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Published on: October 20, 2023
Short-term hemodynamic effect of angiotensin-converting enzyme inhibition in patients with severe aortic stenosis: a
Morten Dalsgaard1, Kasper Iversen2, Jesper Kjaergaard1
1Department of Cardiology, The Heart Centre, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
Insights
Angiotensin-converting enzyme inhibitors (ACEi) may improve left ventricular unloading in severe aortic stenosis (AS) without adverse hemodynamic effects. This study found ACEi reduced left ventricular end-systolic volume and N-terminal pro-brain natriuretic peptide in AS patients.
Area of Science:
- Cardiology
- Pharmacology
- Clinical Medicine
Background:
- Severe aortic stenosis (AS) traditionally contraindicates angiotensin-converting enzyme inhibitor (ACEi) use.
- Limited clinical data exists on the hemodynamic risks and benefits of ACEi in severe AS.
Purpose of the Study:
- To investigate the hemodynamic effects and clinical outcomes of trandolapril, an ACEi, in patients with severe AS.
Main Methods:
- Forty-four severe AS patients were randomized to trandolapril or placebo.
- Right heart catheterization and echocardiography were performed at rest and during exercise at baseline and follow-up.
- Hemodynamic parameters, left ventricular end-systolic volume (LVESV), and N-terminal pro-brain natriuretic peptide were assessed.
Main Results:
- Trandolapril significantly decreased systolic blood pressure and increased systemic arterial compliance at day 3.
- At follow-up, trandolapril significantly reduced LVESV and N-terminal pro-brain natriuretic peptide compared to placebo.
- No symptomatic hypotension occurred, and other hemodynamic parameters remained stable.
Conclusions:
- ACE inhibition in severe AS leads to left ventricular unloading, indicated by decreased LVESV and N-terminal pro-brain natriuretic peptide.
- Hemodynamic parameters are preserved at rest and during exercise, suggesting a potential benefit of ACEi in severe AS.
Background:
In patients with severe aortic stenosis (AS), treatment with angiotensin-converting enzyme inhibitors has previously been considered contraindicated. However, there is a lack of clinical evidence to confirm these potential hemodynamic risks and benefits.
Methods:
Forty-four patients with severe AS (aortic valve area <1 cm(2)) were randomized to treatment with trandolapril 22 mg daily/placebo (1:1). Right heart catheterization and echocardiography were performed at rest and during exercise at baseline and on day 3. Follow-up was performed before valve replacement or after a maximum of 8 weeks, when exercise echocardiography was repeated.
Results:
Compared with placebo, systolic blood pressure and systemic arterial compliance significantly changed at day 3 (-14 ± 11 vs -5 ± 13 mm Hg, P = .02, and 0.08 ± 0.16 vs -0.05 ± 0.86 mL/m(2) per mm Hg, P = .03, respectively). Changes in left ventricular end systolic volume (LVESV) was nonsignificant (-8 ± 9 vs -3 ± 11 mL, P = .17). At a median of 49 days of follow-up, changes in LVESV and N-terminal pro-brain natriuretic peptide were even lower revealing significant differences between the groups (-7.8 ± 2.6 vs -0.5 ± 2.5 mL, P = .04, and -19 ± 7 vs 0.8 ± 6 pmol/L, P = .04, respectively). No episodes of symptomatic hypotension were noted, and other hemodynamic parameters remained unchanged.
Conclusion:
Angiotensin-converting enzyme inhibition in severe AS caused a decrease in LVESV and N-terminal pro-brain natriuretic peptide with other hemodynamic parameters preserved both at rest and during exercise implying hemodynamic improvement with left ventricular unloading.
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