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Association of Lipoprotein(a) Levels With Myocardial Infarction in Patients With Low-Attenuation Plaque
Meng-Meng Yu1, Ming-Liang Wang2, Jin-Jin Wang3
1Department of Radiology, Zhongshan Hospital, Fudan University, and Shanghai Institute of Medical Imaging, Shanghai, China.
Background:
Lipoprotein(a) (Lp[a]) is associated with an increased risk of myocardial infarction (MI). However, the mechanism underlying this association has yet to be fully elucidated.
Objectives:
This multicenter study aimed to investigate whether association between Lp(a) and MI risk is reinforced by the presence of low-attenuation plaque (LAP) identified by coronary computed tomography angiography (CCTA).
Methods:
In a derivation cohort, a total of 5,607 patients with stable chest pain suspected of coronary artery disease who underwent CCTA and Lp(a) measurement were prospectively enrolled. In validation cohort, 1,122 patients were retrospectively collected during the same period. High Lp(a) was defined as Lp(a) ≥50 mg/dL. The primary endpoint was a composite of time to fatal or nonfatal MI. Associations were estimated using multivariable Cox proportional hazard models.
Results:
During a median follow-up of 8.2 years (Q1-Q3: 7.2-9.3 years), the elevated Lp(a) levels were associated with MI risk (adjusted HR [aHR]: 1.91; 95% CI: 1.46-2.49; P < 0.001). There was a significant interaction between Lp(a) and LAP (Pinteraction <0.001) in relation to MI risk. When stratified by the presence or absence of LAP, Lp(a) was associated with MI in patients with LAP (aHR: 3.03; 95% CI: 1.92-4.76; P < 0.001). Mediation analysis revealed that LAP mediated 73.3% (P < 0.001) for the relationship between Lp(a) and MI. The principal findings remained unchanged in the validation cohort.
Conclusions:
Elevated Lp(a) augmented the risk of MI during 8 years of follow-up, especially in patients with LAP identified by CCTA. The presence of LAP could reinforce the relationship between Lp(a) and future MI occurrence.
Insights
Elevated Lipoprotein(a) (Lp[a]) significantly increases myocardial infarction (MI) risk, particularly when low-attenuation plaque (LAP) is present. LAP reinforces the link between Lp[a] and future MI events.
Area of Science:
- Cardiology
- Biochemistry
- Medical Imaging
Background:
- Lipoprotein(a) (Lp[a]) is a known risk factor for myocardial infarction (MI).
- The precise mechanisms linking Lp[a] to MI, especially in conjunction with plaque characteristics, require further elucidation.
Purpose of the Study:
- To investigate if low-attenuation plaque (LAP), identified via coronary computed tomography angiography (CCTA), amplifies the association between Lp[a] and MI risk.
- To explore the mediating role of LAP in the Lp[a]-MI relationship.
Main Methods:
- A multicenter study involving a derivation cohort (5,607 patients) and a validation cohort (1,122 patients).
- Patients with suspected coronary artery disease underwent CCTA and Lp[a] measurement.
- High Lp[a] defined as ≥50 mg/dL; primary endpoint was composite of fatal or nonfatal MI.
- Multivariable Cox proportional hazard models and mediation analysis were employed.
Main Results:
- Elevated Lp[a] was associated with increased MI risk (aHR: 1.91).
- A significant interaction between Lp[a] and LAP on MI risk was observed (P<0.001).
- Lp[a] markedly increased MI risk in patients with LAP (aHR: 3.03), with LAP mediating 73.3% of this relationship.
Conclusions:
- Elevated Lp[a] significantly augments MI risk over 8 years.
- The presence of LAP, identified by CCTA, substantially reinforces the association between Lp[a] and future MI.
- LAP plays a critical mediating role in the Lp[a]-driven MI pathway.
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