松村 貴由

BACKGROUND: Recent studies on the etiology of aortic valve disease in the US showed a decrease in rheumatic valve disease and an increase in age-related degenerative disease. The purpose of this study was to describe the etiology of aortic valve disease and its temporal changes in Japan, based on a large number of cases. METHODS: The medical charts of all patients who underwent aortic valve replacement at our institute between 1977 and 1999 were reviewed. Among the 600 patients analyzed, 213 (36%) had pure aortic stenosis, 265 (44%) had pure aortic regurgitation, and 122 (20%) had combined stenosis and regurgitation. RESULTS: The causes were rheumatic change (49%), degenerative change (19%), bicuspid valves (18%), infective endocarditis (5%) and others (9%). Rheumatic disease continued to be the most common cause of aortic stenosis, but its frequency decreased from 100% in 1977-1979 to 37% in 1995-1999. In contrast, the frequency of degenerative change among stenotic valves increased recently from 11% in 1990-1994 to 30% in 1995-1999. Similarly, rheumatic disease remained to be the leading cause of aortic regurgitation, with a decline in frequency from 46% in 1985-1989 to 27% in 1995-1999. The percentage of degenerative change among regurgitant valves did not change appreciably. CONCLUSIONS: There was a shift in the causes of aortic valve disease, with a decrease in rheumatic disease and an increase in degenerative disease. This trend was similar to that observed in the US. These findings suggest the increasing importance of aortic valve disease due to degenerative change.

OBJECTIVES: Whether beta-blocker therapy changes the circulating levels of cytokines as congestive heart failure improves remains uncertain. METHODS: Nine patients with idiopathic dilated cardiomyopathy, who had previously received conventional treatment and were classified as New York Heart Association (NYHA) functional class II, received carvedilol by stepwise dose increase up to 20 mg daily, and the plasma interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels were measured. RESULTS: IL-6 was significantly reduced from 0.80 +/- 0.49 pg/ml before therapy to 0.21 +/- 0.08 pg/ml after carvedilol was increased to 20 mg daily (p < 0.05). Moreover, IL-6 level had already decreased significantly compared to the baseline when the dose of carvedilol had reached 10 mg daily (0.28 +/- 0.12 pg/ml, p < 0.05). TNF-alpha levels did not change significantly. CONCLUSIONS: These results demonstrate that IL-6 concentration is significantly decreased by beta-blocker therapy. The efficacy for heart failure may be related to the change of IL-6 concentration.