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Published on: February 17, 2013
Functional approach to investigate Lp(a) in ischaemic heart and cerebral diseases
A de la Peña-Díaz1, G Cardoso-Saldaña, J Zamora-González
1Instituto Nacional de Cardiología Ignacio Chávez, México.
Insights
Lipoprotein(a) [Lp(a)] binding to fibrin is linked to athero-thrombotic disease. Higher Lp(a) fibrin-binding was observed in patients with cerebrovascular disease compared to ischemic cardiopathy.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Thrombosis Research
Background:
- Lipoprotein(a) [Lp(a)] is a significant cardiovascular risk factor.
- Apolipoprotein(a) [apo(a)] in Lp(a) inhibits plasmin formation, impacting fibrinolysis.
- Lp(a) is implicated in atherothrombosis by hindering fibrinolysis.
Purpose of the Study:
- To develop a functional assay for detecting pathogenic Lp(a).
- To quantify Lp(a) binding to fibrin.
- To investigate the association between Lp(a) fibrin-binding and athero-thrombotic diseases.
Main Methods:
- Developed an assay using a fibrin surface and apo(a)-specific monoclonal antibody.
- Assay measures competitive binding of Lp(a) and plasminogen to fibrin.
- Conducted a case-control study of 248 individuals (ischemic cardiopathy, cerebrovascular disease, controls).
Main Results:
- High Lp(a) fibrin-binding was observed in cerebrovascular disease (CVD) cases (0.268 +/- 0.15 nmol L-1).
- Lp(a) fibrin-binding was lower in ischemic cardiopathy (IC) cases (0.155 +/- 0.12 nmol L-1).
- Differences suggest distinct pro- or anti-thrombotic mechanisms in cerebral vs. coronary arteries.
Conclusions:
- Lp(a) fibrin-binding is associated with athero-thrombotic disease.
- Small Apo(a) isoforms are also linked to athero-thrombotic conditions.
- Findings highlight Lp(a) fibrin-binding as a marker for thrombotic risk.
Background:
Lp(a), a major cardiovascular risk factor, contains a specific apolipoprotein, apo(a), which by virtue of structural homology with plasminogen inhibits the formation of plasmin, the fibrinolytic enzyme. A number of clinical reports support the role of Lp(a) as a cardiovascular or cerebral risk factor, and experimental data suggest that it may contribute to atherothrombosis by inhibiting fibrinolysis.
Design:
A well-characterized model of a fibrin surface and an apo(a)-specific monoclonal antibody were used to develop a functional approach to detect pathogenic Lp(a). The assay is based on the competitive binding of Lp(a) and plasminogen for fibrin, and quantifies fibrin-bound Lp(a). High Lp(a) binding to fibrin is correlated with decreased plasmin formation. In a transversal case-control study we studied 248 individuals: 105 had a history of ischaemic cardiopathy (IC), 52 had cerebro-vascular disease (CVD) of thrombotic origin, and 91 were controls.
Results:
The remarkably high apo(a) fibrin-binding in CVD (0.268 +/- 0.15 nmol L-1) compared with IC (0.155 +/- 0.12 nmol L-1) suggests the existence of peculiar and poorly understood differences in pro- or anti-thrombotic mechanisms in either cerebral and/or coronary arteries.
Conclusions:
Our results demonstrated that Lp(a) fibrin-binding and small Apo(a) isoforms are associated with athero-thrombotic disease.
