Influence of aortic impedance on the development of pressure-overload left ventricular hypertrophy in rats
Aortic input impedance, which represents LV afterload, is considered to be a major determinant for the development of pressure-overload left ventricular (LV) hypertrophy. To test whether the sustained change in aortic input impedance might affect the mode of development of LV hypertrophy, coarctatio...
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Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1996-12, Vol.94 (12), p.3362-3368 |
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Zusammenfassung: | Aortic input impedance, which represents LV afterload, is considered to be a major determinant for the development of pressure-overload left ventricular (LV) hypertrophy.
To test whether the sustained change in aortic input impedance might affect the mode of development of LV hypertrophy, coarctation of either the ascending aorta (G1, n = 13) or suprarenal abdominal aorta (G2, n = 12) was performed over 4 weeks in 6-weeks-old Wistar rats. Although peak LV pressure and total systemic resistance were increased similarly in G1 and G2, time to peak LV pressure was decreased by 24% (P < .01) in G1 compared with G2. The aortic input impedance spectra revealed that the early systolic loading in G1 was characterized by an increase in characteristic impedance, whereas the late systolic loading in G2 was by an augmented arterial wave reflection. G1 showed a smaller increase (P < .01) in either the ratio of LV weight (mg) to body weight (g) or LV wall thickness than G2 after aortic banding. Myocyte diameter was also smaller (P < .05) in G1 (14.3 +/- 0.7 mm) than in G2 (16.1 +/- 1.2 mm). The ex vivo passive pressure-volume relation had a rightward shift in G1 compared with G2, suggesting less concentric LV hypertrophy in G1.
The sustained early systolic loading due to the increase in characteristic impedance was accompanied by less concentric, reduced hypertrophy, whereas the sustained late systolic loading due to the augmented arterial wave reflection was accompanied by concentric, adequate hypertrophy. |
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ISSN: | 0009-7322 1524-4539 |
DOI: | 10.1161/01.cir.94.12.3362 |