Prospective association of a genetic risk score with major adverse cardiovascular events in patients with coronary artery disease

Zhao, Chen; Zhu, Ping; Shen, Qile; Jin, Li

doi:10.1097/md.0000000000009473

Cited by 13 publications

(17 citation statements)

References 33 publications

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“…Study participants with CHD receiving statin therapy and with hypertension manifested an association between weighted GRS and MACEs. Such individuals with a medium or high risk according to the GRS also had a 2.138- and 4.048-fold higher risk of a MACE, respectively [ 69 ].…”

Section: Modern Models Of Genetic Risk Calculators (2016–2020)mentioning

confidence: 99%

Genetic Risk Score for Coronary Heart Disease: Review

Semaev

Shakhtshneider

2020

JPM

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The present review deals with the stages of creation, methods of calculation, and the use of a genetic risk score for coronary heart disease in various populations. The concept of risk factors is generally recognized on the basis of the results of epidemiological studies in the 20th century; according to this concept, the high prevalence of diseases of the circulatory system is due to lifestyle characteristics and associated risk factors. An important and relevant task for the healthcare system is to identify the population segments most susceptible to cardiovascular diseases (CVDs). The level of individual risk of an unfavorable cardiovascular prognosis is determined by genetic factors in addition to lifestyle factors.

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Section: Modern Models Of Genetic Risk Calculators (2016–2020)mentioning

confidence: 99%

Genetic Risk Score for Coronary Heart Disease: Review

Semaev

Shakhtshneider

2020

JPM

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“…К настоящему времени идентифицировано множество полиморфных вариантов генов, ассоциированных с риском развития полигенных форм ИБС [11]. Наиболее выраженными эффектами в отношении риска развития болезни обладали такие гены, как PCSK9 [11][12][13][14], LPA [10], NPC1L1 [15], ST3GAL4 [16], генный кластер APOE-C1-C2-C4 [17], COBLL1 [15], LRP4 [10], STARD3 [18], ABCA1 [10,19], SCARB1 [20][21][22], CETP [23,24], PLTP [25,26], LCAT [10]. Продукты экспрессии идентифицированных генов не ограничены влияниями на липидный обмен, а вовлечены в разнообразные молекулярные механизмы развития ИБС.…”

Section: ибсunclassified

“…Апо-C3 экспрессируется в составе ЛПОНП. Установлено, что полиморфизм rs4420638 ассоциирован с риском развития ИБС в китайской популяции [17]. Установлена ассоциация данного полиморфизма с уровнями общего холестерина, ЛПВП, ЛПНП и ТГ в популяции северных финнов [37].…”

Section: Apoe-c1-c2-c4unclassified

Lipid metabolism genes and predisposition to ischemic heart disease

Churilin¹,

Kononov²,

Маль³

et al. 2019

Medical news of the North Caucasus

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Анализируется литература последних лет, посвященная изучению генов, ответственных за регуляцию липидного обмена и развитие коронарного атеросклероза. Ключевые слова: GWAS, полногеномное ассоциативное исследование, липидный обмен, ИБС This review deals with the analysis of foreign and domestic literature of recent years on the search for genes involved in the regulation of lipid metabolism and responsible for the development of coronary atherosclerosis.

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“…It also found that TWIST1 rs2107595 was associated with an increased risk of MACE such as large artery stroke, CAD, and ischemic stroke. 9 Routine genetic testing for hyperlipidemia and CVD risk is limited to patients with history of familial hypercholesterolemia (FH), predicted by variation in LDLR, APOB, or PCSK9. 1 CVD nevertheless shows strong heritability in patients without FH, suggesting an underlying genetic component.…”

Section: Introductionmentioning

confidence: 99%

Genome Wide Epistasis Study of On-Statin Cardiovascular Events with Iterative Feature Reduction and Selection

Feroze

Nguyen

et al. 2020

Preprint

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Background Predicting risk for major adverse cardiovascular events (MACE) is an evidence-based practice that incorporates lifestyle, history, and other risk factors. Statins reduce risk for MACE by decreasing lipids, but it is difficult to stratify risk following initiation of a statin. Genetic risk determinants for on-statin MACE are low-effect size and impossible to generalize. Our objective was to determine high-level epistatic risk factors for on-statin MACE with GWAS-scale data. Methods Controlled-access data for 5,980 subjects taking a statin collected from Vanderbilt University Medical Center's BioVU were obtained from dbGaP. We used Random Forest Iterative Feature Reduction and Selection (RF-IFRS) to select highly informative genetic and environmental features from a GWAS-scale dataset of patients taking statin medications. Variant-pairs were distilled into overlapping networks and assembled into individual decision trees to provide an interpretable set of variants and associated risk. Results 1,718 cases who suffered MACE and 4,172 controls were obtained from dbGaP. Pathway analysis showed that variants in genes related to vasculogenesis (FDR=0.024), angiogenesis (FDR=0.019), and carotid artery disease (FDR=0.034) were related to risk for on-statin MACE. We identified six gene-variant networks that predicted odds of on-statin MACE. The most elevated risk was found in a small subset of patients carrying variants in COL4A2, TMEM178B, SZT2, and TBXAS1 (OR=4.53, p<0.001). Conclusions The RF-IFRS method is a viable method for interpreting complex "black-box" findings from machine-learning. In this study, it identified epistatic networks that could be applied to risk estimation for on-statin MACE. Further study will seek to replicate these findings in other populations.

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Prospective association of a genetic risk score with major adverse cardiovascular events in patients with coronary artery disease

Abstract: Supplemental Digital Content is available in the text

Cited by 13 publications

References 33 publications

Genetic Risk Score for Coronary Heart Disease: Review

Genetic Risk Score for Coronary Heart Disease: Review

Lipid metabolism genes and predisposition to ischemic heart disease

Genome Wide Epistasis Study of On-Statin Cardiovascular Events with Iterative Feature Reduction and Selection

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