Heart failure & cardiomyopathies
The Effect of Trimetazidine On Cardiac Haemodynamics and Mitochondrial Function in Wild-Type Transthyretin Amyloidosis
Authors' conclusion
In ATTRwt, treatment with trimetazidine did not improve mPAWP or cardiac mitochondrial oxidative phosphorylation capacity compared with placebo.
Study context
- Population
- Patients with wild-type transthyretin cardiac amyloidosis (ATTRwt)crossover
- Participants
- 22 patients
- Comparison
- Trimetazidine vs placebo
- Primary endpoint
- Mean pulmonary artery wedge pressure (mPAWP) during peak exercise
- Follow-up
- After each 4-week treatment period
Methodological detailsdouble-blind, placebo-controlled, crossover
- Double-blind
- Placebo-controlled
- Crossover
Primary result
As reported in the abstract
mPAWP during peak exercise
P = 0.61
Secondary outcomes
Cardiac mitochondrial oxidative phosphorylation capacity
P = 0.81
EF, global longitudinal strain, N-terminal pro-brain natriuretic peptide (NT-proBNP), quality of life (exploratory)
- No improvement in EF
- P = 0.93
- No improvement in global longitudinal strain
- P = 0.23
- No improvement in NT-proBNP
- P = 0.92
- No improvement in quality of life
- P = 0.98
Original publication
The Effect of Trimetazidine On Cardiac Haemodynamics and Mitochondrial Function in Wild-Type Transthyretin Amyloidosis. ESC Heart Fail. Published 3 December 2024. doi:10.
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