Electronic cigarette use in relation to changes in smoking status and respiratory symptoms.

INTRODUCTION: How e-cigarette use relates to changes in smoking status and respiratory symptoms in the population remains controversial. The aim was to study the association between e-cigarette use and, changes in smoking status and changes in respiratory symptoms. METHODS: A prospective, population-based study of random samples of the population (age 16-69 years) was performed within The Obstructive Lung Disease in Northern Sweden (OLIN) study and West Sweden Asthma Study (WSAS). A validated postal questionnaire containing identical questions was used in OLIN and WSAS at baseline in 2006-2008 and at follow-up in 2016. In total, 17325 participated on both occasions. Questions about respiratory symptoms and tobacco smoking were included in both surveys, while e-cigarette use was added in 2016. RESULTS: In 2016, 1.6% used e-cigarettes, and it was significantly more common in persistent tobacco smokers (10.6%), than in those who quit smoking (2.1%), started smoking (7.8%), or had relapsed into tobacco smoking at follow-up (6.4%) (p<0.001). Among current smokers at baseline, tobacco smoking cessation was less common in e-cigarette users than e-cigarette non-users (14.2% vs 47.6%, p<0.001) and there was no association with a reduction in the number of tobacco cigarettes smoked per day. Those who were persistent smokers reported increasing respiratory symptoms. In contrast, the symptoms decreased among those who quit tobacco smoking, but there was no significant difference in respiratory symptoms between quitters with and without e-cigarette use. CONCLUSIONS: E-cigarette use was associated with persistent tobacco smoking and reporting respiratory symptoms. We found no association between e-cigarette use and tobacco smoking cessation, reduction of number of tobacco cigarettes smoked per day or reduction of respiratory symptoms.

Use of heated tobacco products (IQOS) causes an acute increase in arterial stiffness and platelet thrombus formation.

BACKGROUND AND AIMS: Heated tobacco products (HTPs) are novel alternative tobacco products being promoted as an alternative to cigarettes. To evaluate the impact of HTP use on vascular function, we investigated the effects of a brief HTP usage on arterial stiffness and platelet thrombus formation in healthy volunteers. METHODS: In a randomised crossover study, twenty-four healthy young adults with occasional tobacco use smoked the HTP IQOS 3 Multi (Phillip Morris Int.) and "no-exposure" was used as a control, with a wash-out period of at least one week in-between. Arterial stiffness was assessed through pulse wave velocity and pulse wave analysis. Blood samples, collected at baseline and 5 min following exposure, were analysed with the Total-Thrombus-formation analysis system evaluating platelet and fibrin-rich thrombus formation tendency. RESULTS: HTP exposure caused immediate heightened pulse wave velocity (+0.365 m/s, 95% CI: +0.188 to 0.543; p = 0.004) and enhanced augmentation index corrected to heart rate (+6.22%, 95% CI: +2.33 to 10.11; p = 0.003) compared to the no-exposure occasion. Similarly, blood pressure and heart rate transiently increased immediately following HTP inhalation. Platelet thrombus formation significantly increased following HTP exposure (area under the curve +59.5, 95% CI: +25.6 to 93.4; p < 0.001) compared to no-exposure. No effect was seen on fibrin-rich thrombus formation following HTP-exposure. CONCLUSIONS: Brief HTP use in healthy young adults had immediate adverse effects on vascular function resulting in increased arterial stiffness and platelet thrombus formation, known risk factors for the development of atherosclerosis. Further research is needed to address long term health impacts.

Electronic Cigarette Vaping with Nicotine Causes Increased Thrombogenicity and Impaired Microvascular Function in Healthy Volunteers: A Randomised Clinical Trial.

Electronic cigarette (EC) vaping is increasingly popular, despite growing evidence of adverse health effects. To further evaluate the impact of EC use on vascular health, we investigated the effects of brief EC inhalation on flow-dependent thrombus formation and microcirculation in healthy volunteers. The study was performed with a randomised double-blind crossover design. Twenty-two healthy subjects aged between 18 and 45 years with occasional tobacco use were recruited. Subjects inhaled 30 puffs of EC aerosol with and without nicotine on two occasions separated by a wash-out period of at least 1 week. Blood samples were collected at baseline and at 15 and 60 min following exposure and analysed with the Total-Thrombus-formation analysis system evaluating fibrin-rich thrombus formation and platelet thrombus formation in whole blood under flow. Microvascular function was assessed at baseline and 30 min after exposure by laser speckle contrast imaging and iontophoresis of acetylcholine and sodium nitroprusside (SNP) to evaluate the endothelium-dependent and independent pathways of vasodilation. Compared with nicotine free EC aerosol, exposure to EC aerosol with nicotine significantly increased platelet thrombus formation and fibrin-rich thrombus formation at 15 min (p = 0.017 and p = 0.037, respectively) with normalisation after 60 min. Peak SNP-mediated microvascular perfusion, i.e. endothelium-independent vasodilation, was reduced following EC vaping with nicotine compared with baseline (p = 0.006). Thirty puffs of EC aerosol with nicotine increased platelet and fibrin-dependent thrombus formation and reduced microvascular dilatation capacity. No compelling effects of EC vaping without nicotine were observed, indicating nicotine as the main effector. Trial registration: ClinicalTrials.gov Identifier: NCT04175457 URL: https://clinicaltrials.gov/ct2/show/NCT04175457.

Admission glucose as a prognostic marker for all-cause mortality and cardiovascular disease.

BACKGROUND: Diabetes and prediabetes are known risk factors for cardiovascular disease and associated with increased mortality risk. Whether patients with a random elevated blood glucose level but no history of diabetes are at a higher mortality and cardiovascular risk is not entirely known. METHODS: A retrospective cohort study where patients (18-80 years) with no history of diabetes between 2006 and 2016 attending the emergency department (ED) in Sweden were included. Based on the first (index) blood glucose level patients were categorized into four groups: hypoglycemia (< 3.9 mmol/L), normal glucose tolerance (NGT) (3.9-7.8 mmol/L), dysglycemia (7.8-11.1 mmol/L), and hyperglycemia (> 11.1 mmol/L). Data was collected from four nationwide registers (National Patient Register, National Cause of Death Register, Prescribed Drug Register and Statistics Sweden). Cox regression was used to calculate adjusted hazard ratios (HR) with 95% confidence intervals (CI) for all-cause mortality and cardiovascular outcomes using NGT as reference. RESULTS: 618,694 patients were included during a mean follow-up time of 3.9 years. According to the index blood glucose level: 1871 (0.3%) had hypoglycemia, 525,636 (85%) had NGT, 77,442 (13%) had dysglycemia, and 13,745 (2%) patients had hyperglycemia, respectively. During follow-up 44,532 (7.2%) deaths occurred. After multiple adjustments, mortality risk was highest in patients with hypoglycemia HR 2.58 (2.26-2.96) followed by patients with hyperglycemia HR 1.69 (1.63-1.76) and dysglycemia HR 1.16 (1.13-1.19). Risk for cardiovascular events: i.e., myocardial infarction, stroke and heart failure, were highest among patients with hyperglycemia HR 2.28 (2.13-2.44), HR 1.62 (1.51-1.74) and HR 1.60 (1.46-1.75), respectively. CONCLUSION: Patients with disturbed blood glucose level at ED admission have a higher mortality risk than patients with NGT. Patients with hyperglycemia have almost a two folded increased long-term mortality risk and more than a doubled risk for cardiovascular events compared to patients with NGT.

Chronic snus use in healthy males alters endothelial function and increases arterial stiffness.

BACKGROUND: Snus usage is commonly touted as a safer alternative to cigarette smoking. However, recent studies have demonstrated possible adverse cardiovascular effects in chronic snus users. The present study evaluates the effects of chronic snus use on vascular function by assessing central arterial stiffness and endothelial vasodilatory function in healthy chronic snus users as compared to matched non-users. METHODS AND RESULTS: Fifty healthy males (24 snus users, 26 age-matched controls) with a mean age of 44 years were included in the study. Arterial stiffness was assessed employing both pulse wave velocity and pulse wave analysis. Endothelial vasodilatory function was measured by venous occlusion plethysmography, utilizing intra-arterial administration of acetylcholine, glyceryl trinitrate and bradykinin to further gauge endothelium-dependent and -independent vasodilatory function. Arterial stiffness was significantly higher in chronic snus users as compared to controls: pulse wave velocity [m/s]: 6.6±0.8 vs 7.1±0.9 resp. (p = 0.026), augmentation index corrected for heart rate [%]: 0.1±13.2 vs 7.3±7.8 resp. (p = 0.023). Endothelial independent vasodilation, i.e. the reaction to glyceryl trinitrate, was significantly lower in snus users as measured by venous occlusion plethysmography. CONCLUSIONS: The results of this study show an increased arterial stiffness and an underlying endothelial dysfunction in daily snus users as compared to matched non-tobacco controls. These findings indicate that long-term use of snus may alter the function of the endothelium and therefore reinforces the assertion that chronic snus use is correlated to an increased risk of development of cardiovascular disease.

Predictors of electronic cigarette use among Swedish teenagers: a population-based cohort study.

OBJECTIVES: The aim was to identify predictors of electronic cigarette (e-cigarette) use among teenagers. DESIGN AND SETTING: A prospective population-based cohort study of schoolchildren in northern Sweden. PARTICIPANTS: In 2006, a cohort study about asthma and allergic diseases among schoolchildren started within the Obstructive Lung Disease in Northern Sweden studies. The study sample (n=2185) was recruited at age 7-8 years, and participated in questionnaire surveys at age 14-15 and 19 years. The questionnaire included questions about respiratory symptoms, living conditions, upper secondary education, physical activity, diet, health-related quality of life, parental smoking and parental occupation. Questions about tobacco use were included at age 14-15 and 19 years. PRIMARY OUTCOME: E-cigarette use at age 19 years. RESULTS: At age 19 years, 21.4% had ever tried e-cigarettes and 4.2% were current users. Among those who were daily tobacco smokers at age 14-15 years, 60.9% had tried e-cigarettes at age 19 years compared with 19.1% of never-smokers and 34.0% of occasional smokers (p<0.001). Among those who had tried e-cigarettes, 28.1% were never smokers both at age 14-15 and 19 years, and 14.4% were never smokers among the current e-cigarette users. In unadjusted analyses, e-cigarette use was associated with daily smoking, use of snus and having a smoking father at age 14-15 years, as well as with attending vocational education, physical inactivity and unhealthy diet. In adjusted analyses, current e-cigarette use was associated with daily tobacco smoking at age 14-15 years (OR 6.27; 95% CI 3.12 to 12.58), attending a vocational art programme (OR 2.22; 95% CI 1.04 to 4.77) and inversely associated with eating a healthy diet (OR 0.74; 95% CI 0.59 to 0.92). CONCLUSIONS: E-cigarette use was associated with personal and parental tobacco use, as well as with physical inactivity, unhealthy diet and attending vocational upper secondary education. Importantly, almost one-third of those who had tried e-cigarettes at age 19 years had never been tobacco smokers.

Electronic cigarettes containing nicotine increase endothelial and platelet derived extracellular vesicles in healthy volunteers.

BACKGROUND AND AIMS: E-cigarette use is increasingly common. Whether e-cigarettes are harmful to human health is an intensely debated subject. In order to investigate whether e-cigarettes with and without nicotine cause different vascular responses, we obtained blood samples from healthy young volunteers who performed brief active e-cigarette inhalations. Extracellular vesicles (EVs) of endothelial and platelet origin were measured to determine vascular changes. METHODS: Using a randomized, double-blind, crossover design, 17 healthy occasional smokers inhaled 30 puffs of e-cigarette vapor during 30 min. Blood samples were collected at baseline, as well as at 0, 2, 4 and 6 h post-exposure. EVs from platelets and endothelial cells were measured by flow cytometry. RESULTS: Platelet and endothelial derived EVs were significantly increased with peak levels seen at 4 h following exposure to active inhalation of e-cigarette vapor with nicotine. Moreover, platelet derived EVs, expressing platelet activation marker P-selectin and the inflammation marker, CD40 ligand, were also significantly increased following inhalation of e-cigarette vapor with nicotine. In addition, platelet derived EVs expressing CD40 ligand was increased after inhalation of e-cigarette vapor without nicotine. CONCLUSION: As few as 30 puffs of nicotine-containing e-cigarette vapor caused an increase in levels of circulating EVs of endothelial and platelet origin, which may signify underlying vascular changes. Although e-cigarette vapor without nicotine caused an increase in platelet EVs expressing CD40 ligand, nicotine, as a component in the vapor, seems to have a more compelling effect on extracellular vesicle formation and protein composition.

Acute versus chronic myocardial injury and long-term outcomes.

OBJECTIVE: There is a paucity of data regarding prognosis in patients with acute versus chronic myocardial injury for long-term outcomes. We hypothesised that patients with chronic myocardial injury have a similar long-term prognosis as patients with acute myocardial injury. METHODS: In an observational cohort study of 22 589 patients who had high-sensitivity cardiac troponin T (hs-cTnT) measured in the emergency department during 2011-2014, we identified all patients with level >14 ng/L and categorised them as acute myocardial injury, type 1 myocardial infarction (T1MI), type 2 myocardial infarction (T2MI) or chronic myocardial injury through adjudication. We estimated adjusted HRs with 95% CIs for the primary outcome all-cause mortality and secondary outcomes MI, and heart failure in patients with acute myocardial injury, T1MI and T2MI compared with chronic myocardial injury. RESULTS: In total, 3853 patients were included. During 3.9 (±2) years of follow-up, 48%, 24%, 44% and 49% of patients with acute myocardial injury, T1MI, T2MI and chronic myocardial injury died, respectively. Patients with acute myocardial injury had higher adjusted risks of death (1.21, 95% CI 1.08 to 1.36) and heart failure (1.24, 95% CI 1.07 to 1.43), but a similar risk for myocardial infarction (MI) compared with the reference group. Patients with T1MI had a lower adjusted risk of death (0.86, 95% CI 0.74 to 1.00) and higher risk of MI (2.09, 95% CI 1.62 to 2.68), but a similar risk of heart failure. Patients with T2MI had a higher adjusted risk of death (1.46, 95% CI 1.18 to 1.80) and heart failure (1.30, 95% CI 1.00 to 1.69) compared with patients with chronic myocardial injury. CONCLUSIONS: Absolute long-term risks for death are similar, and adjusted risks are slightly higher, among patients with acute myocardial injury and T2MI, respectively, compared with chronic myocardial injury. The lowest risk of long-term mortality was found in patients with T1MI. Both acute and chronic myocardial injury are associated with very high risks of adverse outcomes.

Acute Effects of Electronic Cigarette Inhalation on the Vasculature and the Conducting Airways.

The use of electronic cigarettes has increased exponentially since its introduction onto the global market in 2006. However, short- and long-term health effects remain largely unknown due to the novelty of this product. The present study examines the acute effects of e-cigarette aerosol inhalation, with and without nicotine, on vascular and pulmonary function in healthy volunteers. Seventeen healthy subjects inhaled electronic cigarette aerosol with and without nicotine on two separate occasions in a double-blinded crossover fashion. Blood pressure, heart rate, and arterial stiffness measured by pulse wave velocity and pulse wave analysis were assessed at baseline, and then at 0 h, 2 h, and 4 h following exposure. Dynamic spirometry and impulse oscillometry were measured following vascular assessments at these time points, as well as at 6 h following exposure. e-Cigarette aerosol with nicotine caused a significant increase in heart rate and arterial stiffness. Furthermore, e-cigarette aerosol-containing nicotine caused a sudden increase in flow resistance as measured by impulse oscillometry, indicating obstruction of the conducting airways. Both aerosols caused an increase in blood pressure. The present study indicates that inhaled e-cigarette aerosol with nicotine has an acute impact on vascular and pulmonary function. Thus, chronic usage may lead to long-term adverse health effects. Further investigation is warranted.

The toxic potential of a fourth-generation E-cigarette on human lung cell lines and tissue explants.

The use of electronic cigarettes (E-cigs) is rapidly increasing. The latest generation of E-cigs is highly customizable, allowing for high heating coil temperatures. The aim of this study was to assess the toxic potential of a fourth-generation E-cig. Aerosols generated from E-liquid with (24 mg/mL) and without nicotine, using a fourth-generation E-cig, were chemically analysed and compared with cigarette smoke (K3R4F). Human lung epithelial cell lines and distal lung tissue explants were exposed to E-cig vapour extract (EVE) and cigarette smoke extract for 24 hours and assessed for viability, inflammation, oxidative stress and genotoxicity. E-cig aerosols contained measurable levels of volatile organic compounds, aldehydes and polycyclic aromatic hydrocarbons, in general, to a much lesser extent than cigarette smoke. Higher levels of certain carbonyls, e.g. formaldehyde, were detected in the E-cig aerosols. EVEs decreased cell viability of BEAS-2B cells, whereas little effect was seen in A549 cells and distal lung tissue. The nicotine-containing EVE caused a greater decrease in cell viability and significant increase in DNA damage than the nicotine-free EVE. Increased cytotoxicity, reactive oxygen species production and genotoxicity were seen with cells and tissue exposed to cigarette smoke extract compared with EVEs. Although E-cig aerosols were less toxic than cigarette smoke, it was not benign. Moreover, the EVE containing nicotine was more toxic than the nicotine-free EVE. More research is needed on the short- and long-term health effects of vaping and the usage of newly emerging E-cig devices to evaluate better the potential negative effects of E-cigs on human health.

Brief exposure to Swedish snus causes divergent vascular responses in healthy male and female volunteers.

INTRODUCTION: The use of Swedish oral moist snuff, known as snus, has for a long time been limited to the Scandinavian countries. With declining cigarette sales in the western world, tobacco companies have looked to the development of alternative tobacco products. In 2006 snus products were launched in the US. Even though several studies have demonstrated negative health effects, snus is often depicted as harmless. The aim of the present study was to investigate acute vascular effects of snus as measured by arterial stiffness as well as blood pressure and heart rate. METHODS: Two separate randomized double-blind crossover studies with the same study design were pooled for analysis. Twenty-nine healthy snus-users (17 females, 12 males) were included. Snus (Göteborgs Rapé) and tobacco free snus (Onico) were administered in a randomized order at two separate visits. Arterial stiffness, blood pressure and heart rate were measured at baseline as well as every five minutes for 40 minutes during exposure. Following snus removal, measurements continued for 30 minutes post exposure. Arterial stiffness was measured using pulse wave velocity (Vicorder) and pulse wave analysis (Sphygmocor). RESULTS: Compared to placebo, snus significantly increased systolic and diastolic blood pressure as well as heart rate, however, only in females (p = 0.004, p = 0.006 and p<0.001 respectively). No changes were seen in arterial stiffness measurements in either gender. CONCLUSION: We observed an increase in blood pressure and heart rate only in females, but not in males due to snus usage as compared to placebo. This novel finding was surprising and needs to be further investigated considering most of the earlier studies have mainly focused on male snus users and the increasing usage of snus among females.

Association of Electronic Cigarette Use With Smoking Habits, Demographic Factors, and Respiratory Symptoms.

Importance: There is an ongoing debate about whether electronic cigarettes (e-cigarettes) are the solution to the tobacco epidemic or a new public health threat. Large representative studies are needed to study e-cigarette use in the general population, but hardly any have been published. Objectives: To estimate the prevalence of e-cigarette use and to investigate the association of e-cigarette use with smoking habits, demographic factors, and respiratory symptoms. Design, Setting, and Participants: Cross-sectional, population-based study of random samples of the population, performed within the Obstructive Lung Disease in Northern Sweden (OLIN) study and West Sweden Asthma Study (WSAS). The same validated questionnaire including identical questions was used in OLIN and WSAS. In 2016, OLIN and WSAS conducted postal questionnaire surveys in random samples of adults aged 20 to 75 years. In OLIN, 6519 participated (response rate, 56.4%); in WSAS, 23 753 participated (response rate, 50.1%). Main Outcomes and Measures: Electronic cigarette use, smoking habits, and respiratory symptoms. Results: Of 30 272 participants (16 325 women [53.9%]), 3897 (12.9%) were aged 20 to 29 years; 4242 (14.0%), 30 to 39 years; 5082 (16.8%), 40 to 49 years; 6052 (20.0%), 50 to 59 years; 6628 (21.9%), 60 to 69 years; and 4371 (14.4%), 70 to 75 years. The number of current smokers was 3694 (12.3%), and 7305 (24.4%) were former smokers. The number of e-cigarette users was 529 (2.0%), and e-cigarette use was more common among men (275 of 12 347 [2.2%; 95% CI, 2.0%-2.5%]) than women (254 of 14 022 [1.8%; 95% CI, 1.6%-2.0%]). Among current smokers, 350 of 3566 (9.8%; 95% CI, 8.8%-10.8%) used e-cigarettes compared with 79 of 6875 (1.1%; 95% CI, 0.9%-1.3%) in former smokers and 96 of 15 832 (0.6%; 95% CI, 0.5%-0.7%) in nonsmokers (P < .001). Among e-cigarette users who answered the survey question about cigarette-smoking habits (n = 525), 350 (66.7%; 95% CI, 62.7%-70.7%) were current smokers, 79 (15.0%; 95% CI, 11.9%-18.1%) were former smokers, and 96 (18.3%; 95% CI, 15.0%-21.6%) were nonsmokers (P < .001 for trend). In a regression analysis, e-cigarette use was associated with male sex (odds ratio [OR], 1.35; 95% CI, 1.12-1.62); age groups 20 to 29 years (OR, 2.77; 95% CI, 1.90-4.05), 30 to 39 years (OR, 2.27; 95% CI, 1.53-3.36), 40 to 49 years (OR, 1.65; 95% CI, 1.11-2.44), and 50 to 59 years (OR, 1.47; 95% CI, 1.01-2.12); educational level at primary school (OR, 1.99; 95% CI, 1.51-2.64) and upper secondary school (OR, 1.57; 95% CI, 1.25-1.96); former smoking (OR, 2.37; 95% CI, 1.73-3.24); and current smoking (OR, 18.10; 95% CI, 14.19-23.09). All respiratory symptoms were most common among dual users and former smokers and nonsmokers who used e-cigarettes. Conclusions and Relevance: Use of e-cigarettes was most common among smokers, and dual users had the highest prevalence of respiratory symptoms. On a population level, this study indicates that the present use of e-cigarettes does not adequately serve as a smoking cessation tool.

Stable High-Sensitivity Cardiac Troponin T Levels and Outcomes in Patients With Chest Pain.

BACKGROUND: There is a paucity of data on the association between high-sensitivity cardiac troponin (hs-cTn) levels and outcomes in patients with chest pain but no myocardial infarction (MI), or any other condition that may lead to acutely elevated troponin levels. OBJECTIVES: The authors hypothesized that any detectable high-sensitivity cardiac troponin T (hs-cTnT) level is associated with adverse outcomes. METHODS: All patients (N = 22,589) >25 years of age with chest pain and hs-cTnT analyzed concurrently in the emergency department of Karolinska University Hospital, Stockholm, Sweden from 2011 to 2014 were eligible for inclusion. After excluding all patients with acute conditions that may have affected hs-cTnT, or MI associated with the visit, or insufficient information to determine whether troponin levels were stable, Cox regression was used to estimate risks for all-cause, cardiovascular, and noncardiovascular mortality, MI, and heart failure at different levels of troponins. RESULTS: A total of 19,460 patients with a mean age of 54 ± 17 years were included. During a mean follow-up of 3.3 ± 1.2 years, 1,349 (6.9%) patients died. Adjusted hazard ratios (with 95% confidence intervals) for all-cause mortality were 2.00 (1.66 to 2.42), 2.92 (2.38 to 3.59), 4.07 (3.28 to 5.05), 6.77 (5.22 to 8.78), and 9.68 (7.18 to 13.00) in patients with hs-cTnT levels of 5 to 9, 10 to 14, 15 to 29, 30 to 49, and ≥50 ng/l, respectively, compared with patients with hs-cTnT levels <5 ng/l. There was a strong and graded association between all detectable levels of hs-cTnT and risk for MI, heart failure, and cardiovascular and noncardiovascular mortality. CONCLUSIONS: Among patients with chest pain and stable troponin levels, any detectable level of hs-cTnT is associated with an increased risk of death and cardiovascular outcomes and should merit further attention.

Sex-specific risk of emergency department revisits and early readmission following myocardial infarction.

BACKGROUND: Readmissions within 30days after hospitalization have been introduced as a measure of quality of care. There is a paucity of data regarding sex-specific risk of early readmissions after myocardial infarction (MI). OBJECTIVES: To investigate the association between sex and revisits to the emergency department (ED), and readmissions after MI. METHODS: All patients with chest pain, diagnosed with MI at the Karolinska University Hospital during 2011 and 2012 were included. National Health care registers were used for information about patient characteristics, outcomes, and medication. We calculated risk ratios (RR) with 95% confidence intervals (CI) in women versus men, for revisits to the ED, readmission to hospital within 30, and 180days, and to undergo coronary angiography, or revascularization, and to receive guideline-directed cardiovascular medication. RESULTS: In total there were 667 patients with MI during the study period, of whom 197 (30%) were women. Women were older (mean age 73 vs. 65years), and had more comorbidities than men. The 30-day risk of revisits to the ED was 1.56 times greater in women than men (adjusted RR 1.56 (1.09-2.25)). Throughout the first year; women were more likely to be readmitted than men, with the most striking difference found within 30days (22% vs. 13%) of discharge (adjusted RR 1.54 (95% CI, 1.00-2.36)). There were no differences between men and women in new cardiovascular medication, coronary angiographies or revascularizations. CONCLUSIONS: Women have an increased risk of revisits to the ED, and readmissions to hospital during the first year after a MI.

Trends in admissions for chest pain after the introduction of high-sensitivity cardiac troponin T.

BACKGROUND: The aim was to describe temporal trends in admission rates for chest pain and patient outcomes after the clinical introduction of the high-sensitivity cardiac troponin T (hs-cTnT) assay. METHODS: We included all patients aged >25years presenting with chest pain to the emergency department (ED) at our hospital during 2011-2014. For each year, rates of admissions, coronary angiographies, and revascularizations were determined. After adjustment for confounders, hazard ratios (HR) with 95% confidence intervals (CI) were calculated for mortality or major adverse cardiac events (MACE) within 1year of the ED visit per year, using 2011 as referent. RESULTS: In total, 15,472 chest pain patients were accountable for 18,237 visits to the ED. The chest pain admission rate in 2011 was 44%; 2012, 39%; 2013, 33%; and 2014, 28%, with an overall decrease in 36%. Coronary angiographies within 1year of the ED visit increased from 6.8% in 2011 to 9.6% in 2013, but the proportion of revascularizations was virtually unchanged. The risk of death within 1year of the visit increased by 51% (HR 1.51, 95% CI, 1.18-1.92) in 2014, compared with 2011. Only non-cardiovascular mortality was significantly increased (HR 1.85, 95% CI, 1.34-2.55), with no increase in MACE. CONCLUSION: Admissions for chest pain were reduced by 36% the first 4years of hs-cTnT use. We observed no increase in MACE, but all-cause mortality increased significantly for non-cardiovascular causes only which was paralleled by a significant increase in the use of coronary angiographies.

Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers.

BACKGROUND AND AIMS: The use of electronic cigarettes is increasing dramatically on a global scale and its effects on human health remain uncertain. In the present study, we measured endothelial progenitor cells (EPCs) and microvesicles (MVs) in healthy young volunteers following short-term exposure to inhalation of e-cigarette vapor (ECV) to determine vascular changes. METHODS: Sixteen healthy seldom smokers were randomized into two groups either exposed or not exposed to 10 puffs of ECV for 10 min, in a crossover design. Blood samples were obtained at baseline and 1, 4 and 24 h following exposure. EPCs (CD34 + CD309) and MVs were analyzed by flow cytometry. MVs were phenotyped according to origin (platelet (CD41), endothelial (CD144), leukocytes (CD45), monocytes (CD14)) and nuclear content (SYTO 13 dye). In addition, expression of inflammation markers such P-selectin (CD62P), E-selectin (CD62E), CD40-ligand (CD154) and HMGB1 was investigated. Fractional exhaled nitric oxide (FeNO) was also measured at baseline and after 24 h. RESULTS: EPC levels in blood were significantly increased 1 h following exposure to ECV and returned to baseline values after 24 h. Only E-selectin positive MVs (endothelial origin) were slightly elevated (p < 0.038). FeNO was unaffected by exposure to ECV. CONCLUSIONS: In healthy volunteers, ten puffs of e-cigarette vapor inhalation caused an increase in EPCs. This increase was of the same magnitude as following smoking of one traditional cigarette, as we previously demonstrated. Taken together, these results may represent signs of possible vascular changes after short e-cigarette inhalation. Further studies analyzing potential cardiovascular health effects are critical as the e-cigarette market continues to burgeon.

Controlled exposures to air pollutants and risk of cardiac arrhythmia.

BACKGROUND: Epidemiological studies have reported associations between air pollution exposure and increases in cardiovascular morbidity and mortality. Exposure to air pollutants can influence cardiac autonomic tone and reduce heart rate variability, and may increase the risk of cardiac arrhythmias, particularly in susceptible patient groups. OBJECTIVES: We investigated the incidence of cardiac arrhythmias during and after controlled exposure to air pollutants in healthy volunteers and patients with coronary heart disease. METHODS: We analyzed data from 13 double-blind randomized crossover studies including 282 participants (140 healthy volunteers and 142 patients with stable coronary heart disease) from whom continuous electrocardiograms were available. The incidence of cardiac arrhythmias was recorded for each exposure and study population. RESULTS: There were no increases in any cardiac arrhythmia during or after exposure to dilute diesel exhaust, wood smoke, ozone, concentrated ambient particles, engineered carbon nanoparticles, or high ambient levels of air pollution in either healthy volunteers or patients with coronary heart disease. CONCLUSIONS: Acute controlled exposure to air pollutants did not increase the short-term risk of arrhythmia in participants. Research employing these techniques remains crucial in identifying the important pathophysiological pathways involved in the adverse effects of air pollution, and is vital to inform environmental and public health policy decisions.

The effects of smoking on levels of endothelial progenitor cells and microparticles in the blood of healthy volunteers.

BACKGROUND: Cigarette smoking, both active and passive, is one of the leading causes of morbidity and mortality in cardiovascular disease. To assess the impact of brief smoking on the vasculature, we determined levels of circulating endothelial progenitor cells (EPCs) and circulating microparticles (MPs) following the smoking of one cigarette by young, healthy intermittent smokers. MATERIALS AND METHODS: 12 healthy volunteers were randomized to either smoking or not smoking in a crossover fashion. Blood sampling was performed at baseline, 1, 4 and 24 hours following smoking/not smoking. The numbers of EPCs and MPs were determined by flow cytometry. MPs were measured from platelets, leukocytes and endothelial cells. Moreover, MPs were also labelled with anti-HMGB1 and SYTO 13 to assess the content of nuclear molecules. RESULTS: Active smoking of one cigarette caused an immediate and significant increase in the numbers of circulating EPCs and MPs of platelet-, endothelial- and leukocyte origin. Levels of MPs containing nuclear molecules were increased, of which the majority were positive for CD41 and CD45 (platelet- and leukocyte origin). CD144 (VE-cadherin) or HMGB1 release did not significantly change during active smoking. CONCLUSION: Brief active smoking of one cigarette generated an acute release of EPC and MPs, of which the latter contained nuclear matter. Together, these results demonstrate acute effects of cigarette smoke on endothelial, platelet and leukocyte function as well as injury to the vascular wall.