Research

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

Elisa Giacomin¹ , Elisabetta Palmerini¹ , Piercarlo Ballo² , Valerio Zac๠, Giovanni Bova¹ and Sergio Mondillo¹

¹Department of Cardiovascular Disease, University of Siena, Italy

²Cardiology Operative Unit, S. Andrea Hospital, La Spezia, Italy

author email corresponding author email

Cardiovascular Ultrasound 2008, 6:9doi:10.1186/1476-7120-6-9

Published:	4 March 2008

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 (S_a), early diastolic E_a, and late diastolic (A_a) 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 A_a (+12.1%, p = 0.0026), tricuspid S_a (+9.8%, p = 0.012) and TAPSE (+7.9%, p = 0.017), and a decrease in the mitral E_a/A_a ratio (-8.5%, p = 0.0084). Sequential caffeine assumption and cigarette smoking in group 3 was associated with an acute increase in mitral A_a (+13.0%, p = 0.015) and tricuspid A_a (+11.6%, p < 0.0001) and a reduction in mitral E_a/A_a ratio (-8.5%, p = 0.0084) tricuspid E_a (-6.6%, p = 0.048) and tricuspid E_a/A_a 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 A_a and E_a/A_a ratio, and for tricuspid A_a and E_a/A_a 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.