Aortic Stenosis and Statins

Abstract

Aortic stenosis (AS) is a relatively common cause of cardiac debility and death, increasing in frequency and severity with age; indeed, AS of at least moderate severity may affect almost 8% of people ≥75 years of age.1 The natural history of AS is dependent on the myocardial response to the abnormal left ventricular pressure load caused by the stenotic valve, involving cardiomyocyte hypertrophy, hyperproduction of extracellular matrix collagen by cardiac fibroblasts, and other alterations in myocardial biology. When these changes become critically severe, symptoms develop (angina pectoris, syncope, exertional dyspnea, and other manifestations of pulmonary vascular congestion) followed predictably by cardiac death at an annual rate of 25% unless aortic valve replacement surgery is performed. See page 592 The basis of the lifesaving effect of aortic valve replacement is clear: the ventricular myocardium is unloaded, enabling myocardial remodeling toward normal, generally with recovery of normal myocardial performance.2 A more satisfactory solution than surgery would be prevention of the stenotic process itself. To achieve this goal, the pathophysiology …