title: Medical therapy for rheumatic heart disease: is it time to be proactive rather than reactive?
abstract: Rheumatic Heart Disease (RHD) is well known to be an active inflammatory process which develops progressive calcification and leaflet thickening over time. The potential for statin therapy in slowing the progression of valvular heart disease is still controversial. Retrospective studies have shown that medical therapy is beneficial for patients with calcific aortic stenosis and recently for rheumatic valve disease. However, the prospective randomized clinical trials have been negative to date. This article discusses the epidemiologic risk factors, basic science, retrospective and prospective studies in valvular heart disease and a future clinical trial to target RHD with statin therapy to slow the progression of this disease. Recent epidemiological studies have revealed the risk factors associated with valvular disease include male gender, smoking, hypertension and elevated serum cholesterol and are similar to the risk factors for vascular atherosclerosis. An increasing number of models of experimental hypercholesterolemia demonstrate features of atherosclerosis in the aortic valve (AV), which are similar to the early stages of vascular atherosclerotic lesions. Calcification, the end stage process of the disease, must be understood as a prognostic indicator in the modification of this cellular process before it is too late. This is important in calcific aortic stenosis as well as in rheumatic valve disease. There are a growing number of studies that describe similar pathophysiologic molecular markers in the development of rheumatic valve disease as in calcific aortic stenosis. In summary, these findings suggest that medical therapies may have a potential role in patients in the early stages of this disease process to slow the progression of RHD affecting the valves. This review will summarize the potential for statin therapy for this patient population.
authors.affiliation: Bluhm Cardiovascular Institute, Nortwestern University Feinberg School of Medicine, Tarry, Chicago IL, USA. n-rajamannan@northwestern.edu
authors.forename: Nalini M
authors.initials: NM
authors.lastname: Rajamannan
authors.forename: Francesco
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authors.lastname: Antonini-Canterin
authors.forename: Luis
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authors.lastname: Moura
authors.forename: Jose L
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authors.forename: Patricia Jm
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authors.lastname: Chandra
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authors.lastname: Alfieri
authors.forename: Patrizio
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authors.lastname: Lancellotti
authors.forename: Pilar
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authors.lastname: Tornos
authors.forename: Ragavendra R
authors.initials: RR
authors.lastname: Baliga
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authors.lastname: Wang
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authors.lastname: Shuvy
authors.forename: Ronen
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authors.lastname: Beeri
authors.forename: Chaim
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authors.forename: Jassim Al
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authors.lastname: Suwaidi
authors.forename: Vinay
authors.initials: V
authors.lastname: Bahl
authors.forename: Luc A
authors.initials: LA
authors.lastname: Pierard
authors.forename: Gerald
authors.initials: G
authors.lastname: Maurer
authors.forename: Gian Luigi
authors.initials: GL
authors.lastname: Nicolosi
authors.forename: Shahbudin H
authors.initials: SH
authors.lastname: Rahimtoola
authors.forename: K
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authors.lastname: Chopra
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authors.lastname: Pandian
mesh_terms: D000818:Animals; D001024:Aortic Valve Stenosis / Q000453:epidemiology / Q000517:prevention & control*; D015984:Causality; D015897:Comorbidity; D006801:Humans; D008946:Mitral Valve Stenosis / Q000453:epidemiology / Q000517:prevention & control*; D012214:Rheumatic Heart Disease / Q000453:epidemiology / Q000517:prevention & control*; D012307:Risk Factors