Genetically Elevated Lipoprotein(a) and Increased Risk of Myocardial Infarction

Kamstrup, Pia R.

doi:10.1001/jama.2009.801

Cited by 1,090 publications

(798 citation statements)

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“…GENESIS‐PRAXY indicates GENdEr and Sex determInantS of cardiovascular disease: from bench to beyond‐Premature Acute Coronary Syndrome; Lp(a), lipoprotein(a); OR, odds ratio. P ‐value calculated by χ 2 test for continuous variables.aIn the Copenhagen General Population Study (CGPS) (N=5543), 20% of the population had elevated Lp(a) 2…”

Section: Resultsmentioning

confidence: 99%

“…aIn the Copenhagen General Population Study (CGPS) (N=5543), 20% of the population had elevated Lp(a) 2…”

Section: Resultsmentioning

confidence: 99%

“…High Lp(a) has been determined as the strongest independent genetic risk factor of CV disease,27, 28 and a causal role for circulating Lp(a) in cardiovascular events has been demonstrated by Mendelian randomization 2. Lp(a) has also been shown to be a potential causal factor for valve calcification and aortic stenosis in a large genome‐wide association study,3 and in several subsequent reports 29, 30.…”

Section: Discussionmentioning

confidence: 98%

“…Second, our study was cross‐sectional and may not fully consider the lifelong impact of elevations of both Lp(a) and LDL‐C on ACS risk. However, because Lp(a) levels are primarily genetically mediated, Lp(a) has been shown to remain constant over time 2. Third, use of the case‐only approach precludes reporting the direct association of Lp(a) or LDL‐C with MI; however, both of these lipid markers have been shown to be strongly associated with MI and cardiovascular events in large meta‐analyses and have recently been shown to be causal using Mendelian randomization.…”

Section: Discussionmentioning

confidence: 99%

“…Lp(a) has recently been confirmed as a causal factor for cardiovascular disease including myocardial infarction (MI)2 and aortic stenosis 3. To date, the appropriate management of high Lp(a) is not known as there are limited therapeutic options to directly lower Lp(a) 4.…”

Section: Introductionmentioning

confidence: 99%

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Lipoprotein(a) Interactions With Low‐Density Lipoprotein Cholesterol and Other Cardiovascular Risk Factors in Premature Acute Coronary Syndrome (ACS)

Afshar

Pilote

Dufresne

et al. 2016

JAHA

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BackgroundCurrent recommendations for lipoprotein(a) (Lp[a]) focus on the control of other risk factors, including lowering low‐density lipoprotein cholesterol (LDL‐C), with little evidence to support this approach. Identifying interactions between Lp(a) and other risk factors could identify individuals at increased risk for Lp(a)‐mediated disease.Methods and ResultsWe used a case‐only study design and included 939 participants (median age=49 years, interquartile range 46–53, women=33.1%) from the GENdEr and Sex determInantS of cardiovascular disease: from bench to beyond‐Premature Acute Coronary Syndrome (GENESIS‐PRAXY) study, a multicenter prospective cohort study of premature acute coronary syndrome. There was a higher prevalence of elevated Lp(a) levels (>50 mg/dL; 80th percentile) in PRAXY participants as compared to the general population (31% versus 20%; P<0.001). Lp(a) was strongly associated with LDL‐C (adjusted β 0.17; P<0.001). Individuals with high Lp(a) were more likely to have LDL‐C >2.5 mmol/L, indicating a synergistic interaction (adjusted odds ratio 1.51; 95% CI 1.08–2.09; P=0.015). The interaction with high Lp(a) was stronger at increasing LDL‐C levels (LDL‐C >3.5, adjusted odds ratio 1.87; LDL‐C >4.5, adjusted odds ratio 2.72). In a polytomous logistic model comparing mutually exclusive LDL‐C categories, the interaction with high Lp(a) became attenuated at LDL‐C ≤3.5 mmol/L (odds ratio 1.16; 95% CI 0.80–1.68, P=0.447). Other risk factors were not associated with high Lp(a).ConclusionsIn young acute coronary syndrome patients, high Lp(a) is more prevalent than in the general population and is strongly associated with high LDL‐C, suggesting that Lp(a) confers greater risk for acute coronary syndrome when LDL‐C is elevated. Individuals with high Lp(a) and LDL‐C >3.5 mmol/L may warrant aggressive LDL‐C lowering.

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