Transition from compensated hypertrophy to intrinsic myocardial dysfunction during development of left ventricular pressure-overload hypertrophy in conscious sheep. Systolic dysfunction precedes diastolic dysfunction.

Circulation ◽  
1993 ◽  
Vol 88 (5) ◽  
pp. 2415-2425 ◽  
Author(s):  
T Aoyagi ◽  
A M Fujii ◽  
M F Flanagan ◽  
L W Arnold ◽  
K W Brathwaite ◽  
...  
2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Brian R. Weil ◽  
Cody Smith ◽  
Christian G. Cavalieri ◽  
Rebeccah F. Young ◽  
Ruogang Zhao ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e72651 ◽  
Author(s):  
Anne Margreet De Jong ◽  
Isabelle C. Van Gelder ◽  
Inge Vreeswijk-Baudoin ◽  
Megan V. Cannon ◽  
Wiek H. Van Gilst ◽  
...  

1993 ◽  
Vol 264 (4) ◽  
pp. H1307-H1314 ◽  
Author(s):  
P. S. Pollack ◽  
B. A. Bailey ◽  
R. Budjak ◽  
E. Fernandez ◽  
S. R. Houser

Serial echocardiography and Doppler were used to monitor the progression of pressure-overload produced by banding the ascending aortas of young cats. The peak Doppler gradient across the band increased (as the animals grew in size) from 42 +/- 4.2 mmHg at 1 wk to 78 +/- 4.5 mmHg at 2-3 mos. Echocardiographic measurements of septal wall thickness increased significantly at 1 wk. Global ventricular function was unaltered in banded cats versus shams at each time point. However, in the subgroup of animals with an aortic-constricted area of < 0.025 cm2 at 1 wk, fractional shortening decreased by 40% at 2-3 mos. Contractile abnormalities were present in isolated myocytes from hypertrophied hearts. Mechanical function was more profoundly depressed in cells from hearts with echocardiographic evidence of ventricular decompensation. Echocardiographic and Doppler studies assessed cardiac size and function and identified indexes predictive of global and cellular myocardial dysfunction. The use of noninvasive techniques as a predictor of failure makes the feline model of progressive left ventricular pressure-overload useful for studies of cellular and molecular factors regulating not only the development of cardiac hypertrophy but also the transition from compensated hypertrophy to myocardial failure.


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