Key result
Trimetazidine fails to reduce peak exercise wedge pressure vs placebo in wild-type ATTR amyloidosis.
Why the study?
ATTRwt causes myocardial hypoperfusion and impaired mitochondrial function, prompting investigation into whether trimetazidine, which improves contractility and mitochondrial function in stable angina, impacts invasive haemodynamics and cardiac mitochondrial function in ATTRwt.
Does oral trimetazidine 20 mg three times daily for 4 weeks improve peak exercise mean pulmonary artery wedge pressure and cardiac mitochondrial oxidative phosphorylation capacity compared with placebo in patients with early-stage wild-type transthyretin cardiac amyloidosis?
RCT (n=22)
Double-blind
Blocks of four patients, crossover order
No
Does oral trimetazidine 20 mg three times daily for 4 weeks improve peak exercise mean pulmonary artery wedge pressure and cardiac mitochondrial oxidative phosphorylation capacity compared with placebo in patients with early-stage wild-type transthyretin cardiac amyloidosis?
Answers are grounded in this paper and cite their sources.
Four weeks of trimetazidine therapy failed to improve exercise haemodynamics, cardiac mitochondrial oxidative phosphorylation capacity, echocardiographic function, or quality of life in patients with early-stage wild-type transthyretin cardiac amyloidosis.
AIMS: Wild-type transthyretin cardiac amyloidosis (ATTRwt) is a cardiomyopathy causing myocardial hypoperfusion and impaired cardiac mitochondrial function. Trimetazidine is an antianginal agent used in patients with stable angina pectoris, which improves cardiac contractility and mitochondrial function. The aim of the study was to investigate the effect of trimetazidine on invasive haemodynamics and cardiac mitochondrial function in ATTRwt. METHODS: In a randomized, double-blind, placebo-controlled, crossover trial, 22 patients with ATTRwt received 4 weeks of trimetazidine and placebo in randomized order. After each treatment period followed examinations with endomyocardial biopsies taken for high-resolution respirometry and right heart catheterization at rest and during a cardiopulmonary exercise test. The primary endpoint was mean pulmonary artery wedge pressure (mPAWP) during peak exercise. The secondary endpoint was cardiac mitochondrial oxidative phosphorylation capacity. Exploratory endpoints were echocardiographic parameters, cardiac biomarker levels and quality of life. RESULTS: /(mg*s), P = 0.81) compared with placebo, nor did treatment with trimetazidine improve ejection fraction (P = 0.93), global longitudinal strain (P = 0.23), N-terminal pro-brain natriuretic peptide (NT-proBNP) levels (P = 0.92) or the patients' quality of life (P = 0.98). CONCLUSIONS: In ATTRwt, treatment with trimetazidine did not improve mPAWP or cardiac mitochondrial oxidative phosphorylation capacity compared with placebo.
No takes yet. Share an insight, caveat, or question.
Ladefoged et al. (2024) conducted an RCT in Early-stage wild-type transthyretin cardiac amyloidosis (ATTRwt) (n=22). Trimetazidine vs. Placebo was evaluated on Mean pulmonary artery wedge pressure (mPAWP) during peak exercise (p=0.61). Trimetazidine did not reduce peak exercise mean pulmonary artery wedge pressure compared to placebo in patients with wild-type transthyretin cardiac amyloidosis.
Synapse has enriched 10 related papers. Consider them for comparative context: