Key result
Acute MI linked to ~6-fold higher peak serum LPA levels vs controls.
Case-Control (n=43)
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In this study the relation between lysophosphatidic acid (LPA) and myocardial infarction was investigated, the typical and simplified methods for measuring serum LPA concentration by dot immunogold filtration assay (DIFA) based on a polyclonal antibody to LPA were developed, and serum LPA concentrations were measured in 31 patients with acute myocardial infarction (AMI) and 12 controls (blood donors) by DIFA. Serum LPA levels were raised more than twofold 8 h after the onset of AMI. Maximal elevation (10.43 mg/L) was found at 48-72 h following onset and remained higher than the control concentration (1.66 mg/L) 7 days after AMI. The rise in serum LPA concentration in AMI patients suggests that LPA might be involved in AMI-related pathophysiology in the cardiovascular system. The simplified DIFA developed in the present study for measuring serum LPA concentration is convenient and highly sensitive.
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Chen et al. (2003) conducted a case-control in Acute myocardial infarction (n=43). Acute myocardial infarction (measured via dot immunogold filtration assay) vs. Healthy blood donor controls was evaluated on Serum lysophosphatidic acid (LPA) concentration (mg/L). Acute myocardial infarction was associated with elevated serum lysophosphatidic acid levels, peaking at 10.43 mg/L at 48-72 hours vs 1.66 mg/L in controls.
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