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.

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.

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...

SUMMARYPrevious studies have suggested that microvascular abnormalities and endothelial dysfunction cause slow coronary flow (SCF). The objective of this study was to assess the plasma nitric oxide (NO) level and determine its role in the pathogenesis of SCF phenomenon. Thirty-six patients with SCF (group 1) and otherwise patent coronary arteries and 34 subjects with normal coronary flow (group 2) were included in the study. Coronary flow was quantified according to the TIMI Frame Count (TFC) method. Brachial artery endothelium-dependent flow-mediated dilatation (FMD) and nitroglycerin (NTG)-induced endothelium-independent dilatation were studied in both groups. In addition, plasma NO levels were measured and their contribution to FMD was determined. The sex, age, body mass index, arterial blood pressure, and heart rate distributions were similar in both groups. TFC was significantly higher in group 1 compared to group 2 for each artery. The plasma NO level was lower in patients with SCF than in control subjects (18.4 ± 4.4 versus 25.2 ± 6.3 µmol/L P = 0.001). FMD was significantly smaller in group 1 than in group 2 (4.0 ± 3.2% versus 10.6 ± 5.8%, P = 0.0001). The percent NTG-induced dilatation was similar in the two groups (16.8 ± 1.1% versus 17.1 ± 1.1%, P = 0.42). In group 1, the plasma NO level was correlated with percent of FMD. Also, the plasma NO level was inversely correlated with TFC for each artery. Reduced NO bioactivity as well as impaired FMD support the presence of endothelial damage in the pathogenesis of SCF phenomenon. (Int Heart J 2005; 46: 373-382)

he vascular endothelium plays an integral role not only in regulation of vascular tonus, but also in prevention and formation of thrombus and inflammation. 1 It is known that endothelial dysfunction is associated with coronary risk factors and atherosclerosis, and has a close pathophysiological relation with acute coronary syndromes. [2][3][4] Endothelial dysfunction has been shown in patients with documented atherosclerosis, but it is also an early step in the pathogenesis of the atherosclerotic cascade. [5][6][7] Among various methods to assess endothelial function, endothelium-dependent vasodilatation (EDV) is a noninvasive, highly reproducible, simple method based on high-sensitivity ultrasound waves. 7,8 In this study we assessed the relationship between EDV in systemic arteries and coronary risk factors in patients with documented coronary artery disease (CAD). Methods Patient PopulationOne hundred and fifty patients with angiographically proven CAD (103 males, 47 females), age ranging between 29 and 78 years (mean: 58±10), were recruited. CAD was defined as the presence of angiographically demonstrated ≥70% stenosis in at least 1 major epicardial coronary artery. Hypertension (HT) was defined as blood pressure ≥140/ 90 mmHg or use of antihypertensive drugs and diabetes mellitus (DM) as fasting blood glucose level ≥126 mg/dl or use of antidiabetic agents. All study subjects underwent a complete physical examination, and biochemical, electrocardiographic and body mass index (BMI) measurements. Vascular endothelial function in the brachial artery was measured by the flow-mediated dilatation (FMD) technique. Patients with acute coronary syndromes, severe left ventricular dysfunction (ejection fraction <35%) or old myocardial infarction were excluded from the study. Vascular StudyEach subject was studied in the morning, after abstaining from alcohol, caffeine and tobacco, as well as food, within 8 h before the study. High-resolution echocardiography Doppler ultrasound (Technos MPX ultrasound ESOTA Inc) with an 8.0 MHz transducer was used to measure the Circ J 2007; 71: 698 -702 (Received August 1, 2006; revised manuscript received January 22, 2007; accepted February 9, 2007 Background Results of experimental and clinical studies suggest that both coronary artery disease (CAD) itself and its traditional risk factors lead to endothelial dysfunction. The aim of the present study was to determine which CAD risk factors sustain their contribution to endothelial dysfunction despite the presence of established CAD. Methods and ResultsThe study group comprised 150 patients with CAD. Using a high-resolution ultrasound, the diameter of the brachial artery at rest and during reactive hyperemia (flow-mediated dilatation, FMD%: endothelial-dependent stimulus to vasodilatation), as well as after sublingual administration of nitroglycerin (NTG%: endothelium-independent vasodilatation), was measured.