Key result
Angiotensin II infusion prolongs tau ~20% coincident with asynchronous wall motion in normal dog hearts.
Why the study?
It was unclear whether impaired left ventricular relaxation caused by increased afterload is due to regional dyssynchrony.
Does increased afterload via angiotensin II infusion impair left ventricular relaxation and cause regional dyssynchrony in normal dogs?
Population
7 normal dogs
Comparison
Baseline vs angiotensin II infusion
Design
Preclinical study with simultaneous ventriculography and pressure measurement
Authors
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May implicate afterload in impaired relaxation via dyssynchrony; leaves open human translation.
Does increased afterload via angiotensin II infusion impair left ventricular relaxation and cause regional dyssynchrony in normal dogs?
Absolute Event Rate: 39.2% vs 32.7%
p-value: p=< 0.01
In normal dog hearts, increased afterload impairs left ventricular relaxation, which is coincident with asynchronous wall motion, particularly in the apical-inferior region.
Miura et al. (1993) studied Normal dog heart (animal model) (n=7). Angiotensin II infusion vs. Control (before infusion) was evaluated on Isovolumic pressure time constant (tau) (p=< 0.01). Angiotensin II infusion prolonged the isovolumic pressure time constant (tau) from 32.7 to 39.2 ms (P < 0.01), coincident with asynchronous wall motion in normal dog hearts.
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