Editorial [Hot Topic: One Century of Triglycerides, but there is Still Lots to Learn(Guest Editors: K. Anagnostopoulou, D.P. Mikhailidis and G. Kolovou)]

In 1901 Eijkman developed a method to test the presence of lipase in animal fat [1]. In 1912 Wells and Corper tested 5 different esters of ethyl butyrate, triacetin and olive oil and suggested that all esters are attacked by the same enzyme [2]. Triglycerides (TGs) were first described by Trussell and Weed in 1937 [3]. Since then, serum TG concentrations are often measured in clinical practice. However, Garber and Avins believe that their use in screening for cardiovascular risk should be rather experimental than practical [4]. Other researchers also believe that low and high density lipoprotein cholesterol concentrations are better markers of cardiovascular risk [4]. The relevance of low density lipoprotein cholesterol has been emphasized by survival trials of statins [5,6]. A causal role for TGs in coronary heart disease has been never conclusively proved and TGs have not been found in atherosclerotic plaques. The biological variability in fasting TGs, which can be easily influenced by a fat meal for the next 4-8 h (nonfasting hyperlipidaemia, discussed in this issue by Nordestgaard et al.) [7], and the failure of many investigators to control for confounding by high density lipoprotein cholesterol, which has a strong inverse correlation with serum TGs, exaggerate this problem. Hypertriglyceridaemia may be due to genetic factors (primary hypertriglyceridaemia) or to causes like medication or disease (secondary hypertriglyceridaemia) [8]. The primary and secondary causes of hypertriglyceridaemia are considered in the current issue by Kolovou et al. [9]. There are indirect mechanisms by which TGs may promote the progression of atherosclerosis, such as endothelial function, thrombogenesis and low and high density lipoprotein particle size (smaller, denser and more atherogenic) [10]. In this issue Tziomalos et al. consider these mechanisms and the role of TGs in the progression of atherosclerosis [11]. In 1994, the PROCAM study presented evidence for an independent contribution from TGs to coronary risk [12]. In a cohort from the Physicians' Health Study, TGs were a strong and independent risk factor for cardiovascular disease, independently of high density lipoprotein cholesterol [13]. Moreover, data from a meta-analysis showed that for every 1 mmol/l (88 mg/dl) increase in TG concentration, the relative risk of coronary heart disease increased by 14% in men and 37% in women [14]. Additionally, available prospective studies in Western populations consistently indicate moderate and highly significant associations between TG values and coronary heart disease risk [15]. A large number of studies have shown that treatment with hypolipidaemic drugs significantly reduces deaths from coronary heart disease but a large proportion of cardiovascular events are still not prevented [16-19]. Hypolipidaemic and non-hypolipidaemic drugs affecting hypertriglyceridaemia (e.g. weight reducing, diabetes mellitus, antihypertensives) are discussed in the current issue by AS Wierzbicki [20]. A multi-factorial intervention for all risk factors, including weight reduction, dietary modification and increased physical exercise, is also discussed by Manfredini et al. [21]. The authors focus on the influence of diet, sedentary lifestyle and negative habits (such as excessive alcohol intake and smoking) on hypertriglyceridaemia as well as the effects of lifestyle change. This points to the need for a better understanding of lipid metabolism. An extensive review on TG properties and metabolism is presented by Karantonis et al. [22].