Abstract

With evidence for efficacy in such diverse clinical settings such as stable coronary artery disease, reperfusion injury, and contrast-induced nephropathy, trimetazidine (TMZ) is novel among cardiovascular agents. In spite of this and almost half a century of clinical experience with the drug, it remains licensed only as an adjunct in the management of angina pectoris in patients who are inadequately controlled by or intolerant to first-line therapies. Although no single pharmacological mechanism has been hitherto universally accepted, TMZ is known to target deranged cellular energetics particularly in ischaemic myocardial tissue. Mechanistically, this separates the drug from conventional anti-anginal therapies, namely beta-adrenergic antagonists, calcium channel blockers, and nitrates. Moreover, a haemodynamically neutral side-effect profile should make TMZ a much more attractive therapeutic agent in this setting. Such ostensibly beneficial pharmacodynamics notwithstanding, the drug has a limited role in angina pectoris treatment algorithms. Concerns regarding a potential for new onset movement disorder further complicate its use and have led to a licensing revocation in some jurisdictions for the treatment of vestibular disorders. In this review article, we examine the pertinent literature and assess the evidence base for TMZ as a viable treatment option in a number of clinical settings.

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