2019
DOI: 10.1016/j.atherosclerosis.2019.06.265
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Monogenic Familial Hypercholesterolemia, Polygenic Hypercholesterolemia, And The Risk Of Premature Atherosclerotic Cardiovascular Disease

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Cited by 1 publication
(4 citation statements)
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“…This confirms that the CAD risk caused by elevated Lp(a) concentrations follows a distinct pathomechanism from LDL-C. 36 Current risk models for cardiovascular disease primarily rely on clinical data, but evidence that genome-wide variation contributes to this risk is widely investigated. 3,15,30,31,[37][38][39][40] In accordance with the literature, 41 only 46.6% of HC patients in our cohort have a detectable monogenic cause of FH, and therefore, a clear disease etiology. This leaves a large proportion of "idiopathic" patients with undetermined clear genetic cause.…”
Section: Monogenic Hcsupporting
confidence: 91%
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“…This confirms that the CAD risk caused by elevated Lp(a) concentrations follows a distinct pathomechanism from LDL-C. 36 Current risk models for cardiovascular disease primarily rely on clinical data, but evidence that genome-wide variation contributes to this risk is widely investigated. 3,15,30,31,[37][38][39][40] In accordance with the literature, 41 only 46.6% of HC patients in our cohort have a detectable monogenic cause of FH, and therefore, a clear disease etiology. This leaves a large proportion of "idiopathic" patients with undetermined clear genetic cause.…”
Section: Monogenic Hcsupporting
confidence: 91%
“…With a positive predictive value of 90%, the LPA genetic score can be used as a valuable surrogate for biochemical Lp(a) measurements in large genetic screening efforts and therefore complement monogenic testing within a single intervention. We also detected HC individuals with a combination of monogenic and multi‐allelic predisposition (Table 1), which was shown to result in an increased cumulative risk for CAD 31,38 as multiple alleles might act as modulators both at the very high and very low risk level and could therefore provide valuable information for individualized treatment. In our population control cohort, 21.6% of individuals showed elevated LPA genetic scores; considering the high positive predictive value of 90%, 19.4% of our population control individuals are expected to have high Lp(a) concentrations and might benefit from clinical surveillance and future treatments for Lp(a) associated dyslipidemia to prevent CAD risk.…”
Section: Discussionmentioning
confidence: 99%
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