Abstract
BackgroundLipoprotein(a) is genetically determined and increasingly recognized as a major risk factor for arteriosclerotic cardiovascular disease. We examined whether plasma lipoprotein(a) concentrations were associated with intraplaque neovascularization (IPN) grade in patients with carotid stenosis and in terms of increasing plaque susceptibility to haemorrhage and rupture.MethodsWe included 85 patients diagnosed with carotid stenosis as confirmed using carotid ultrasound who were treated at Guangdong General Hospital. Baseline data, including demographics, comorbid conditions and carotid ultrasonography, were recorded. The IPN grade was determined using contrast-enhanced ultrasound through the movement of the microbubbles. Univariate and multivariate binary logistic regression analyses were used to evaluate the association between lipoprotein(a) and IPN grade, with stepwise adjustment for covariates including age, sex, comorbid conditions and statin therapy (model 1), total cholesterol, triglyceride, low-density lipoprotein cholesterol calculated by Friedwald's formula, high-density lipoprotein cholesterol, apolipoprotein A and apolipoprotein B (model 2), maximum plaque thickness and total carotid maximum plaque thickness, degree of carotid stenosis and internal carotid artery (ICA) occlusion (model 3).ResultsLipoprotein(a) was a significant predictor of higher IPN grade in binary logistic regression before adjusting for other risk factors (odds ratio [OR] 1.238, 95% confidence interval [CI] (1.020, 1.503), P = 0.031). After adjusting for other risk factors, lipoprotein(a) still remained statistically significant in predicting IPN grade in all model. (Model 1: OR 1.333, 95% CI 1.074, 1.655, P = 0.009; Model 2: OR 1.321, 95% CI 1.059, 1.648, P = 0.014; Model 3: OR 1.305, 95% CI 1.045, 1.628, P = 0.019). Lp(a) ≥ 300 mg/L is also significantly related to IPN compare to < 300 mg/L (OR 2.828, 95% CI 1.055, 7.580, P = 0.039) as well as in model 1, while in model 2 and model 3 there are not significant difference.ConclusionsPlasma lipoprotein(a) concentrations were found to be independently associated with higher IPN grade in patients with carotid stenosis. Lowering plasma lipoprotein(a) levels may result in plaque stabilization by avoiding IPN formation.
Highlights
Lipoprotein(a) is genetically determined and increasingly recognized as a major risk factor for arteriosclerotic cardiovascular disease
Lipoprotein(a) (Lp(a)), formed from an apolipoprotein B-100 covalently linked to apo(a), is a low-density lipoprotein (LDL)-like protein which is genetically determined and increasingly recognised as a major risk factor for Arteriosclerotic cardiovascular disease (ASCVD) [5]
While other 35.3% patients admitted for cerebral ischemia-related reasons including dizzy, blurred vision or unilateral limb weakness and 8.2% patients suffered from asymptomatic carotid stenosis
Summary
Lipoprotein(a) is genetically determined and increasingly recognized as a major risk factor for arteriosclerotic cardiovascular disease. We examined whether plasma lipoprotein(a) concentrations were associated with intraplaque neovascularization (IPN) grade in patients with carotid stenosis and in terms of increasing plaque susceptibility to haemorrhage and rupture. Few methods can detect intraplaque neovascularization (IPN), which increases the susceptibility to haemorrhage and rupture of the plaque [2] that are expensive and inconvenient to deal with in terms of repeated examinations. Lipoprotein(a) (Lp(a)), formed from an apolipoprotein (apo) B-100 covalently linked to apo(a), is a low-density lipoprotein (LDL)-like protein which is genetically determined and increasingly recognised as a major risk factor for ASCVD [5]. Previous studies have demonstrated a strong and independent association between Lp(a) and carotid artery disease [6] and Lp(a) independently predict carotid atherosclerosis progression [7]. Whether Lp(a) is associate with IPN across the plaque, affecting its stability, is worth pondering
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
