Exposure to secondhand smoke promotes sympathetic activity and cardiac muscle cachexia.

Recent trials demonstrated that a single brief exposure to secondhand smoke (SHS) generates acute adverse health effects. We evaluated the acute (immediately after exposure) and short-term (0.5, 1, 2, 3 and 4 h after exposure) effects of SHS on cardiac autonomic control and myocardial integrity. Nineteen adult healthy never-smokers underwent a 1 h exposure to SHS at bar/restaurant levels and a 1 h control exposure. Heart rate variability (HRV), serum cotinine, and six cardiac protein markers were assessed before, during, and up to four hours following each exposure. SHS reduced the standard deviation of normal-to-normal intervals and increased cotinine levels, creatine kinase (CK)-MB, and myoglobin (p < 0.05). We conclude that acute exposure to SHS suppresses HRV and augments CK-MB and myoglobin. The SHS-induced elevations in CK-MB and myoglobin may reflect a generalized lytic state, especially of the cardiac muscle, which is apparent for at least 2 h following the SHS exposure.

Acute effects of second-hand smoke on complete blood count.

We assessed the acute effects of a 1-h exposure to second-hand smoke (SHS) on complete blood count (CBC) markers in a controlled simulated bar/restaurant environment. Nineteen adult never-smokers completed a 1-h .exposure to SHS at bar/restaurant levels, and a 1-h exposure to normal room air. Blood samples were collected at the baseline at 30 min during each exposure, and at 0, 0.5, 1, 2, 3, and 4 h after each exposure. The values of white blood cells (WBC) at 1 h (p = 0.010), 3 h (p = 0.040), and 4 h (p = 0.008) following SHS were significantly increased compared with the baseline values. Also, there was a positive association between the WBC and cotinine levels (r = 0.28, p = 0.007). A 1-h exposure to SHS at bar/restaurant levels significantly increased the WBC for at least 4 h following the exposure time. This effect of SHS on WBC has dose-response characteristics and should be considered to prescribing CBC.

Individualised aerobic and resistance exercise training improves cardiorespiratory fitness and reduces cardiovascular risk in patients with rheumatoid arthritis.

BACKGROUND AND OBJECTIVES: Low cardiorespiratory fitness (CRF) is a significant predictor of cardiovascular disease (CVD), and interventions aiming at increasing CRF are known to reduce CVD risk. The effects of such interventions on CVD risk have not been studied in patients with rheumatoid arthritis (RA). METHODS: 40 age, gender, body mass index (BMI) and disease duration matched RA patients were allocated to either an exercise (receiving 6 months individualised aerobic and resistance high intensity exercise intervention, three times per week), or control (receiving advice on exercise benefits and lifestyle changes) arm. Participants were assessed at baseline, 3 and 6 months for aerobic capacity (VO2max), individual CVD risk factors (blood pressure, lipids, insulin resistance, body composition), 10-year CVD event probability and RA characteristics (C-reactive protein (CRP), Disease Activity Score 28 (DAS28) and Health Assessment Questionnaire (HAQ)). RESULTS: There were no differences between groups at baseline in any of the assessed variables. VO2max (p=0.001), blood pressure (systolic: p<0.001; diastolic: p=0.003), triglycerides (p=0.030), high density lipoprotein (HDL; p=0.042), total cholesterol:HDL ratio (p=0.005), BMI (p=0.001), body fat (p=0.026), 10-year CVD event probability (p=0.012), CRP (p=0.042), DAS28 (p=0.008) and HAQ (p=0.003) were all significantly improved in the exercise versus the control group. The change in VO2max was the strongest predictor for the observed improvements in all of the assessed CVD risk factors and disease characteristics. CONCLUSIONS: Individualised aerobic and resistance exercise intervention can lead to significantly improved CRF, individual CVD risk factors, composite CVD risk, and disease activity and severity in RA patients.

Secondhand smoke exposure induces acutely airway acidification and oxidative stress.

Previous studies have shown that secondhand smoke induces lung function impairment and increases proinflammatory cytokines. The aim of the present study was to evaluate the acute effects of secondhand smoke on airway acidification and airway oxidative stress in never-smokers. In a randomized controlled cross-over trial, 18 young healthy never-smokers were assessed at baseline and 0, 30, 60, 120, 180 and 240 min after one-hour secondhand smoke exposure at bar/restaurant levels. Exhaled NO and CO measurements, exhaled breath condensate collection (for pH, H(2)O(2) and NO(2)(-)/NO(3)(-) measurements) and spirometry were performed at all time-points. Secondhand smoke exposure induced increases in serum cotinine and exhaled CO that persisted until 240 min. Exhaled breath condensate pH decreased immediately after exposure (p < 0.001) and returned to baseline by 180 min, whereas H(2)O(2) increased at 120 min and remained increased at 240 min (p = 0.001). No changes in exhaled NO and NO(2)/NO(3) were observed, while decreases in FEV(1) (p < 0.001) and FEV(1)/FVC (p < 0.001) were observed after exposure and returned to baseline by 180 min. A 1-h exposure to secondhand smoke induced airway acidification and increased airway oxidative stress, accompanied by significant impairment of lung function. Despite the reversal in EBC pH and lung function, airway oxidative stress remained increased 4 h after the exposure. Clinical trial registration number (EudraCT): 2009-013545-28.

Anti-tumour necrosis factor alpha therapy improves insulin sensitivity in normal-weight but not in obese patients with rheumatoid arthritis.

INTRODUCTION: Insulin resistance (IR), a risk factor for the development of cardiovascular disease, is common among patients with rheumatoid arthritis (RA). Inflammation, and especially tumour necrosis factor alpha (TNFα), has been associated with IR, and the administration of anti-TNFα agents is suggested to improve insulin sensitivity. However obesity, a potent contributor to IR, may limit the beneficial effects of anti-TNFα medication on IR. The aim of this study is to compare the effects of anti-TNFα therapy on IR between normal-weight and obese patients with RA. METHODS: Patients who were normal-weight with IR (N+IR) or obese with IR (O+IR) and had embarked on anti-TNFα treatment, participated. Assessments included body mass index (BMI), insulin sensitivity (Homeostasis Model Assessment of insulin resistance, HOMA and the Quantitative Insulin sensitivity Check Index, QUICKI), and RA disease characteristics before and following six months of anti-TNFα treatment. Their results were compared to matched (for age, gender, BMI, disease duration and smoking status) normal-weight patients without IR (N-IR) and obese without IR (N-IR), respectively. In total, 32 patients were assessed for this study, with 8 in each group. RESULTS: Following six months of treatment, disease activity was significantly reduced in all groups (P < 0.05) to a similar extent (P for differences between groups > 0.05 in all cases). In the total population, changes in HOMA (mean reduction at 6 m = -0.2 ± 0.1; P = 0.088) and QUICKI (mean increase at 6 m = 0.03 ± 0.022; P = 0.092) after treatment were not statistically significant, though a trend towards improvement was observed. However, N+IR patients showed a significant decrease in HOMA (mean reduction at 6 m = -0.54 ± 0.2; P = 0.002) and increase in QUICKI (mean increase at 6 m = 0.046 ± 0.02; P = 0.011). These changes were significantly different compared to the other groups (P < 0.05 in all cases). Multivariable analyses showed that the change in Erythrocyte Sedimentation Rate (ESR), and the change in C-Reactive Protein (CRP) associated with the improvement in HOMA (ESR: F1₋7 = 5.143, P = 0.019; CRP: F1₋7 = 3.122, P = 0.022) and QUICKI (ESR: F1₋7 = 3.814, P = 0.021; CRP: F1₋7 = 2.67; P = 0.041) only in the N+IR group. CONCLUSIONS: Anti-TNFα therapy, through controlling inflammation, seems to improve insulin sensitivity in normal-weight RA patients with insulin resistance, but is not sufficient to achieving the same beneficial effect in obese RA patients with insulin resistance.

Respiratory and immune response to maximal physical exertion following exposure to secondhand smoke in healthy adults.

We assessed the cardiorespiratory and immune response to physical exertion following secondhand smoke (SHS) exposure through a randomized crossover experiment. Data were obtained from 16 (8 women) non-smoking adults during and following a maximal oxygen uptake cycling protocol administered at baseline and at 0-, 1-, and 3- hours following 1-hour of SHS set at bar/restaurant carbon monoxide levels. We found that SHS was associated with a 12% decrease in maximum power output, an 8.2% reduction in maximal oxygen consumption, a 6% increase in perceived exertion, and a 6.7% decrease in time to exhaustion (P<0.05). Moreover, at 0-hours almost all respiratory and immune variables measured were adversely affected (P<0.05). For instance, FEV(1) values at 0-hours dropped by 17.4%, while TNF-α increased by 90.1% (P<0.05). At 3-hours mean values of cotinine, perceived exertion and recovery systolic blood pressure in both sexes, IL4, TNF-α and IFN-γ in men, as well as FEV(1)/FVC, percent predicted FEV(1), respiratory rate, and tidal volume in women remained different compared to baseline (P<0.05). It is concluded that a 1-hour of SHS at bar/restaurant levels adversely affects the cardiorespiratory and immune response to maximal physical exertion in healthy nonsmokers for at least three hours following SHS.

Inverted BMI rather than BMI is a better proxy for percentage of body fat.

BACKGROUND: Percentage of body fat (BF%) is a known risk factor for a range of healthcare problems but is difficult to measure. An easy to measure proxy is the weight/height(2) ratio known as the Body Mass Index (BMI kg/m(2)). However, BMI does have some inherent weaknesses which are readily overcome by its inverse iBMI (1000/BMI, cm(2)/kg). METHODS: The association between BF% and both BMI and iBMI together with their distributional properties was explored using previously published data from healthy (n = 2993) and diseased populations (n = 298). RESULTS: BMI is skewed whereas iBMI is symmetrical and so is better approximated by the normal distribution. The relationship between BF% and BMI is curved, but that of iBMI and BF% is linear and thus iBMI explains more of the variation in BF% than BMI. For example a unit increase in BMI for a group of thin women represents an increase of 2.3% in BF, but for obese women this represents only a 0.3% increase in BF-a 7-fold difference. The curvature stems from body mass being the numerator in BMI but the denominator in BF% resulting in a form of hyperbolic curve which is not the case with iBMI. Furthermore, BMI and iBMI have different relationships (interaction) with BF% for men and women, but these differences are less marked with iBMI. CONCLUSIONS: Overall, these characteristics of iBMI favour its use over BMI, especially in statistical models.

Rheumatoid arthritis susceptibility genes associate with lipid levels in patients with rheumatoid arthritis.

INTRODUCTION: Rheumatoid arthritis (RA), a systemic inflammatory disease with complex genetic aetiology, associates with excess cardiovascular morbidity and mortality. Dyslipidaemia, a major cardiovascular risk factor has been reported to predate the onset of RA, thus suggesting a potential genetic link between the two conditions. The authors assessed whether RA susceptibility genes associate with the presence of dyslipidaemia in RA patients. METHODS: 400 well-characterised RA patients were included in this cross-sectional study. Fasting lipid profile (total cholesterol, high-density lipoproteins (HDL), low-density lipoproteins (LDL), triglycerides, apolipoproteins (ApoA and ApoB) and lipoprotein (a)) and four RA susceptibility genes (PTPN22, TRAF1/C5, STAT4 and human leucocyte antigen shared epitope (HLA-SE)) were assessed and associations were sought in both univariate and multivariate analyses. RESULTS: Following adjustment for age, sex and erythrocyte sedimentation rate, the G allele of TRAF1/C5 associated with lower total cholesterol (p=0.010), LDL (p=0.022) and ApoB (p=0.014); one or more copies of the shared epitope associated with lower ApoA (p=0.035) and higher ApoB:ApoA ratio (p=0.047); while STAT4 TT homozygotes had higher lipoprotein (a) (p=0.004). CONCLUSIONS: RA susceptibility genes (TRAF1/C5, STAT4 and HLA-DRB1-SE) may be involved in the regulation of lipid metabolism in RA patients, thus contributing to cardiovascular disease (CVD) risk and adverse outcome. If these findings are replicated, such genotyping could be used to identify and target for prevention those RA patients most at risk of CVD. It will also be interesting to study the association of these genes with lipid levels in the general population and identify mechanisms to explain the link.

Obesity in rheumatoid arthritis.

Obesity is a major threat for public health and its study has attracted significant attention in the general population, predominantly due to its association with significant metabolic and cardiovascular complications. In RA research, BMI is frequently reported as a demographical variable, but obesity, as such, has received little interest. This is surprising, in view of the clear associations of obesity with other arthritides, particularly OA, but also in view of the now-clear association of RA with increased cardiovascular morbidity and mortality. In this review, we summarize the studies that have looked into obesity in the RA population, evaluate their findings, identify knowledge gaps and propose directions for future research. We also pose a question of high clinical and research significance: is the use of BMI still a valid way of assessing obesity in RA?

Passive smoking and the development of cardiovascular disease in children: a systematic review.

Passive smoking may be implicated in the development of cardiovascular disease (CVD) in children because of their partially developed physiological systems. The aim of the present systematic paper is to investigate whether passive smoking is associated with factors that influence the development of CVD in children. Data sources included Medline, Cochrane Library, Cumulative Index to Nursing & Allied Health (CINAHL) research database, Google Scholar, Excerpta Medica database (EMBASE), the 2006 Office of the Surgeon General's report, and the 2005 report from the California Environmental Protection Agency. We identified a total of 42 relevant articles (i.e., 30 reviews and 12 observational). Results revealed that passive smoking may be implicated in deteriorating cardiovascular status in children in terms of unfavorable high-density lipoprotein levels and deteriorated vascular function.

Rheumatoid cachexia and cardiovascular disease.

Both cachexia and cardiovascular disease are strongly associated with rheumatoid arthritis (RA) and linked to the chronic inflammatory process. Typically, rheumatoid cachexia occurs in individuals with normal or increased BMI (reduced muscle mass and increased fat mass). Classic cachexia (reduced muscle mass and reduced fat mass) is rare in RA but is associated with high inflammatory activity and aggressive joint destruction in patients with a poor cardiovascular prognosis. Conversely, obesity is linked to hypertension and dyslipidemia but, paradoxically, lower RA disease activity and less cardiovascular disease-related mortality. Rheumatoid cachexia might represent the 'worst of both worlds' with respect to cardiovascular outcome, but until diagnostic criteria for this condition are agreed upon, its effect on cardiovascular disease risk remains controversial.

Cardiorespiratory and immune response to physical activity following exposure to a typical smoking environment.

OBJECTIVE: Millions of non-smokers suffer daily passive smoking (PS) at home or at work, many of whom then have to walk fast for several minutes or climb a few sets of stairs. We conducted a randomised single-blind crossover experiment to assess the cardiorespiratory and immune response to physical activity following PS. DESIGN: Data were obtained from 17 (eight women) non-smoking adults during and following 30 minutes of moderate cycling administered at baseline and at 0 hour, 1 hour and 3 hours following a 1-hour PS exposure set at bar/restaurant PS levels. RESULTS: We found that PS was associated with a 36% and 38.7% decrease in mean power output in men and women, respectively, and that this effect persisted up to 3 hours (p<0.05). Moreover, at 0 hour almost all cardiorespiratory and immune variables measured were markedly reduced (p<0.05). For instance, FEV(1) values at 0 hour dropped by 10.2% in men and 10.8% in women, while IL-5 increased by 59.2% in men and 44% in women, respectively (p<0.05). At 3-hour mean values of respiratory quotient, mean power, perceived exertion, cotinine, FEV(1), IL-5, IL-6 and INFgamma in both sexes, recovery diastolic and mean arterial pressure, IL-4 and TNFalpha in men, as well as percentage predicted FEV(1) in women remained different compared to baseline (p<0.05). Also, some of the PS effects were exacerbated in less fit individuals. CONCLUSION: It is concluded that 1 hour of PS at bar/restaurant levels adversely affects the response to moderate physical activity in healthy non-smokers for at least 3 hours following PS.

Biological evidence for the acute health effects of secondhand smoke exposure.

A vast number of studies on the unfavorable effects of secondhand smoke (SHS) exist within the international literature, the majority of which evaluate longitudinal epidemiological data. Although limited, the experimental studies that assess the acute and short-term effects of exposure to SHS are also increasing in number. They include cellular, animal, and human studies that indicate a number of pathophysiological mechanisms through which the deleterious effects of SHS may arise. This current review evaluates the existing biological evidence regarding the acute health effects of SHS exposure. Analyses on the inhaled toxicants and the carcinogenicity of SHS are included as well as in-depth discussions on the evidence for acute SHS-induced respiratory, cardiovascular, metabolic, endocrine and immune effects, and SHS-induced influences on oxygen delivery and exercise. The influence of the length of exposure and the duration of the observed effects is also described. Moreover, recent findings regarding the underlying pathophysiological mechanisms related to SHS are depicted so as to generate models that describe the SHS-induced effects on different systems within the human body. Based on the presented biological evidence, it is concluded that brief, acute, transient exposures to SHS may cause significant adverse effects on several systems of the human body and represent a significant and acute health hazard. Future research directions in this area include research on the concentrations of tobacco smoke constituents in the alveolar milieu following SHS exposure, individual susceptibility to SHS, as well as the effects of SHS on neurobehavioral activity, brain cell development, synaptic development, and function.

Target organ damage in patients with rheumatoid arthritis: the role of blood pressure and heart rate.

BACKGROUND: Rheumatoid arthritis (RA) is characterised by increased cardiovascular morbidity and mortality. Even though hypertension (HT) is highly prevalent in RA, the extent of target organ damage (TOD) caused by it remains unknown. Inflammation and sympathetic overdrive may also associate with TOD. We investigated the prevalence and associations of TOD in RA. METHODS: In this cross-sectional, observational study, 251 RA patients with no overt cardiovascular or renal disease had extensive clinical and laboratory evaluations, including a 12-lead electrocardiogram and urine albumin:creatinine ratio. Pulse pressure (PP) was used as a proxy of arterial stiffness and heart rate (HR) of autonomic activity. TOD was defined as described in the European guidelines for the management of arterial hypertension. Binary logistic regression analysis was used to evaluate the independence of the variables that associated with the presence of TOD. RESULTS: TOD prevalence was 23.5% (59/251). Of the 59 patients with TOD, 45.8% had suboptimally controlled HT, whereas 32.3% had undiagnosed HT. In univariable analysis, TOD was significantly associated with higher age (64.2+/-11.7 years vs. 58.0+/-12.4 years, p=0.001), HT prevalence (89.8% vs. 60.4%, p<0.001), systolic blood pressure (SBP) (150.3+/-18.8mmHg vs. 139.7+/-20.7mmHg, p=0.001), PP (70.6+/-16.6mmHg vs. 60.3+/-17.3mmHg, p<0.001), HR (77.1+/-15.4bpm vs. 72.2+/-12.2bpm, p<0.001), serum uric acid (320.6+/-88.8mumol/l vs. 285.0+/-74.9mumol/l, p=0.03) and type 2 diabetes mellitus prevalence (13.6% vs. 4.7%, p=0.019). Binary logistic regression analysis revealed that only hypertension indices and HR associated independently with TOD. CONCLUSIONS: TOD is highly prevalent in patients with RA and associates independently with hypertension, arterial stiffness and heart rate. Further prospective studies are needed to confirm these findings and examine the role of beta-blockers in this particular population.

Prediction of VO2max from a new field test based on portable indirect calorimetry.

We assessed the validity and reliability of the new 15m square shuttle run test (SST) for predicting laboratory treadmill test (TT) maximal oxygen uptake (VO(2 max)) compared to the 20 m multistage shuttle run test (MST) in 45 adult males. Thirty participants performed a TT and a SST once to develop a VO( 2max) prediction model. The remaining 15 participants performed the TT and MST once and the SST twice for cross-validation purposes. Throughout testing V O(2max) was determined via portable indirect calorimetry while blood lactate concentration was assessed at the fifth recovery minute. Comparisons of TT V O(2 max) (51.3+/-3.1 ml kg(-1)min(-1)) with SST measured (51.2+/-3.2 ml kg(-1)min(-1)) and predicted (50.9+/-3.3 ml kg(-1)min(-1)) V O(2 max) showed no differences while TT blood lactate was higher compared to SST (10.3+/-1.7 mmol vs. 9.7+/-1.7 mmol, respectively). In contrast, MST measured (53.4+/-3.5 ml kg(-1)min(-1)) and predicted (57.0+/-4.5 ml kg(-1)min(-1)) V O(2 max) and blood lactate (11.2+/-2.0 mmol) were significantly higher compared to TT. No test-retest differences were detected for SST measured and predicted V O(2 max) and blood lactate. It is concluded that the SST is a highly valid and reliable predictive test for V O(2 max).

Passive smoking, asthma and allergy in children.

Despite the recent campaigns to eliminate smoking and hinder the detrimental effects of passive smoking (PS), actual smoking rates still increase worldwide. Several physiological systems, with the respiratory being the primary, are disrupted by PS and progressively deteriorate through chronic exposures. This is of particular importance in children, given that respiratory complications during childhood can be transferred to adulthood, lead to significantly inferior health profiles. Hence, it is no surprise that children that are exposed to PS either in utero or during their adulthood may have an increased prevalence of allergies and asthma. However, investigating the acute effects of PS in children is inherently limited by complexities pertaining mainly to ethical constrains. Knowledge of the acute effects could be very important as it is the dose-dependant acute effects of passive smoking that lead to the long-term adaptations linked with the development of allergy and asthma. Current available data show that the chemical and carcinogenic constituents of tobacco have profound effects on children's health as they may disrupt normal biological development. PS appears to have pronounced effects on respiratory parameters that promote asthma development and persistent wheezing rather than other allergies. As such, PS exposure has to be eliminated and researchers have to develop interventions for supporting smoking cessation as well as minimised PS exposure either this is in utero or during childhood.

Effects of secondhand smoke on thyroid function.

Growing evidence suggests that the effects of second hand smoke (SHS) exposure contribute to disruptions in thyroid function. Toxic elements contained in cigarette smoke, such as thiocyanate, may be partially responsible for impaired thyroid hormonogenesis. SHS-induced inflammatory stress, namely interleukin 1beta (IL-1beta), impairs thyroid hormonogenesis and iodine uptake; initiates interleukin 6 (IL-6) production from thyroid epithelial cells and stimulates the expression of molecules that exacerbate thyroid autoimmunity. The link between SHS exposure and thyroid autoimmune disease is not well documented and thus, remains to be fully understood. Elevated inflammatory stress and thyroid hormone secretion in response to SHS exposure initiates catabolic processes that alter body composition via lean body mass breakdown; translating to an elevation in resting energy expenditure of approximately 10%. The combination of certain biological factors, such as sex and/or existing thyroid disease may stimulate differential SHS-induced effects on thyroid function. Nevertheless, exposure to SHS disturbs vital human processes via thyroid disruption.

Acute and short-term effects of secondhand smoke on lung function and cytokine production.

RATIONALE: The acute effect of secondhand smoke (SHS) on lung function and the duration of system disruption remain unknown. OBJECTIVES: To assess the SHS effects and their duration on lung function and inflammatory markers. METHODS: In a randomized single-blind crossover experiment data were obtained from 16 (8 women) nonsmoking adults at baseline and at 0, 1, and 3 hours after a 1-hour SHS exposure set at bar/restaurant SHS levels. MEASUREMENTS AND MAIN RESULTS: Serum and urine cotinine, lung function, and cytokines IL-4, IL-5, IL-6, tumor necrosis factor (TNF)-alpha, and IFN-gamma. At 0 hours most lung function parameters were significantly reduced (indicative: FEV(1), 4.3 +/- 0.4 vs. 3.8 +/- 0.3 L; FEV(1)/FVC, 0.9 +/- 0.1 vs. 0.8 +/- 0.1; P < 0.05) but at 3 hours they were at baseline levels. In contrast, cotinine (serum, 8.9 +/- 3.2 vs. 35.5 +/- 10.2 ng x ml(-1)), IL-4 (41.3 +/- 5.8 vs. 44.2 +/- 4.5 pg x ml(-1)), IL-5 (36.1 +/- 3.2 vs. 60.1 +/- 7.0 pg x ml(-1)), IL-6 (2.5 +/- 0.3 vs. 7.6 +/- 1.4 pg x ml(-1)) and IFN-gamma (0.3 +/- 0.2 vs. 0.6 +/- 0.2 IU x ml(-1)) at 3 hours were higher than at baseline (P < 0.05). IL-4 and TNF-alpha increased only in men, whereas IL-5, IL-6, and IFN-gamma were different between sexes after exposure (P < 0.05). Regression analyses revealed inverse associations of FEV(1) and FEV(1)/FVC ratio with IL-5 (P < 0.05) in men and with IL-5 (P = 0.01), IL-6 (P < 0.001), IFN-gamma (P = 0.034) and serum cotinine (P < 0.001) in women. CONCLUSIONS: We conclude that 1 hour of SHS exposure at bar/restaurant levels is accompanied by significant decrements on lung function and marked increases in inflammatory cytokines, particularly in men. More importantly, whereas most smoke-induced effects on lung function appear to recede within 60 minutes, inflammatory cytokines remain elevated for at least 3 hours after exposure to SHS.

Association of physical inactivity with increased cardiovascular risk in patients with rheumatoid arthritis.

OBJECTIVE: Patients with rheumatoid arthritis (RA) are characterized by reduced physical activity and increased morbidity and mortality from cardiovascular disease (CVD). The aim of this study was to investigate associations between levels of physical activity and CVD risk profile in RA patients. METHODS: Levels of physical activity were assessed in 65 RA patients (43 females). Using the International Physical Activity Questionnaire, patients were allocated into three groups: active, moderately active and inactive. Anthropometric characteristics, RA activity/severity, multiple classical and novel CVD risk factors and 10-year CVD event probability were assessed and compared among the three groups. RESULTS: Significant differences were detected among groups in systolic blood pressure (P=0.006), cholesterol (P<0.001), low-density lipoprotein (P=0.01), homeostasis model assessment (P=0.001), type-I plasminogen activator inhibitor antigen (P<0.001), tissue-type plasminogen activator antigen (P=0.019), homocysteine (P=0.027), fibrinogen (P=0.001), apolipoprotein B (P=0.002) and von Willebrand Factor (P=0.001), with a consistent deterioration from the physically active to the physically inactive group. Multivariate analysis of variance revealed that levels of physical activity were significantly associated with the differences in all of the above variables (P<0.05) after adjustment for age, weight, sex, smoking status, as well as RA disease activity and severity. CONCLUSION: This cross-sectional study suggests that physically inactive RA patients have significantly worse CVD risk profile compared with physically active patients. The possible beneficial impact of increased physical activity, including structured exercise, to the CVD risk of RA patients needs to be accurately assessed in prospective studies.

Underweight and obese states both associate with worse disease activity and physical function in patients with established rheumatoid arthritis.

Obesity is characterised by low-grade inflammation and could potentially affect disease activity and severity in patients with rheumatoid arthritis (RA). Body mass index (BMI), body fat (BF), erythrocyte sedimentation rate, C-reactive protein, disease activity score 28, physical function (health assessment questionnaire) and presence of erosions and joint surgery were assessed in 294 (female=219) volunteers with established RA [age 63.3 (56.2-69.6); disease duration 13 (7-20) years]. Smoking status, rheumatoid factor and anti-cyclic citrullinated peptide positivity were also assessed. BMI and BF independently associated with disease characteristics. Compared to normal-weight patients, underweight and obese had higher C-reactive protein (p=0.046) and physical dysfunction (p=0.034). BMI or BF did not associate with presence of erosions or joint surgery. In patients with established RA, both very low and very high BMI and BF associate independently with increased disease activity and physical dysfunction; however, this does not seem to associate with presence of erosions or joint surgery. Further longitudinal studies are required to address this apparent dissociation.