Abstract 14606: Endothelial Injury Biomarkers and Risk Factors Associated With Discordant Risk of Acute Coronary Syndrome Despite Controlled Low-density Lipoprotein Cholesterol Identified by a Novel Coronary Artery Disease Predictive Algorithm

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Ned Premyodhin ◽  
WENJUN FAN ◽  
Masood Younus ◽  
Douglas S Harrington ◽  
Nathan D Wong
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoprotein Cholesterol ◽  
Predictive Algorithm ◽  
Coronary Syndrome ◽  
History Of ◽  
Artery Disease

Background: Individuals with no history of coronary artery disease can develop acute coronary syndrome (ACS), often in the absence of major risk factors including low-density lipoprotein cholesterol (LDL-C). We identified risk factors and biomarkers that can help identify those at discordantly high risk of ACS who have normal LDL-C using a novel coronary artery disease predictive algorithm (CADPA) incorporating biomarkers of endothelial injury validated in the Multi-Ethnic Study of Atherosclerosis cohort. Methods: Five-year predicted ACS risk was calculated using the CADPA for 8589 patients. Common risk factors and serum levels of 9 biomarkers utilized by the CADPA were tracked. We identified a “discordant high ACS” risk group with serum LDL-C < 130 mg/dL but 5-year CADPA predicted risk ≥ 7.5% and a “discordant low ACS” risk group defined as LDL-C ≥ 130 mg/dL but 5-year CADPA risk of < 7.5%. Multiple logistic regression identified risk factors and biomarkers that predicted discordance in two separate models. Results: The average age and percent male of the high ACS discordant group was higher compared to non-discordant (68±10 vs 54±13 years and 61% vs 43%, respectively). Diabetes (OR 2.84 [2.21-3.66]), male sex (OR 2.83 [2.40-3.35]), family history (OR 2.23 [1.88-2.64]) and active smoking (OR 1.99 [1.50-2.62]) exhibited greatest odds of high ACS discordance compared to other risk factors (all p < 0.01). Increased serum soluble FAS (OR 2.12 [1.97-2.29]), Hemoglobin A1c (OR 1.60 [1.48-1.72]) and interleukin-16 (OR 1.40 [1.32-1.48]) were the biomarkers most associated with discordant risk, independent of global risk factors. Conclusion: Men with diabetes and family history of myocardial infarction who are actively smoking may be at highest risk of developing ACS despite controlled LDL-C. Future studies should examine whether using the CADPA can help identify such individuals that could benefit from earlier targeting of risk factor modification for prevention of ACS.

scholarly journals Baseline Low-Density-Lipoprotein Cholesterol Modifies the Risk of All-Cause Death Associated With Elevated Lipoprotein(a) in Coronary Artery Disease Patients

2022 ◽  
Vol 8 ◽  
Author(s):  
Younan Yao ◽  
Jin Liu ◽  
Bo Wang ◽  
Ziyou Zhou ◽  
Xiaozhao Lu ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Penalized Spline ◽  
All Cause Mortality ◽  
Artery Disease

Background: The prognostic value of elevated lipoprotein(a) [Lp(a)] in coronary artery disease (CAD) patients is inconsistent in previous studies, and whether such value changes at different low-density-lipoprotein cholesterol (LDL-C) levels is unclear.Methods and Findings: CAD patients treated with statin therapy from January 2007 to December 2018 in the Guangdong Provincial People's Hospital (NCT04407936) were consecutively enrolled. Individuals were categorized according to the baseline LDL-C at cut-off of 70 and 100 mg/dL. The primary outcome was 5-year all-cause death. Multivariate Cox proportional models and penalized spline analyses were used to evaluate the association between Lp(a) and all-cause mortality. Among 30,908 patients, the mean age was 63.1 ± 10.7 years, and 76.7% were men. A total of 2,383 (7.7%) patients died at 5-year follow-up. Compared with Lp(a) &lt;50 mg/dL, Lp(a) ≥ 50 mg/dL predicted higher all-cause mortality (multivariable adjusted HR = 1.19, 95% CI 1.07–1.31) in the total cohort. However, when analyzed within each LDL-C category, there was no significant association between Lp(a) ≥ 50 mg/dL and higher all-cause mortality unless the baseline LDL-C was ≥ 100 mg/dL (HR = 1.19, 95% CI 1.04–1.36). The results from penalized spline analyses were robust.Conclusions: In statin-treated CAD patients, elevated Lp(a) was associated with increased risks of all-cause death, and such an association was modified by the baseline LDL-C levels. Patients with Lp(a) ≥ 50 mg/dL had higher long-term risks of all-cause death compared with those with Lp(a) &lt;50 mg/dL only when their baseline LDL-C was ≥ 100 mg/dL.

scholarly journals Risk of Coronary Artery Disease Conferred by Low-Density Lipoprotein Cholesterol Depends on Polygenic Background

Circulation ◽  
2021 ◽  
Vol 143 (14) ◽  
pp. 1452-1454
Author(s):  
Alessandro Bolli ◽  
Paolo Di Domenico ◽  
Roberta Pastorino ◽  
George B. Busby ◽  
Giordano Bottà
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Artery Disease

Plasma homocyst(e)ine as a risk factor for early familial coronary artery disease

1994 ◽  
Vol 40 (4) ◽  
pp. 552-561 ◽  
Author(s):  
L L Wu ◽  
J Wu ◽  
S C Hunt ◽  
B C James ◽  
G M Vincent ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Coronary Risk Factors ◽  
Low Density Lipoprotein Cholesterol ◽  
Relative Odds ◽  
The Mean ◽  
High Concentrations ◽  
Artery Disease

Abstract We measured plasma homocyst(e)ine [H(e)] and other coronary risk factors in 266 patients with early coronary artery disease from 170 families in which two or more siblings were affected and in 168 unmatched controls. The mean H(e) concentration adjusted for significant correlates (serum creatinine, uric acid, and low-density lipoprotein cholesterol) was 12.0 mumol/L in proband cases compared with 10.1 mumol/L in controls (P = 0.0001). Many (17.6%) of the proband cases had H(e) concentrations exceeding the 95th percentile for the controls (relative odds = 4.9, P &lt; 0.001). H(e) among cases was bimodally distributed even after adjustment for concentrations of plasma vitamins. Concordant high H(e) was seen in at least 10 (12%) of 85 families with two or more affected siblings. We conclude that a substantial proportion of early familial coronary artery disease is probably related to production of high concentrations of H(e) by one or more major genes.

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