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咖啡因与吸烟对健康受试者心室长轴功能的急性影响。

Acute effects of caffeine and cigarette smoking on ventricular long-axis function in healthy subjects.

作者信息

Giacomin Elisa, Palmerini Elisabetta, Ballo Piercarlo, Zacà Valerio, Bova Giovanni, Mondillo Sergio

机构信息

Cardiology Operative Unit, S, Andrea Hospital, La Spezia, Italy.

出版信息

Cardiovasc Ultrasound. 2008 Mar 4;6:9. doi: 10.1186/1476-7120-6-9.

DOI:10.1186/1476-7120-6-9
PMID:18318902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2288591/
Abstract

BACKGROUND

Few data exist regarding the direct effects of caffeine and smoking on cardiac function. We sought to explore the acute effects of caffeine assumption, cigarette smoking, or both on left ventricular (LV) and right ventricular (RV) function in a population of young normal subjects.

METHODS

Forty-five healthy subjects aged 25 +/- 2 years underwent echocardiography. Fifteen of them were non-smokers and habitual coffee consumers (group 1), 15 were smokers and not habitual coffee consumers (group 2), and 15 were smokers and habitual coffee consumers (group 3). Peak systolic (Sa), early diastolic Ea, and late diastolic (Aa) velocity of mitral annulus were measured by pulsed Tissue Doppler, and left atrioventricular plane displacement was determined by M-mode. Tricuspid annular velocities and systolic excursion (TAPSE) were also determined. Measurements were performed at baseline and after oral assumption of caffeine 100 mg in group 1, one cigarette smoking in group 2, and both in group 3.

RESULTS

No changes in ventricular function were observed in group 1 after caffeine administration. In group 2, cigarette smoking yielded an acute increase in mitral Aa (+12.1%, p = 0.0026), tricuspid Sa (+9.8%, p = 0.012) and TAPSE (+7.9%, p = 0.017), and a decrease in the mitral Ea/Aa ratio (-8.5%, p = 0.0084). Sequential caffeine assumption and cigarette smoking in group 3 was associated with an acute increase in mitral Aa (+13.0%, p = 0.015) and tricuspid Aa (+11.6%, p < 0.0001) and a reduction in mitral Ea/Aa ratio (-8.5%, p = 0.0084) tricuspid Ea (-6.6%, p = 0.048) and tricuspid Ea/Aa ratio (-9.6%, p = 0.0003). In a two-way ANOVA model controlling for hemodynamic confounding factors, changes in the overall population remained significant for mitral Aa and Ea/Aa ratio, and for tricuspid Aa and Ea/Aa ratio.

CONCLUSION

In young healthy subjects, one cigarette smoking is associated to an acute impairment in LV diastolic function and a hyperdynamic RV systolic response. Caffeine assumption alone does not exert any acute effect on ventricular long-axis function, but potentiates the negative effect of cigarette smoking by abolishing RV supernormal response and leading to a simultaneous impairment in both LV and RV diastolic function.

摘要

背景

关于咖啡因和吸烟对心脏功能的直接影响,现有数据较少。我们试图探讨在年轻正常受试者群体中,摄入咖啡因、吸烟或两者兼而有之对左心室(LV)和右心室(RV)功能的急性影响。

方法

45名年龄在25±2岁的健康受试者接受了超声心动图检查。其中15名是非吸烟者且有喝咖啡的习惯(第1组),15名是吸烟者且无喝咖啡的习惯(第2组),15名是吸烟者且有喝咖啡的习惯(第3组)。通过脉冲组织多普勒测量二尖瓣环的收缩期峰值速度(Sa)、舒张早期Ea和舒张晚期(Aa)速度,并通过M型超声确定左房室平面位移。还测定了三尖瓣环速度和收缩期偏移(TAPSE)。在基线时以及第1组口服100毫克咖啡因后、第2组吸一支烟后、第3组同时进行这两项操作后进行测量。

结果

第1组摄入咖啡因后未观察到心室功能变化。在第2组中,吸烟使二尖瓣Aa急性增加(+12.1%,p = 0.0026)、三尖瓣Sa增加(+9.8%,p = 0.012)和TAPSE增加(+7.9%,p = 0.017),并使二尖瓣Ea/Aa比值降低(-8.5%,p = 0.0084)。第3组先后摄入咖啡因和吸烟与二尖瓣Aa急性增加(+13.0%,p = 0.015)和三尖瓣Aa增加(+11.6%,p < 0.0001)以及二尖瓣Ea/Aa比值降低(-8.5%,p = 0.0084)、三尖瓣Ea降低(-6.6%,p = 0.048)和三尖瓣Ea/Aa比值降低(-9.6%,p = 0.0003)有关。在控制血流动力学混杂因素的双向方差分析模型中,总体人群中二尖瓣Aa和Ea/Aa比值以及三尖瓣Aa和Ea/Aa比值的变化仍然显著。

结论

在年轻健康受试者中,吸一支烟与左心室舒张功能急性受损和右心室收缩反应亢进有关。单独摄入咖啡因对心室长轴功能没有任何急性影响,但通过消除右心室超常反应并导致左心室和右心室舒张功能同时受损,增强了吸烟的负面影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/83ccd7ca61cf/1476-7120-6-9-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/d11a9c74d8bf/1476-7120-6-9-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/0f0dfb5b1d57/1476-7120-6-9-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/ee17ec7c61f7/1476-7120-6-9-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/aa098a4b39eb/1476-7120-6-9-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/09580431aed3/1476-7120-6-9-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/83ccd7ca61cf/1476-7120-6-9-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/d11a9c74d8bf/1476-7120-6-9-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/0f0dfb5b1d57/1476-7120-6-9-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/ee17ec7c61f7/1476-7120-6-9-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/aa098a4b39eb/1476-7120-6-9-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/09580431aed3/1476-7120-6-9-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0546/2288591/83ccd7ca61cf/1476-7120-6-9-6.jpg

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