Lipoprotein(a): from Causality to Treatment

Kronenberg, Florian

doi:10.1007/s11883-024-01187-6

Cited by 12 publications

(2 citation statements)

References 54 publications

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“…Interestingly, PCSK9 R46L carriers were observed an allele-dependent lower effect on lipoprotein(a) (Lp(a)) levels versus non-carriers (9 mg/dL in heterozygote, 8 mg/dL in homozygous vs. 10 mg/dL in non-carriers). The application of results regarding the link among PCSK9, LDLR, and Lp(a) metabolism is questionable, especially since Lp(a) plasma levels differ among different ethnic groups [47][48][49].…”

Section: Loss-of-function Mutationsmentioning

confidence: 99%

PCSK9 and Lipid Metabolism: Genetic Variants, Current Therapies, and Cardiovascular Outcomes

Grejtakova,

Boronova,

Bernasovska

et al. 2024

Cardiovasc Drugs Ther

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Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a crucial role in the modulation of lipid metabolism as a critical negative regulator of hepatic low-density lipoprotein receptor (LDLR) levels and circulating low-density lipoprotein (LDL) clearance. Numerous gain-of-function (GOF) mutations in PCSK9 have been identified as causing familial hypercholesterolemia (FH) by reducing LDLR levels, and loss-of-function (LOF) mutations associated with a hypercholesterolemia phenotype protective against atherosclerosis. PCSK9 represents an example of successful translational research resulting in the identification of PCSK9 as a major drug target for a lipid-lowering therapy. To explore the genetic constitution of PCSK9 and its biologic role, in this review, we summarize the current evidence of clinically significant PCSK9 genetic variants involved in lipid metabolism as well as emphasize the importance of PCSK9 inhibition for the improvement of cardiovascular outcomes by conducting a meta-analysis of the available data on the incidence of cardiovascular disease events.

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Section: Loss-of-function Mutationsmentioning

confidence: 99%

PCSK9 and Lipid Metabolism: Genetic Variants, Current Therapies, and Cardiovascular Outcomes

Grejtakova,

Boronova,

Bernasovska

et al. 2024

Cardiovasc Drugs Ther

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“…Lipoprotein (a) [Lp(a)] is approximately 6-fold more atherogenic compared to low-density lipoprotein (LDL) on a per-particle basis [ 1 ]. Strong evidence has shown an independent, causal association between Lp(a) levels and atherosclerotic cardiovascular disease (ASCVD) [ 2 ]. Moreover, high Lp(a) levels are a risk factor for aortic valve calcification and stenosis [ 3 ].…”

mentioning

confidence: 99%

Lipoprotein (a) measurement: potential for personalized cardiovascular disease management in a patient with acute myocardial infarction

Zimodro,

Gąsecka,

Arski

et al. 2024

Arch Med Sci

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P r e p r i n tLipoprotein (a) [Lp(a)] is approximately 6-fold more atherogenic compared to low-density lipoprotein (LDL) on a per-particle basis [1]. Strong evidence has shown an independent, causal association between Lp(a) levels and atherosclerotic cardiovascular disease (ASCVD) [2]. Moreover, high Lp(a) levels are a risk factor for aortic valve calcification and stenosis [3]. Recommendations for the diagnosis and management of elevated Lp(a) levels have been recently published by experts from the Polish Cardiac Society and the Polish Lipid Association [4], following the European Atherosclerosis Society consensus statement (2022) [5]. Here, we describe how Lp(a) measurement allowed for personalized lipid-lowering therapy (LLT) in a very high-risk patient with acute myocardial infarction (MI).A 58-year-old male triathlete without prior medical history or medication use was referred to the cardiology department due to deteriorating anginal symptoms.Negative T waves in the inferior electrocardiographic leads (II, III, aVF), along with the elevated concentration of high-sensitivity cardiac troponin T (1564 pg/ml) in the initial measurement confirmed the diagnosis of non-ST-elevation MI. Immediate coronary angiography revealed a total occlusion in the proximal segment of the right coronary artery (RCA), followed by 80% stenosis in the left anterior descending artery (LAD), and 50% stenosis in the circumflex branch. Drug-eluting stents were implanted in the RCA and LAD with good angiographic results. Simultaneously, 12-month dual antiplatelet therapy was initiated. Further diagnostic workup showed mild aortic valve sclerosis with a peak velocity of 1.5 m/s, and bilateral atherosclerotic plaques in the carotid arteries with intima-media thickness of 0.68 mm and 1.04 mm on the left and right side, respectively. Lp(a) measurement was incorporated in the initial lipid profile, and hence, the LDL cholesterol (LDL-C) level of 132 mg/dl (3.41 mmol/l) and Lp(a) P r e p r i n t level of 90 mg/dl (225 nmol/l) were found. Other modifiable CVD risk factors were in the optimal range with blood pressure of 132/79 mmHg, heart rate of 50 beats per minute, body mass index of 21.4 kg/m 2 , and glycated hemoglobin of 5.4%, accompanied by no history of smoking, and negative family history.

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Exploring the Interplay between Diabetes and Lp(a): Implications for Cardiovascular Risk

Pablo,

Matías,

Lavalle Cobo

et al. 2024

Curr Diab Rep

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Lipoprotein(a): from Causality to Treatment

Cited by 12 publications

References 54 publications

PCSK9 and Lipid Metabolism: Genetic Variants, Current Therapies, and Cardiovascular Outcomes

PCSK9 and Lipid Metabolism: Genetic Variants, Current Therapies, and Cardiovascular Outcomes

Lipoprotein (a) measurement: potential for personalized cardiovascular disease management in a patient with acute myocardial infarction

Exploring the Interplay between Diabetes and Lp(a): Implications for Cardiovascular Risk

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