Aortic valve stenosis is the most common valvular heart disease and the most frequent cardiovascular disease after hypertension and coronary artery disease. Of all people over age 65 years, stenosis is present in 2% to 7% of this population. With the growing elderly population, the prevalence of this disease will continue to increase.

Aortic stenosis may be caused by: (1) senile calcification of a morphologically normal tricuspid valve, (2) progressive calcification of a congenitally bicuspid valve, or (3) rheumatic fever which causes mixed stenotic and regurgitant lesions and is commonly associated with mitral valve disease. AS is rarely associated with systemic diseases such as Paget disease of bone and end-stage renal disease. Degenerative calcification is an active process with similarities to atherosclerosis and is mediated by inflammation, mechanical stress, and lipid deposition with macrophage infiltration. Atherosclerotic coronary artery disease is present in nearly 50% of patients with calcific aortic stenosis. Stenotic, bicuspid valves present primarily in the fourth and fifth decade of life, while calcified tricuspid valves usually present later in the seventh to ninth decade.

The normal human aortic valve area (AVA) is between 3 and 4 cm² with minimal to no gradient. Acquired aortic stenosis is characterized by gradual calcification of the cusps and increasing reduction of the orifice cross-sectional area. Cardiac output is from the start maintained through left ventricular (LV) hypertrophy and increase of the gradient across the valve. LV hypertrophy acts as a compensatory mechanism to restore wall stress and preserve cardiac output under increasing pressure afterload caused by the stenotic valve. During this stage, LV diastolic filling and LV longitudinal shortening are
already decreased. When the stenosis restricts the increase in cardiac output during physical activity, dyspnea, hypotension, angina and syncope may occur. Continuing cardiomyocyte death and replacement with fibrosis and LV hypertrophy leads to development of LV dysfunction and heart failure (HF) symptoms. Patients with aortic stenosis remain asymptomatic for several years but development of symptoms signals an inflection point in the survival and mortality rate is around 50% after 3 years. In asymptomatic patients with a severe aortic stenosis, sudden cardiac death is around 1.5% per year. Differentiating between asymptomatic and mildly symptomatic patients is often challenging, although symptom onset is a key factor in the indication for intervention. Predictors of symptom development in asymptomatic patients are older age, rate of hemodynamic progression, peripheral vascular disease, increase in gradient with exercise, excessive LV hypertrophy, and symptoms occurring during exercise testing. The onset of symptoms is not the only indication for intervention. A reduced LV function ejection fraction of less than 50% is also a class I (level of evidence B) indication for aortic valve replacement.

Aortic stenosis is defined as mild, moderate, and severe, and the corresponding AVA, mean gradients, and peak jet velocities are shown in Table 1.1. In the presence of normal cardiac output, the transvalvular gradient is typically greater than 50 mm Hg when the AVA is less than 1 cm². A rapid increase in transvalvular gradient is seen when the AVA is less than 0.8 to 1.0 cm².

Despite the absence of data from a randomized clinical trial, symptomatic severe aortic stenosis is considered a class 1 indication for surgery.

The average AVA is 0.6 to 0.8 cm² at the onset of symptoms. Gradual progression of outflow obstruction and ventricular hypertrophy leads to symptoms of aortic stenosis, which are: (1) angina, (2) syncope, and (3) dyspnea or congestive HF. Various studies have demonstrated that average life expectancy in patients with hemodynamically significant aortic stenosis is 4 years with angina, 3 years with syncope, and 2 years with congestive HF.

Patients with infective endocarditis and aortic dissection may suffer from acute severe aortic regurgitation and without intervention their prognosis is bad. In patients with chronic severe aortic regurgitation the most common causes are calcific valve disease and bicuspid aortic valve. Aortic regurgitation may also be associated with dilatation of the ascending aorta or sinuses of Valsalva. The disease course is over a longer time and LV volume overload increases slowly with LV dilatation. Symptoms of HF develop over time and are linked with a poor long-term prognosis. Patients with mild to moderate aortic regurgitation are generally asymptomatic and the likelihood of adverse events is low.

Patients with chronic aortic regurgitation should be monitored with clinical assessment and echocardiography, for alterations in symptoms, severity of aortic regurgitation, and LV systolic dysfunction. Aortic valve replacement improves survival, reduces symptoms, prevents development of HF, and avoids aortic complications in patients with dilatation of the ascending aorta. AVR is indicated for symptomatic patients with severe regurgitation regardless of LV systolic function or in asymptomatic patients with chronic severe regurgitation and LV systolic dysfunction.

Prosthetic valves are generally grouped as mechanical or biologic. Many prosthetic valves have been developed over the years with the aim of improving hemodynamic function, increasing durability, and reducing complications. Nevertheless, there is no perfect valve, and all prosthetic valves carry complications.

The most commonly implanted mechanical valves are the bileaflet valves. The major benefit of mechanical prosthesis is their durability. However, their Achilles heel is the need for lifelong anticoagulation, frequent INR tests, difficulties in starting interaction with other drugs, maintaining an adequate level of anticoagulation, and high chances of bleeding. The risk of a bleeding complication from anticoagulation is between 1% and 2% per year. Anticoagulation risk is higher in aging patients and in patients with comorbidities like congestive HF, hypertension, diabetes mellitus, and stroke or transient ischemic attack. The closure clicks of mechanical heart valve prostheses’ leaflets are quite often audible. However, only a small minority (6%) of mechanical heart valve recipients complain about the valve noise.

The most frequently implanted biologic valve is a stented xenograft. The leaflets of stented pericardial xenografts are made from bovine or porcine pericardium. Biologic valves are at risk for structural valve deterioration. The age of the patient at the time of implant is the most critical risk factor, the younger the patients, the faster the valve deterioration. Life expectancy is therefore an essential aspect of valve selection taking into account that in patients with a prosthetic heart valve, life expectancy is reduced compared to the general population.

Patients older than 65 years usually do not outlive the life expectancy of a tissue valve and implanting a bioprosthesis precludes anticoagulation. For patients younger than 60 to 65 years undergoing aortic valve replacement, a bileaflet mechanical valve seems to be the best choice. However, there is an increase in the use of bioprosthetic heart valves also in patients aged 60 years or younger because of an improved quality of life without warfarin and without the clear noise of the mechanical prosthesis. The
durability of tissue valves with low rates of structural valve deterioration, improved surgical techniques and postoperative care have diminished the risk of a redo aortic valve replacement procedure. The outlook of a valve-in-valve procedure with a transcatheter aortic valve may also influence the age at which a bioprosthetic valve is recommended. Patients with bioprostheses will also need anticoagulation if they develop atrial fibrillation. However, for atrial fibrillation one can keep the international normalized ratio at a lower level compared to a mechanical prosthesis.

If valve replacement is necessary in women of childbearing age, the choice of the type of prosthetic valve is difficult. Mechanical valves mean that anticoagulation with warfarin, phenprocoumon or acenocoumarol is needed with an increased risk of fetal loss or malformation and an increased risk of maternal prosthetic valve thrombosis and peripartum bleeding.