(a) Pathogenesis of aortic stenosis : relationship to valvular endothelial function. [ 2002 - 2004 ]

Research Grant

Researchers: Prof John Horowitz (Principal investigator) ,  A/Pr Jennifer Kennedy ,  A/Pr Margaret Arstall ,  Dr Yuliy Chirkov ,  Prof Peter Macdonald

Brief description In the 21st century, heart disease will continue to be a major cause of disability and death in Western society. However, the relative decline in the frequency of premature death due to coronary disease (such as heart attacks) combined with increases in longevity, will see the emergence of new disease states. Aortic stenosis (AS) is likely to be one of the most important of these: progressive aortic valvular narrowing, culminating in the development of heart failure, and cardiac death. To date, the only established treatment for severe AS is valve replacement. The incidence of AS increases with age: approximately 40% of individuals over the age of 80 have some AS, while 4% have severe AS. Studies to date have revealed that AS is more likely to occur (and to progress rapidly) in patients with impaired kidney function, and that some coronary risk factors (high cholesterol levels and diabetes, for example) also predispose to AS. The planned research will examine the potential role of the (endothelial) cells lining the aortic valve in protecting against the development of AS. In particular, we will try to identify which chemicals interfere with endothelial function, and how this leads to thickening of the valve. The ulitmate objective of this research is to delineate the chemical factors causing AS, in order to help in the development of preventative strategies for this disease.

Funding Amount $AUD 254,995.38

Funding Scheme NHMRC Project Grants

Notes Standard Project Grant