Relationship between Two AMI Risk Factors: Low Serum Lipoprotein Lipase Mass and Hypoadiponectinemia

Abstract

Aim: Recent clinical studies have reported that low lipoprotein lipase mass in preheparin serum (s-LpL) and hypoadiponectinemia are important risk factors for acute myocardial infarction (AMI). The aim of this study was to elucidate the relationship between low s-LpL and hypoadiponectinemia, both of which are risk factors for AMI. Methods: One hundred and thirty-seven male patients with AMI and fifty-three males with normal coronary arteries (NCA) were enrolled in the study. Coronary risk factors, including s-LpL and serum total adiponectin concentrations (t-adiponectin), were compared. Results: Both s-LpL and t-adiponectin were significantly lower in patients with AMI than in subjects with NCA (s-LpL, NCA: 48.1 11.0 ng/mL, AMI: 38.9 11.1 ng/mL, p 0.01; t-adiponectin, NCA: 7.7 2.9 g/mL, AMI: 6.

Comparison of the effect of post-heparin and pre-heparin lipoprotein lipase and hepatic triglyceride lipase on remnant lipoprotein metabolism

“…Although the RLP-TG/RLP-C ratio in pre-heparin plasma exhibited a trend of being inversely correlated with the LPL concentration in the fasting plasma, it was not statistically significant, probably because of a low TG concentration in the fasting plasma. Adiponectin is a plasma protein expressed in adipose tissue that is known to be closely associated with LPL and cardiovascular risk [38]. Interestingly, adiponectin in pre-heparin plasma was inversely and significantly correlated with the RLP-TG/RLP-C ratio and positively correlated with LPL concentration, but adiponectin was not correlated with LPL activity in post-heparin plasma.…”

Serum Triglyceride Lipase Concentrations are Independent Risk Factors for Coronary Artery Disease and In-Stent Restenosis

“…Plasma EL concentration was shown to be associated with inflammation 27, 28) . Some studies showed that HL was associated with insulin resistance and inflammation 29, 36) , and LPL was significantly associated with insulin resistance, adiponectin, and inflammation 30, 37, 38) . Therefore, in our study, we like to propose that triglyceride lipases affecting CAD or in-stent restenosis could work through other mechanisms such as inflammation.…”