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Published on: October 12, 2017
[The importance of lipoprotein(a) in pathogenesis of the high risk unstable angina]
Mustafa Yazici1, Sabri Demircan, Firdovsi Ibrahimli
1Ondokuz Mayis Universitesi Tip Fakültesi, Kardiyoloji Anabilim Dali, Kurupelit 55139 - Samsun-Türkiye. drmeyaz@hotmail.com
Insights
Elevated lipoprotein (a) [Lp(a)] levels correlate with higher cardiac troponin-I (cTn-I) in unstable angina patients. This suggests Lp(a) may indicate plaque instability and myocardial injury.
Area of Science:
- Cardiology
- Biochemistry
- Clinical Medicine
Background:
- Unstable angina pectoris is a critical cardiovascular condition.
- Lipoprotein (a) [Lp(a)] is an emerging biomarker in cardiovascular disease.
- Cardiac troponin-I (cTn-I) is a key indicator of myocardial damage.
Purpose of the Study:
- To compare Lp(a) levels in patients with low versus high-risk unstable angina, stratified by cTn-I levels.
- To investigate the relationship between Lp(a) and myocardial damage in unstable angina.
- To explore the association of Lp(a) with coronary artery disease severity.
Main Methods:
- Blood samples were collected from chest pain patients for Lp(a), C-reactive protein (CRP), and cTn-I measurements.
- Patients were categorized into negative (cTn-I <1.0 ng/ml) and positive (cTn-I ≥1.0 ng/ml) unstable angina groups.
- Coronary artery disease severity was assessed using angiography.
Main Results:
- Lp(a) levels were significantly higher in the cTn-I positive group compared to the negative group (52.9±6.0 mg/dl vs 15.7±2.5 mg/dl, p<0.0001).
- A significant positive correlation was observed between Lp(a) and cTn-I levels (r=0.870, p=0.0001).
- No significant correlation was found between Lp(a) and Gensini score or between Lp(a) and multi-vessel disease.
Conclusions:
- Elevated Lp(a) levels in high-risk unstable angina patients are linked to myocardial injury.
- Lp(a) may serve as a risk factor for plaque destabilization and thrombosis in unstable angina.
- Lp(a) appears more related to plaque instability than to the severity of coronary artery disease in this context.
Objective:
The aim of this study is to compare lipoprotein (a) [Lp(a)] levels in patients with low and high risk unstable angina pectoris, which is defined according to the cardiac troponin-I (Tn-I) levels and to investigate their relation with myocardial damage.
Methods:
From patients with chest pain; venous blood samples were collected for measuring serum Lp(a) and C-reactive protein (CRP) levels on admission and serum cTn-I levels 12 and 24 hours after admission. Fifty-nine patients with serum cTn-I levels <1.0 ng/ml were assigned as negative unstable angina group and 53 patients with serum cTn-I levels >or=1.0 ng/ml were assigned as positive unstable angina groups, respectively. Severity of coronary artery disease was determined by angiography in all patients.
Results:
Compared with cTn-I negative group, Lp(a) levels were significantly higher in cTn-I positive group (52.9+/-6.0 mg/dl vs 15.7+/-2.5 mg/dl, p<0.0001). There was a significant correlation between Lp(a) and cTn-I levels (r=0.870, p=0.0001). We could not establish any correlation between Lp(a) levels and Gensini score or between multiple vessel disease and low density lipoprotein cholesterol levels (p>0.05). Also, there was no significant difference between cTn-I positive and negative groups with respect to Gensini score (p>0.05).
Conclusion:
Increased Lp(a) levels and significant relation between Lp(a) and cTn-I levels support the opinion that Lp(a) can be a risk factor for plaque destabilization and thrombosis rather than severity of coronary artery disease in patients with high risk unstable angina. Furthermore, high levels of Lp(a) may be related with myocardial injury in patients with unstable angina.
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