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Valvular Heart Disease: Difference between revisions
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Calcified degenerative aortic valve stenosis was previously considered to be the result of a passive degenerative process due to longterm mechanical stress in combination with calcium accumulation. Recently this concept is revised. Calcified degenerative aortic stenosis is considered an active pathobiological process, including proliferative and inflammatory changes, lipid accumulation, renin-angiotensin system activation, valular interstitial cell transformation, ultimately resulting in calcification of the aortic valve <cite>RajamannanGershBonow</cite><cite>Rajamannan2</cite> <cite>OBrien</cite> <cite>Mohler</cite>. Risk factors for development of calcific aortic stenosis are similar to those for vascular atherosclerosis such as diabetes, hypertension, and cholesterol levels. <cite>Stewart</cite> <cite>Stritzke</cite> Progressive calcification leads to immobilization of the cusps causing stenosis. | Calcified degenerative aortic valve stenosis was previously considered to be the result of a passive degenerative process due to longterm mechanical stress in combination with calcium accumulation. Recently this concept is revised. Calcified degenerative aortic stenosis is considered an active pathobiological process, including proliferative and inflammatory changes, lipid accumulation, renin-angiotensin system activation, valular interstitial cell transformation, ultimately resulting in calcification of the aortic valve <cite>RajamannanGershBonow</cite><cite>Rajamannan2</cite> <cite>OBrien</cite> <cite>Mohler</cite>. Risk factors for development of calcific aortic stenosis are similar to those for vascular atherosclerosis such as diabetes, hypertension, and cholesterol levels. <cite>Stewart</cite> <cite>Stritzke</cite> Progressive calcification leads to immobilization of the cusps causing stenosis. | ||
Severity of outflow obstruction gradually increases in aortic valve stenosis. Left ventricular output is maintained by the adaptation of the increasingly hypertrophic left ventricle. This compensational mechanism serves to normalize the left ventricle wall stress. Left ventricular hypertrophy in combination with the prolonged systolic phase of the cardiac cycle results in increased myocardial oxygen demand. The mismatch between oxygen demand and supply is the main mechanism for angina pectoris in aortic stenosis. | |||
As the stenosis progresses, the left ventricle becomes less compliant with subsequent limited preload reserve. Eventually, the left ventricle will decompensate with a decline in cardiac output and rise in pulmonary artery pressure. | |||
Aortic stenosis is assessed by estimating the mean systolic pressure gradient and aortic valve area (AVA) Measurement of valve area is an important part of the assessment of the severity of aortic stenosis. The normal aortic valve area is 3-4 cm2. A valve area of <1 cm2 implies severe aortic stenosis The valve area may decrease by as much as 0.12 ± 0.19 cm 2 per year. <cite>OttoBurwaskLegget</cite> In late stages of severe aortic stenosis, cardiac output declines due to systolic dysfunction of the left ventricle, with a decline in the transvalvular gradient. | |||
== Clinical Presentation == | |||
Symptoms of degenerative aortic stenosis manifest with progression of the disease. The first symptoms usually commence in the seventh or eight decade. Symptoms are typically noted on exertion. Dyspnoea on exertion is the most common encountered first symptom. Other symptoms are angina, precipitated by exertion and relieved by rest, syncope and heart failure. The findings on physical examination vary with the severity of aortic stenosis. On auscultation, a systolic ejection crescendo-decrescendo murmur, radiating to the neck is audible, often accompanied by a thrill. An elevated left ventricular pressure in patients with aortic stenosis, in conjunction with mitral annulus calcifications predisposes to rupture of mitral chordae tendineae, which may produce a regurgitant systolic murmur. <cite>Brener</cite> <cite>Mihaljevic</cite> | |||
The first heart sound is usually normal or soft in patients with aortic stenosis. The second heart sound may be delayed due to prolongation of systolic ejection time. The S 2 also may be single because of superimposed aortic and pulmonic valve components, or the aortic valve component is absent or soft because the aortic valve is too calcified and has become immobile. If the aortic component is audible, this may give rise to a paradoxical splitting of S2. A pronounced atrial contraction can give rise to a palpable and audible S4. | |||
When stroke volume and systolic pulse pressures fall in severe aortic stenosis, a pulsus parvus (small pulse) may be present. A wide pulse pressure is also characteristic of aortic stenosis. A pulsus parvus et tardus (the arterial pulse is slow to increase and has a reduced peak) can be appreciated by palpating the carotid pulse of patients with severe aortic stenosis. The stenotic valve decreases the amplitude and delays the timing of the carotid upstroke. The rigidity of the vasculature may hamper this sign in the elderly. | |||
== Diagnostic options == | |||
=== Chest Radiography === | |||
In aortic stenosis, cardiac silhouette and pulmonary vascular distribution are normal unless cardiac decompensation is present. Post-stenotic dilatation of the ascending aorta is frequent. Calcification of the valve is found in almost all adults with severe aortic stenosis; however, fluoroscopy may be necessary to detect it. A late feature in patients with aortic valve stenosis is cardiomegaly. In patients with heart failure, the heart is enlarged, with congestion of pulmonary vasculature. | |||
The right atrium and right ventricle may also be enlarged in advanced heart failure. | |||
=== Electrocardiography === | |||
In approximately 85% of patients with aortic stenosis, left ventricle hypertrophy, with or without repolarization abnormalities is seen on electrocardiography (ECG). Left atrial enlargement, left axis deviation and conduction disorders are also common. Atrial fibrillation can be seen at late state and in older patients or those with hypertension. | |||
=== Echocardiography === | |||
The best non-invasive diagnostic tool to confirm the diagnosis of aortic stenosis, assess the number of cusps and the annular size, is ultrasonic examination of the heart. Quantification of valvular calcification is possible. In 1998, the American college of cardiology/American Heart Association (ACC/AHA) task force <cite>Bonow</cite> recommended the diagnostic use of echocardiography. | |||
Echocardiographic imaging evaluates the severity and etiology of the primary valvular lesion, secondary lesions, and coexisting abnormalities. The size and function of the atria and ventricles can be evaluated as well as hemodynamic characteristics. Echocardiography is also performed for postprocedural evaluation of patients. | |||
To assess the severity of aortic stenosis, transvalvular gradients and maximum jet velocity is measured using Doppler echocardiography, and aortic valve area is calculated. The systolic gradient across the stenotic aortic valve depends on stroke volume, systolic ejection period, and systolic pressure in the ascending aorta. The stenotic valve area is inversely related to the square root of the mean systolic gradient. Due to their flow-dependency these measurements are most valuable in normotensive patients. | |||
Valve thickening and calcification, as well as reduced leaflet motion can also be assessed using Doppler. | |||
=== Computed tomography === | |||
Although the role of computed tomography (CT) in clinical management is currently not well defined, This imaging modality could improve assessment of the ascending aorta. CT has an established role in evaluating the presence and severity of aortic root and ascending aortic dilatation in patients with associated aortic aneurysms. The high sensitivity and specificity of CT in detecting high-grade coronary artery stenosis could be useful to preoperatively rule out coronary artery disease. | |||
Both electron beam and multislice cardiac CT can be useful in quantifying valve calcification, which have been shown to correlate with echocardiographic assessment and clinical outcome. Prior to transcatheter aortic valve implantations, CT provides information concerning the aortic valve area, annulus size, and the distance between the aortic cusps and the coronary ostia. | |||
=== Cardiac Magnetic Resonance Imaging === | |||
Cardiac MRI (CMR) has an established role in evaluating aortic root and ascending aorta anatomy. This imaging modality can be used to measure the aortic valve area, but the role of CMR in the management of aortic stenosis is currently not well defined. | |||
=== Cardiac Catheterization === | |||
Cardiac catheterization remains the gold standard to detect coronary artery disease. Currently, in patients with aortic stenosis, cardiac catheterization is most often performed to identify the presence of concomitant coronary artery disease (CAD). In patients with inconclusive noninvasive tests, hemodynamic abnormalities can be assessed by cardiac catheterization. Coronary angiography is recommended prior to aortic valve replacement. | |||
=== Exercise Testing === | |||
Since aortic stenosis is a progressive disease, most common in the elderly population, many patients with aortic stenosis do not recognize gradually developing symptoms and cannot differentiate fatigue and dyspnea from aging and physical deconditioning. Lifestyle modification may mask symptoms. Although contraindicated in patients with severe aortic stenosis, Exercise testing is useful for risk stratification and eliciting symptoms. Under supervision, it is reasonable to propose exercise testing in patients >70 years who are still highly active. | |||
== Treatment == | |||
=== Medical treatment === | |||
For many years the standard of care for patients with significant aortic valve stenosis has been to provide antibiotic prophylaxis against infective endocarditis. However, current AHA guidelines for prevention of infective endocarditis no longer recommend antibiotic prophylaxis for this group of patients. Exceptions are patients with a prior episode of endocarditis, patients with prosthetic valves or with additional complex cardiac lesions inducing with consequently a high risk for the development of endocarditis. Patients who have had rheumatic fever should still receive antibiotic prophylaxis against recurrences of rheumatic fever. | |||
No medical treatment has proven to delay the progression of aortic stenosis. Surgery is inevitable for symptomatic patients. Patients at prohibitive risk for intervention may benefit from medical treatment including digitalis, diuretics, ACE inhibitors, or angiotensin receptor blockers, if experiencing heart failure. Beta-blockers should be avoided in these circumstances. | |||
=== Surgery === | |||
The infinitive treatment for aortic valve stenosis is aortic valve replacement. | |||
The first cardiac valve surgery under direct vision was an aortic valve replacement, performed in 1960 by dr. Dwight Harken <cite>Stephenson</cite> The aortic valve was replaced by a caged ball valve, which became the standard for aortic valve replacement. <cite>Emery</cite> <cite>Chaikof</cite> | |||