Wild-type transthyretin cardiac amyloidosis (ATTRwt) is a deposition disorder in which one of the proteins of the body misfolds and accumulates at various places in the body, including the heart, leading to both mechanical and cellular damage. The gradual development of the disease will ultimately lead to heart failure and death

The protein which deposits in the heart of patients, damages both the heart mechanically as the myocardium becomes rigid and hypertrophic over time but also at the cellular level. Cell damage can be observed by elevated blood tests for cell damage (Troponin) and during exercise tests that show patients' hearts burning oxygen inefficiently when exposed to physical stress compared with the hearts of healthy individuals . No one has, however, intimately studied this cellular damage.

Vastarel® (Trimetazidine, TMZ) is an already known drug for the treatment of chest pain. The mechanism of action indicates that it may have an effect on patients with cardiac amyloidosis.

The study aims to investigate the effects of TMZ on the mitochondrial function, myocardial performance, and invasive hemodynamics in patients with ATTRwt with a randomized, double-blinded, crossover-trial.

Inclusion Criteria:

• Wild-type transthyretin cardiac amyloidosis
• NAC stage I
• NYHA class of I or II
• Informed consent

Exclusion Criteria:

• Other, similar diagnoses
• Hereditary transthyretin cardiac amyloidosis
• Light chain amyloidosis
• Morbus Waldenstrøm
• Myelomatosis
• Medical treatment with loop diuretics in standard doses (40 mgx1 daily)
• Contraindications to trimetazidine
• Significant comorbidity assessed by the investigators
• Unable to provide informed consent