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as most people eat regularly throughout the day&#44; non-fasting lipids may be a better indicator of mean lipid concentrations in the blood&#44; and individuals are exposed to post-prandial TG most of the time&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">1&#44;2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Genome-wide association studies &#40;GWAS&#41; have also found a causal association between TG and CVD&#46; Mutations in at least six different genes including <span class="elsevierStyleItalic">APOC2</span>&#44; <span class="elsevierStyleItalic">APOA5</span>&#44; <span class="elsevierStyleItalic">LMF1</span>&#44; <span class="elsevierStyleItalic">GPIHBP1</span>&#44; and <span class="elsevierStyleItalic">GPD1</span> can substantially increase TG and are identified as monogenic disorders&#46; Some GWAS have clearly linked high TG with increased CV risk&#44; and conversely a significantly reduced risk for ischemic CVD has been found with genetically reduced TG&#46; The main TG-metabolizing enzyme is lipoprotein lipase &#40;LPL&#41;&#44; the function of which is modulated by apolipoproteins A-V &#40;APOA5&#41; and C-III&#46; In this regard&#44; studies have found relative risk reductions of 24&#37; and 46&#37; in ischemic CVD for APOA5 and LPL gain-of-function mutations&#44; respectively &#40;with corresponding reductions of 35-36&#37; in non-fasting TG&#41;&#44; compared with non-TG-reducing alleles&#46;<a class="elsevierStyleCrossRefs" href="#bib0140"><span class="elsevierStyleSup">3&#8211;6</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">No large-scale randomized trials have directly examined the effect of reducing TG on CV risk in people with raised TG&#46; Thus&#44; only secondary subgroup analyses from other trials have been used to assess CV risk in patients with high TG&#44; with or without low HDL-C&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">2</span></a> The question is whether lowering TG reduces CV risk in clinical trials&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The Scandinavian Simvastatin Survival Study &#40;4S&#41; and Cholesterol and Recurrent Events &#40;CARE&#41; found a greater CV risk reduction in high TG subgroups with statin therapy&#46; By contrast&#44; in the Long-Term Intervention with Pravastatin in Ischaemic Disease &#40;LIPID&#41; trial&#44; the Heart Protection Study and the West of Scotland Coronary Prevention Study &#40;WOSCOPS&#41;&#44; CVD reductions were similar across all baseline TG levels&#44; and the Anglo-Scandinavian Cardiac Outcome Trial &#40;ASCOT&#41; actually found higher CVD reduction in those without the features of metabolic syndrome&#46; The LIPID study found an 11&#37; decrease in CV risk &#40;14&#37; after adjustment for other risk factors&#41; with each 1 mmol&#47;l decrease in TG with pravastatin&#44; and in the Pravastatin or Atorvastatin Evaluation and Infection Therapy&#58; Thrombolysis in Myocardial Infarction &#40;PROVE IT-TIMI&#41; trial&#44; each 10 mg&#47;dl decrease in on-treatment TG level was associated with a 1&#46;8&#37; reduction in CVD &#40;1&#46;4&#37; after adjustment for other risk factors&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">7&#8211;16</span></a> There are conflicting data concerning the relationship between fibrate therapy and CVD&#46; The Helsinki Heart Study &#40;HHS&#41; &#40;gemfibrozil monotherapy in primary prevention&#41; and the Veterans Affairs HDL Intervention Trial &#40;VA-HIT&#41; &#40;gemfibrozil monotherapy in secondary prevention&#41; found a significant benefit in CV outcomes&#46; However&#44; the Bezafibrate Infarction Prevention trial and others failed to show any significant CVD reduction in secondary prevention in monotherapy&#46; In two trials with fenofibrate in combination with statins&#44; Fenofibrate Intervention and Event Lowering in Diabetes &#40;FIELD&#41; and Action to Control Cardiovascular Risk in Diabetes &#40;ACCORD Lipid&#41;&#44; the benefit was only observed in subgroups with increased baseline TG and low HDL&#46;<a class="elsevierStyleCrossRefs" href="#bib0210"><span class="elsevierStyleSup">17&#8211;20</span></a> On the other hand&#44; for secondary prevention in patients with established CVD or with diabetes and other risk factors and with fasting TG of 135-499 mg&#47;dl&#44; icosapent ethyl reduced the risk of ischemic events&#44; including CV death&#46;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">21</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">While there is still controversy concerning the relationship between TG and CVD&#44; the value of non-HDL-C as a CV risk factor is universally accepted&#46; Non-HDL-C is defined as all the cholesterol present in potentially atherogenic lipoprotein particles that include very-low-density cholesterol&#44; intermediate-density cholesterol&#44; lipoprotein&#40;a&#41;&#44; and low-density lipoprotein cholesterol &#40;LDL-C&#41;&#46; Non-HDL-C is therefore sometimes considered an even better marker than LDL-C&#46; Measurement of non-HDL-C has the advantage of not requiring fasting&#44; and is more practical&#44; reliable&#44; and inexpensive than assessment of other lipid fractions&#46; Non-HDL-C is thus potentially an important risk marker&#44; particularly in patients with diabetes&#44; metabolic syndrome or obesity&#59; the UK National Institute of Health and Care Excellence considers non-HDL-C a better CVD risk indicator than LDL-C&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In some cases&#44; even with the maximum dose of more potent statins&#44; associated with ezetimibe and proprotein convertase subtilisin&#47;kexin type 9 &#40;PCSK-9&#41; inhibitors&#44; a significant CV risk remains&#44; known as residual risk&#46; It is consensual that non-HDL-C&#44; given its relationship with TG-rich remnant lipoproteins&#44; is one of the main causes of this residual risk&#46; When high non-HDL-C is associated with low HDL-C and high levels of TG and small dense LDL particles&#44; this phenotype&#44; which is characteristic of diabetes&#44; metabolic syndrome and obesity&#44; is known as atherogenic dyslipidemia&#46;<a class="elsevierStyleCrossRefs" href="#bib0135"><span class="elsevierStyleSup">2&#44;22</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The current issue of the <span class="elsevierStyleItalic">Journal</span> sees the publication of a multidisciplinary consensus among Portuguese experts on the definition&#44; detection and management of atherogenic dyslipidemia&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">23</span></a> In the CODAP study&#44; a questionnaire was applied to an expert panel composed of specialists in internal medicine&#44; endocrinology&#44; cardiology and family and general medicine&#44; following a modified Delphi methodology&#46; The panel acknowledged the importance of the atherogenic dyslipidemia phenotype and the role played by LDL-C and HDL-C as risk markers and therapeutic targets&#46; Around 72&#37; of the participants considered that non-HDL-C is a better risk marker for atherogenic dyslipidemia than LDL-C&#46; By contrast&#44; there was no consensus on the role played by TG in CV risk and the therapeutic value of fibrates&#46; So&#44; is the role of TG as a CV risk factor still in doubt&#63; We do not believe this to be the case&#46; Recent studies have shown that high TG levels &#40;200-600 mg&#47;dl&#41; are associated with high levels of remnant lipoproteins and with significant CV risk&#46;<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">24</span></a> In a substudy of the Copenhagen General Population Study that included 58 547 individuals aged 40-65 years and free of atherosclerotic CVD&#44; diabetes&#44; and statin use at baseline&#44; 14&#37; were definitely statin eligible&#44; 7&#37; were not eligible and had TG&#8805;264 mg&#47;&#47;l&#44; and 79&#37; were not statin eligible and had TG&#60;264 mg&#47;l&#46; The estimated 10-year risk of major adverse cardiovascular events was 2&#46;8&#37; and 5&#46;7&#37; in statin non-eligible individuals with TG &#60;264 mg&#47;l and &#8805;264 mg&#47;l&#44; respectively&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">25</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">The authors of the CODAP study conclude that in patients at high or very high cardiovascular risk and atherogenic dyslipidemia&#44; after LDL-C targets have been achieved with a statin&#44; fenofibrate should be associated&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">23</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Does lowering triglycerides reduce cardiovascular risk?
Será que a diminuição dos triglicéridos reduz o risco cardiovascular?
José Pereira de Mouraa,b,c
a AHG de Medicina Interna, Centro Hospitalar Universitário de Coimbra, Coimbra, Portugal
b Consulta de Aterosclerose do Serviço de Medicina Interna, Centro Hospitalar Universitário de Coimbra, Coimbra, Portugal
c Professor Convidado da Faculdade de Medicina da Universidade de Coimbra, Coimbra, Portugal
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Triglycerides &#40;TG&#41; have long been the ugly duckling of lipidology&#46; The relationship between TG and cardiovascular &#40;CV&#41; risk has been fraught with multiple issues&#58; from the variability of TG levels&#44; to their inverse association with high-density lipoprotein cholesterol &#40;HDL-C&#41; and whether to measure them in a fasting or non-fasting state&#46; Many large studies have found a significant association between TG and cardiovascular disease &#40;CVD&#41;&#46; The Paris Prospective Study&#44; the Lipid Research Clinics Follow-up Study&#44; the Reykjavik study&#44; and the European Prospective Investigation of Cancer &#40;EPIC Norfolk&#41; study showed a relationship between TG levels and CVD&#44; while the Multiple Risk Factor Intervention Trial&#44; the Copenhagen City Heart Study&#44; the Copenhagen General Population Study and the Women&#39;s Health Study found an even stronger relationship between non-fasting TG levels and CVD&#59; as most people eat regularly throughout the day&#44; non-fasting lipids may be a better indicator of mean lipid concentrations in the blood&#44; and individuals are exposed to post-prandial TG most of the time&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">1&#44;2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Genome-wide association studies &#40;GWAS&#41; have also found a causal association between TG and CVD&#46; Mutations in at least six different genes including <span class="elsevierStyleItalic">APOC2</span>&#44; <span class="elsevierStyleItalic">APOA5</span>&#44; <span class="elsevierStyleItalic">LMF1</span>&#44; <span class="elsevierStyleItalic">GPIHBP1</span>&#44; and <span class="elsevierStyleItalic">GPD1</span> can substantially increase TG and are identified as monogenic disorders&#46; Some GWAS have clearly linked high TG with increased CV risk&#44; and conversely a significantly reduced risk for ischemic CVD has been found with genetically reduced TG&#46; The main TG-metabolizing enzyme is lipoprotein lipase &#40;LPL&#41;&#44; the function of which is modulated by apolipoproteins A-V &#40;APOA5&#41; and C-III&#46; In this regard&#44; studies have found relative risk reductions of 24&#37; and 46&#37; in ischemic CVD for APOA5 and LPL gain-of-function mutations&#44; respectively &#40;with corresponding reductions of 35-36&#37; in non-fasting TG&#41;&#44; compared with non-TG-reducing alleles&#46;<a class="elsevierStyleCrossRefs" href="#bib0140"><span class="elsevierStyleSup">3&#8211;6</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">No large-scale randomized trials have directly examined the effect of reducing TG on CV risk in people with raised TG&#46; Thus&#44; only secondary subgroup analyses from other trials have been used to assess CV risk in patients with high TG&#44; with or without low HDL-C&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">2</span></a> The question is whether lowering TG reduces CV risk in clinical trials&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The Scandinavian Simvastatin Survival Study &#40;4S&#41; and Cholesterol and Recurrent Events &#40;CARE&#41; found a greater CV risk reduction in high TG subgroups with statin therapy&#46; By contrast&#44; in the Long-Term Intervention with Pravastatin in Ischaemic Disease &#40;LIPID&#41; trial&#44; the Heart Protection Study and the West of Scotland Coronary Prevention Study &#40;WOSCOPS&#41;&#44; CVD reductions were similar across all baseline TG levels&#44; and the Anglo-Scandinavian Cardiac Outcome Trial &#40;ASCOT&#41; actually found higher CVD reduction in those without the features of metabolic syndrome&#46; The LIPID study found an 11&#37; decrease in CV risk &#40;14&#37; after adjustment for other risk factors&#41; with each 1 mmol&#47;l decrease in TG with pravastatin&#44; and in the Pravastatin or Atorvastatin Evaluation and Infection Therapy&#58; Thrombolysis in Myocardial Infarction &#40;PROVE IT-TIMI&#41; trial&#44; each 10 mg&#47;dl decrease in on-treatment TG level was associated with a 1&#46;8&#37; reduction in CVD &#40;1&#46;4&#37; after adjustment for other risk factors&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">7&#8211;16</span></a> There are conflicting data concerning the relationship between fibrate therapy and CVD&#46; The Helsinki Heart Study &#40;HHS&#41; &#40;gemfibrozil monotherapy in primary prevention&#41; and the Veterans Affairs HDL Intervention Trial &#40;VA-HIT&#41; &#40;gemfibrozil monotherapy in secondary prevention&#41; found a significant benefit in CV outcomes&#46; However&#44; the Bezafibrate Infarction Prevention trial and others failed to show any significant CVD reduction in secondary prevention in monotherapy&#46; In two trials with fenofibrate in combination with statins&#44; Fenofibrate Intervention and Event Lowering in Diabetes &#40;FIELD&#41; and Action to Control Cardiovascular Risk in Diabetes &#40;ACCORD Lipid&#41;&#44; the benefit was only observed in subgroups with increased baseline TG and low HDL&#46;<a class="elsevierStyleCrossRefs" href="#bib0210"><span class="elsevierStyleSup">17&#8211;20</span></a> On the other hand&#44; for secondary prevention in patients with established CVD or with diabetes and other risk factors and with fasting TG of 135-499 mg&#47;dl&#44; icosapent ethyl reduced the risk of ischemic events&#44; including CV death&#46;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">21</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">While there is still controversy concerning the relationship between TG and CVD&#44; the value of non-HDL-C as a CV risk factor is universally accepted&#46; Non-HDL-C is defined as all the cholesterol present in potentially atherogenic lipoprotein particles that include very-low-density cholesterol&#44; intermediate-density cholesterol&#44; lipoprotein&#40;a&#41;&#44; and low-density lipoprotein cholesterol &#40;LDL-C&#41;&#46; Non-HDL-C is therefore sometimes considered an even better marker than LDL-C&#46; Measurement of non-HDL-C has the advantage of not requiring fasting&#44; and is more practical&#44; reliable&#44; and inexpensive than assessment of other lipid fractions&#46; Non-HDL-C is thus potentially an important risk marker&#44; particularly in patients with diabetes&#44; metabolic syndrome or obesity&#59; the UK National Institute of Health and Care Excellence considers non-HDL-C a better CVD risk indicator than LDL-C&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In some cases&#44; even with the maximum dose of more potent statins&#44; associated with ezetimibe and proprotein convertase subtilisin&#47;kexin type 9 &#40;PCSK-9&#41; inhibitors&#44; a significant CV risk remains&#44; known as residual risk&#46; It is consensual that non-HDL-C&#44; given its relationship with TG-rich remnant lipoproteins&#44; is one of the main causes of this residual risk&#46; When high non-HDL-C is associated with low HDL-C and high levels of TG and small dense LDL particles&#44; this phenotype&#44; which is characteristic of diabetes&#44; metabolic syndrome and obesity&#44; is known as atherogenic dyslipidemia&#46;<a class="elsevierStyleCrossRefs" href="#bib0135"><span class="elsevierStyleSup">2&#44;22</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The current issue of the <span class="elsevierStyleItalic">Journal</span> sees the publication of a multidisciplinary consensus among Portuguese experts on the definition&#44; detection and management of atherogenic dyslipidemia&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">23</span></a> In the CODAP study&#44; a questionnaire was applied to an expert panel composed of specialists in internal medicine&#44; endocrinology&#44; cardiology and family and general medicine&#44; following a modified Delphi methodology&#46; The panel acknowledged the importance of the atherogenic dyslipidemia phenotype and the role played by LDL-C and HDL-C as risk markers and therapeutic targets&#46; Around 72&#37; of the participants considered that non-HDL-C is a better risk marker for atherogenic dyslipidemia than LDL-C&#46; By contrast&#44; there was no consensus on the role played by TG in CV risk and the therapeutic value of fibrates&#46; So&#44; is the role of TG as a CV risk factor still in doubt&#63; We do not believe this to be the case&#46; Recent studies have shown that high TG levels &#40;200-600 mg&#47;dl&#41; are associated with high levels of remnant lipoproteins and with significant CV risk&#46;<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">24</span></a> In a substudy of the Copenhagen General Population Study that included 58 547 individuals aged 40-65 years and free of atherosclerotic CVD&#44; diabetes&#44; and statin use at baseline&#44; 14&#37; were definitely statin eligible&#44; 7&#37; were not eligible and had TG&#8805;264 mg&#47;&#47;l&#44; and 79&#37; were not statin eligible and had TG&#60;264 mg&#47;l&#46; The estimated 10-year risk of major adverse cardiovascular events was 2&#46;8&#37; and 5&#46;7&#37; in statin non-eligible individuals with TG &#60;264 mg&#47;l and &#8805;264 mg&#47;l&#44; respectively&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">25</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">The authors of the CODAP study conclude that in patients at high or very high cardiovascular risk and atherogenic dyslipidemia&#44; after LDL-C targets have been achieved with a statin&#44; fenofibrate should be associated&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">23</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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