LAUSR

In this month’s issue of the Netherlands Heart Journal, van de Bovenkamp et al. [1] describe their study design of the DoPING-HFpEF trial, a placebo-controlled cross-over trial that studies the effect of trimetazidine on diastolic function and cardiac energetics in heart failure with preserved ejection fraction (HFpEF). It seems that in the absence of specific therapies for HFpEF, cardiologists might have to resort to using doping substances to treat their patients. Trimetazidine was added to the World Anti-Doping Agency (WADA) Prohibited List on 1 January 2014, and 2 years later its analogue meldonium caused turmoil in international sports when it was added to the list of forbidden substances and contributed to the banning of an unprecedented number of top-level sportsmen and women. Both drugs are known for their cardioprotective effects and enhancement of glucose oxidation by limiting beta-oxidation through the inhibition of synthesis or carnitine-facilitated transport of fatty acids. Conventional heart failure therapies that alter haemodynamics have a limited effect on HFpEF, so instead a therapy is being sought in metabolic modulation: altering the metabolic state of the cardiac cell in order to improve its function. Trimetazidine does not alter haemodynamics; instead it provides the heart muscle with more energy (adenosine triphosphate, ATP) per molecule of oxygen. Subsequently the heart is provided with more energy for the same amount of heart muscle perfusion. The idea is not new, since trimetazidine is used as a therapy for angina pectoris and was marketed in the 1970s, around the same time as atenolol, the haemodynamic-altering therapy for