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Lipoprotein(a) as a novel therapeutic target for preventing cardiovascular disease: A whiter shade of pale?
Lp(a) como um novo alvo terapêutico na prevenção da doença cardiovascular: uma luz ao fundo do túnel?
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"tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "495" "paginaFinal" => "496" ] ] "autores" => array:1 [ 0 => array:3 [ "autoresLista" => "Manuela Fiuza" "autores" => array:1 [ 0 => array:4 [ "nombre" => "Manuela" "apellidos" => "Fiuza" "email" => array:1 [ 0 => "manuela.fiuza@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Serviço de Cardiologia do CHULN, Lisboa, Portugal" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Faculdade de Medicina de Lisboa, Lisboa, Portugal" "etiqueta" => "b" "identificador" => "aff0010" ] ] ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Lp(a) como um novo alvo terapêutico na prevenção da doença cardiovascular: uma luz ao fundo do túnel?" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Research on the importance of lipoprotein(a) [Lp(a)] gained new momentum when it became a potential therapeutic target. Our understanding of this mysterious circulating lipoprotein particle has undergone advances and setbacks since its discovery in 1963 by Kåre Berg's group.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Lp(a) is composed of liver-derived apolipoprotein A and apolipoprotein B-100, and has a similar structure to both low-density lipoprotein cholesterol (LDL-C) and plasminogen. Lp(a) thus has a proatherogenic and a prothrombotic component, and is associated with the pathogenesis of cardiovascular disease (CVD).</p><p id="par0015" class="elsevierStylePara elsevierViewall">Findings from epidemiological, genetic and clinical studies<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">2–4</span></a> have provided compelling evidence establishing Lp(a) as a marker of increased CVD risk in both primary and secondary prevention, including myocardial infarction (MI), stroke, and calcific aortic valve disease (CAVD).</p><p id="par0020" class="elsevierStylePara elsevierViewall">However, significant gaps in knowledge remain about the biology and pathophysiology of Lp(a). To address these gaps, a National Heart, Lung, and Blood Institute working group identified several challenges to fully understand the role of Lp(a) in CVD/CAVD.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">5</span></a> These include its metabolism and pathophysiological mechanisms, how to measure it, current and emerging therapies for elevated Lp(a), and identification of patients at high Lp(a)-mediated risk.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Joaquim Menezes-Brandão carried out a single-center retrospective observational study, published in this issue of the <span class="elsevierStyleItalic">Journal</span>,<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">6</span></a> of 516 patients (224 male; 292 female; 98.6% Caucasian) with at least two cardiovascular risk factors who regularly attended outpatient consultations at a cardiovascular risk and metabolism clinic for primary prevention. The aim was to analyze the effect of combined standard pharmacological therapy along with lifestyle interventions for managing Lp(a) levels in patients at high cardiovascular risk but who had not suffered major adverse cardiovascular events. The patients were followed for a mean of 11.35±4.32 years.</p><p id="par0030" class="elsevierStylePara elsevierViewall">The results show that, in this well-controlled population under different drug therapies (statins, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, oral antidiabetics, antiplatelets, calcium channel blockers and allopurinol) there was a reduction in Lp(a) values during the follow-up period.</p><p id="par0035" class="elsevierStylePara elsevierViewall">There was also a significant association between Lp(a) and cardiovascular risk scores in patients with high vascular risk. In a previous work in the same population,<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">7</span></a> the author reported that increased Lp(a) levels were also strongly associated with cardiovascular risk factors, such as carotid intima-media thickness, LDL-C and homocysteine, as well as with non-alcoholic hepatic steatosis.</p><p id="par0040" class="elsevierStylePara elsevierViewall">This study points to the need to measure Lp(a) in routine assessment of at-risk patients, because as a marker of cardiovascular risk, Lp(a) should be recognized as a therapeutic target. It may be useful to initiate combined drug therapies and to promote healthy lifestyles in primary prevention, targeting various cardiovascular risk factors, in order to delay the atherosclerotic process.</p><p id="par0045" class="elsevierStylePara elsevierViewall">These results may lead to better identification of target populations who will benefit most from Lp(a)-lowering therapies.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Several other studies have addressed this question. Among them, the BiomarCaRE project<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">8</span></a> confirmed Lp(a) as a marker of cardiovascular risk in the European population, demonstrating increased cardiovascular risk for Lp(a) >50 mg/dl, which is in line with the target level of <50 mg/dl recommended by the guidelines. Further, it showed a north-south gradient of Lp(a) levels across Europe, with lower levels in northern European cohorts.</p><p id="par0055" class="elsevierStylePara elsevierViewall">Another study in different ethnic groups worldwide also showed that high Lp(a) concentrations (>50 mg/dl) were associated with significantly increased risk of MI in all populations except Arabs and Africans.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">9</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Nevertheless, Lp(a) is not routinely tested in clinical practice, and there is a widespread lack of awareness of its role in accelerating atherosclerotic CVD.</p><p id="par0065" class="elsevierStylePara elsevierViewall">Which patient groups should be screened for Lp(a)? The European Atherosclerosis Society Consensus Panel<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">10</span></a> recommends that Lp(a) should be measured in patients with intermediate or high risk for CVD or coronary heart disease (CHD). In particular, those patients presenting with (i) premature CVD, (ii) familial hypercholesterolemia, (iii) a family history of premature CVD and/or elevated Lp(a), (iv) recurrent CVD despite statin treatment, (v) 3% 10-year risk of fatal CVD according to the European guidelines<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">11</span></a> and (vi) 10% 10-year risk of fatal and/or non-fatal CHD according to the US guidelines. The measurement needs to be taken only once per patient life, and repeated measurements of Lp(a) are only indicated if a treatment for elevated Lp(a) levels is initiated in order to monitor therapeutic response.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">12</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Screening for elevated Lp(a) will enable standard preventative measures to be introduced, including optimal control of blood pressure, diabetes and LDL-C levels and smoking cessation, and in the future the use of novel therapies that effectively lower Lp(a). Several agents are currently in development to lower Lp(a), such as proprotein convertase subtilisin/kexin type 9 inhibitors, antisense oligonucleotides targeting apolipoprotein B, and microsomal triglyceride transfer protein inhibitors.<a class="elsevierStyleCrossRefs" href="#bib0135"><span class="elsevierStyleSup">13–15</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Early detection and intervention, preferably before the onset of atherosclerotic CVD, offers the best opportunity to reduce the time-dependent risk associated with this important cardiovascular risk factor. However, it should not be forgotten that there is to date no strong clinical evidence that lowering Lp(a) has any beneficial effects in preventing cardiovascular disease.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0080" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Conflicts of interest" ] 1 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:15 [ 0 => array:3 [ "identificador" => "bib0075" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "A new serum type system in man: the LP system" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "K. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 5 | 3 | 8 |
| 2024 October | 44 | 25 | 69 |
| 2024 September | 43 | 29 | 72 |
| 2024 August | 37 | 26 | 63 |
| 2024 July | 37 | 32 | 69 |
| 2024 June | 26 | 21 | 47 |
| 2024 May | 34 | 17 | 51 |
| 2024 April | 22 | 28 | 50 |
| 2024 March | 35 | 25 | 60 |
| 2024 February | 29 | 21 | 50 |
| 2024 January | 32 | 20 | 52 |
| 2023 December | 24 | 22 | 46 |
| 2023 November | 33 | 39 | 72 |
| 2023 October | 18 | 11 | 29 |
| 2023 September | 24 | 19 | 43 |
| 2023 August | 24 | 11 | 35 |
| 2023 July | 17 | 18 | 35 |
| 2023 June | 21 | 13 | 34 |
| 2023 May | 38 | 27 | 65 |
| 2023 April | 20 | 6 | 26 |
| 2023 March | 44 | 23 | 67 |
| 2023 February | 32 | 24 | 56 |
| 2023 January | 22 | 23 | 45 |
| 2022 December | 42 | 30 | 72 |
| 2022 November | 44 | 22 | 66 |
| 2022 October | 38 | 34 | 72 |
| 2022 September | 18 | 43 | 61 |
| 2022 August | 25 | 38 | 63 |
| 2022 July | 24 | 38 | 62 |
| 2022 June | 19 | 39 | 58 |
| 2022 May | 29 | 23 | 52 |
| 2022 April | 21 | 35 | 56 |
| 2022 March | 22 | 43 | 65 |
| 2022 February | 36 | 37 | 73 |
| 2022 January | 36 | 30 | 66 |
| 2021 December | 28 | 37 | 65 |
| 2021 November | 34 | 38 | 72 |
| 2021 October | 30 | 56 | 86 |
| 2021 September | 25 | 35 | 60 |
| 2021 August | 27 | 41 | 68 |
| 2021 July | 24 | 24 | 48 |
| 2021 June | 23 | 21 | 44 |
| 2021 May | 32 | 46 | 78 |
| 2021 April | 51 | 31 | 82 |
| 2021 March | 21 | 22 | 43 |
| 2021 February | 28 | 20 | 48 |
| 2021 January | 28 | 18 | 46 |
| 2020 December | 22 | 3 | 25 |
| 2020 November | 24 | 18 | 42 |
| 2020 October | 21 | 12 | 33 |
| 2020 September | 15 | 10 | 25 |
| 2020 August | 7 | 11 | 18 |
| 2020 July | 11 | 9 | 20 |
| 2020 June | 22 | 14 | 36 |
| 2020 May | 12 | 9 | 21 |
| 2020 April | 9 | 6 | 15 |
| 2020 March | 15 | 12 | 27 |
| 2020 February | 24 | 19 | 43 |
| 2020 January | 8 | 7 | 15 |
| 2019 December | 48 | 11 | 59 |
| 2019 November | 51 | 11 | 62 |
| 2019 October | 59 | 21 | 80 |
| 2019 September | 5 | 2 | 7 |
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