哮喘联盟

   摘要
   背景：吸烟是一种重要的心血管疾病的危险因素，但关于吸烟对血压的影响机制却知之甚少。
   方法和结果：141317名参与者（62666未曾吸烟，40669曾经吸烟，37982目前吸烟者），来自23个基于人口的研究中。采用孟德尔随机化（MR）META分析方法，研究吸烟状况和吸烟严重程度与血压（收缩压和舒张压）（SBP，DBP），高血压和静息心率之间的关系。在MR分析中，吸烟者中重度吸烟者采用遗传变异RS16969968/RS1051730作为一个代理参数。在监测分析中，与未曾吸烟者相比，目前吸烟者收缩压，舒张压降低，高血压的风险降低，但静息心率增高。目前吸烟者的分析中，重度吸烟者每天吸烟数量越多，静息心率增加越高（0.21次/分钟; 95％CI 0.19- 0.24），DBP轻度增高（0.05MMHG; 95％CI0.02-0.08），SBP轻度增高（0.08MMHG; 95％CI0.03-0.13）。然而，在MR对于目前吸烟者的分析中，每位吸烟者吸烟等位基因RS16969968/RS1051730增加和静息心率增加（0.36 次/分/等位基因; 95% CI 0.18- 0.54)相关，但和DBP、SBP或高血压相关不明显。提示每天吸烟20支，心率将会增加7次/分钟。
   结论：本次MR META分析结果提示重度吸烟与静息心率增高有因果关系，但与血压关系不明显。这些结果表明，部分吸烟产生的心血管疾病的风险是通过增加静息心率实现的。

 

（苏欣 审校）
Circ Cardiovasc Genet. 2015 Nov 4. pii: CIRCGENETICS.115.001225. [Epub ahead of print]
 

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

Linneberg A1, Jacobsen RK2, Skaaby T2, Taylor AE3, Fluharty ME3, Jeppesen JL4, Bjørngaard JH5, Åsvold BO6,Gabrielsen ME7, Campbell A8, Marioni RE9, Kumari M10, Marques-Vidal P11, Kaakinen M12, Cavadino A13,Postmus I14, Ahluwalia TS15, Wannamethee SG16, Lahti J17, Räikkönen K18, Palotie A19, Wong A20, Dalgård C21,Ford I22, Ben-Shlomo Y23, Christiansen L24, Kyvik KO25, Kuh D20, Eriksson JG26, Whincup PH27, Mbarek H28, de Geus EJ28, Vink JM29, Boomsma DI29, Davey Smith G30, Lawlor DA30, Kisialiou A22, McConnachie A22,Padmanabhan S31, Jukema JW32, Power C33, Hyppönen E34, Preisig M35, Waeber G11, Vollenweider P11,Korhonen T36, Laatikainen T37, Salomaa V38, Kaprio J39, Kivimäki M40, Smith BH41, Hayward C42, Sørensen TI43,Thuesen BH2, Sattar N44, Morris RW45, Romundstad PR46, Munafò MR3, Jarvelin MR47, Husemoen LL2.
 

Abstract
BACKGROUND:Smoking is an important cardiovascular disease risk factor, but the mechanisms linking smoking to blood pressure are poorly understood.
METHODS AND RESULTS: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, onecigarette/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.
CONCLUSIONS: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.
 

Circ Cardiovasc Genet. 2015 Nov 4. pii: CIRCGENETICS.115.001225. [Epub ahead of print]