Insights Into Aortic Sclerosis and Its Relationship With Coronary Artery Disease

A ortic valve (AV) sclerosis (AVS) is a form of AV disease affecting an estimated 1 in 4 people above the age of 65 in the United States. 1 An aging population and more widespread use of noninvasive imaging are increasing the incidence of AVS.AVS is typically defined as calcification of the aortic leaflets without impairment in leaflet excursion or a significant transvalvular pressure gradient. 2It is characterized by a gradual progression beginning with calcium deposition that may ultimately transform to aortic stenosis (AS) with obstruction of outflow from the left ventricle.Severe AS eventually leads to ventricular remodeling and hemodynamic compromise with a high morbidity and mortality if not treated.Long considered an incidental age-related degenerative process as a result of progressive wear and tear, there is substantial emerging evidence related to AVS that challenges this assumption.Recent observations have shown that the development of AVS and AS may involve chronic inflammatory infiltrates, deposition of atherosclerotic lipoproteins, and calcification, akin to coronary artery disease (CAD).However, AVS has unique features, including a calcium predominance on histology, gradual progression, and location at a site of high pressure that serves as a gateway from the heart to the systemic circulation.Some investigators have reported the frequent coexistence of either AVS or AS in patients with underlying CAD. 3 Several studies have demonstrated that independent risk factors in the progression of CAD, such as dyslipidemia, hypertension, and male sex, may also affect development of AVS and its progression to AS. 456 These observations not only highlight the many shared characteristics of CAD and AVS but have also prompted investigators to test the efficacy of medical interventions that may have salutary effects on both conditions.Heart disease is the leading cause of death in the United States.The majority of these deaths are attributed to CAD. 7 Improvements in treatment for CAD, such as statins, angiotensin inhibitors (ACEI), and revascularization, have resulted in a larger proportion of the population living with CAD. 8 Realizing the potential similarities between the underlying pathophysiology for AVS and CAD, many clinically relevant questions remain unanswered. 9,10For instance, does the presence of AVS suggest existence or progression of underlying CAD?Should AVS be considered a novel risk factor for the development of CAD?Does the finding of AVS warrant the initiation and careful titration of medications with lifestyle changes analogous to current strategies used in treating patients with diabetes mellitus?In this review, we discuss the shared pathophysiological aspects of AVS and CAD, summarize the present literature on mechanisms that lead to disease progression, and provide insights for future research to identify novel therapeutic targets.