15289-s-bos

102 | Chapter 7 Life style and diet Healthy lifestyle and a prudent diet are cornerstones of CVD prevention. Recently two studies have addressed the effect of lifestyle intervention on Lp(a) levels. Both showed that Lp(a) levels are not influenced by rigorous exercise[8, 9]. Studies on the influence of diet on Lp(a) have produced conflicting result for a long time, and it remains to be established if diet indeedmodifies Lp(a) or not [9, 10]. Themain shortcomings of most of these studies include the small sample size, the use of firmly isoform dependent assays for measuring Lp(a), and improper use of statistics. Recently, the Copenhagen Heart study established that Lp(a)levels are not directly influenced by food intake: No difference in Lp(a) levels was observed between fasting and non-fasting blood samples [11]. In conclusion, these studies reinforce that the influence of exercise and food intake on Lp(a) levels is limited at best. Drug Treatment Next to life style, weight control and dietary hygiene, pharmacological treatment plays a crucial role in CVD prevention. The remainder of this review focusses on the effect of different compounds on circulating Lp(a) levels. Estrogens Hormone replacement therapy containing estrogens favourably influences Lp(a), LDL-cholesterol (LDL-C), and high dense lipoprotein-cholesterol (HDL-C) levels in postmenopausal women. Recently, Howard et al. [12], provided an excellent overview of all cardiovascular effects of hormone replacement therapy, including Lp(a). These authors concluded that despite the Lp(a) lowering effect of estrogens, there is no place for hormone replacement therapy in CVD prevention because it did not lead to a decrease in CVD events. Reversely, Lp(a) levels increase when the action of estrogens is blocked [13]. A recent double blinded randomized controlled trial (RCT) investigated the effect of Letrozole (Novartis, Basel, Switzerland), an aromatase inhibitor which inhibits the conversion of testosterone to estrogens, on lipoprotein levels. After 60 months of follow-up Lp(a) was measured in 103 postmenopausal women with breast cancer, showing that Lp(a) levels where 106% higher compared to baseline in those randomized to Letrozole treatment [13]. Although, the mechanism is uncertain Hoover- Plow and Menggui Huang proposed influence of estrogen on the LPA promoter[14]. This is highly suggestive of an association between estrogens and Lp(a) levels. Given the outcome of the hormone replacement therapy trials on CVD endpoints it is unlikely that