Lipoprotein (a) and aortic valve calcium in South Asians compared to other race/ethnic groups

Makshood, Minhal; Joshi, Parag H.; Kanaya, Alka M.; Ayers, Colby; Budoff, Matthew J.; Tsai, Michael Y.; Blaha, Michael J.; Michos, Erin D.; Post, Wendy S.

doi:10.1016/j.atherosclerosis.2020.09.010

Cited by 17 publications

(5 citation statements)

References 29 publications

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“…41,42 For several SNPs that are in linkage disequilibrium with LPA allele sizes, the associations with Lp(a) levels in plasma differ between different ancestry groups. 43,44 Recently published data from diverse cohorts, such as the ARIC study (Atherosclerosis Risk in Communities), 45,46 the MESA study (Multi-Ethnic Study of Atherosclerosis), 47 and the MASALA study (Mediators of Atherosclerosis in South Asians Living in America), 48 link high plasma Lp(a) levels to increased ASCVD risk in various populations. However, there is large variability between studies in the methods used to measure Lp(a), making it difficult to compare findings across different populations.…”

Section: Determinants Of Plasma Lp(a) Levels: Genetics Production And...mentioning

confidence: 99%

Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association

Reyes‐Soffer¹,

Ginsberg²,

Berglund³

et al. 2022

ATVB

231

130

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High levels of lipoprotein(a) [Lp(a)], an apoB100-containing lipoprotein, are an independent and causal risk factor for atherosclerotic cardiovascular diseases through mechanisms associated with increased atherogenesis, inflammation, and thrombosis. Lp(a) is predominantly a monogenic cardiovascular risk determinant, with ≈70% to ≥90% of interindividual heterogeneity in levels being genetically determined. The 2 major protein components of Lp(a) particles are apoB100 and apolipoprotein(a). Lp(a) remains a risk factor for cardiovascular disease development even in the setting of effective reduction of plasma low-density lipoprotein cholesterol and apoB100. Despite its demonstrated contribution to atherosclerotic cardiovascular disease burden, we presently lack standardization and harmonization of assays, universal guidelines for diagnosing and providing risk assessment, and targeted treatments to lower Lp(a). There is a clinical need to understand the genetic and biological basis for variation in Lp(a) levels and its relationship to disease in different ancestry groups. This scientific statement capitalizes on the expertise of a diverse basic science and clinical workgroup to highlight the history, biology, pathophysiology, and emerging clinical evidence in the Lp(a) field. Herein, we address key knowledge gaps and future directions required to mitigate the atherosclerotic cardiovascular disease risk attributable to elevated Lp(a) levels.

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Section: Determinants Of Plasma Lp(a) Levels: Genetics Production And...mentioning

confidence: 99%

Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association

Reyes‐Soffer¹,

Ginsberg²,

Berglund³

et al. 2022

ATVB

231

130

View full text Add to dashboard Cite

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“…The association between Lp(a) and CAVD/AS appears similar between sexes and has been reported in individuals with bicuspid AV, and individuals with familial hypercholesterolaemia (FH) [32 ▪▪ ,37,38 ▪ ]. However, there may be differences among ethnicities; an association between Lp(a) and CAVD has been demonstrated in White and Black individuals but not in South Asians, Hispanic or Chinese individuals [32 ▪▪ ,39]. The ASCVD risk associated with Lp(a) may be modulated by inflammation, whereby Lp(a) is associated with ASCVD in individuals with elevated high-sensitivity C-reactive protein (CRP) levels (≥2 mg/l) [40 ▪ ].…”

Section: Reviewmentioning

confidence: 64%

Lipoprotein(a) and calcific aortic valve disease: current evidence and future directions

Lan,

Khan,

Watts

2023

Current Opinion in Clinical Nutrition &Amp; Metabolic Care

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Purpose of review Calcific aortic valve disease (CAVD), the most common cause of aortic stenosis (AS), is characterized by slowly progressive fibrocalcific remodelling of the valve cusps. Once symptomatic, severe AS is associated with poor survival unless surgical or transcatheter valve replacement is performed. Unfortunately, no pharmacological interventions have been demonstrated to alter the natural history of CAVD. Lipoprotein(a) [Lp(a)], a low-density lipoprotein-like particle, has been implicated in the pathophysiology of CAVD. Recent findings The mechanisms by which Lp(a) results in CAVD are not well understood. However, the oxidized phospholipids carried by Lp(a) are considered a crucial mediator of the disease process. An increasing number of studies demonstrate a causal association between plasma Lp(a) levels and frequency of AS and need for aortic valve replacement, which is independent of inflammation, as measured by plasma C-reactive protein levels. However, not all studies show an association between Lp(a) and increased progression of calcification in individuals with established CAVD. Summary Epidemiologic, genetic, and Mendelian randomization studies have collectively suggested that Lp(a) is a causal risk factor for CAVD. Whether Lp(a)-lowering can prevent initiation or slow progression of CAVD remains to be demonstrated.

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“…Instead, Makshood et al found that while South Asians from MASALA had lower Lp(a) levels than Black subjects from MESA, those Black subjects had a lower prevalence of aortic valve calcification. Additionally, while South Asians from MASALA had higher Lp(a) levels than White subjects from MESA, both groups had a similar prevalence of aortic valve calcification 21. Therefore, they believed the relationship between Lp(a) and aortic valve calcification is ‘likely multifactorial.’ Specifically, they hypothesised that ‘race specific factors’ might explain their findings, such as ‘racial/ethnic differences in the composition of Lp(a) particles or in Lp(a) associated factors.’ Their assumptions regarding ‘race-specific factors’ are highly speculative and may even be irresponsible if they further entrench beliefs about innate genetic or molecular features among South Asians compared with other populations.…”

Section: Resultsmentioning

confidence: 99%

Constructing a South Asian cardiovascular disease: a qualitative analysis on how researchers study cardiovascular disease in South Asians

Kawano

2022

J Med Ethics

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BackgroundDebates on the use of race in biomedical research have typically overlooked immigrant groups outside of the black-white racial dichotomy. Recent biomedical research on South Asians and cardiovascular disease provides an opportunity to understand how scientists define race and interpret racial health disparities from an underexamined perspective.PurposeTo examine how researchers in the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study defined a South Asian population, and then compared health differences between South Asians and other populations.MethodsQualitative content analysis was performed on eleven articles from August 2013 to January 2021 that directly compared the South Asian cohort in MASALA to four other groups. The MASALA study design article was also included in this analysis. Articles were analysed for how South Asians were defined, and for how health differences between South Asians and other populations were studied and discussed.ResultsResearchers in MASALA were neither clear nor precise in defining South Asians as either an ancestral group or ethnic group. Their studies also prioritised investigating genetic and molecular causes of the cardiovascular health disparity between South Asians and other populations and failed to examine possible social factors.ConclusionsThese findings reflect a broader trend in biomedical research in which race and racial health disparities are poorly defined and studied, limiting scientists’ understanding of the relationship between race and health. I propose methodologies to help researchers define populations and design studies without relying on biologically reductive assumptions.

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Lipoprotein (a) and aortic valve calcium in South Asians compared to other race/ethnic groups

Cited by 17 publications

References 29 publications

Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association

Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association

Lipoprotein(a) and calcific aortic valve disease: current evidence and future directions

Constructing a South Asian cardiovascular disease: a qualitative analysis on how researchers study cardiovascular disease in South Asians

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