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Modifying the Natural History of Aortic Valve Stenosis

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Cardiac Valvular Medicine

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Abstract

Aortic valve stenosis (AS) is the most common heart valve disease with a prevalence up to 3% of adults over the age of 75 years (Nkomo et al. 2006). One-third of US adults ≥65 years has aortic valve sclerosis and of these at least one-third will develop some degree of AS within 5 years (Faggiano et al. 2003; Otto et al. 1999). The natural history, diagnosis, and cellular mechanisms of this disease process have evolved over the past several decades. Over the last 10 years, the scientific progress in the field of calcific aortic valve stenosis has increased exponentially. A critical discovery in our understanding of calcification as the end-stage pathogenesis of a congenital bicuspid or normal tricuspid aortic valve is the osteogenic process (Rajamannan et al. 2003; Otto 2006; Rosenhek et al. 2000a). Progressive calcification of the leaflets usually leads to severe narrowing of the aortic valve orifice and fibrosis of the left ventricular wall, finally resulting in left ventricular outflow tract obstruction and severe aortic stenosis. After a prolonged asymptomatic period with low morbidity and mortality, the development of the classic triad of symptoms including: angina, syncope, or heart failure marks the critical point in the natural history of aortic valve disease. AS is a progressive disease and without intervening treatment associated with high morbidity and mortality rates within a few years of diagnosis (Horstkotte and Loogen 1988). Survival declines when a patient with AS develops angina or syncope, and is even more limited when the patient develops congestive heart failure. Because AS is a disease of the elderly, it can be difficult to distinguish the gradual decrease in physical functioning attributed to advanced age and multiple co-morbidities such as frailty, lung disease, neurological disease, and symptoms from the worsening AS disease. It is not uncommon that patients will lower their activity level below their symptom threshold, to accommodate to the progressive left ventricular outflow tract obstruction. This chapter will outline the studies in the field of diagnosis and the impact of the evolving science of clinical risk factors for calcific aortic valve disease to further understand the complexity of monitoring this disease process in this patient population.

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Authors and Affiliations

  1. Department of Cardio-Thoracic Surgery, Erasmus University Medical Center, Rotterdam, The Netherlands

    Helena J. Heuvelman M.D. & Johanna J. M. Takkenberg M.D., Ph.D.

  2. Department of Molecular Biology and Biochemistry, Mayo Clinic, Rochester, MN, USA

    Nalini Marie Rajamannan M.D.

  3. Department of Aerospace Engineering, University of Notre Dame, South Bend, IN, USA

    Nalini Marie Rajamannan M.D.

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  1. Helena J. Heuvelman M.D.
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Correspondence to Helena J. Heuvelman M.D. .

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  1. , Molecular Biology and Biochemistry, Mayo Clinic, Rochester, 55905, Minnesota, USA

    Nalini M. Rajamannan

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Heuvelman, H.J., Rajamannan, N.M., Takkenberg, J.J.M. (2013). Modifying the Natural History of Aortic Valve Stenosis. In: Rajamannan, N. (eds) Cardiac Valvular Medicine. Springer, London. https://doi.org/10.1007/978-1-4471-4132-7_1

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