AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol (October 23, 2009). doi:10.1152/ajpheart.00824.2009
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Submitted on August 28, 2009
Accepted on October 16, 2009

Mechanisms of Aortic Valve Calcification: The LDL-Density-Radius Theory A Translation from Cell Signaling to Physiology

Nalini Marie Rajamannan1*

1 Division of Cardiology and Cardiothoracic Surgery, Northwestern University

* To whom correspondence should be addressed. E-mail: n-rajamannan{at}northwestern.edu.

Recent epidemiological studies have revealed the risk factors associated for vascular atherosclerosis, including male gender, smoking, hypertension and elevated serum cholesterol, are similar to the risk factors associated with development of aortic valve stenosis. An increasing number of models of experimental hypercholesterolemia demonstrates features of atherosclerosis in the aortic valve(AV), which are similar to the early stages of vascular atherosclerotic lesions. The experimental and clinical studies demonstrate that the hypercholesterolemic AV develops an atherosclerotic lesion which is proliferative, and expresses high levels of osteoblast bone markers which mineralize over time to form bone. Calcification, the end stage process of the disease is necessary to understand as a prognostic indicator in the modification of this cellular process before it is too late. 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 to severe aortic stenosis(AS) and to delay the timing of the need for surgery. Translation of these experimental studies to clinical practice will be important to understand the potential for medical therapy for this disease process.







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