Coenzyme Q10 (CoQ10), first identified by Moor et al in 1940, is a fat soluble quinone with characteristics common to vitamins [1]. It is found in the organs of various animal species with highest concentrations in the heart, liver, kidney, muscles and pancreas [2, 3]. Festenstein et al in 1955 named the substance ubiquinone [2] while Crane et al in 1957 choose the name coenzyme Q [4]. Ubiquinone is a component of the mitochondrial respiratory chain, participating in electron transport in NADH-coenzyme Q reductase (complex I), succinate coenzyme Q reductase (complex II) and the cytochrome system [4, 5]. Folkers and his group determined the structure of the quinone moiety which was found identical to that described by Morton and his team, and suggested the name “ubiquinone” referring to the ubiquitous occurrence of this compound in various tissues [2-5]. It is also rich in pancreas and may be protective against type 2 diabetes [6]. In 1957, Crane et al demonstrated that it has an important role as a redox carrier in the mammalian respiratory transport chain [4]. A high concentration of CoQ10 observed in healthy human myocardium has led to the assumption that a myocardial deficiency of CoQ10 is detrimental to cardiac function [7]. In 1972, Littarru, of Italy and the late Prof. Folkers from Texas, documented a deficiency of CoQ10 in human heart disease, particularly among patients subjected to bypass surgery in Houston, USA [8-10].

Lower than normal levels of CoQ10 have also been found in blood samples from patients with cardiovascular diseases (CVDs) compared with levels in healthy human subjects [9, 10]. Yamamura and his group were the first to use CoQ10 for the treatment of cardiovascular disease (CVD) in the 1960’s [11] and later Folkers et al. presented the rationale for using CoQ10 in treating congestive heart failure (CHF) [8].