Background Lipoprotein(a) [Lp(a)] elevation is an important risk factor for coronary artery disease (CAD). However, the correlation between Lp(a) elevations and the risk of recurrent cardiovascular events in patients with established cardiovascular disease is controversial. Some studies have shown that Low-density lipoprotein cholesterol (LDL-C) levels may influence the association between Lp(a) and cardiovascular risk. Our study aims to explore the correlation between Lp(a) elevations and cardiovascular risk in patients with different LDL-C levels. Methods We included 516 patients who received coronary stents due to acute coronary syndrome (ACS) and followed them for three years. They were divided into low-Lp(a) group and high-Lp(a) group according to Lp(a) levels, and the incidence of major adverse cardiovascular events (MACE) and acute coronary events (ACE) was compared between the two groups. Then the patients were divided into three subgroups (S1:LDL-C ≥ 1.8 mmol/L; S2:1.4 ≤ LDL-C < 1.8 mmol/L; S3:LDL-C < 1.4 mmol/L). The correlation between Lp(a) elevations and cardiovascular risk in different subgroups was analysed by Cox proportional hazards models. Results The incidence of MACE and ACE in the high-Lp(a) group was significantly higher than those in the low-Lp(a) group (P < 0.05). Lp(a) elevations had independent prognostic value from the statistical point of view (MACE: HR = 1.63, 95%CI = 1.12–2.38, P = 0.012; ACE: HR = 1.70, 95%CI = 1.03–2.81, P = 0.037). Subgroup analysis showed that Lp(a) elevations increased cardiovascular risk when LDL-C ≥ 1.4 mmol/L. However, this correlation no longer existed when LDL-C levels were very low (< 1.4 mmol/L) (MACE: HR = 0.49, 95%CI = 0.17–1.42, P = 0.186; ACE: HR = 0.68, 95%CI = 0.18–2.61, P = 0.570). Conclusions Lp(a) elevations are associated with recurrent cardiovascular events when LDL-C levels are high, but this association may change when LDL-C levels are extremely low. CAD patients with combination of LDL-C ≥ 1.4 mmol/L and Lp(a) elevations shall be considered as high-risk groups and require further medication for the reduction of their LDL-C levels.

Background Lipoprotein (a) [Lp(a)] is an independent risk factor for coronary artery disease (CAD). Recent studies have indicated that statins tend to increase Lp(a) levels by 10–20%. However, the association of statin-mediated increases in Lp(a) levels with CAD has not been determined.  Methods This study included 488 patients with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI). Lp(a) levels were measured at baseline and 1 month after statin therapy. The study endpoints were major adverse cardiovascular events (MACE). Hazard ratios for the MACE were adjusted for potential confounder using Cox regression. Results After statin therapy, the mean level of Lp(a) increased by 19.3% from baseline. Lp(a) levels increased in 307 patients (62.9%) with a median elevation of 4.1 mg/dL. Patients with an increase in Lp(a) were at higher risk for MACE than those without an increase in Lp(a) (p = 0.044). Subgroup analyses revealed that a mild-to-moderate increase in Lp(a) was not associated with MACE, whereas there was a strong correlation between the highest quartile increase in Lp(a) (≥ 10.1 mg/dL) and MACE (HR = 2.29, 95%CI = 1.36–3.84, p = 0.002). This correlation was independent of baseline Lp(a) levels but not independent of on-statin Lp(a) levels. Conclusions Severe increases in Lp(a) following statin therapy raise the risk of MACE, but a mild-to-moderate increase in Lp(a) may not affect the cardiovascular prognosis of CAD patients. Even if the baseline Lp(a) levels are low, it is necessary to continue testing for Lp(a) concentration at least once after statin.

BackgroundEpicardial adipose tissue (EAT) is directly related to coronary artery disease (CAD), but little is known about its role in hemodynamically significant CAD. Therefore, our goal is to explore the impact of EAT volume on hemodynamically significant CAD.MethodsPatients who underwent coronary computed tomography angiography (CCTA) and received coronary angiography within 30 days were retrospectively included. Measurements of EAT volume and coronary artery calcium score (CACs) were performed on a semi-automatic software based on CCTA images, while quantitative flow ratio (QFR) was automatically calculated by the AngioPlus system according to coronary angiographic images.ResultsThis study included 277 patients, 112 of whom had hemodynamically significant CAD and showed higher EAT volume. In multivariate analysis, EAT volume was independently and positively correlated with hemodynamically significant CAD [per standard deviation (SD) cm3; odds ratio (OR), 2.78; 95% confidence interval (CI), 1.86–4.15; P &lt; 0.001], but negatively associated with QFRmin (per SD cm3; β coefficient, −0.068; 95% CI, −0.109 to −0.027; P = 0.001) after adjustment for traditional risk factors and CACs. Receiver operating characteristics curve analysis demonstrated a significant improvement in predictive value for hemodynamically significant CAD with the addition of EAT volume to obstructive CAD alone (area under the curve, 0.950 vs. 0.891; P &lt; 0.001).ConclusionIn this study, we found that EAT volume correlated substantially and positively with the existence and severity of hemodynamically significant CAD in Chinese patients with known or suspected CAD, which was independent of traditional risk factors and CACs. In combination with obstructive CAD, EAT volume significantly improved diagnostic performance for hemodynamically significant CAD, suggesting that EAT could be a reliable noninvasive indicator of hemodynamically significant CAD.