Effect of Smoking on Blood Pressure and Resting Heart RateCLINICAL PERSPECTIVE

A. Linneberg, R. Jacobsen, T. Skaaby, Amy E Taylor, M. Fluharty, J. Jeppesen, J. Bjørngaard, B. Åsvold, M. Gabrielsen, A. Campbell, R. Marioni, M. Kumari, P. Marques-Vidal, M. Kaakinen, A. Cavadino, I. Postmus, T. Ahluwalia, S. Wannamethee, J. Lahti, K. Räikkönen, A. Palotie, A. Wong, C. Dalgård, I. Ford, Y. Ben-Shlomo, L. Christiansen, K. Kyvik, D. Kuh, J. Eriksson, P. Whincup, H. Mbarek, E. D. Geus, J. Vink, D. Boomsma, G. Smith, D. Lawlor, A. Kisialiou, A. McConnachie, S. Padmanabhan, J. Jukema, C. Power, E. Hyppönen, M. Preisig, G. Waeber, P. Vollenweider, T. Korhonen, T. Laatikainen, V. Salomaa, J. Kaprio, M. Kivimäki, Blair H. Smith, C. Hayward, T. Sørensen, B. Thuesen, N. Sattar, R. Morris, P. Romundstad, M. Munafo, M. Järvelin, L. Husemoen
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引用次数: 20

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 randomization meta-analyses of the associations of smoking status and smoking heaviness with systolic and diastolic blood pressure, hypertension, and resting heart rate. For the Mendelian randomization 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 systolic blood pressure and diastolic blood pressure and lower hypertension risk, but with higher resting heart rate. In observational analyses among current smokers, 1 cigarette/day higher level of smoking heaviness was associated with higher (0.21 bpm; 95% confidence interval 0.19; 0.24) resting heart rate and slightly higher diastolic blood pressure (0.05 mm Hg; 95% confidence interval 0.02; 0.08) and systolic blood pressure (0.08 mm Hg; 95% confidence interval 0.03; 0.13). However, in Mendelian randomization analyses among current smokers, although each smoking increasing allele of rs16969968/rs1051730 was associated with higher resting heart rate (0.36 bpm/allele; 95% confidence interval 0.18; 0.54), there was no strong association with diastolic blood pressure, systolic blood pressure, or hypertension. This would suggest a 7 bpm higher heart rate in those who smoke 20 cigarettes/day. Conclusions— This Mendelian randomization 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.
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吸烟对血压和静息心率的影响
吸烟是一个重要的心血管疾病危险因素,但吸烟与血压之间的联系机制尚不清楚。方法和结果:来自23项基于人群的研究的14317名参与者(62666名从不吸烟者,40669名戒烟者,37982名目前吸烟者)的数据被纳入观察性和孟德尔随机化荟萃分析,研究吸烟状况和吸烟严重程度与收缩压和舒张压、高血压和静息心率的关系。在孟德尔随机化分析中,基因变异rs16969968/rs1051730被用作当前吸烟者吸烟严重程度的代表。在观察性分析中,与从不吸烟相比,吸烟与较低的收缩压和舒张压以及较低的高血压风险相关,但与较高的静息心率相关。在当前吸烟者的观察性分析中,每天1支烟的吸烟严重程度与更高的(0.21 bpm;95%置信区间0.19;0.24)静息心率和稍高的舒张压(0.05 mm Hg;95%置信区间0.02;0.08 mm Hg)和收缩压(0.08 mm Hg;95%置信区间0.03;0.13)。然而,在目前吸烟者的孟德尔随机分析中,尽管rs16969968/rs1051730的每个吸烟增加等位基因都与较高的静息心率相关(0.36 bpm/等位基因;95%置信区间0.18;0.54),与舒张压、收缩压或高血压无强相关性。这意味着每天抽20支烟的人心率要高出7 bpm。结论:这项孟德尔随机荟萃分析支持重度吸烟与较高静息心率水平的因果关系,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。
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来源期刊
Circulation-Cardiovascular Genetics
Circulation-Cardiovascular Genetics CARDIAC & CARDIOVASCULAR SYSTEMS-GENETICS & HEREDITY
CiteScore
3.95
自引率
0.00%
发文量
0
期刊介绍: Circulation: Genomic and Precision Medicine considers all types of original research articles, including studies conducted in human subjects, laboratory animals, in vitro, and in silico. Articles may include investigations of: clinical genetics as applied to the diagnosis and management of monogenic or oligogenic cardiovascular disorders; the molecular basis of complex cardiovascular disorders, including genome-wide association studies, exome and genome sequencing-based association studies, coding variant association studies, genetic linkage studies, epigenomics, transcriptomics, proteomics, metabolomics, and metagenomics; integration of electronic health record data or patient-generated data with any of the aforementioned approaches, including phenome-wide association studies, or with environmental or lifestyle factors; pharmacogenomics; regulation of gene expression; gene therapy and therapeutic genomic editing; systems biology approaches to the diagnosis and management of cardiovascular disorders; novel methods to perform any of the aforementioned studies; and novel applications of precision medicine. Above all, we seek studies with relevance to human cardiovascular biology and disease. Manuscripts are examined by the editorial staff and usually evaluated by expert reviewers assigned by the editors. Both clinical and basic articles will also be subject to statistical review, when appropriate. Provisional or final acceptance is based on originality, scientific content, and topical balance of the journal. Decisions are communicated by email, generally within six weeks. The editors will not discuss a decision about a manuscript over the phone. All rebuttals must be submitted in writing to the editorial office.
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