Meldonium (Mildronate) is used as a cardioprotective drug; however, it has not been officially approved anywhere outside the former Soviet Union (SU). The supposed action mechanism is based on the carnitine (Lcarnitine) lowering effect in muscular and cardiac tissues. Carnitine deficiency was reported to be associated with muscle ache, fatigue, muscular weakness and cramps; it can induce hypoketotic hypoglycemia, which is potentially unfavorable both for the nervous and muscular functions. There is a considerable evidence from clinical and experimental studies that carnitine exerts a cardioprotective effect in cardiomyopathy, lessens infarct size, prevents arrhythmias and improves survival in myocardial infarction. Oral administration of meldonium to healthy volunteers at the recommended dose brought about a lowering of plasma carnitine by 18%. Administration of meldonium to rats decreased L-carnitine concentration in myocardium. In a series of studies from the former SU, efficiency of meldonium was uniformly confirmed in cardiac insufficiency, myocardial infarction and stroke also in elderly patients. Considering potential decrease in availability of ATP as energy carrier, mildronate could have contributed to a decline in the cardiac function in some patients with myocardial infarction and heart failure. There is an opinion that lowering the acylcarnitine concentration can be a promising approach to prevent the development and progression of some cardiovascular diseases. It can be argued that carnitine and its derivatives are available from meat and synthesized by the body e.g., in vegetarians, so that an occasional pharmacological suppression of their levels seems to have not much sense for the cardiovascular disease prevention. The problem should be seen within the scope of placebo marketing under the guise of evidence-based medications, which seems to be on the increase these days. © 2018 Nova Science Publishers, Inc. All rights reserved.