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Lipoprotein(a) and Cardiovascular Diseases ― Revisited
Circulation Journal, 2020/05/25, Vol.84(6), pp.867-874
[Peer Reviewed Journal]
2020 THE JAPANESE CIRCULATION SOCIETY ;ISSN: 1346-9843 ;EISSN: 1347-4820 ;DOI: 10.1253/circj.CJ-20-0051 ;PMID: 32336721
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Title:
Lipoprotein(a) and Cardiovascular Diseases ― Revisited
Author:
Jang, Albert Youngwoo
;
Han, Seung Hwan
;
Sohn, Il Suk
;
Oh, Pyung Chun
;
Koh, Kwang Kon
Subjects:
Animals
;
Atherothrombotic traits
;
Biomarkers - blood
;
Cardiovascular diseases
;
Cardiovascular Diseases - etiology
;
Cardiovascular Diseases - genetics
;
Cardiovascular Diseases - prevention & control
;
Dyslipidemias - blood
;
Dyslipidemias - complications
;
Dyslipidemias - drug therapy
;
Dyslipidemias - genetics
;
Humans
;
Hypolipidemic Agents - therapeutic use
;
Lipoprotein(a)
;
Lipoprotein(a) - blood
;
Lipoprotein(a) - genetics
;
Prognosis
;
Residual risk
;
Risk Factors
;
Up-Regulation
Is Part Of:
Circulation Journal, 2020/05/25, Vol.84(6), pp.867-874
Description:
Two decades ago, it was recognized that lipoprotein(a) (Lp(a)) concentrations were elevated in patients with cardiovascular disease (CVD). However, the importance of Lp(a) was not strongly established due to a lack of both Lp(a)-lowering therapy and evidence that reducing Lp(a) levels improves CVD risk. Recent advances in clinical and genetic research have revealed the crucial role of Lp(a) in the pathogenesis of CVD. Mendelian randomization studies have shown that Lp(a) concentrations are causal for different CVDs, including coronary artery disease, calcified aortic valve disease, stroke, and heart failure, despite optimal low-density lipoprotein cholesterol (LDL-C) management. Lp(a) consists of apolipoprotein (apo) B100 covalently bound to apoA. Thus, Lp(a) has atherothrombotic traits of both apoB (from LDL) and apoA (thrombo-inflammatory aspects). Although conventional pharmacological therapies, such as statin, niacin, and cholesteryl ester transfer protein, have failed to significantly reduce Lp(a) levels, emerging new therapeutic strategies using proprotein convertase subtilisin-kexin type 9 inhibitors or antisesnse oligonucleotide technology have shown promising results in effectively lowering Lp(a). In this review we discuss the revisited important role of L(a) and strategies to overcome residual risk in the statin era.
Publisher:
Japan: The Japanese Circulation Society
Language:
English
Identifier:
ISSN: 1346-9843
EISSN: 1347-4820
DOI: 10.1253/circj.CJ-20-0051
PMID: 32336721
Source:
Geneva Foundation Free Medical Journals at publisher websites
MEDLINE
Alma/SFX Local Collection
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