Abstract 15487: Combined Effects of Lipoprotein(a) and Hypertension in Predicting Cardiovascular Outcomes in Patients With Coronary Artery Disease

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Huihui Liu ◽  
Yexuan Cao ◽  
Jinglu Jin ◽  
Hui-Wen Zhang ◽  
Qi Hua ◽  
...  

Introduction: Although emerging data have suggested that circulating lipoprotein(a) [Lp(a)] could predict cardiovascular events (CVEs) in patients with cardiovascular disease, no study is currently available regarding the prognostic significance of Lp(a) in patients with hypertension. Hypothesis: We assessed the hypothesis that there is a prognostic linkage between hypertension and Lp(a) concentrations in patients with coronary artery disease (CAD). Methods: A total of 8668 patients with stable CAD were consecutively enrolled. Baseline Lp(a) concentrations of them were measured. All subjects were categorized according to Lp(a) levels of <10 (low), 10-30 (medium) and 30 mg/dL (high) and were further stratified by hypertension status. They were regularly followed-up for the occurrence of cardiovascular death, non-fatal myocardial infarction and stroke. Results: Over an average of 54.81±18.60 months follow-up, 584 (6.7%) CVEs occurred. Kaplan-Meier and multivariate Cox regression analyses showed that elevated Lp(a) levels had a significant association with CVEs in hypertensive patients, regardless of the control status of blood pressure, but not in normotensive subjects. Moreover, when subgrouping according to both Lp(a) categories and hypertension status, the risk for CVEs was only significantly elevated in high Lp(a) plus hypertension group compared with the reference group with low Lp(a) levels and normotension (hazard ratio: 1.85, 95% confidence interval: 1.19-2.85). Conclusions: In conclusion, elevated Lp(a) was associated with higher risk for CVEs in CAD patients with hypertension and the coexistence of high Lp(a) concentrations and hypertension greatly worsened the clinical prognosis. Our findings may present a prognostic linkage between hypertension and Lp(a) concentrations in patients with CAD.

2020 ◽  
Author(s):  
Yan Zhang ◽  
Jing-Lu Jin ◽  
Ye-Xuan Cao ◽  
Hui-Hui Liu ◽  
Hui-Wen Zhang ◽  
...  

Abstract Background: Elevated lipoprotein(a) [Lp(a)] and fibrinogen (Fib) are both associated with coronary artery disease (CAD) and the atherogenicity of Lp(a) can be partly due to the potentially antifibrinolytic categories. We hypothesize that patients with higher Lp(a) and Fib may have worse outcomes. Methods: In this prospective study, we consecutively enrolled 8,417 patients with stable CAD from March 2011 to March 2017. All subjects were divided into 9 groups according to Lp(a) (Lp(a)-Low, Lp(a)-Medium, Lp(a)-High) and Fib levels (Fib-Low, Fib-Medium, Fib-High) and followed up for CVEs, including nonfatal acute myocardial infarction, stroke, and cardiovascular mortality. Caplan-Meier, Cox regression and C-statistic analyses were performed.Results: During a median of 37.1 months’ follow-up, 395 (4.7%) CVEs occurred. The occurrence of CVEs increased by Lp(a) (3.5% vs. 5.3% vs. 5.6%, p=0.001) and Fib (4.0% vs. 4.4% vs. 6.1%, p<0.001) categories. When further classified into 9 groups by Lp(a) and Fib levels, the CVEs were highest in the 9th (Lp(a)-High and Fib-High) compared with the 1st (Lp(a)-Low and Fib-Low) group (7.2% vs. 3.3%, p<0.001). The highest risk of subsequent CVEs was found in the 9th group (HRadjusted 2.656, 95% CI 1.628-4.333, p<0.001), which was more significant than Lp(a)-High (HRadjusted 1.786, 95% CI 1.315-2.426, p<0.001) or Fib-High (HRadjusted 1.558, 95% CI 1.162-2.089, p=0.003) group. Moreover, adding the combined Lp(a) and Fib increased the C-statistic by 0.013.Conclusion: Combining Fib and Lp(a) enhance the prognostic value for incident CVEs beyond Lp(a) or Fib alone.


2020 ◽  
Author(s):  
Yan Zhang ◽  
Jing-Lu Jin ◽  
Ye-Xuan Cao ◽  
Hui-Hui Liu ◽  
Hui-Wen Zhang ◽  
...  

Abstract Background: Elevated lipoprotein(a) [Lp(a)] and fibrinogen (Fib) are both associated with coronary artery disease (CAD). The atherogenicity of Lp(a) can be partly due to the potentially antifibrinolytic categories. We hypothesize that patients with higher Lp(a) and Fib may have worse outcomes. Methods: In this prospective study, we consecutively enrolled 8,417 Chinese patients with stable CAD from March 2011 to March 2017. All subjects were divided into 9 groups according to Lp(a) (Lp(a)-Low, Lp(a)-Medium, Lp(a)-High) and Fib levels (Fib-Low, Fib-Medium, Fib-High) and followed up for CVEs, including nonfatal acute myocardial infarction, stroke, and cardiovascular mortality. Kaplan-Meier, Cox regression and C-statistic analyses were performed.Results: During a median of 37.1 months’ follow-up, 395 (4.7%) CVEs occurred. The occurrence of CVEs increased by Lp(a) (3.5% vs. 5.3% vs. 5.6%, p=0.001) and Fib (4.0% vs. 4.4% vs. 6.1%, p<0.001) categories. When further classified into 9 groups by Lp(a) and Fib levels, the CVEs were highest in the 9th (Lp(a)-High and Fib-High) compared with the 1st (Lp(a)-Low and Fib-Low) group (7.2% vs. 3.3%, p<0.001). The highest risk of subsequent CVEs was found in the 9th group (HRadjusted 2.656, 95% CI 1.628-4.333, p<0.001), which was more significant than Lp(a)-High (HRadjusted 1.786, 95% CI 1.315-2.426, p<0.001) or Fib-High (HRadjusted 1.558, 95% CI 1.162-2.089, p=0.003) group. Moreover, adding the combined Lp(a) and Fib increased the C-statistic by 0.013.Conclusion: Combining Fib and Lp(a) enhance the prognostic value for incident CVEs beyond Lp(a) or Fib alone.


2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Yan Zhang ◽  
Jing-Lu Jin ◽  
Ye-Xuan Cao ◽  
Hui-Hui Liu ◽  
Hui-Wen Zhang ◽  
...  

Abstract Background Elevated lipoprotein(a) [Lp(a)] and fibrinogen (Fib) are both associated with coronary artery disease (CAD). The atherogenicity of Lp(a) can be partly due to the potentially antifibrinolytic categories. We hypothesize that patients with higher Lp(a) and Fib may have worse outcomes. Methods In this prospective study, we consecutively enrolled 8,417 Chinese patients with stable CAD from March 2011 to March 2017. All subjects were divided into 9 groups according to Lp(a) (Lp(a)-Low, Lp(a)-Medium, Lp(a)-High) and Fib levels (Fib-Low, Fib-Medium, Fib-High) and followed up for CVEs, including nonfatal acute myocardial infarction, stroke, and cardiovascular mortality. Kaplan–Meier, Cox regression and C-statistic analyses were performed. Results During a median of 37.1 months’ follow-up, 395 (4.7%) CVEs occurred. The occurrence of CVEs increased by Lp(a) (3.5 vs. 5.3 vs. 5.6%, p = 0.001) and Fib (4.0 vs. 4.4 vs. 6.1%, p < 0.001) categories. When further classified into 9 groups by Lp(a) and Fib levels, the CVEs were highest in the 9th (Lp(a)-High and Fib-High) compared with the 1st (Lp(a)-Low and Fib-Low) group (7.2 vs. 3.3%, p < 0.001). The highest risk of subsequent CVEs was found in the 9th group (HRadjusted 2.656, 95% CI 1.628–4.333, p < 0.001), which was more significant than Lp(a)-High (HRadjusted 1.786, 95% CI 1.315–2.426, p < 0.001) or Fib-High (HRadjusted 1.558, 95% CI 1.162–2.089, p = 0.003) group. Moreover, adding the combined Lp(a) and Fib increased the C-statistic by 0.013. Conclusion Combining Fib and Lp(a) enhance the prognostic value for incident CVEs beyond Lp(a) or Fib alone.


Heart ◽  
2020 ◽  
Vol 106 (16) ◽  
pp. 1228-1235 ◽  
Author(s):  
Hui-Hui Liu ◽  
Ye-Xuan Cao ◽  
Jing-Lu Jin ◽  
Hui-Wen Zhang ◽  
Qi Hua ◽  
...  

ObjectiveWhether lipoprotein(a) (Lp(a)) is a predictor for recurrent cardiovascular events (RCVEs) in patients with coronary artery disease (CAD) has not been established. This study, hence, aimed to examine the potential impact of Lp(a) on RCVEs in a real-world, large cohort of patients with the first cardiovascular event (CVE).MethodsIn this multicentre, prospective study, 7562 patients with angiography-diagnosed CAD who had experienced a first CVE were consecutively enrolled. Lp(a) concentrations of all subjects were measured at admission and the participants were categorised according to Lp(a) tertiles. All patients were followed-up for the occurrence of RCVEs including cardiovascular death, non-fatal myocardial infarction and stroke.ResultsDuring a mean follow-up of 61.45±19.57 months, 680 (9.0%) RCVEs occurred. The results showed that events group had significantly higher Lp(a) levels than non-events group (20.58 vs 14.95 mg/dL, p<0.001). Kaplan-Meier analysis indicated that Lp(a) tertile 2 (p=0.001) and tertile 3 (p<0.001) groups had significantly lower cumulative event-free survival rates compared with tertile 1 group. Moreover, multivariate Cox regression analysis further revealed that Lp(a) was independently associated with RCVEs risk (HR: 2.01, 95% CI: 1.44 to 2.80, p<0.001). Moreover, adding Lp(a) to the SMART risk score model led to a slight but significant improvement in C-statistic (∆C-statistic: 0.018 (95% CI: 0.011 to 0.034), p=0.002), net reclassification (6.8%, 95% CI: 0.5% to 10.9%, p=0.040) and integrated discrimination (0.3%, 95% CI: 0.1% to 0.7%, p<0.001).ConclusionsCirculating Lp(a) concentration was indeed a useful predictor for the risk of RCVEs in real-world treated patients with CAD, providing additional information concerning the future clinical application of Lp(a).


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Said ◽  
Y.J Van De Vegte ◽  
N Verweij ◽  
P Van Der Harst

Abstract Background Caffeine is the most widely consumed psychostimulant and is associated with lower risk of coronary artery disease (CAD) and type 2 diabetes (T2D). However, whether these associations are causal remains unknown. Objectives This study aimed to identify genetic variants associated with caffeine intake, and to investigate possible causal links between genetically determined caffeine intake and CAD or T2D. Additionally, we aimed to replicate previous observational findings between caffeine intake and CAD or T2D. Methods Genome wide associated studies (GWAS) were performed on caffeine intake from coffee, tea or both in 407,072 UK Biobank participants. Identified variants were used in a two-sample Mendelian randomization (MR) approach to investigate evidence for causal links between caffeine intake and CAD in CARDIoGRAMplusC4D (60,801 cases; 123,504 controls) or T2D in DIAGRAM (26,676 cases; 132,532 controls). Observational associations were tested within UK Biobank using Cox regression analyses. Results Moderate observational caffeine intakes from coffee or tea were associated with lower risks of CAD or T2D compared to no or high intake, with the lowest risks at intakes of 120–180 mg/day from coffee for CAD (HR=0.77 [95% CI: 0.73–0.82; P&lt;1e-16]), and 300–360 mg/day for T2D (HR=0.76 [95% CI: 0.67–0.86]; P=1.57e-5). GWAS identified 51 novel genetic loci associated with caffeine intake, enriched for central nervous system genes. In contrast to observational analyses, MR analyses in CARDIoGRAMplusC4D and DIAGRAM yielded no evidence for causal links between caffeine intake and the development of CAD or T2D. Conclusions MR analyses indicate caffeine intake might not protect against CAD or T2D, despite protective associations in observational analyses. Manhattan_plot_CaffeineIntake Funding Acknowledgement Type of funding source: None


2011 ◽  
Vol 29 (10) ◽  
pp. 1889-1896 ◽  
Author(s):  
Hisashi Kai ◽  
Takafumi Ueno ◽  
Takeshi Kimura ◽  
Hisashi Adachi ◽  
Yutaka Furukawa ◽  
...  

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