Abstract
Lipoprotein (a) (Lp(a)) is considered a genetic factor for cardiovascular disease playing an important role in atherogenesis and thrombosis, but the evidence about its association with sleep duration is controversial. We evaluated the relation between self-reported sleep duration and Lp(a). Among 1600 participants of the population-based sample, we selected 1427 subjects without previously known cardiovascular events, who answered the questions about their sleep duration; had valid lipid profile results (total cholesterol, low- and high-density lipoproteins, Lp(a), apolipoprotein AI (ApoAI), ApoB, and ApoB/ApoAI); and did not take lipid-lowering drugs (mean age 46 ± 12 years). We performed a structured interview, which included questions about lifestyle, medical history, complaints, and sleep duration (How long have you been sleeping per night during the last month?). Sleep duration was classified as follows: <6 h/night—short, 6–9 h/night—normal, and ≥10 h/night—long. Overall, 73 respondents (5.2%) were short-sleepers and 69 (4.8%) long-sleepers. Males were slightly more prevalent among short-sleepers. The groups matched by age, body mass index, blood pressure, diabetes mellitus, and hypertension rate. Short-sleepers had lower rates of high total cholesterol (≥5.0 mmol/L), lower Lp(a) levels and lower rates of increased Lp(a) ≥0.5 g/L, and higher insulin and insulin resistance (assessed by the homeostatic model assessment for insulin resistance (HOMA-IR)). ApoAI, ApoB, their ratio, and other lab tests were similar in the groups. The multinomial logistic regression demonstrated that only the short sleep duration was independently (odds ratio (OR) 0.29, 95% confidence interval (CI) (0.09–0.91), p = 0.033) associated with Lp(a) (χ2 = 41.58, p = 0.003). Other influencing factors were smoking and HOMA-IR. Such an association was not found for long-sleepers. In conclusion, a short-sleep duration is associated with Lp(a). The latter might mediate the higher insulin resistance and higher cardiometabolic risks in short-sleepers.
Highlights
The traditional, well-known cardiovascular risk factors include blood pressure (BP), total cholesterol and low-density lipoproteins, smoking, and sex [1,2]
The distribution of subjects depending on sleep duration is presented on Figure 1
The discrepancy between the published studies and our results can be explained by the different definitions of short and long-sleep durations applied in various studies
Summary
The traditional, well-known cardiovascular risk factors include blood pressure (BP), total cholesterol and low-density lipoproteins, smoking, and sex [1,2]. Current evidence and guidelines establish that risk stratification can be improved when additional factors are assessed, especially for those at low or moderate risk, according to the traditional risk stratification. Isnut.gJ.gMesotl.eSdci.a2s02p0o, 2te1,nxtiFaOlRmPoEEdRifiReErVsI.EAWmong biochemical additional factors, the apolipoprotein B2 oafn1d4 alippoolpiprootperiont(eai)n(LBp(aa)n)darleipcoopnrsoidteeirne(da)po(Ltepn(tai)a)llyarme ocdoinfisaibdleer,eadlbepiottleenstsiainllvyesmtigoadtiefida,brlies,kaflabcetoitrslefossr icnavrdesiotivgaastceudl,arrisdkisfeaacstoesrs[1fo,2r].cardiovascular diseases [1,2]. EStlaebeopliqcuahleitayl,thsl.eeSpledepuraqtuioanli,tyan, dslseleepepdduisraotridoenr,s aanreddsislceuepsseddisaosrpdoertesnatirael dtairsgcuetsssefdorasmpeodteicnatliailnttaerrgveetns tfioornm[3ed].icaElpinidteermveionltoiognica[3l].sEtupdidieesmdioelmogoincsatlrsattuedtihesatdebmotohnssthroartet tahnadt bloonthg sshleoerpt aanredalsosnogcisalteeedpwaritehaussnofacivaoteradbwleitcharudniofavvaosrcaublaler coaurtdcioomvaessc(ucolarroonuartcyoamrteesry(cdoirsoenaasrey, satrrtoekrye, danisdeacsaerd, siotrvoaksecu, alanrddecaarthd)io[4v,a5s]caunldarmdeetaatbho)li[c4d,5i]soarndderms [e6t]a.bHoloiwc deviseor,rdtheersev[6id].eHncoewabevouert,atnhaesesvoicdiaetniocne abbeotwuteeann salseseopcidautiroantiboentwanedendsylseleippidduemraitaioins raantdhedryssclaiprcideeamndiaciosnrtartahdeircstocaryrcaenadndlacckoinntgraidnifcotromryaatinodn laabcokuintgLpin(fao)ramnadtiaopnoalibpoouptroLtpe(ian)sa[n7–d1a1p].olipoproteins [7,8,9,10,11]. TThhee aaiimm ooffththeecucrurrernetnatnaanlyaslyissiws aws athsethesetiemstaitmioantioofnthoef athsseocaisastoiocniabtieotnwbeeentwseeelfn-respelofr-rteedposrleteedp sdlueeraptidounrsaatinodnsthaenldiptihdeplirpoifidlep,rionfcilleu,diinncgluLdpin(ag) Lanpd(aa)paonldipaopporloipteoinpsroAteIi(naspAoAI (Ia)paonAdIB) a(AndpoBB()A, ipnotBh)e, ignentheeraglepnoepraullaptoiopnu.lation AAmmoonngg bbehehavavioiroarlarlisrkisfakctofarcst,osrlese, psalenedpsleaenpdpastlteeerpnsparaettienrvnesstiagraeteidnavseismtigpaotretdantadsetiemrmpoinrtaanntst dofetcearrmdiionmanettsaboofliccahredailothm. eStlaebeopliqcuahleitayl,thsl.eeSpledepuraqtuioanli,tyan, dslseleepepdduisraotridoenr,s aanreddsislceuepsseddisaosrpdoertesnatirael dtairsgcuetsssefdorasmpeodteicnatliailnttaerrgveetns tfioornm[3ed].icaElpinidteermveionltoiognica[3l].sEtupdidieesmdioelmogoincsatlrsattuedtihesatdebmotohnssthroartet tahnadt bloonthg sshleoerpt aanredalsosnogcisalteeedpwaritehaussnofacivaoteradbwleitcharudniofavvaosrcaublaler coaurtdcioomvaessc(ucolarroonuartcyoamrteesry(cdoirsoenaasrey, satrrtoekrye, danisdeacsaerd, siotrvoaksecu, alanrddecaarthd)io[4v,a5s]caunldarmdeetaatbho)li[c4d,5i]soarndderms [e6t]a.bHoloiwc deviseor,rdtheersev[6id].eHncoewabevouert,atnhaesesvoicdiaetniocne abbeotwuteeann salseseopcidautiroantiboentwanedendsylseleippidduemraitaioins raantdhedryssclaiprcideeamndiaciosnrtartahdeircstocaryrcaenadndlacckoinntgraidnifcotromryaatinodn laabcokuintgLpin(fao)ramnadtiaopnoalibpoouptroLtpe(ian)sa[n7–d1a1p].olipoproteins [7,8,9,10,11].
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