ReviewEffects of active and passive tobacco cigarette smoking on heart rate variability☆
Introduction
A vast number of studies have demonstrated that active smoking generates a number of unfavorable health effects, including an increased risk for stroke, multiple cancers, lung cancer, emphysema, and heart disease [[1], [2], [3]]. Based on recent evidence, there will be more than 8 million smoking-related deaths every year by 2030, while the total smoking-induced deaths during the 21st century will reach one billion [4]. This is because, despite the adoption of stricter antismoking campaigns in many countries, more people smoke today than during any other time in human history [estimated to > 1.25 billion adults] [1], [5]. Indeed, the prevalence rates of smoking are steadily increasing [1], [6] primarily among young girls [[7], [8], [9]] and a further global expansion of the tobacco epidemic is projected in the near future [1].
Given the widespread incidence of smoking as well as its deleterious health effects, it is crucial to examine practical and cost effective prognostic markers assessing the impact of smoking on cardiovascular health. Heart rate variability (HRV) is a straightforward and cost effective technique to foresee health issues of cardiovascular nature and can be used to predict in advance smoking-induced health effects that may arise in the future [10]. Indeed, HRV abnormalities are linked with many cardiovascular diseases, including ischemic disease [11] and heart failure [12], and provide prognostic information for adverse outcomes [13]. However, to our knowledge the evidence linking smoking with changes in HRV and, in turn, cardiovascular abnormalities have not been critically reviewed. Therefore, the aim of this review is to critically evaluate the existing biological evidence regarding the effects of smoking (both active and passive) on HRV and their associated cardiovascular consequences. In addition, we summarize fundamental information on the various HRV indicators and their diagnostic significance. We envisage that the information provided will be valuable not only to physicians and scientists, but also to those interested in personal or public health, politics and economics. In order to achieve the above, a comprehensive search in PubMed was conducted using MeSH terms that are germane to active and passive smoking, HRV, autonomic function, and health effects (particularly of cardiovascular nature). The search also included the articles cited in the identified papers.
Section snippets
Heart rate variability (HRV)
HRV is calculated based on the time difference between repeated heart beats [3], [14]. As such, it characterizes changes in the activation of the autonomic nervous system which comprises a neural network that automatically controls a number of bodily actions (e.g., circulation, digestion) through a series of positive and negative feedback loops [[14], [15], [16]]. The autonomic nervous system is divided anatomically into the sympathetic nervous system (SNS) and the parasympathetic nervous
Indicators of HRV analysis
Wolf et al. [29] first recognized that reduced HRV is linked with an increased risk for postinfarction mortality. Consequently, power spectral analysis of heart rate fluctuations was introduced to quantitatively evaluate beat-to-beat cardiovascular control [30]. These analyses provided with indicators that enhanced knowledge regarding the autonomic background of RR interval fluctuations in the heart rate record [31], [32]. At present, measurements of HRV are fundamentally composed of average,
Chronic effects
The influence of chronic active smoking on HRV has been studied extensively (Table 1). The first published evidence was provided by Penny and Mir [43] demonstrating a decreased HRV in chronic cigarette smokers compared to non-smokers. In the following years, a number of epidemiological studies were conducted, the vast majority of which confirmed that HRV is decreased in chronic active smokers. Specifically, Hayano and colleagues found a decreased vagal activation in heavy smokers compared to
Chronic effects
To the best of our knowledge, only one study has assessed the chronic effects of passive smoking on HRV (Table 2). In this experiment, Felber Dietrich and colleagues measured HRV through 24-h electrocardiogram recordings in 1218 nonsmokers aged ≥ 50 years [42]. The results demonstrated that individuals who were passively exposed to smoke at home or at work for more than 2 h/day revealed decreased total power, LF and LF/HF as well as increased HF. These results suggest that chronic passive smoking
Mechanisms
As observed in the previous sections, the vast majority of evidence provided to date suggests that acute and chronic active and passive smoking generate marked disruptions in the normal autonomic nervous system functioning characterized by increased SNS drive and reduced PNS modulation and overall HRV. Two main mechanistic pathways have been proposed to explain this smoking-induced effect on neurocardiovascular regulation. The principal biomarker in the first mechanism put forth is nicotine,
Clinical implications
The mechanism(s) by which the smoking-induced reduction in autonomic function contributes to cardiovascular-related mortality is not well understood. A recent study in mice suggests that the smoking-induced reduction in autonomic function increases arrhythmia susceptibility (atrial fibrillation, ventricular fibrillation or tachycardia), abnormalities in cardiac electrical conduction, and AV block [25]. This may account for the findings in the epidemiological data linking active and passive
Concluding remarks
This review attempts to critically evaluate the existing biological evidence regarding the effects of smoking (both active and passive) on HRV and their associated cardiovascular problems. Overall, the vast majority of published evidence suggests that acute and chronic active and passive smoking generate marked disruptions in the normal autonomic nervous system functioning characterized by increased SNS drive and reduced PNS modulation and overall HRV. This phenomenon is partly attributed to an
Acknowledgments
This work was supported in part by funding from the European Union 7th Framework Program (FP7-PEOPLE-IRG-2008 grant no. 239521). The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology (Shewan and Coats 2010;144:1-2).
References (93)
- et al.
Short- and long-term effects of cigarette smoking on heart rate variability
Am J Cardiol
(Jan. 1 1990) - et al.
Prognostic value of heart rate variability in chronic congestive heart failure (Veterans Affairs' Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure)
Am J Cardiol
(Jul 1 2002) - et al.
Fractal analysis of heart rate variability and mortality after an acute myocardial infarction
Am J Cardiol
(Aug 15 2002) - et al.
Software for advanced HRV analysis
Comput Methods Programs Biomed
(Oct 2004) - et al.
Decreased heart rate variability and its association with increased mortality after acute myocardial infarction
Am J Cardiol
(1987) - et al.
The relationship between heart rate variability and inflammatory markers in cardiovascular diseases
Psychoneuroendocrinology
(Nov 2008) - et al.
Cardiorespiratory response to exercise before and after acute beta-adrenoreceptor blockade in nonsmokers and chronic smokers
Int J Cardiol
(Jun 1986) - et al.
Autonomic functioning and cigarette smoking: heart rate spectral analysis
Biol Psychiatry
(Mar 15 1992) - et al.
Short-term heart rate variability and factors modifying the risk of coronary artery disease in a population sample
Am J Cardiol
(Oct 15 1993) - et al.
Combined effect of cigarette smoking and sulfur dioxide on heart rate variability
Int J Cardiol
(Mar 20 2009)