This meta- analysis shows that oral tibolone treatment significantly lowers circulating Lp(a ) levels in postmenopausal women .
INTRODUCTION Circulating lipoprotein ( a ) ( Lp(a ) ) is a recognized risk factor for cardiovascular disease ( CVD ) .
Tibolone , a synthetic steroid , may lower Lp(a ) levels ; however , evidence of the effects of tibolone on Lp(a ) still remain to be defined .
Therefore , we investigated the effects of tibolone treatment on circulating Lp(a ) levels in postmenopausal women .
Lipoprotein(a) as a potential causal genetic risk factor of cardiovascular disease: a rationale for increased efforts to understand its pathophysiology and develop targeted therapies.
Recent published studies have provided increasing evidence that lipoprotein(a ) [ Lp(a ) ] may be a potential causal , genetic , independent risk factor for cardiovascular disease ( CVD ) . Lp(a ) levels > 25 mg/dl are present in ∼30 % of Caucasians and 60 % to 70 % of Blacks . Lp(a ) is composed of apolipoprotein B-100 and apolipoprotein ( a ) [ ( apo(a ) ] . Circulating Lp(a ) levels are primarily influenced by the LPA gene without significant dietary or environmental effects , mediating CVD risk throughout the patient 's lifetime . Recent clinical outcomes studies , meta-analyses , and Mendelian r and omization studies , in which r and omization of Lp(a ) levels is achieved through the r and om assortment of LPA gene variants thereby removing confounders , have shown that genetically determined Lp(a ) levels are continuously and linearly related to risk of CVD . Currently , Lp(a ) pathophysiology is not fully understood , and specifically targeted therapies to lower Lp(a ) are not available . We provide a rationale for increased basic and clinical investigational efforts to further underst and Lp(a ) pathophysiology and assess whether reducing Lp(a ) levels minimizes CVD risk . First , a detailed underst and ing of Lp(a ) synthesis and clearance has not been realized . Second , several mechanisms of atherogenicity are known to varying extent , but the relative contributions of each are not known . Lp(a ) may be atherothrombotic through its low-density lipoprotein moiety , but also through apo(a ) , including its ability to be retained in the vessel wall and mediate pro-inflammatory and proapoptotic effects including those potentiated by its content of oxidized phospholipids , and antifibrinolytic effects . Finally , development of specific Lp(a)-lowering agents to potently lower Lp(a ) will allow testing of mechanistic hypotheses in animal models and the design of r and omized clinical trials to assess reduction in CVD . A convergence of academic , scientific , pharmaceutical , and National Institutes of Health priorities and efforts can make this a reality in the next decade
This meta- analysis shows that oral tibolone treatment significantly lowers circulating Lp(a ) levels in postmenopausal women .
INTRODUCTION Circulating lipoprotein ( a ) ( Lp(a ) ) is a recognized risk factor for cardiovascular disease ( CVD ) .
Tibolone , a synthetic steroid , may lower Lp(a ) levels ; however , evidence of the effects of tibolone on Lp(a ) still remain to be defined .
Therefore , we investigated the effects of tibolone treatment on circulating Lp(a ) levels in postmenopausal women .