Effect of Smoking on Blood Pressure and Resting Heart Rate: A Mendelian Randomization Meta-Analysis in the CARTA Consortium.

Effect of Smoking on Blood Pressure and Resting Heart Rate: A Mendelian Randomization Meta-Analysis in the CARTA Consortium.
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DOI:
10.1161/circgenetics.115.001225
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发表时间:
2015-12
期刊:
Circulation. Cardiovascular genetics
影响因子:
--
通讯作者:
Husemoen LL
Husemoen LL
中科院分区:
其他
文献类型:
--
作者:
Linneberg A;Jacobsen RK;Skaaby T;Taylor AE;Fluharty ME;Jeppesen JL;Bjorngaard JH;Åsvold BO;Gabrielsen ME;Campbell A;Marioni RE;Kumari M;Marques-Vidal P;Kaakinen M;Cavadino A;Postmus I;Ahluwalia TS;Wannamethee SG;Lahti J;Räikkönen K;Palotie A;Wong A;Dalgård C;Ford I;Ben-Shlomo Y;Christiansen L;Kyvik KO;Kuh D;Eriksson JG;Whincup PH;Mbarek H;de Geus EJ;Vink JM;Boomsma DI;Smith GD;Lawlor DA;Kisialiou A;McConnachie A;Padmanabhan S;Jukema JW;Power C;Hyppönen E;Preisig M;Waeber G;Vollenweider P;Korhonen T;Laatikainen T;Salomaa V;Kaprio J;Kivimaki M;Smith BH;Hayward C;Sørensen TI;Thuesen BH;Sattar N;Morris RW;Romundstad PR;Munafò MR;Jarvelin MR;Husemoen LL

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吸烟是一个重要的心血管疾病风险因素,但吸烟与血压之间的联系机制却知之甚少。来自23项基于人群的研究的141,317名参与者(从未吸烟者62,666人,以前吸烟者40,669人,现在吸烟者37,982人)的数据被纳入观察性和孟德尔随机化(MR)荟萃分析,分析吸烟状况和吸烟重量与收缩和舒张压(SBP、DBP)、高血压和静息心率的关系。在MR分析中,基因变异rs16969968/rs1051730被用作当前吸烟者吸烟严重程度的替代。在观察分析中,与从不吸烟相比,经常吸烟与较低的SBP、DBP和较低的高血压风险相关,但与较高的静息心率相关。在当前吸烟者中的观察分析中,每天吸烟重量增加一支与较高的静息心率(0.21次/分钟;95%可信区间0.19;0.24)相关,并略高于舒张压(0.05毫米汞;95%可信区间0.02;0.08)和收缩压(0.08毫米汞;95%可信区间0.03;0.13)。然而,在当前吸烟者的MR分析中,虽然rs16969968/rs1051730的每个吸烟增加等位基因与较高的静息心率(0.36次/分钟/等位基因;95%可信区间0.18;0.54)相关,但与DBP、SBP或高血压没有很强的关联。这表明每天抽20支烟的人心率要高出7次/分钟。这项MR荟萃分析支持吸烟过重与较高的静息心率水平之间的因果联系,但与血压无关。这些发现表明,吸烟的部分心血管风险可能是通过增加静息心率来实现的。
Smoking is an important cardiovascular disease risk factor, but the mechanisms linking smoking to blood pressure are poorly understood. Data on 141,317 participants (62,666 never, 40,669 former, 37,982 current smokers) from 23 population-based studies were included in observational and Mendelian randomisation (MR) meta-analyses of the associations of smoking status and smoking heaviness with systolic and diastolic blood pressure (SBP, DBP), hypertension, and resting heart rate. For the MR analyses, a genetic variant rs16969968/rs1051730 was used as a proxy for smoking heaviness in current smokers. In observational analyses, current as compared with never smoking was associated with lower SBP, DBP, and lower hypertension risk, but with higher resting heart rate. In observational analyses amongst current smokers, one cigarette/day higher level of smoking heaviness was associated with higher (0.21 beats/minute; 95% CI 0.19; 0.24) resting heart rate, and slightly higher DBP (0.05 mmHg; 95% CI 0.02; 0.08) and SBP (0.08 mmHg; 95% CI 0.03; 0.13). However, in MR analyses amongst current smokers, while each smoking increasing allele of rs16969968/rs1051730 was associated with higher resting heart rate (0.36 beats/minute/allele; 95% CI 0.18; 0.54), there was no strong association with DBP, SBP, or hypertension. This would suggest a 7 beats/minute higher heart rate in those who smoke 20 cigarettes/day. This MR meta-analysis supports a causal association of smoking heaviness with higher level of resting heart rate, but not with blood pressure. These findings suggest that part of the cardiovascular risk of smoking may operate through increasing resting heart rate.