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Acute cigarette smoking enhances adrenergic activity and thus may be associated with hemodynamic changes in the cardiovascular system. In this study, the acute effect of cigarette smoking on heart rate variability (HRV) was studied. Fifteen subjects were included in the study. Time domain (the mean R-R interval, the standard deviation of R-R interval, and the root mean square of successive R-R interval differences) and frequency domain (high-frequency, low-frequency ratio, and low-frequency/high-frequency ratio) parameters of HRV were obtained from all participants for each 5-minute segment: 5 minutes before and 5, 10, 15, 20, 25, and 30 minutes after smoking a cigarette. The mean R-R interval, the standard deviation of R-R interval, and the root mean square of successive R-R interval differences significantly decreased within the first 5-minute period compared with baseline, and then the standard deviation of R-R interval increased within the 20- to 30-minute period. The low-frequency high-frequency ratio significantly decreased within the first 5 minutes after smoking and then remained unchanged throughout the study period. Similarly, low-frequency and high-frequency power increased within the first 5 minutes compared with baseline. Acute cigarette smoking alters HRV parameters, particularly within the first 5 to 10 minutes after smoking.

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igarette smoking is a well-known cardiovascular risk factor, and it affects both the coronary and peripheral circulation. [1][2][3][4] Because cigarette smoke contains a large number of oxidants, it has been hypothesized that the adverse effect of smoking could result in oxidative damage to vascular endothelium. 5 Indeed, endothelial dysfunction in brachial and coronary arteries has been demonstrated in long-term smokers and even in passive smokers. [6][7][8] However, it has also been found that acute cigarette smoking causes vasoconstriction of the epicardial coronary artery and increases the coronary resistance vessel tone. 9,10 Acute cigarette smoking has also been shown to cause a transient increase in pulse rate and blood pressure. 11 Although previous studies have apparently found that chronic cigarette smoking is associated with endothelial dysfunction, data regarding the dose-dependent effects of smoking on endothelial dependent vasodilatation are limited and inconclusive. 6-8, 12,13 Flow mediated dilatation in systemic as well as coronary arteries is mediated by the endothelium through the release of dilator substances that act on the underlying smooth muscle; these endothelium-derived relaxing factors have Circulation Journal Vol. 68, December 2004 been identified as nitric oxide. 14 Anderson et al 15 found that coronary artery endothelium dependent vasomotor responses to acetylcholine and flow-mediated vasodilatation in the brachial artery were similar. Thus, endothelial function in peripheral vessels such as the brachial artery can be measured noninvasively and inferentially correlated to responses within the coronary vasculature. In addition, Weideinger et al 16 recently showed that brachial artery wall thickness (BA-WT) is independently correlated with the presence of coronary artery disease (CAD) and that BA-WT can provide a novel noninvasive marker of atherosclerosis.Therefore, the purpose of this study was to determine chronic as well as instantaneous effects of smoking on brachial artery endothelial function in long-term smokers and non-smokers, and the effect of chronic smoking on BA-WT. Methods SubjectsTwenty healthy long-term heavy smokers (15 males, 5 females, mean age 27±9 years, smoking average of 25 cigarettes/day) and age-matched 20 healthy nonsmoking hospital staff (14 males, 6 females, mean age 25±7 years) were studied. A complete physical and echocardiographic examination was performed prior to the study. The participants were free from the other risk factors for CAD and none were taking any any medication during the study (Table 1). All participants gave their informed consent and the institutional review board approved the study protocol. Background Impaired flow mediated dilatation (FMD) and increased wall thickness (WT) of the brachial artery have been associated with atherosclerosis and its risk factors. In this study we sought to determine brachial artery wall thickness in chronic smokers and the instantaneous effect of smoking on brachial artery endothelium dependent vaso...

Cardiac involvement in rheumatoid arthritis (RA) has been reported previously. However, evaluation of ventricular function in this disease by the use of recently proposed Doppler echocardiographic methods has not been reported before. Thus, the aim of this study was to evaluate ventricular function by measurement of myocardial performance index (MPI) and transmitral flow propagation velocity (TFPV). Thirty-two patients with long-standing RA and 32 control subjects (mean ages 52 +/- 11 and 50 +/- 10 years, respectively) participated in this study. Systolic function was assessed by subjective evaluation of wall motion for both ventricles and by fractional shortening for the left ventricle (LV). LV diastolic function was evaluated by standard pulsed-wave Doppler echocardiography, MPI and TFPV. Right ventricular (RV) function was evaluated by MPI. No subject had signs or symptoms of clinically overt heart failure. Systolic function was normal in all subjects. Among the echocardiographic indices of LV diastolic function the peak E velocity, E velocity/A velocity ratio, isovolumetric relaxation time, MPI and TFPV in the RA group were significantly different from those of the controls ( P < 0.05). However, we did not observe a significant difference in RV echocardiographic indices between the two groups. Our results show that there is LV diastolic dysfunction in patients with long-standing RA. The lack of a history of cardiotoxic antirheumatic drug use among our patients suggests that this abnormality is due to RA itself.