Lipoprotein(a), Interleukin-10, C-Reactive Protein, and 8-Year Outcome After Percutaneous Coronary Intervention

Thoraxcenter, Erasmus Medical Center, Rotterdam, The Netherlands.
Clinical Cardiology (Impact Factor: 2.59). 08/2012; 35(8):482-9. DOI: 10.1002/clc.21988
Source: PubMed


This prospective study investigated the association between preprocedural biomarker levels and incident major adverse cardiac events (MACE) in complex patients undergoing percutaneous coronary intervention (PCI) with sirolimus-eluting stenting.
Lipoprotein(a) (Lp[a]), interleukin-10 (IL-10), and high-sensitivity C-reactive protein (CRP) have long-term prognostic value in patients undergoing PCI.
Between April 2002 and February 2003, 161 patients were included in the study. Blood was drawn before the procedure, and biomarkers were measured. Patients were followed-up for MACE (death, nonfatal myocardial infarction, and repeat revascularization). Cox proportional hazard models were used to determine risk of MACE for tertiles of biomarkers. Both 1-year and long-term follow-up (median, 6 years; maximum, 8 years) were evaluated.
Mean age was 59 years, and 68% were men. During long-term follow-up, 72 MACE occurred (overall crude cumulative incidence: 45% [95% confidence interval (CI): 37%-52%]). Lp(a) was associated with a higher 1-year risk of MACE, with an adjusted hazard ratio (HR) of 3.1 (95% CI: 1.1-8.6) for the highest vs the lowest tertile. This association weakened and lost significance with long-term follow-up. IL-10 showed a tendency toward an association with MACE. The 1-year HR was 2.1 (95% CI: 0.92-5.0). Long-term follow-up rendered a similar result. The association of CRP with MACE did not reach statistical significance at 1-year follow-up. However, CRP was associated with long-term risk of MACE, with an HR of 1.9 (95% CI: 1.0-3.5).
In this prospective study, preprocedural Lp(a) level was associated with short-term prognosis after PCI. The preprocedural CRP level was associated with long-term prognosis after PCI.

Download full-text


Available from: Patrick W Serruys, Sep 03, 2014
  • Source
    • "Substantial studies consistently show that plasma Lp(a) level is predominantly dependent on the isoform size variability of Apo(a) in terms of small isoform size of Apo(a) which results in higher Lp(a) level and vice versa [18–21]. And previous epidemiological studies also firmly demonstrate that, with Lp(a) elevation, the risk for cardiovascular risk is significantly increased [22–24]. For example, Kardys et al. observed that Lp(a) was associated with a higher 1-year risk of cardiovascular events, with an adjusted hazard ratio (HR) of 3.1 (95% confidence interval (CI): 1.1–8.6) "
    [Show abstract] [Hide abstract]
    ABSTRACT: Atherosclerotic cardiovascular diseases (CVD) are still the leading cause of morbidity and mortality worldwide, although optimal medical therapy has been prescribed for primary and secondary preventions. Residual cardiovascular risk for some population groups is still considerably high although target low density lipoprotein-cholesterol (LDL-C) level has been achieved. During the past few decades, compelling pieces of evidence from clinical trials and meta-analyses consistently illustrate that lipoprotein(a) (Lp(a)) is a significant risk factor for atherosclerosis and CVD due to its proatherogenic and prothrombotic features. However, the lack of effective medication for Lp(a) reduction significantly hampers randomized, prospective, and controlled trials conducting. Based on previous findings, for patients with LDL-C in normal range, Lp(a) may be a useful marker for identifying and evaluating the residual cardiovascular risk, and aggressively lowering LDL-C level than current guidelines' recommendation may be reasonable for patients with particularly high Lp(a) level.
    Full-text · Article · Oct 2013 · Disease markers
  • Source
    • "Previous studies demonstrated that elevated Lp(a) levels are associated with increasing incidence and severity of cardiovascular diseases [2-7]. Furthermore, elevated baseline Lp(a) levels predict the subsequent cardiovascular event incidence in patients with coronary artery disease (CAD) after percutaneous coronary intervention (PCI) [8-10]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Elevated lipoprotein(a) [Lp(a)] levels predict cardiovascular events incidence in patients with coronary artery disease (CAD). Genetic variants in the rs3798220, rs10455872 and rs6415084 single-nucleotide polymorphisms (SNPs) in the Lp(a) gene (LPA) correlate with elevated Lp(a) levels, but whether these SNPs have prognostic value for CAD patients is unknown. The present study evaluated the association of LPA SNPs with incidence of subsequent cardiovascular events in CAD patients after percutaneous coronary intervention (PCI). TaqMan SNP genotyping assays were performed to detect the rs6415084, rs3798220 and rs10455872 genotypes in 517 Chinese Han patients with CAD after PCI. We later assessed whether there was an association of these SNPs with incidence of major adverse cardiovascular events (MACE: cardiac death, nonfatal myocardial infarction, ischemic stroke and coronary revascularization). Serum lipid profiles were also determined using biochemical methods. Only the rs6415084 variant allele was associated with higher Lp(a) levels [41.3 (20.8, 74.6) vs. 18.6 (10.3, 40.9) mg/dl, p < 0.001]. During a 2-year follow-up period, 102 patients suffered MACE, and Cox regression analysis demonstrated that elevated Lp(a) (>=30 mg/dl) levels correlated with increased MACE (adjusted HR, 1.69; 95% CI 1.13-2.53), but there was no association between LPA genetic variants (rs6415084 and rs3798220) and MACE incidence (p > 0.05). Our data did not support a relationship between genetic LPA variants (rs6415084 and rs3798220) and subsequent cardiovascular events after PCI in Chinese Han CAD patients.
    Full-text · Article · Aug 2013 · Lipids in Health and Disease
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The incremental predictive value of red cell distribution width (RDW) for major adverse cardiac events (MACEs) has not been fully investigated in patients with acute myocardial infarction (AMI). The aim of this study was to determine the incremental value of RDW to the established risk factors in predicting clinical outcomes after AMI. Between November 2005 and January 2010, 1596 patients with AMI (1070 male; mean age, 64.5 ± 11.9 years) were analyzed in this study. Baseline levels of RDW were measured at the time of admission. The 12-month MACEs were defined as death and nonfatal MI. The RDW levels were significantly higher in patients with 12-month MACEs (13.8 ± 1.3% vs 13.3 ± 1.2%, P < 0.001). In a Cox proportional hazards model, RDW (hazard ratio [HR]: 1.19, P = 0.016) was an independent predictor for 12-month MACEs. Adding RDW to established risk factors and hemoglobin levels significantly improved prediction for 12-month MACEs, as shown by the net reclassification improvement (0.297; P = 0.012) and integrated discrimination improvement (0.0143; P = 0.042). The likelihood ratio test showed that RDW added incremental predictive value to the combination of hemoglobin and established risk factors (P = 0.005). Patients were categorized into 4 groups according to quartiles of RDW at baseline. Adjusted HRs for 12-month MACEs were 1 (RDW ≤12.6%, reference), 4.24 (RDW 12.7%–13.1%, P = 0.01), 4.36 (RDW 13.2%–13.9%, P = 0.008), and 6.18 (RDW 13.2%–13.9%, P = 0.001), respectively. In post-myocardial infarction patients, baseline RDW levels at admission could provide incremental predictive value to established risk factors for predicting 12-month MACEs.
    Full-text · Article · Jun 2013 · Clinical Cardiology
Show more