This chapter provides an overview of aortic valve replacement (AVR) with stented bioprostheses. The indications for aortic valve surgery are reviewed, with an emphasis on current evidence-based guidelines, and currently available stented aortic bioprostheses are described. Clinical and physiologic outcomes of aortic valve surgery are critically evaluated to create a rational basis for prosthesis selection.
Aortic stenosis (AS) may be caused by: (1) degenerative calcification; (2) congenital malformations, most commonly bicuspid aortic valve; or (3) rheumatic fever. It is uncommonly associated with systemic diseases such as Paget's disease of bone and end-stage renal disease. Degenerative calcification is common in the elderly population and moderate to severe calcific AS is the most common pathology among patients undergoing AVR. The incidence of calcific AS is expected to rise with the increase in age of population in developed countries.
Valvular degenerative calcification is characterized as a progressive reduction of orifice cross-sectional area caused by calcification of the cusps. The pathogenesis of inflammation and lipid accumulation is reminiscent of atherosclerosis.1 The normal human aortic valve area (AVA) is between 3.0 and 4.0 cm2 with minimal to no gradient. Aortic stenosis is defined as mild, moderate, and severe AS, and the corresponding AVA, mean gradients, and peak jet velocities are shown in Table 33-1. In the presence of normal cardiac output, transvalvular gradient is usually greater than 50 mm Hg when the AVA is less than 1.0 cm2.2 A rapid increase in transvalvular gradient is seen when AVA is less than 0.8 to 1.0 cm2.
Table 33-1 Classification of Aortic Stenosis (AS) ||Download (.pdf)
Table 33-1 Classification of Aortic Stenosis (AS)
|Mean gradient (mm Hg)||<25||25–40||>40|
|Peak jet velocity (m/s)||<3.0||3.0–4.0||>4.0|
Obstruction to flow created by the reduced orifice area of the aortic valve elevates intracavitary pressures, and resultant wall stress leads to compensatory concentric hypertrophy to maintain normal cardiac output.3 With progressive hypertrophy, ventricular compliance progressively decreases and end-diastolic pressure rises.4 In this situation, the contribution of atrial contraction to preload becomes more significant and loss of sinus rhythm may lead to rapid progression of symptoms.
As AS progresses to become hemodynamically significant, initial compensation occurs by left ventricular hypertrophy (LVH). The average AVA is 0.6 to 0.8 cm2 at the onset of symptoms.3 Gradual progression of outflow obstruction and ventricular hypertrophy lead to the cardinal symptoms of AS, which are: (1) angina, (2) syncope, and (3) dyspnea or congestive heart failure (CHF). Classic natural history studies have demonstrated that average life expectancy in patients with hemodynamically significant AS is 4 years with angina, 3 years with syncope, and 2 years ...