Effect of hypertriglyceridaemia on lipoprotein (a) serum concentrations

Abstract

Numerous studies have shown lipoprotein (a) [Lp(a)] serum levels above 0.3 gL-1 to be a genetically determined and independent risk factor for atherosclerotic vascular disease. In this study of sera from 1009 patients attending our lipid clinics, multivariate regression analysis revealed an inverse correlation between the serum concentrations of triglycerides (TG) and Lp(a) (r = -0.31; P < 0.001) as determined by electroimmunodiffusion. This was not observed in 1237 controls from a random population. Detailed analysis of the frequency distribution of Lp(a) levels at different degrees of hypertriglyceridaemia (HTG) revealed a decreasing dosage effect of HTG on Lp(a) serum levels. In 60% of patients with TG > 9.12 mmol L-1, this effect led to undetectable serum Lp(a) levels. Dilution of hypertriglyceridaemic samples with normotriglyceridaemic sera containing high levels of Lp(a) revealed that analytical interference in part accounts for the decreasing effect of TG-rich lipoproteins on Lp(a). Re-evaluation of 45 hypertriglyceridaemic samples by enzyme immunoassay and immunoblotting revealed the presence of small amounts of Lp(a) in several samples which were considered to be free of Lp(a) upon electroimmunodiffusion. We conclude that TG-rich lipoproteins interfere with the quantification of Lp(a), at least by electroimmunodiffusion. However, HTG may also decrease Lp(a) plasma concentrations in vivo, possibly by increased clearance of TG-rich Lp(a).

Lipoprotein(a), tissue plasminogen activator and plasminogen activator inhibitor 1 levels in hyperlipidaemic patients in Kuwait

“…However, in confirmation of earlier reports [39,40], Lp(a) levels were higher only in those patients with hypercholesterolaemia, not unexpectedly, as Lp(a) is derived from the LDL molecule [13,16]. Levels of Lp(a) were reduced in hypertriglyceridaemia [39], probably as a result of a reported predominance of the null apo(a) isoform in that disorder [41] reduction in the apo(a) fractional synthesis rates by elevated plasma TG levels [42]. The implications of this negative association between Lp(a) and TG levels (also observed in the whole group here) in the pathogenesis of CHD are currently unknown.…”

“…It is thus likely that the increase in blood levels of these prothrombotic factors, Lp(a), tPA and PAI-1, in patients with hyperlipidaemia might constitute an additional mechanism for the accelerated atherosclerosis observed in these patients. However, in confirmation of earlier reports [39,40], Lp(a) levels were higher only in those patients with hypercholesterolaemia, not unexpectedly, as Lp(a) is derived from the LDL molecule [13,16]. Levels of Lp(a) were reduced in hypertriglyceridaemia [39], probably as a result of a reported predominance of the null apo(a) isoform in that disorder [41] reduction in the apo(a) fractional synthesis rates by elevated plasma TG levels [42].…”

“…However, in confirmation of earlier reports [39,40], Lp(a) levels were higher only in those patients with hypercholesterolaemia, not unexpectedly, as Lp(a) is derived from the LDL molecule [13,16]. However, in confirmation of earlier reports [39,40], Lp(a) levels were higher only in those patients with hypercholesterolaemia, not unexpectedly, as Lp(a) is derived from the LDL molecule [13,16].…”

Lipoprotein(a) as a risk factor for maternal cardiovascular disease mortality in kindreds with familial combined hyperlipidemia or familial hypertriglyceridemia

“…In addition, we observed no significant correlation between Lp(a) levels and any of these other risk factors. In particular, there was no association with TG levels, in contrast to several studies reporting an inverse association between these two risk factors in hyperlipidemic subjects [62,63].…”