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A New Face for an Old Disease

Arch Intern Med. 2003;163:1769-1770.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

WHEN I WAS a second-year medical student in the 1960s, one of the first patients I was shown was a man with severe aortic stenosis secondary to rheumatic heart disease. I still remember this patient's face and the distinctive, rough, systolic ejection murmur that filled systole, obliterating the second heart sound. Since then, rheumatic cases of aortic stenosis have become rare, but severe aortic stenosis is still one of the commonest causes of valvular heart disease seen in hospitalized patients. In the more than 30 years since I saw my first patient with aortic stenosis, much has been learned concerning the pathophysiology of this condition. Indeed, there are studies currently under way seeking to alter the pathological sequence in this disease that eventually leads to aortic valve replacement.

PATHOPHYSIOLOGY OF AORTIC STENOSIS

Today, most cases of aortic stenosis are the result of bicuspid aortic valves (BAVs) or so-called calcific involvement of an originally tricuspid . . . [Full Text of this Article]

WHEN DO PATIENTS WITH BAV AND/OR AORTIC SCLEROSIS DEVELOP CLINICALLY IMPORTANT AORTIC STENOSIS?

MANAGEMENT IMPLICATIONS FOR CLINICIANS

CONCLUSIONS
Joseph S. Alpert, MD
Department of Medicine
University of Arizona Health Sciences Center
1501 N Campbell Ave
Tucson, AZ 85724-5035

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