.
Surgical intervention may be a necessary component of treatment for symptomatic severe aortic stenosis. Aortic valve replacement is the mainstay of treatment of symptomatic aortic stenosis, as it improves both the symptoms and life expectancy in aortic stenosis patients, in contrast to medical therapy alone which may improve the symptoms without prolonging life expectancy.
Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty
Surgical aortic valve replacement is the mainstay of the treatment of aortic stenosis as it improves both symptoms and life expectancy. However, some patients may not be surgical candidates due to coexisting comorbidities. Hence, minimally invasive treatment such as percutaneous aortic balloon valvotomy (PABV) maybe an alternative to surgery as a palliative strategy. PABV is a procedure during which one or more balloons are placed across a stenotic valve and then inflated in order to cause a decrease the severity of aortic stenosis. This is to be distinguished from transcatheter aortic valve implantation (TAVI) which is a different method that involves replacement of the valve percutaneously.
Transcatheter Aortic Valve Implantation
Until recently, aortic valve replacement (AVR) was the only effective treatment for severe symptomatic aortic stenosis. However, over the past decade percutaneous treatment of aortic valve disease with the implantation of a stent-based valve prosthesis has been introduced as a new treatment in patients considered inoperable because of severe co-morbidities. In Transcatheter Aortic Valve Implantation (TAVI) also known as Percutaneous Aortic Valve Replacement (PAVR), a synthetic valve is advanced to the heart through a small hole made in the groin. This procedure is similar in its mechanism to the insertion of a stent, or performing balloon angioplasty albeit with much larger equipment. Traditional aortic valve replacement is an invasive surgical procedure, with considerable mortality and morbidity, especially in more fragile patients. In the newly developed TAVI procedure, the dysfunctional aortic valve is replaced percutaneously, which obviates the need for open heart surgery.
Follow up is recommended for all patients with operated and unoperated aortic stenosis. Asymptomatic patients with aortic stenosis should undergo follow up since aortic stenosis is an ongoing disease that progresses with time. In fact, asymptomatic patients should undergo follow up every 1 year, 3 years and 5 years in case of severe, moderate and mild aortic stenosis respectively.
Aortic stenosis associated with rheumatic heart disease can be minimized with antibiotic therapy in patients with documented streptococcal pharyngitis (strep throat). Bicuspid aortic valve disease is a congenital variant and cannot be prevented. Calcific degeneration of the valve can potentially be minimized by rosouvistatin and other measures targeting prevention of atherosclerosis.
Precautions and Prophylaxis
People with aortic stenosis of any etiology are at risk for the development of infection of their stenosed valve, i.e. infective endocarditis and antibiotic prophylaxis should be considered. Patients with severe aortic stenosis should avoid strenuous exercise and any exercise that greatly increases afterload such as weight lifting.
- ↑ 1.0 1.1 1.2 1.3 Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al. (2008). "2008 Focused update incorporated into the ACC/AHA 2006 guidelines 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 (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.". Circulation 118 (15): e523-661. doi:10.1161/CIRCULATIONAHA.108.190748. PMID 18820172.
- ↑ Dweck MR, Boon NA, Newby DE (2012). "Calcific aortic stenosis: a disease of the valve and the myocardium.". J Am Coll Cardiol 60 (19): 1854-63. doi:10.1016/j.jacc.2012.02.093. PMID 23062541.
- ↑ Stewart BF, Siscovick D, Lind BK, Gardin JM, Gottdiener JS, Smith VE, Kitzman DW, Otto CM (March 1997). "Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study". Journal of the American College of Cardiology 29 (3): 630–4. PMID 9060903. Retrieved on 2012-04-11.
- ↑ Ross J, Braunwald E (1968). "Aortic stenosis.". Circulation 38 (1 Suppl): 61-7. PMID 4894151.
- ↑ Kelly TA, Rothbart RM, Cooper CM, Kaiser DL, Smucker ML, Gibson RS (1988). "Comparison of outcome of asymptomatic to symptomatic patients older than 20 years of age with valvular aortic stenosis.". Am J Cardiol 61 (1): 123-30. PMID 3337000.
- ↑ Iivanainen AM, Lindroos M, Tilvis R, Heikkilä J, Kupari M (1996). "Natural history of aortic valve stenosis of varying severity in the elderly.". Am J Cardiol 78 (1): 97-101. PMID 8712130.
- ↑ Charlson E, Legedza A, Hamel M (2006). "Decision-making and outcomes in severe symptomatic aortic stenosis.". J Heart Valve Dis 15 (3): 312-21. PMID 16784066.
- ↑ "Survival in elderly patients with severe aortic stenosis is dramatically improved by aortic valve replacement: results from a cohort of 277 patients aged >/=80 years.". Eur J Cardiothorac Surg. PMID 16950629.
- ↑ Grube E, Laborde JC, Gerckens U, Felderhoff T, Sauren B, Buellesfeld L, Mueller R, Menichelli M, Schmidt T, Zickmann B, Iversen S, Stone GW (October 2006). "Percutaneous implantation of the CoreValve self-expanding valve prosthesis in high-risk patients with aortic valve disease: the Siegburg first-in-man study". Circulation 114 (15): 1616–24. doi:10.1161/CIRCULATIONAHA.106.639450. PMID 17015786. Retrieved on 2011-03-17.
- ↑ 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.
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