Repeat Measures of Lipoprotein(a) Molar Concentration and Cardiovascular Risk

Trinder, Mark; Paruchuri, Kaavya; Haidermota, Sara; Bernardo, Rachel; Zekavat, Seyedeh M.; Gilliland, Thomas; Januzzi, James L.; Natarajan, Pradeep

doi:10.1016/j.jacc.2021.11.055

Cited by 49 publications

(41 citation statements)

References 41 publications

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“…Our data support this notion that one measurement during the life is adequate to identify individuals at risk. This is in line with a recent investigation of repeated measurements in more than 15,000 participants of the UK Biobank which showed that a single measurement of Lp(a) is efficient to inform about the coronary artery disease risk [25]. Furthermore, we found that tracking was strong already from childhood and adolescence suggesting that measurements done in early life may reliably reflect the Lp(a) levels later in mid-adulthood.…”

Section: Discussionsupporting

confidence: 91%

“…Similarly, Routi et al [48] found a strong correlation between Lp(a) levels at 7 and 36 months of age (r = 0.88) in 430 children participating in the STRIP Study. In middle-aged adult population of the UK Biopank, the 4-year tracking of Lp(a) was r = 0.96 25 . Strong tracking reflects the fact that Lp(a) levels are genetically determined and not much influenced by extrinsic factors.…”

Section: Discussionmentioning

confidence: 97%

“…This is based on the current understanding that the levels remain largely stable throughout life because they are under strong genetic control. The stability or tracking of Lp(a) levels have previously been studied, both in children and adults [21][22][23][24][25]. These earlier results have shown that Lp(a) levels are stable, at least up to five years [24].…”

Section: Introductionmentioning

confidence: 99%

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Long-term tracking and population characteristics of lipoprotein (a) in the Cardiovascular Risk in Young Finns Study

Raitakari¹,

Kivelä²,

Pahkala³

et al. 2022

Atherosclerosis

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Long-term tracking and population characteristics of lipoprotein (a) in the Cardiovascular Risk in Young Finns Study

Raitakari¹,

Kivelä²,

Pahkala³

et al. 2022

Atherosclerosis

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“…[ 154 , 155 , 156 ] Until therapies that lower Lp(a) are proven to provide health benefits, a single accurate measure of Lp(a) may be sufficient to inform on CVD risk. [157] Statins are the most recommended drug treatment for hypercholesterolemia due to their cholesterol-lowering efficacy, safety, and ASCVD benefits supported by numerous cardiovascular outcomes trials. [93] “High intensity statins” (atorvastatin 40 - 80 mg or rosuvastatin 20 – 40 mg) may lower LDL-C ≥ 50%, and are often recommended as first-line therapy in patients with ASCVD or at high risk for ASCVD.…”

Section: Introductionmentioning

confidence: 99%

“…[ 154 , 155 , 156 ] Until therapies that lower Lp(a) are proven to provide health benefits, a single accurate measure of Lp(a) may be sufficient to inform on CVD risk. [157] …”

Section: Introductionmentioning

confidence: 99%

Ten things to know about ten cardiovascular disease risk factors – 2022

Bays

Kulkarni

German

et al. 2022

American Journal of Preventive Cardiology

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Lipoprotein(a) and its Significance in Cardiovascular Disease

2022

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ipoprotein(a) (Lp[a]) is a low-density lipoprotein (LDL) cholesterol-like particle that was first identified by Kåre Berg, MD, in 1963. 1 Its concentration is largely genetically determined, with marked variations across populations. 2 Epidemiologic and observational studies suggest a potential causal association between elevated Lp(a) and an increased risk of atherosclerotic cardiovascular disease (ASCVD) 3,4 and calcific aortic valve stenosis (AS). 5,6 These findings have been recently supported by genetic studies. 7,8 While no universally accepted absolute risk threshold exists, approximately 20% to 25% of the global population have an Lp(a) level of 50 mg/dL (to convert to milligrams per liter, multiply by 10) or greater, 2 which according to the European Atherosclerosis Society (EAS) confers an increased cardiovascular risk 9 despite traditional risk factor optimization. 10 This article aims to review Lp(a) biology and pathophysiology, data with current therapies, and novel therapies under development. Structure and MetabolismLp(a) assembly occurs either on the hepatocyte surface or in the space of Disse. Its core composition resembles LDL and consists of triglycerides and cholesteryl esters surrounded by an outer membrane of phospholipids and free cholesterol. Its protein moiety comprises a single copy of apolipoprotein B-100 (apoB) bound to a single apolipoprotein(a) (apo[a]) particle through covalent and noncovalent bonds (Figure 1). 11 Lp(a) synthesis is primarily determined through the LPA gene, which codes for 2 kringle domains (kringles IV-V [KIV-KV]). KIV expands into 10 subtypes (KIV 1 -KIV 10 ), while KV is attached to both KIV 10 and an inactive protease domain. Expansion of KIV 2 results in a variable intragenic copy number variation resulting in 1 to more than 40 identically repeated copies. This leads to heterogeneous apo(a) isoform sizes, a unique occurrence among proteins. The other KIV IMPORTANCE Lipoprotein(a) (Lp[a]) is a low-density lipoprotein (LDL) cholesterol-like particle bound to apolipoprotein(a). This novel marker of cardiovascular disease acts through induction of vascular inflammation, atherogenesis, calcification, and thrombosis. While an absolute risk threshold remains to be universally accepted, an estimated 20% to 25% of the global population have Lp(a) levels of 50 mg/dL or higher, a level noted by the European Atherosclerosis Society to confer increased cardiovascular risk.OBSERVATIONS Compelling evidence from pathophysiological, observational, and genetic studies suggest a potentially causal association between high Lp(a) levels, atherosclerotic cardiovascular disease, and calcific aortic valve stenosis. Additional evidence has demonstrated that elevated Lp(a) levels are associated with a residual cardiovascular risk despite traditional risk factor optimization, including LDL cholesterol reduction. These findings have led to the formulation of the Lp(a) hypothesis, namely that Lp(a) lowering leads to cardiovascular risk reduction, intensifying the search for Lp(a)-reducing...

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Repeat Measures of Lipoprotein(a) Molar Concentration and Cardiovascular Risk

Cited by 49 publications

References 41 publications

Long-term tracking and population characteristics of lipoprotein (a) in the Cardiovascular Risk in Young Finns Study

Long-term tracking and population characteristics of lipoprotein (a) in the Cardiovascular Risk in Young Finns Study

Ten things to know about ten cardiovascular disease risk factors – 2022

Lipoprotein(a) and its Significance in Cardiovascular Disease

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