Lipoprotein(a) [Lp(a)] has been considered as a causal risk factor for cardiovascular disease (CVD) in the general population and levels vary in different ethnicities.
Recent evidence underscores the importance of LDL-C lowering in CVD prevention by mechanisms that increase the hepatic clearance of apolipoprotein B-containing lipoproteins from the plasma.
The greatest frequency of cardiovascular disease (CVD; 69%) was observed in DM[-]EOCHD[+] patients, whose lipoprotein(a) and insulinemia were also highest (81 nmol/L and 140 pmol/L, respectively).
Recently, lipoprotein(a) has emerged as an important cardiovascular risk factor and lipoprotein apheresis has been used to decrease lipoprotein(a) concentrations in patients with marked elevations and cardiovascular disease.
Lipid-lowering medications can attenuate anti-inflammatory medication-induced increases in ApoB and LDL-C, but can also reduce CVD risk due to cumulative lifetime exposure.
Clinical trials are under way to lower the lipoprotein (a) (Lp(a)) and its associated oxidized phospholipids, which will provide clinical evidence that targeting inflammation caused by oxidized lipids is a viable approach for CVD.
In patients who cannot be treated adequately by drugs it is possible to reduce increased LDL-C and/or lipoprotein(a) (Lp(a)) values by the use of lipoprotein apheresis (LA) with the potential to decrease severe CVD events in the range of 70%->80%.
We found in separate models that women were significantly more likely to have AD and CVD pathology than men, and men were more likely to have "pure" Lewy Body disease, in models adjusted for age at death, education, race, and the APOE-e4 allele.
Background Elevated lipoprotein(a) (Lp(a)), a low-density lipoprotein-like particle bound to the polymorphic apolipoprotein(a) (apo(a)), may be causal for cardiovascular disease.
Homocysteine and education but not lipoprotein (a) predict estimated 10-year risk of cardiovascular disease in blood donors: a community based cross-sectional study.
Low levels of HDL cholesterol, adjusted for ApoE and the above mentioned variables, associated with higher prevalence of CVD (aOR=1.35, 95%CI 1.00, 1.83) and all-cause mortality (aHR=1.42, 95%CI 1.14, 1.78).