Genetically elevated lipoprotein(a) and increased risk of myocardial infarction.

By P. Kamstrup, A. Tybjaerg-hansen, R. Steffensen, Børge G. Nordestgaard. Journal of the American Medical Association (JAMA), 2009

1,305 citations recorded by the source corpus.

Subfields: Cancer Research, Endocrinology, Diabetes and Metabolism, Surgery

View Paper: https://www.semanticscholar.org/paper/aa6673e551c2243945f2afc25cb569b9570cb5be

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Citations in the corpus

Mendelian Randomization Analysis With Multiple Genetic Variants Using Summarized Data (2013, methodology): “It has recently been used to strengthen the evidence for causal roles in coronary heart disease of interleukin-6 [Swerdlow et al., 2012] and lipoprotein(a) [Kamstrup et al., 2009].”
Triglyceride-Rich Lipoproteins and Atherosclerotic Cardiovascular Disease: New Insights From Epidemiology, Genetics, and Biology. (2016, positive): “Importantly, when the effect size for the causal estimate is much larger than the observational for the same increase in a lipoprotein, then this represents additional strong evidence for a causal life-long exposure, exactly as observed for high lipoprotein(a) levels and increased risk of MI.(65) Fo”
A Test in Context: Lipoprotein(a): Diagnosis, Prognosis, Controversies, and Emerging Therapies. (2017, positive): “In contrast, genetic studies, which reflect life-long elevated Lp(a) and less confounding by the multiple heterogeneous limitations in meta-analyses, show a more potent and linear risk, with odds ratios as high as 4 relative to subjects with low levels (27,30).”
Using published data in Mendelian randomization: a blueprint for efficient identification of causal risk factors (2015, background): “Evidence from Mendelian randomization has been used to prioritize investigation of certain biomarkers as causal risk factors for cardiovascular disease: for example lipoprotein(a) [7], and interleukin-6 receptor [8]; and to de-prioritize others: fibrinogen [9], C-reactive protein (CRP) [10], and uri”
Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points—a joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Med (2016, background): “Este factor de riesgo cardiovascular genético causal (11)(22) debe medirse al menos una vez en todos los pacientes evaluados para detectar riesgo cardiovascular (11); hay que destacar que en cualquier individuo las concentraciones de Lp(a) varían poco con el tiempo (<10%).”
Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease (2013, background): “a well-established causal risk factor for cardiovascular disease irrespective of LDL cholesterol concentration.(29,30) Elevated Lp(a) is Figure 6 Overlap of clinical and mutation diagnosis of heterozygous familial hypercholesterolaemia.”
Distribution and Medical Impact of Loss-of-Function Variants in the Finnish Founder Population (2014, background): “In addition to a strong correlation between circulating lipoprotein(a) levels and cardiovascular disease, it has been previously reported that genetic variants that elevate circulating lipoprotein(a) levels are cardiovascular risk factors [22,23].”
2016 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in the Adult. (2016, background): “The Copenhagen Heart Study determined the risk of MI according to Lp(a) concentrations in the general population including 7524 subjects followed for 17 years.(53) Subjects with an Lp(a) concentration between 30 and 76 mg/dL had a 1.”
Lipoprotein(a) as a cardiovascular risk factor: current status (2010, methodology): “The significant similar trend tests in three separate studies all point to increased CVD risk when the number of kringles is low and thus plasma levels of Lp(a) elevated.(2)”