Remnant cholesterol as a cause of ischemic heart disease: Evidence, definition, measurement, atherogenicity, high risk patients, and present and future treatment

2014 ◽  
Vol 141 (3) ◽  
pp. 358-367 ◽  
Author(s):  
Anette Varbo ◽  
Marianne Benn ◽  
Børge G. Nordestgaard
2005 ◽  
Vol 58 (8) ◽  
pp. 934-940 ◽  
Author(s):  
Antonio Tello ◽  
Francisco Marín ◽  
Vanessa Roldán ◽  
Ana García-Herola ◽  
Sofía Lorenzo ◽  
...  

2003 ◽  
Vol 104 (s48) ◽  
pp. 9P-9P
Author(s):  
F Marín ◽  
V Roldán ◽  
GJ Caine ◽  
A García-Herola ◽  
V Climent ◽  
...  

2010 ◽  
Vol 139 (1) ◽  
pp. 95-97 ◽  
Author(s):  
Ángel López-Cuenca ◽  
Francisco Marín ◽  
Vanessa Roldán ◽  
Vicente E. Climent ◽  
Mariano Valdés ◽  
...  

1993 ◽  
Vol 76 (3) ◽  
pp. 298-300 ◽  
Author(s):  
M. Findler ◽  
D. Galili ◽  
Z. Meidan ◽  
V. Yakirevitch ◽  
A.A. Garfunkel

2016 ◽  
Vol 62 (4) ◽  
pp. 593-604 ◽  
Author(s):  
Anne-Marie K Jepsen ◽  
Anne Langsted ◽  
Anette Varbo ◽  
Lia E Bang ◽  
Pia R Kamstrup ◽  
...  

Abstract BACKGROUND Increased concentrations of remnant cholesterol are causally associated with increased risk of ischemic heart disease. We tested the hypothesis that increased remnant cholesterol is a risk factor for all-cause mortality in patients with ischemic heart disease. METHODS We included 5414 Danish patients diagnosed with ischemic heart disease. Patients on statins were not excluded. Calculated remnant cholesterol was nonfasting total cholesterol minus LDL and HDL cholesterol. During 35836 person-years of follow-up, 1319 patients died. RESULTS We examined both calculated and directly measured remnant cholesterol; importantly, however, measured remnant cholesterol made up only 9% of calculated remnant cholesterol at nonfasting triglyceride concentrations <1 mmol/L (89 mg/dL) and only 43% at triglycerides >5 mmol/L (443 mg/dL). Multivariable-adjusted hazard ratios for all-cause mortality compared with patients with calculated remnant cholesterol concentrations in the 0 to 60th percentiles were 1.2 (95% CI, 1.1–1.4) for patients in the 61st to 80th percentiles, 1.3 (1.1–1.5) for the 81st to 90th percentiles, 1.5 (1.1–1.8) for the 91st to 95th percentiles, and 1.6 (1.2–2.0) for patients in the 96th to 100th percentiles (trend, P < 0.001). Corresponding values for measured remnant cholesterol were 1.0 (0.8–1.1), 1.2 (1.0–1.4), 1.1 (0.9–1.5), and 1.3 (1.1–1.7) (trend, P = 0.006), and for measured LDL cholesterol 1.0 (0.9–1.1), 1.0 (0.8–1.2), 1.0 (0.8–1.3), and 1.1 (0.8–1.4) (trend, P = 0.88). Cumulative survival was reduced in patients with calculated remnant cholesterol ≥1 mmol/L (39 mg/dL) vs <1 mmol/L [log-rank, P = 9 × 10−6; hazard ratio 1.3 (1.2–1.5)], but not in patients with measured LDL cholesterol ≥3 mmol/L (116 mg/dL) vs <3 mmol/L [P = 0.76; hazard ratio 1.0 (0.9–1.1)]. CONCLUSIONS Increased concentrations of both calculated and measured remnant cholesterol were associated with increased all-cause mortality in patients with ischemic heart disease, which was not the case for increased concentrations of measured LDL cholesterol. This suggests that increased concentrations of remnant cholesterol explain part of the residual risk of all-cause mortality in patients with ischemic heart disease.


2018 ◽  
Vol 36 (1) ◽  
pp. 44-52 ◽  
Author(s):  
Eric J. Chow ◽  
Yan Chen ◽  
Melissa M. Hudson ◽  
Elizabeth A.M. Feijen ◽  
Leontien C. Kremer ◽  
...  

Purpose We aimed to predict individual risk of ischemic heart disease and stroke in 5-year survivors of childhood cancer. Patients and Methods Participants in the Childhood Cancer Survivor Study (CCSS; n = 13,060) were observed through age 50 years for the development of ischemic heart disease and stroke. Siblings (n = 4,023) established the baseline population risk. Piecewise exponential models with backward selection estimated the relationships between potential predictors and each outcome. The St Jude Lifetime Cohort Study (n = 1,842) and the Emma Children’s Hospital cohort (n = 1,362) were used to validate the CCSS models. Results Ischemic heart disease and stroke occurred in 265 and 295 CCSS participants, respectively. Risk scores based on a standard prediction model that included sex, chemotherapy, and radiotherapy (cranial, neck, and chest) exposures achieved an area under the curve and concordance statistic of 0.70 and 0.70 for ischemic heart disease and 0.63 and 0.66 for stroke, respectively. Validation cohort area under the curve and concordance statistics ranged from 0.66 to 0.67 for ischemic heart disease and 0.68 to 0.72 for stroke. Risk scores were collapsed to form statistically distinct low-, moderate-, and high-risk groups. The cumulative incidences at age 50 years among CCSS low-risk groups were < 5%, compared with approximately 20% for high-risk groups ( P < .001); cumulative incidence was only 1% for siblings ( P < .001 v low-risk survivors). Conclusion Information available to clinicians soon after completion of childhood cancer therapy can predict individual risk for subsequent ischemic heart disease and stroke with reasonable accuracy and discrimination through age 50 years. These models provide a framework on which to base future screening strategies and interventions.


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