Vagal modulation of the heart is blunted in heavy smokers, particularly during a parasympathetic maneuver. Blunted autonomic control of the heart may partly be associated with adverse event attributed to cigarette smoking.

No abstract

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.

Background: Vitamin D deficiency is associated with cardiovascular disease such as coronary artery disease, heart failure, and hypertension. Vitamin D deficiency activates the renin-angiotensin-aldosterone system, which affects the cardiovascular system. For this reason, it could be suggested that there is a relationship between vitamin D deficiency and atrial fibrillation (AF). In our study, we compared 25-hydroxyvitamin D (25-OHD) levels between nonvalvular AF, valvular AF, and control groups in sinus rhythm. Method: A total of 102 patients with nonvalvular chronic AF without any other cardiovascular disease (mean age 62.51 + 5.88; group I) and 96 patients with AF, which is associated with mitral valve disease (mean age 61.51 + 5; group II) were included in our study. Of all, 100 age-matched healthy people with sinus rhythm were accepted as control groups (mean age 61.35 + 5.44). Routine biochemical parameters, 25-OHD and parathormone levels were performed. Results: Baseline characteristics of the study groups were comparable. Group I patients had a lower vitamin D level than group II and the control group (6.51 + 4.89, 9.24 + 7.39, and 11.18 + 6.98 ng/mL, P < .001, respectively). In groups I and II, the patients' left atrium diameter and systolic pulmonary artery pressure are higher than the control group. Conclusion: As a result, our study revealed a relationship between vitamin D deficiency and nonvalvular AF.

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...