Key result
Trandolapril reduces proarrhythmic remodeling and mortality in volume overload HF rats despite preserved eccentric hypertrophy.
Why the study?
Chronic volume overload induces cardiac remodeling leading to eccentric hypertrophy and heart failure, and it was hypothesized that ACE inhibition by trandolapril might affect remodeling processes differentially.
Does trandolapril reduce cardiac remodeling and mortality in a rat model of volume overload heart failure?
Does trandolapril reduce cardiac remodeling and mortality in a rat model of volume overload heart failure?
In a rat model of volume overload heart failure, trandolapril reduces mortality and proarrhythmic electrical remodeling independently of its antihypertrophic effects.
Answers are grounded in this paper and cite their sources.
Supports mortality benefit without reversing eccentric hypertrophy in rat volume-overload HF; hypothesis-generating, requires clinical validation.
Chronic volume overload induces multiple cardiac remodeling processes that finally result in eccentric cardiac hypertrophy and heart failure. We have hypothesized that chronic angiotensin-converting enzyme (ACE) inhibition by trandolapril might affect various remodeling processes differentially, thus allowing their dissociation. Cardiac remodeling due to chronic volume overload and the effects of trandolapril were investigated in rats with an aortocaval fistula (ACF rats). The aortocaval shunt was created using a needle technique and progression of cardiac remodeling to heart failure was followed for 24 weeks. In ACF rats, pronounced eccentric cardiac hypertrophy and contractile and proarrhythmic electrical remodeling were associated with increased mortality. Trandolapril substantially reduced the electrical proarrhythmic remodeling and mortality, whereas the effect on cardiac hypertrophy was less pronounced and significant eccentric hypertrophy was preserved. Effective suppression of electrical proarrhythmic remodeling and mortality but not hypertrophy indicates that the beneficial therapeutic effects of ACE inhibitor trandolapril in volume overload heart failure might be dissociated from pure antihypertrophic effects.
No takes yet. Share an insight, caveat, or question.
Jarkovská et al. (2021) studied Experimental volume overload heart failure. Trandolapril was evaluated on Cardiac remodeling (structural, contractile, and electrophysiological) and mortality. Trandolapril substantially reduced electrical proarrhythmic remodeling and mortality in rats with volume overload heart failure, whereas significant eccentric hypertrophy was preserved.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: