Calcific Aortic Stenosis: Current Concepts and Management Options

Calcific aortic stenosis is the most commonly encountered valvular disease in the western countries that needs surgical attention1. It affects approximately 2-3% of the elderly population above 65 years and it is associated with significant morbidity and mortality1. The most common etiology of acquired aortic stenosis is calcific degeneration. The natural history of aortic stenosis is well known. Patients with mild to moderate AS can be asymptomatic for several years even with the presence of obstruction2. Senile degenerative AS is the most common cause for aortic valvular replacement Aortic stenosis can be diagnosed with good physical examination, Doppler echocardiogram and cardiac catheterization3. Management of symptomatic aortic stenosis is replacement of aortic valve. Recent data suggest that statins may be helpful in slowing the hemodynamic progression of calcific aortic stenosis. This review will focus on etiology, pathophysiology, diagnostic evaluation and therapeutic options of acquired aortic stenosis. ETIOLOGY AND PATHOPHYSIOLOGY Calcific aortic stenosis is caused by progressive fibrosis and calfication of valve cusps. The process of calcification appear to be mediated by acute inflammation, lipid deposition and mechanical stress, ultimately vale cusps heavily calcify and cause severe aortic stenosis(4). This disease process shares similar risk factors as atherosclerosis such as smoking, hypercholesterolemia and hypertension and diabetes mellitus ,Lp(a) raised serum creatinine and raised serum calcium(5). Thus, modification of these risk factors may slow the progression of aortic valve calcification. Rheumatic valvular disease is common in the developing countries, but it is rarely seen in the developed countries. Gerber et al, reported inflammatory markers like plasma C reactive protein levels are elevated in patients with tricuspid and Bicuspid AS than normal aortic valves. Study by Sanchez et al, reported that there was high rate of progression of AS in patients with CRP levels greater than 0.3mg/dl (7). These findings suggest that CRP might help in predicting the hemodynamic progression of AS. Calcific aortic stenosis develops gradually and the cardiac output is maintained initially despite increasing gradient across the aortic valve. As a result, left ventricle becomes hypertrophic, and the patient may develop angina, with out any coronary artery disease (6). Eventually left ventricle no longer accommodates the outflow tract obstruction and ultimately starts failing. Gender and age are important factors; Females tend to develop increased concentric wall thickness and small chamber size compared with men (9). Progression of AS with increase in the wall stress and afterload leads to a decrease in the ejection fraction and left ventricular systolic dysfunction. Elderly patients tend to have pronounced diastolic